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Vestibular Migraine

Posted on June 10 2025, By: Cerebral Torque

Vestibular Migraine

Complete Clinical and Patient Guide to Diagnosis, Treatment, and Management of Migraine-Related Dizziness

Updated June 2025

Clinical Definition and Terminology

Vestibular migraine is a neurological condition characterized by repeated episodes of vertigo or other balance problems caused by migraine. The connection between spinning dizziness and migraine was first recognized in 1873, making this one of the longest-known types of migraine variants.

Previously called by various names including migraine-associated vertigo, migraine-associated dizziness, migraine-related balance problems, migrainous vertigo, benign recurrent vertigo, and basilar migraine, the condition is now standardized under the term "vestibular migraine" by international medical organizations. This standardization was adopted by the Bárány Society (international vestibular experts) and International Headache Society to emphasize how migraine affects the vestibular system and avoid confusion with other types of dizziness.

Pediatric Manifestations

Children can have early forms of adult vestibular migraine, including vestibular migraine of childhood, benign paroxysmal vertigo of childhood (sudden episodes of spinning in children), and recurrent vertigo of childhood. These newer terms align with adult vestibular migraine definitions and have been approved by both the International Headache Society and Bárány Society. Many of these children later develop migraine headaches, often years after their spinning episodes have stopped.

Distinction from Migraine with Brainstem Aura

Vestibular migraine is considered different from migraine with brainstem aura (previously called basilar-type migraine). In migraine with brainstem aura, vertigo requires more than one symptom from the brainstem area (the part that controls basic functions) and is never the only aura symptom. Most patients develop migraine headache within 5-60 minutes of the aura starting. Only a small number of vestibular migraine patients meet criteria for migraine with brainstem aura.

Epidemiology and Population Impact

Vestibular migraine is a common balance disorder, though studies have limitations including misdiagnosis, changing diagnostic criteria, and referral biases. Both balance symptoms and migraine are common in the general population, with lifetime prevalence of vertigo estimated at 7% and migraine around 14%. If these were random coincidences, we'd expect 1% to have both, but German survey data showed 3.2% have both conditions, with only one-third actually meeting full criteria for vestibular migraine (1% of the general population).

3.2%

German Survey

Have both migraine and vertigo

2.8%

Children

Ages 6-12 population rate

20-33%

Migraine Patients

Report spinning dizziness

Demographic Characteristics

Patient Demographics and Risk Factors

Female Predominance 1.5:1 to 5:1 ratio

Average Age of Onset Around 40 years

Age Range Any age (oldest first attack: 72 years)

Family Pattern Familial clustering common, less common in men

Correct Diagnosis Rate Only 20% get the right diagnosis

Research Study Results

Vestibular migraine was found in 7% of 200 dizziness clinic patients and 9% of 200 migraine clinic patients. Other studies found it in 13% of patients presenting to headache clinics and 30% of migraine patients. Among patients with migraine, spinning dizziness is reported by 20-33%, compared with less than 8% in tension-type headaches and the general population.

The Diagnosis Challenge

Despite being common, vestibular migraine remains significantly underdiagnosed. While two-thirds of patients with vestibular migraine seek medical care for symptoms, only 20% receive the correct diagnosis. This highlights the need for:

Increased awareness among primary care providers about the migraine-vertigo connection
Systematic symptom history-taking for dizziness complaints including migraine history
Recognition that vestibular symptoms can precede or occur without headache
Appropriate referrals to specialists familiar with vestibular migraine

Pediatric Prevalence

The rate of recurring spinning dizziness related to migraine was estimated at 2.8% in children between 6 and 12 years in population-based studies. Boys and girls are equally affected, and attacks usually last between several minutes and a few hours. Follow-up studies show that most children with benign paroxysmal vertigo will develop migraine later in life, supporting the idea that childhood balance episodes may be early signs of the migraine spectrum.

Pathophysiology and Disease Mechanisms

The pathophysiology of vestibular migraine is still a matter of speculation and is incompletely understood, with different mechanisms suggested by the wide range of symptoms and test findings. Several factors have made study difficult including lack of biological markers, changing diagnostic criteria, and absence of specific tests. The most promising theory is the release of neuropeptides such as calcitonin gene-related peptide (CGRP) that is not only important in migraine headache but also affects the activity of vestibular centers in the brain.

What is CGRP?

CGRP (calcitonin gene-related peptide) is a chemical messenger in the nervous system that plays a key role in both migraine headaches and balance problems. Think of it as a signal that tells blood vessels to widen and pain nerves to become more sensitive. In vestibular migraine, CGRP affects both the pain centers that cause headaches and the balance centers that cause dizziness. This is why newer migraine medications that block CGRP can help with both headaches and dizziness symptoms.

Vestibular System and Migraine Connection

Among patients with migraine, spinning dizziness is reported by 20-33%, compared with less than 8% in tension-type headaches and the general population. One-half to two-thirds of migraine patients also report motion sickness, probably 2-5 times greater than the general population. The vestibular origin of vestibular migraine has been confirmed by observing abnormal eye movements during acute episodes, indicating central vestibular dysfunction in most patients.

20-66%

Between Episodes

Vestibular/oculomotor problems in migraine patients

38-87%

Migraine in Dizziness

Rate among spinning dizziness patients

2-30%

Aura Pattern

Vestibular symptoms as typical migraine aura

Leading Pathophysiologic Theories

Main Disease Mechanisms

Cortical Spreading Depression Brain wave affecting vestibular areas

Trigeminovascular System Neuropeptides CGRP, substance P release

Vasospasm Theory Internal auditory artery problems

Ion Channel Dysfunction Inherited calcium channel abnormalities

Cortical Spreading Depression Mechanisms

Cortical spreading depression is a brain wave phenomenon and could lead to vestibular symptoms when the multisensory brain areas become involved that process vestibular information, which are mainly located in the temporo-parietal junction. Alternatively, a cortical spreading depression affecting the brainstem has been proposed to account for short-lasting episodes of vestibular migraine. However, several features of vestibular migraine such as episode duration and positional nystagmus can hardly be explained by cortical spreading depression alone.

Trigeminovascular System

Trigeminal ganglion activation releases vasoactive neuropeptides including substance P, pituitary adenylate-cyclase-activating polypeptide (PACAP), and CGRP. Vestibular symptoms may result from trigeminovascular activation, with neurogenic inflammation altering vestibular function. Cutaneous trigeminal stimulation can produce abnormal eye movements in migraine patients. Peripheral vestibular and auditory symptoms could be explained by activation of the trigeminovascular system during migraine.

CGRP and Vestibular System

The pathophysiology of migraine involves several neuropeptides such as calcitonin-gene related peptide and serotonin that are also known to affect the activity of central and peripheral vestibular neurons. There is widespread distribution of CGRP-expressing fibers and CGRP receptors in the brainstem and cerebellum, not only in those areas involved in migraine, but also in the vestibular nuclei.

Animal Model Evidence for CGRP Role

Several animal experiments support the role of CGRP in the central vestibular system. The density of CGRP immunoreactivity in the vestibular nuclei increased in rats after exposure to rotational stimulation. In a chronic migraine model with repeated nitroglycerin administration, an increase of CGRP not only in the trigeminal nucleus caudalis but also in the vestibular nuclei has been observed in rats. Blocking CGRP by application of a viral vector prevented imbalance after exposure to the migraine-triggering nitroglycerin.

CGRP Receptor Mechanisms

CGRP expressed in trigeminal ganglion neurons is implicated in migraine pathophysiology, and CGRP receptors in peripheral and central vestibular systems may be relevant to vestibular migraine. The application of the CGRP receptor antagonist olcegepant prevented hyperalgesia and imbalance in the chronic migraine model. Thus, the release of neuropeptides such as CGRP is the most promising theory of vestibular migraine pathophysiology. Bidirectional connections between the vestibular nuclei and the trigeminal system may also be the pathophysiologic basis of the observation that vestibular stimulation can trigger migraine headache.

Vasospasm and Ischemia

Spasm of the internal auditory artery could account for peripheral vestibular and auditory symptoms in migraine with and without vertigo. Vasospasm could account for short attacks of vertigo but hardly for episodes lasting hours or days. Furthermore, central vestibular and oculomotor dysfunction points to another pathophysiologic mechanism. Migraine-induced inner ear ischemia may alter labyrinthine excitability, though given symptom duration and recurrence, inner ear ischemia is unlikely to explain most cases.

Ion Channel Dysfunction and Genetic Factors

A deficit of ion channels expressed in the inner ear or in central vestibular structures could account for vestibular symptoms in vestibular migraine. This theory is the only one systematically tested thus far and appeared to be promising as other episodic disorders presenting with migraine and vertigo such as familial hemiplegic migraine and episodic ataxia type 2 have been found to result from ion channel dysfunction. However, searching for mutations in various candidate genes was negative in patients with vestibular migraine.

Inherited ion channel dysfunction may cause vestibular symptoms in some migraine patients. Episodic ataxia type 2 presents with episodic vertigo, and half of these patients have migraine. Familial hemiplegic migraine involves calcium channel abnormalities on chromosome 19p. Families with inherited syndromes including both migraine and episodic vertigo have been described, though the gene locus remains unidentified.

Central Sensitization and Sensory Processing

Neuronal sensitization involves progressive increased responsiveness to external stimulation, accounting for sensitivities to motion, light, sound, and smell. Some experts believe vestibular migraine relates to both central sensitization and abnormal sensory integration in vestibulo-thalamo-cortical processing, with functional imaging showing altered connectivity between thalamus and visual/vestibular processing regions.

Alternative Peripheral Mechanisms

Damage to the inner ear by repeated activation of the trigeminovascular reflex could account for the observation that several inner ear disorders such as benign paroxysmal positional vertigo are associated with migraine. Endolymphatic hydrops, the pathologic lesion of Meniere disease, may be associated with vestibular migraine through ion channel-induced fluid imbalance or migraine-associated ischemic damage.

Multiple Mechanism Integration

Different findings during acute episodes of vestibular migraine and signs of peripheral vestibular and central oculomotor dysfunction between episodes indicate that more than one mechanism may be involved. The wide spectrum of symptoms and test findings suggests different pathophysiologic mechanisms, with different mechanisms potentially being more important in different patients or even different episodes within the same patient.

Diagnostic Criteria for Vestibular Migraine

International diagnostic criteria developed by the Bárány Society and ICHD-3 for definite and probable vestibular migraine, providing standardized framework for clinical diagnosis.

Requirements	Definite Vestibular Migraine	Probable Vestibular Migraine	Clinical Application
Number of Episodes	≥5 episodes of vestibular symptoms, moderate-severe intensity, 5 min-72 hours	≥5 episodes of vestibular symptoms, same duration criteria	Symptoms must interfere with normal activities
Migraine History	Required: Current or past migraine with or without aura	Either: Migraine history OR migraine features during episodes	Migraine history often precedes vestibular symptoms by years
Migraine Features	Required: ≥50% episodes with migraine characteristics	Either: Migraine features OR migraine history	Migraine headache (unilateral, throbbing, moderate-severe) Photophobia and phonophobia Visual aura
Vestibular Symptoms	Qualifying symptoms: Spontaneous vertigo, positional vertigo, visually triggered vertigo, head motion-triggered vertigo, head motion-triggered dizziness with nausea		Must be moderate-severe, interfering with normal activities
Exclusion Criteria	Not better explained by another vestibular or headache disorder		Requires systematic evaluation for alternative diagnoses

Clinical Presentation and Symptom Patterns

Vestibular migraine is characterized by repeated episodes of episodic vertigo, with most patients also experiencing migraine-type headaches. The clinical presentation changes over time, with migraine headaches typically beginning several years before vestibular symptoms. In adult patients, vestibular migraine usually presents several years after the onset of migraine headaches, though recall bias may contribute to this finding.

Types of Vestibular Symptoms

Patients typically report spontaneous or positional vertigo, or a mixture of both. Some experience a sequence of spontaneous vertigo transforming into positional vertigo after several hours or days. This positional vertigo is different from benign paroxysmal positional vertigo regarding duration of individual attacks (often as long as head position is maintained versus seconds only in BPPV), duration of symptomatic episodes (minutes to days versus weeks in BPPV), and oculomotor findings.

Episode Duration and Severity

Duration of episodes varies widely: about 30% of patients have episodes lasting minutes, 30% have attacks for hours, and another 25% have attacks over several days. The remaining 15% have attacks lasting seconds only, which tend to occur repeatedly during head motion, visual stimulation, or after changes of head position. In these patients, episode duration is defined as the total period during which short attacks recur. At the other end of the spectrum, there are patients who may take 4 weeks to fully recover from an episode. However, the main episode rarely exceeds 72 hours.

30%

Minutes Duration

Episodes lasting minutes

30%

Hours Duration

Episodes lasting hours

25%

Days Duration

Episodes lasting several days

Attacks may be severe enough to force patients to stay in bed for a day or two, where they lie still avoiding the slightest head movement. Patients from large case series rated their vertigo severity at 7 compared to 8 for headaches (on a scale from 0 to 10, with 10 being the worst).

Additional Vestibular Symptoms

A frequent additional symptom is head motion intolerance - imbalance, false sense of motion, and nausea worsened or triggered by head movements. Visually-induced vertigo (triggered by complex or large moving visual scenes like traffic or movies) can be another prominent feature. Nausea and imbalance are frequent but nonspecific accompaniments of acute vestibular migraine.

Common Episode Triggers

Sleep Deprivation Primary trigger

Stress Emotional/physical

Menstruation Hormonal trigger

Certain Foods If there is a comorbid dietary concern (celiac)

Visual Stimuli Fluorescent lights, moving patterns

Relationship to Headaches

Vestibular migraine often lacks not only the temporal requirement for aura as defined by headache specialists, but also the temporal relationship to migraine headaches - vertigo rarely occurs before headache as would be typical for aura. It may begin with the headache, appear late in the headache phase, or be completely unrelated to headaches. Many patients experience attacks both with and without headache. Quite frequently, patients have a milder headache with their vertigo compared to their usual migraine. Misdiagnosis as "cervical vertigo" may occur when accompanying pain is mainly or exclusively located in the neck.

Associated Episode Features

Along with vertigo, patients may experience photophobia, phonophobia, osmophobia, and visual or other auras. These are important for diagnosis since they may be the only obvious connection of vertigo and migraine. Auditory symptoms including hearing loss, tinnitus, and ear pressure have been reported in up to 20-40% of patients with vestibular migraine. Hearing loss is usually mild and transient, without or with only minor progression over time. About 20% develop mild bilateral down-sloping hearing loss over the years. In contrast, unilateral moderate to severe hearing loss starting in the low frequency range would rather favor a diagnosis of Meniere disease.

Motion Sensitivity Patterns

Patients with vestibular migraine often have a history of motion sickness. As persistent vestibular symptoms affect a substantial subgroup of patients, a separate diagnostic category of chronic vestibular migraine has been proposed. Patients are often affected by visual and self-motion sensitivity even between attacks, which may lead to a chronic type of vestibular dizziness. There is an increased prevalence of migraine and vestibular migraine in patients with persistent postural-perceptual dizziness (PPPD).

Psychiatric Comorbidity

Contributing to chronic symptoms is secondary psychiatric morbidity, particularly anxiety disorders in about 50% of patients. This increased prevalence of anxiety and depression compared with controls or those with other vestibular disorders may be a consequence of unpredictable, disabling symptoms and may worsen symptoms during acute episodes.

Physical Examination and Clinical Findings

Physical examination findings during vestibular migraine episodes provide important diagnostic clues, though findings between episodes are typically normal. In most patients, the general neurologic and otologic examination is normal when not having an attack.

Interictal Findings (Between Episodes)

Neuro-ophthalmological evaluation may reveal mild central oculomotor abnormalities such as persistent positional nystagmus and saccadic pursuit, particularly in patients with a long history of vestibular migraine. Spontaneous nystagmus in darkness occurs in only 15% of patients with velocities mostly below 3°/s. In contrast, persistent positional nystagmus seems to be the most common finding between episodes, observed in 55% of patients in a large series.

15%

Spontaneous Nystagmus

Between episodes, very slow velocities

55%

Positional Nystagmus

Most common interictal finding

26%

Head Impulse Test

Abnormal in clinical testing

Ictal Oculomotor Patterns (During Episodes)

During the acute stage of vestibular migraine, nystagmus findings are more pronounced. The most common patterns are spontaneous nystagmus, persistent positional nystagmus, or a mixture of the two. Acute nystagmus is often horizontal but may involve any direction. Nystagmus is typically present during episodes and may suggest peripheral or central origin. Features can be spontaneous, gaze-evoked, or solely positional, identifiable during routine neurologic examination with tools to prevent visual fixation such as Frenzel lenses or video-oculographic recording.

During Episode Characteristics

Spontaneous Horizontal Nystagmus Common during episodes

Intense Horizontal Nystagmus More suggestive of Meniere disease

Vertical Nystagmus More typical in vestibular migraine

Imbalance Usually mild to moderate severity

Vestibular Testing

Clinical head-impulse testing has been reported to be abnormal in up to 26% of patients, but in clinical experience it is almost always normal. Video head-impulse testing is typically normal, thus an abnormal video head-impulse test is suspicious of another disorder. A useful hint for a diagnosis of vestibular migraine is nausea after caloric testing, which was four times more common in affected patients than in those with other vestibular disorders.

What is Caloric Testing?

Caloric testing is a balance test where doctors gently put warm and cool water (or air) into the ear canal to stimulate the balance organs. This causes temporary dizziness and eye movements that doctors can measure to see how well the balance system is working. The test typically takes about 10-15 minutes per ear. People with vestibular migraine often feel more nauseous during this test compared to people with other balance problems, which can actually help with diagnosis.

Understanding Nystagmus

Nystagmus is involuntary eye movement that looks like the eyes are "jumping" or "dancing." It can be side-to-side, up-and-down, or rotary. During vestibular migraine episodes, doctors often observe these abnormal eye movements, which help confirm that the balance system is affected. Most people aren't aware they have nystagmus - it's something doctors look for with special glasses or camera equipment that prevents normal focusing.

Other Examination Findings

Impaired smooth pursuit may be seen on oculomotor examination, and abnormalities of the vestibulo-ocular reflex may be detected during episodes by video head impulse testing. Testing between episodes usually reveals normal symmetric vestibulo-ocular reflex function, though vestibular laboratory tests reveal nonspecific abnormalities in a small minority of patients. Most patients have impaired gait and stance during episodes.

Changes Over Time

Two studies examined the development of vestibular and oculomotor dysfunction over time between episodes. In a group of 61 patients, the prevalence of at least one oculomotor abnormality increased from 15% at initial presentation to 41% after a median follow-up time of 9 years. The most frequent abnormalities were positional nystagmus and head-shaking nystagmus. Interestingly, oculomotor abnormalities between episodes may show variation over time, and in some patients, oculomotor dysfunction may even return to normal at follow-up.

Interictal Symptoms vs. Chronic Vestibular Migraine

Although considered an episodic disorder, many patients report high prevalence of mild vestibular symptoms between attacks. Controversy exists whether these constitute chronic vestibular migraine or comorbid conditions like persistent postural-perceptual dizziness (PPPD). Patients frequently report visually induced and head motion-induced dizziness even when such stimuli don't trigger full episodes. Susceptibility to motion sickness may be more prominent in vestibular migraine than other migraine forms.

Laboratory Testing and Diagnostic Evaluation

The pathophysiology of vestibular migraine is still a matter of speculation, but clinical examination and documentation of eye movements has clarified that the vast majority of patients suffer from central vestibular dysfunction. Neither during acute episodes nor between episodes is there any specific test abnormality in vestibular migraine. However, laboratory testing can be useful to exclude other disorders and to reassure the patient.

Laboratory Findings Between Episodes

The most consistent laboratory finding in vestibular migraine is a unilateral reduced caloric response. In most studies, about 10-20% of patients showed a unilateral canal paresis. The magnitude of caloric asymmetry has been reported in almost none of these studies, making it unclear whether a complete or almost complete canal paresis is compatible with a diagnosis of vestibular migraine.

Testing Indications

Testing is warranted for:

New-onset symptoms not fulfilling diagnostic criteria
Atypical clinical features including very brief (<5 minutes) or prolonged (>72 hours) vestibular symptoms
Sudden or progressive hearing loss
Loss of consciousness during episodes
Systemic signs (fever, rash) or abnormal neurologic examination findings

Laboratory Testing Abnormalities Between Episodes

Frequency of vestibular and oculomotor dysfunction findings in patients with vestibular migraine during asymptomatic periods across multiple research studies.

Research Study	Number of Patients	Spontaneous Nystagmus	Central Positional Nystagmus	Saccadic Pursuit	Unilateral Canal Paresis
Cutrer and Baloh	91	7%	7%	Not reported	21%
Cass et al.	100	7%	13%	3%	18%
Dieterich and Brandt	90	11%	11%	48%	8%
Bir et al.	53	0%	Not reported	24%	12%
Celebisoy et al.	35	0%	Not reported	9%	20%
Wang et al.	62	26%	Not reported	21%	21%
Teggi et al.	30	3%	10%	9%	20%
Young et al.	101	15%	55%	Not reported	16%

Caloric Testing and VOR Findings

Bilateral caloric hyporesponsiveness has been reported in up to 11% of patients, and an isolated directional preponderance of caloric responses in about 10% of patients. Interestingly, patients with vestibular migraine are more likely to experience nausea during caloric stimulation than patients with a vestibular disorder comorbid with migraine and patients with peripheral vestibular disorders.

10-20%

Unilateral Canal Paresis

Most consistent finding

Caloric Nausea

More common than other vestibular disorders

7.5%

Hearing Loss

Average prevalence, unexplained

VEMP Testing

Assessment of cervical and ocular vestibular-evoked myogenic potentials (cVEMPs and oVEMPs) has yielded conflicting results. Whereas in some studies, amplitudes of cVEMPs were reduced in patients with vestibular migraine as compared to controls, they were normal in others. Similarly, amplitudes of oVEMPs were reduced in some studies and normal in others. The latencies of the response were only rarely prolonged in patients with vestibular migraine, being normal in most studies.

What are VEMP Tests?

VEMP stands for Vestibular Evoked Myogenic Potentials. These tests measure how muscles respond to sounds or vibrations, which helps doctors understand if certain parts of the balance system are working properly. During the test, electrodes are placed on the neck or near the eyes, and clicking sounds or vibrations are applied. The muscles should respond in a predictable way if the balance organs are healthy. The test is painless and takes about 30 minutes.

Audiometry

Audiometry revealed sensorineural hearing loss not attributable to any cause in up to 20% of patients. A review on audiometric findings in vestibular migraine summarized results of nine studies and found an average prevalence of unexplained hearing loss of 7.5%. In a large case series, audiometry was age appropriate in 86% of patients and none of those patients with asymmetric audiometric findings had hearing loss involving predominantly the low frequencies. In another case series, 18% of patients had developed mild bilateral sensorineural hearing loss with a down-sloping pattern involving also the low-frequency range after a median follow-up time of 9 years after initial presentation.

Findings During Acute Episodes

Examination during an episode of vestibular migraine usually yields pathological nystagmus, indicating central vestibular dysfunction in most patients. A prospective study of 20 patients during the acute phase recorded pathological nystagmus in 70% of patients. Overall, findings pointed to central vestibular dysfunction in ten patients (50%), peripheral vestibular dysfunction in three patients (15%), and were inconclusive regarding the involved structure in 35%. On follow-up, vestibular and oculomotor abnormalities had disappeared in almost all patients.

Central vs. Peripheral Dysfunction

Recent oculomotor findings in a large case series including 101 patients with acute vestibular migraine showed that eye movements were documented with a portable video-oculographic system. Of those patients with spontaneous nystagmus (71%), the plane of nystagmus was horizontal in 69% and vertical in 31% of patients. In most patients, the intensity of spontaneous nystagmus was low to moderate with a slow phase velocity only rarely exceeding 15°/s. These findings pointed to central vestibular dysfunction in all patients.

Neuroimaging Recommendations

Neuroimaging should evaluate for stroke when acute episodes are new onset, associated with abnormal neurologic findings, or occur in patients with stroke risk factors. Noncontrast head CT is often performed initially but has poor sensitivity for posterior fossa ischemia. Brain MRI with diffusion-weighted sequences is more sensitive for acute stroke, with vascular imaging (CT or MR angiography) performed to identify stenoses or occlusions.

Brain MRI with gadolinium including high-resolution 3D protocols through the internal auditory canal should be performed for patients with acute persisting or chronic vestibular symptoms to evaluate for structural causes like posterior fossa tumors.

Understanding MRI Scans

MRI (Magnetic Resonance Imaging) uses powerful magnets and radio waves to create detailed pictures of the brain and inner ear structures. For vestibular migraine evaluation, doctors sometimes use gadolinium, a contrast dye injected through an IV that helps highlight certain areas. The test is painless but noisy, and takes 30-60 minutes. MRI helps rule out other causes of dizziness like tumors or strokes. Most people with vestibular migraine have normal MRI scans, which is reassuring.

What is Head Impulse Testing?

Head impulse testing checks how well the balance organs in the inner ear work by having the patient focus on a target while the doctor quickly turns their head to one side. In healthy people, the eyes stay locked on the target. If there's inner ear damage, the eyes move with the head and then quickly jump back to the target. Most people with vestibular migraine have normal head impulse tests, which helps distinguish it from other inner ear problems.

Comparison with Migraine Without Vestibular Symptoms

It is important to note that these clinical and laboratory findings are not specific to patients with vestibular migraine but can also be found in migraine patients without a history of vestibular symptoms. A unilateral canal paresis has been described in up to 35% of migraine patients without vertigo. Clinical examination yielded head-shaking nystagmus in 9-25% of migraine patients without vertigo. Only saccadic pursuit seems to be more frequent in vestibular migraine compared to migraine without vertigo.

Differential Diagnosis: Distinguishing Vestibular Migraine from Similar Conditions

Key distinguishing features between vestibular migraine and major differential diagnoses based on clinical characteristics, duration patterns, and specific diagnostic criteria.

Understanding Meniere Disease

Meniere disease is an inner ear disorder caused by excess fluid buildup that causes episodes of vertigo, hearing loss, ear ringing (tinnitus), and ear pressure or fullness. Unlike vestibular migraine, Meniere disease requires all three ear symptoms (hearing loss, tinnitus, and ear fullness) for diagnosis. The hearing loss typically starts in low frequencies and can become permanent over time. Episodes last 20 minutes to 12 hours. Some people can have both Meniere disease and vestibular migraine, which can make diagnosis challenging.

What is BPPV?

BPPV (Benign Paroxysmal Positional Vertigo) is caused by tiny calcium crystals that become dislodged in the inner ear. When these crystals move into the wrong part of the ear, they cause brief but intense spinning sensations triggered by specific head movements like rolling over in bed or looking up. Episodes last only seconds to a minute and can be treated with simple head positioning maneuvers performed by a healthcare provider. Unlike vestibular migraine, BPPV episodes are very brief and purely position-dependent.

Condition	Episode Duration	Associated Features	Key Distinguishing Characteristics
Vestibular Migraine	Minutes to hours (5 min - 72 hr)	Migraine history or features Photophobia/phonophobia Motion sensitivity Mild, temporary hearing symptoms	History of migraine, variable nystagmus patterns, triggered by migraine triggers, vertical nystagmus more common
Meniere Disease	20 min to 12 hours	Progressive unilateral hearing loss Intense aural fullness (required) Prominent tinnitus (required) 45% have migraine-like features Often transient in early stages	Very intense horizontal nystagmus (rarely vertical), asymmetric audiometry, aural fullness precedes attacks, low-frequency hearing loss pattern
BPPV	Seconds to 1 minute	Triggered by specific head movements Improves when remaining still No migraine-like features No auditory symptoms Fatiguability	Very brief duration, specific positional triggers, improvement after head movement ceases, migraine increases BPPV risk 2-fold
Vertebrobasilar TIA	Sudden onset, total attack history <1 year	Other brainstem symptoms common Vascular risk factors Sudden symptom onset Evidence of vascular pathology	Sudden onset, vascular risk factors, total attack history <1 year, vascular imaging shows pathology
Migraine with Brainstem Aura	5-60 minutes (aura), then headache	≥2 brainstem symptoms required Vertigo never only symptom Headache follows within hour Complex aura pattern	Multiple brainstem symptoms, consistent temporal relationship with headache, vertigo as part of aura complex not isolated symptom
Vestibular Paroxysmia	Seconds to 1 minute (up to few minutes)	Brief, frequent attacks Often many times per day Carbamazepine responsive Vascular compression of VIII nerve	Very brief duration, very high frequency, carbamazepine responsive, vascular compression etiology
Psychiatric Dizziness	Variable (situational)	Situational triggers Autonomic activation Catastrophic thinking Avoidance behavior 50% VM patients have comorbid anxiety	Situational triggers, anxiety-related features, motion perception and postural control vigilance, often comorbid with VM

Detailed Differential Diagnosis Considerations

Meniere Disease vs. Vestibular Migraine

Meniere disease presents with vertigo attacks lasting between 20 minutes and 12 hours. Auditory symptoms, including hearing loss, tinnitus, and aural fullness are required for the diagnosis. These symptoms are often transient in the early stages and become permanent later on. Both hearing loss and tinnitus preferentially affect the low-frequency range. Mild hearing loss, tinnitus, and aural fullness may also occur in vestibular migraine, but hearing loss does not progress to profound levels.

Furthermore, when hearing loss develops in vestibular migraine, it is typically bilateral, whereas symmetrical evolution of hearing loss is very rare in Meniere patients. Patients with features of both Meniere disease and vestibular migraine have been repeatedly reported. Similarly, migraine headaches, photophobia, and even migraine auras are common during Meniere attacks. The nosologic relationship between vestibular migraine and Meniere disease remains uncertain, and a future classification may include a VM/Meniere disease overlap syndrome.

BPPV and Positional Symptoms

Vestibular migraine can present with purely positional vertigo, thus mimicking BPPV. Direct observation of nystagmus during the acute phase may be required for differentiation. Positional nystagmus is usually persistent and not aligned with a single semicircular canal in vestibular migraine patients. Symptomatic episodes tend to be shorter with vestibular migraine (minutes to days rather than weeks) and more frequent (several times per year rather than once every few years with BPPV). Clinicians should be aware that a history of migraine increases the risk for BPPV by two-fold.

Transient Ischemic Attacks

A differential diagnosis of vertebrobasilar TIAs can be relevant as vestibular migraine may begin late in life when TIAs become more common. Features suggesting TIA include total history of attacks of less than 1 year, vascular risk factors, sudden onset of symptoms, and angiographic or Doppler ultrasound evidence for vascular pathology in the vertebral or proximal basilar artery. However, labyrinthine TIA or infarction remains particularly challenging as a differential diagnosis, since there is no definite confirmatory test.

Vestibular Paroxysmia

Vestibular paroxysmia presents with brief and frequent attacks of vertigo, usually lasting a few seconds only and occasionally up to 1 minute, which recur many times per day. Attacks can often be prevented by carbamazepine. Vestibular paroxysmia is caused by vascular compression of the vestibular nerve.

Psychiatric Comorbidity

Anxiety and depression may cause dizziness and likewise complicate a vestibular disorder. About 50% of patients with vestibular migraine have comorbid psychiatric disorders. Anxiety-related dizziness is characterized by situational provocation, autonomic activation, catastrophic thinking, avoidance behavior, and increased body vigilance, particularly regarding motion perception and postural control. There is an increased prevalence of migraine and vestibular migraine in patients with persistent postural-perceptual dizziness (PPPD). Both vestibular and psychiatric mechanisms may contribute to chronic dizziness in patients with vestibular migraine.

Acute Treatment Options for Vestibular Migraine Episodes

Evidence-based acute treatment medications with dosing recommendations, onset characteristics, and clinical considerations for episodes lasting longer than 30 minutes or causing significant functional impairment.

Understanding Triptans

Triptans are medications specifically designed for migraine headaches. They work by targeting serotonin receptors in the brain to reduce inflammation and constrict blood vessels. Common names include Imitrex (sumatriptan), Maxalt (rizatriptan), and Zomig (zolmitriptan). While very effective for migraine headaches, research on their effectiveness for dizziness symptoms is limited. They're typically used when vestibular migraine episodes include significant headache pain.

Drug Class	Medication & Dosing	Onset/Duration	Clinical Evidence & Considerations
Antihistamines (First-line)	Meclizine: 12.5-50 mg q6-12h (max 100 mg/day) Diphenhydramine: 25-50 mg q4-6h (max 300 mg/day) Dimenhydrinate: 50 mg q4-6h	Onset: 30-60 min Duration: 4-6 hours Routes: PO, IV, IM	Meta-analysis evidence: superior to benzodiazepines at 2 hours. Preferred first-line for prolonged episodes. Sedation common but generally well-tolerated.
Antiemetics	Prochlorperazine: 5-10 mg q6h Ondansetron: 4 mg q8-12h Promethazine: 12.5-25 mg q4-6h Metoclopramide: 5-10 mg q6h	Onset: 30-45 min Duration: 4-8 hours Routes: PO, IV, IM, PR	Prochlorperazine reduces both nausea and vertigo. Ondansetron for patients unable to tolerate dopamine antagonists. Multiple formulations available.
Benzodiazepines (Limited use)	Lorazepam: 1-2 mg q8h Diazepam: 1-5 mg q12h Alprazolam: 0.5 mg q8h Clonazepam: 0.25-0.5 mg q8-12h	Onset: 15-30 min Duration: 6-12 hours Routes: PO, IV, IM	Limit to 2-3 days maximum for acute vertigo. Dependence risk. Less effective than antihistamines per meta-analysis. Reserve for refractory cases.
Triptans (Limited evidence)	Rizatriptan: 10 mg (may repeat after 2h) Sumatriptan: 50-100 mg PO, 6mg SC Zolmitriptan: 2.5-5 mg PO/nasal	Onset: 30-60 min PO, 10 min SC Duration: 2-4 hours	Limited evidence for vertigo. Rizatriptan trial: similar 1-hour response vs placebo, but improved unsteadiness at 24 hours. Consider when headache accompanies vertigo.
Alternative Approaches	Noninvasive vagal stimulation External trigeminal stimulation	Onset: Variable Duration: Variable Routes: Device-based	Small case series suggest potential for shortening attack duration or reducing vertigo intensity. Limited evidence, requires further study.

Preventive Treatment Approaches

Preventive therapy should be considered for patients with frequent episodes (3-6+ per month) or when acute treatments are ineffective. Indications mirror those for other migraine types, considering frequency, duration, and disabling nature of attacks.

General Measures for All Patients

Lifestyle modification alone can be effective for some patients. Adequate and restful sleep is crucial for reducing episode severity and frequency. Dietary and environmental triggers should be identified and avoided, though research data for this approach in vestibular migraine is limited.

3-6

Episodes/Month

Threshold for preventive treatment

52%

Lifestyle Impact

Reduction possible with modifications

90%

CGRP Response

50%+ reduction with CGRP antagonists

First-Line Prevention Options

Beta-Blockers

Propranolol ER 60 mg daily → 120 mg twice daily

Metoprolol 50 mg daily → 200 mg daily

Research Evidence Randomized controlled trial data

Contraindications Asthma, severe depression, heart block

What are Beta-Blockers?

Beta-blockers are medications originally developed for heart conditions and high blood pressure, but they're also very effective for preventing migraine. They work by blocking certain receptors in the nervous system, which helps stabilize blood vessels in the brain and reduce migraine frequency.

Anticonvulsants

Valproate, topiramate, and lamotrigine are frequently used for migraine prevention and may be effective for vestibular migraine. Evidence comes from small trials and open-label studies, with topiramate showing reduction in vertigo and headache frequency and severity in unblinded trials.

Understanding Anticonvulsants for Migraine

Anticonvulsants (also called antiepileptics) are medications originally developed to prevent seizures, but they're also effective for migraine prevention. Common names include Topamax (topiramate), Depakote (valproate), and Lamictal (lamotrigine). They work by stabilizing electrical activity in the brain, which helps prevent both seizures and migraines. Side effects can include weight loss, tingling in hands and feet, and cognitive changes. These medications require gradual dose increases and regular monitoring.

Detailed Anticonvulsant Dosing

Topiramate: Start 25 mg daily, increase by 25-50 mg weekly to 200 mg in divided doses. Lower 25 mg twice daily dose was better tolerated and equally effective as 50 mg twice daily in studies.

Valproate: Start 500 mg daily, increase by 250-500 mg weekly to 1500 mg daily in divided doses. Avoid in women of childbearing potential due to teratogenicity.

Lamotrigine: Start 25 mg daily, increase by 50 mg after 2 weeks, then 50 mg every 1-2 weeks to target 200 mg daily in divided doses.

Antidepressants

Venlafaxine and amitriptyline are preferred options. Venlafaxine showed similar improvements to propranolol in vertigo frequency and severity with greater improvement in depression measures in unblinded randomized trials. Evidence also supports amitriptyline and nortriptyline in small studies.

Antidepressant Dosing

Venlafaxine 37.5 mg daily → 150 mg daily

Amitriptyline 10 mg at bedtime → 100 mg at bedtime

Side Effects Venlafaxine: hypertension; Amitriptyline: anticholinergic

CGRP Antagonists

Emerging evidence supports CGRP antagonists for vestibular migraine. A randomized controlled trial of galcanezumab showed lower dizziness burden and fewer dizziness days per month versus placebo at three months. Observational studies report 50%+ reduction in vertigo and headache frequency in 90% and 86% of patients, respectively, by 12-month follow-up with various CGRP antagonists.

CGRP Antagonists: The New Generation of Migraine Prevention

CGRP antagonists are newer migraine prevention medications that specifically block the CGRP chemical pathway involved in both headaches and dizziness. Common names include Aimovig (erenumab), Emgality (galcanezumab), and Ajovy (fremanezumab). These are given as monthly or quarterly injections and have shown excellent results for vestibular migraine. They tend to have fewer side effects than older preventive medications and work specifically on migraine pathways. Most people notice improvement within 2-3 months of starting treatment.

Alternative Options

Calcium channel blockers (flunarizine, cinnarizine, lomerizine) have been evaluated in multiple studies, with flunarizine showing the strongest evidence for reducing vertigo frequency and severity. Botulinum toxin showed benefit in non-randomized studies when added to oral preventive medications. Verapamil evidence is modest with some studies failing to show benefit.

Managing Comorbidities

Identifying and treating comorbidities that may mimic or trigger episodes helps guide appropriate therapies. Common comorbidities include anxiety, BPPV, motion sickness, and PPPD. Meniere disease can coexist, warranting careful management of both conditions, sometimes using headache symptoms as treatment response markers for vestibular migraine.

Vestibular Rehabilitation and Non-Pharmacologic Approaches

Vestibular rehabilitation is frequently used for symptomatic vertigo patients, though benefits for purely unprovoked episodic vertigo without chronic interictal symptoms haven't been established.

When Vestibular Therapy Helps

Vestibular therapy may be especially helpful for patients with optokinetic or visual/self-motion triggers or chronic non-vertiginous dizziness between episodes, where habituation-type therapy can be beneficial. Exercises are tailored based on vestibular testing and may include balance exercises, gaze stability training, and habituation exercises to desensitize patients to dizziness triggers.

What is Vestibular Rehabilitation?

Vestibular rehabilitation is a specialized form of physical therapy that helps retrain the brain to process balance information more effectively. A vestibular therapist will assess specific balance problems and design customized exercises to address them. These might include eye movement exercises, balance training, and gradual exposure to movements or visual stimuli that trigger dizziness. The goal is to help the brain adapt and reduce sensitivity to triggers. Sessions typically occur 1-2 times per week for 6-12 weeks, with daily home exercises.

Therapy Applications

Visual Motion Triggers Habituation therapy

Chronic Interictal Dizziness Balance training

Comorbid PPPD Gaze stability exercises

Pure Episodic VM Limited evidence

Current Research Limitations

Studies of vestibular rehabilitation for episodic vestibular migraine have mostly been before-and-after studies without control groups. Most report improvement in vestibular testing, disability measures, vertigo severity, and headache burden, but the possibility of confounding conditions like PPPD is often not reported.

Treatments with Uncertain Benefit

Benzodiazepines: Generally limited to acute symptomatic treatment unless significant anxiety requires daily medication until alternative agents reach therapeutic doses.

Acetazolamide: Effective for episodic ataxia type 2 but not widely used for migraine or vertigo. Two studies explored use in vestibular migraine but showed poor tolerance and high discontinuation rates.

Prognosis and Long-term Outcomes

The natural history of vestibular migraine has not been extensively studied, but available long-term follow-up data provides important insights for patient counseling and management expectations.

87%

Continued Episodes

At median 9-year follow-up

50%+

Reduced Frequency

Experience fewer episodes over time

15→49%

Auditory Symptoms

Increase from baseline to follow-up

Long-term Study Findings

In a long-term follow-up study of 61 patients with vestibular migraine (median nine years), 87% continued to have recurrent vertigo, although episode frequency was reduced in more than half. Cochlear symptoms increased in prevalence from 15% to 49%, signifying an important change in the condition over time.

Diagnostic Stability

In another study, 75 patients diagnosed with vestibular migraine were reassessed after a mean of nine years. More than 80% continued to be considered as having probable or definite vestibular migraine, while the diagnosis was revised in 12 patients, most often to Meniere disease, demonstrating reasonable diagnostic stability over time.

Factors for Better Outcomes

Factors that may improve long-term outcomes include early recognition and appropriate treatment, good adherence to preventive medications, effective trigger identification and avoidance, treatment of comorbidities (anxiety, BPPV), and regular follow-up with healthcare providers familiar with the condition.

Treatment Expectations

Realistic expectations should focus on reducing episode frequency and severity rather than complete elimination of symptoms. Understanding that this is typically a chronic condition helps patients and providers develop appropriate long-term management strategies. The key to successful management lies in matching appropriate treatments to individual patient needs, attack characteristics, and preferences.

"Vestibular migraine is one of the most common causes of episodic vertigo, yet remains significantly underdiagnosed. The condition requires a high index of suspicion and understanding that migraine can affect the vestibular system as prominently as it affects traditional pain pathways." - Cerebral Torque

Important Disclaimer

This information is for educational purposes only and should not replace professional medical advice.

References

Lempert T, Olesen J, Furman J, et al. Vestibular migraine: diagnostic criteria. J Vestib Res. 2012;22(4):167-172.
Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition. Cephalalgia. 2018;38(1):1-211.
Dieterich M, Brandt T. Episodic vertigo related to migraine (90 cases): vestibular migraine? J Neurol. 1999;246(10):883-892.
Neuhauser HK, Radtke A, von Brevern M, et al. Migrainous vertigo: prevalence and impact on quality of life. Neurology. 2006;67(6):1028-1033.
Formeister EJ, Rizk HG, Kohn MA, Sharon JD. The Epidemiology of Vestibular Migraine: A Population-based Survey Study. Otol Neurotol. 2018;39(8):1037-1044.
Furman JM, Marcus DA, Balaban CD. Vestibular migraine: clinical aspects and pathophysiology. Lancet Neurol. 2013;12(7):706-715.
Kayan A, Hood JD. Neuro-otological manifestations of migraine. Brain. 1984;107(Pt 4):1123-1142.
Neuhauser H, Leopold M, von Brevern M, et al. The interrelations of migraine, vertigo, and migrainous vertigo. Neurology. 2001;56(4):436-441.
Hunter BR, Wang AZ, Bucca AW, et al. Efficacy of Benzodiazepines or Antihistamines for Patients With Acute Vertigo: A Systematic Review and Meta-analysis. JAMA Neurol. 2022;79(8):846-854.
Neuhauser H, Radtke A, von Brevern M, Lempert T. Zolmitriptan for treatment of migrainous vertigo: a pilot randomized placebo-controlled trial. Neurology. 2003;60(5):882-883.
Salviz M, Yuce T, Acar H, et al. Propranolol and venlafaxine for vestibular migraine prophylaxis: A randomized controlled trial. Laryngoscope. 2016;126(1):169-174.
Sharon JD, Krauter R, Chae R, et al. A placebo controlled, randomized clinical trial of galcanezumab for vestibular migraine: The INVESTMENT study. Headache. 2024;64(10):1264-1275.
Russo CV, Saccà F, Braca S, et al. Anti-calcitonin gene-related peptide monoclonal antibodies for the treatment of vestibular migraine: A prospective observational cohort study. Cephalalgia. 2023;43(3):03331024231161809.
Liu F, Ma T, Che X, et al. The Efficacy of Venlafaxine, Flunarizine, and Valproic Acid in the Prophylaxis of Vestibular Migraine. Front Neurol. 2017;8:524.
Radtke A, von Brevern M, Neuhauser H, et al. Vestibular migraine: long-term follow-up of clinical symptoms and vestibulo-cochlear findings. Neurology. 2012;79(15):1607-1614.
Young AS, Lechner C, Bradshaw AP, et al. Clinical, oculographic, and vestibular test characteristics of vestibular migraine. Cephalalgia. 2021;41(10):1039-1052.
Neff BA, Staab JP, Eggers SD, et al. Auditory and vestibular symptoms and chronic subjective dizziness in patients with Ménière's disease, vestibular migraine, and Ménière's disease with concomitant vestibular migraine. Otol Neurotol. 2012;33(7):1235-1244.
Smetak MR, Cass ND, Manzoor NF, et al. Vestibular Migraine Confounds Management of Superior Canal Dehiscence Syndrome. Otol Neurotol. 2022;43(7):835-842.
von Brevern M, Zeise D, Neuhauser H, Clarke AH, Lempert T. Acute migrainous vertigo: clinical and oculographic findings. Brain. 2005;128:365-374.
Polensek SH, Tusa RJ. Nystagmus during attacks of vestibular migraine: an aid in diagnosis. Audiol Neurootol. 2010;15:241-246.
Cutrer FM, Baloh RW. Migraine-associated dizziness. Headache. 1992;32:300-304.
Cass SP, Ankerstjerne JKP, Yetiser S, et al. Migraine-related vestibulopathy. Ann Otol Rhinol Laryngol. 1997;106:182-189.
Bir LS, Ardic FN, Kara CO, et al. Migraine patients with or without vertigo: comparison of clinical and electronystagmographic findings. J Otolaryngol. 2003;32:234-238.
Celebisoy N, Gökçay F, Şirin H, Biçak N. Migrainous vertigo: clinical, oculographic and posturographic findings. Cephalalgia. 2007;28:72-77.
Wang CT, Lai MS, Young YH. Relationship between basilar-type migraine and migrainous vertigo. Headache. 2008;49:426-434.
Teggi R, Colombo B, Bernasconi L, et al. Migrainous vertigo: results of caloric testing and stabilometric findings. Headache. 2009;49:435-444.
Casani AP, Sellari-Franceschini S, Napolitano A, et al. Otoneurologic dysfunction in migraine patients with or without vertigo. Otol Neurotol. 2009;30:961-967.
Neugebauer H, Adrion C, Glaser M, Strupp M. Long-term changes of central ocular motor signs in patients with vestibular migraine. Eur Neurol. 2013;69:102-107.
Boldingh MI, Ljostad U, Mygland A, Monstad P. Vestibular sensitivity in vestibular migraine: VEMPs and motion sickness susceptibility. Cephalalgia. 2011;31:1211-1219.
Abu-Arafeh I, Russell G. Paroxysmal vertigo as a migraine equivalent in children: a population-based study. Cephalalgia. 1995;15:22-25.
van de Berg R, Widdershoven J, Bisdorff A, et al. Vestibular migraine of childhood and recurrent vertigo of childhood: diagnostic criteria consensus document of the Committee for the Classification of Vestibular Disorders of the Bárány Society and the International Headache Society. J Vestib Res. 2021;31:1-9.

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