Migraine associated vertigo (vestibular migraine)

By Marcello Cherchi, MD PhD

For patients

Migraine associated vertigo (MAV) is a type of migraine that causes disequilibrium.  This is probably a common cause of disequilibrium in children and adults.  There is no test that “proves” a person has MAV, and since there are numerous illnesses that can cause this same symptom (disequilibrium), your doctor may check several tests to help rule out other diseases.  Treatment of MAV is similar to that of migraines in general.

We usually recommend that patients begin with non-pharmacologic approaches because these have very little risk.  This can include:

Lifestyle modifications:

  • Reducing or eliminating potential dietary triggers, such as alcohol, caffeine, chocolate, aged cheeses, monosodium glutamate and nitrites
  • Having regular mealtimes
  • “Sleep hygiene,” which refers to getting adequate sleep on a regular schedule
  • Having regular aerobic exercise
  • Smoking cessation

Nutritional supplements, herbal supplements and procedures:

For clinicians

Practical summary

Migraine associated vertigo (MAV) is thought to be a version of migraine that manifests with the sensation of disequilibrium, and may or may not involve headaches meeting criteria for migraines.  The disequilibrium itself can have a variety of presentations in terms of quality, frequency, duration and triggers.  MAV is thought to affect nearly 1% of the population.  The underlying cause of MAV is unknown; research has not yet identified specific genes responsible for MAV.  Patients with MAV usually have normal physical examinations, though some may have subtle and variable nystagmus on infrared video oculography.  Like migraines in general, MAV is a diagnosis of exclusion, and the main value of paraclinical testing (otovestibular testing and sometimes imaging) is to exclude competing pathologies from the differential diagnosis.  There is very little literature on treatment specifically for MAV, so most practitioners extrapolate from the existing literature on regular migraine headaches.  We favor starting with non-pharmacological strategies because of their relatively favorable risk profile.

Introduction

The idea that the symptom of disequilibrium can be attributed to an underlying migraine disorder goes by several terms in the literature, including “migraine associated vertigo,” “migrainous vertigo,” “vestibular migraine,” “vertiginous migraine,” and others.  We shall use the phrase “migraine associated vertigo” (MAV) for convenience.

The third edition of the International Headache Society Classification of Headache Disorders (Headache Classification Committee of the International Headache Society 2018) (https://ichd-3.org/1-migraine/, accessed 8/26/23) recognizes 15 types of migraine, 2 types of probable migraine, and two “syndromes that may be associated with migraine.”  Migraine can supposedly present with an impressively broad variety of symptoms (Buchholz and Reich 1996).  The polymorphic phenotype raises the reasonable question of whether these comprise different manifestations of a single pathology, or whether they are different diseases entirely; until tools arise for confirming/disproving the diagnosis, this question will remain fodder for the perennial nosologic debate regarding “lumping” and “splitting” (Endersby 2009; Thaxton et al. 2022).

There is a well-developed literature on MAV (Beh et al. 2019; Cherchi and Hain 2011, 2014; Hain and Cherchi 2018; Hain and Cherchi 2019; Neuhauser and Lempert 2009; Neuhauser et al. 2001; Neuhauser et al. 2006).

Neuhauser and Lempert (Neuhauser and Lempert 2009) proposed the following criteria for “vestibular migraine:”

  • Definite vestibular migraine
    • Episodic vestibular symptoms of at least moderate severity
    • Current or previous history of migraine according to the ICHD‑II (International Headache Society 2004)
    • One of the following migrainous symptoms during two or more attacks of vertigo: migrainous headache, photophobia, phonophobia, visual aura, or other aura
    • Other causes ruled out by appropriate investigations
  • Probable vestibular migraine
    • Episodic vestibular symptoms of at least moderate severity
    • One of the following:
      • Current or previous history of migraine according to the ICHD‑II
      • Migrainous symptoms during vestibular symptoms
      • Migraine precipitants of vertigo in more than 50% of attacks (food triggers, sleep irregularities, or hormonal change)
      • Response to migraine medications in more than 50% of attacks
    • Other causes ruled out by appropriate investigations

Epidemiology

The prevalence of migraine in the general population is about 10% (Stewart et al. 1994).  Approximately one-third of patients with migraines experience some degree of disequilibrium during their migraines (Selby and Lance 1960).  These statistics taken together would lead one to expect a prevalence of migraine-related disequilibrium of about 3%.

However, when using the stricter diagnostic criteria of Neuhauser and Lempert (Neuhauser and Lempert 2009), the prevalence of MAV turns out to be 0.98%.  This leaves another 2.02% unaccounted for.  One interpretation of this discrepancy is that because migraine (broadly speaking) is so common, it is statistically likely that some patients with (non-vestibular) migraine have vestibular symptoms attributable to some non-migrainous disease.  This is important to take into account when considering a differential diagnosis, since a number of “dizzy diseases” have an association with migraine that his higher than what would be expected by chance (10% of the general population, as mentioned earlier).  For example:

To reiterate, this suggests that a patient with migraines and with disequilibrium may have some cause for the disequilibrium other than migraines.  This is why the criteria for MAV discussed earlier explicitly state that the symptoms must not be attributable to another disorder.  Taking this into account along with the fact that migraine is still a disease for which no confirmatory test exists (see below), it should be emphasized that MAV is a clinical diagnosis, and a diagnosis of exclusion.

Genetics

The study of the genetics of migraine (broadly construed) is an emerging discipline (Anttila et al. 2018; Cader 2020; de Boer et al. 2019; Ducros 2021; Grangeon et al. 2023; Sutherland et al. 2019).  For MAV the evidence of heritability is still very limited (Paz-Tamayo et al. 2020), though several genes have been implicated (Bahmad et al. 2009; Oh et al. 2020; Wu et al. 2020).  This field is likely to advance, but as of this writing, genetic testing does not comprise a component of the standard workup.

Pathophysiological mechanism of disease

Despite considerable research, the underlying pathophysiology of migraines (broadly construed) remains uncertain.  Research on the pain associated with migraines, and the positive response to serotonin agonists such as triptans, implicate brainstem dysfunction at the level of the serotonin pathways of the trigeminal system (Goadsby 1997).  Research on migraine aura (in general), and specifically on the circulatory changes in the occipital cortex associated with visual auras, implicates cortical dysfunction, rooted either in vascular dysregulation, or abnormal electrical activity, or both (Leão 1944; Leão and Morison 1945; Olesen et al. 1990).

The same general mechanisms have been proposed for MAV.  The fact that patients with MAV may exhibit nystagmus (see below) implicates dysfunction at the level of the brainstem (particularly the vestibular nuclei).  But the other obvious possibility is cerebral dysfunction at the level of the purported vestibular cortex in the temporal lobe.  These proposals are logical, but remain speculative.

Clinical presentation

Patients offer different descriptors of the disequilibrium they experience during an episode of MAV. Neuhauser and colleagues (Neuhauser et al. 2001) cite the following descriptors and associated frequencies:

  • Sensation of spinning or rotation (70%)
  • Intolerance of head motion (48%)
  • Disequilibrium triggered by changes in position (42%)
  • Less common: motion sickness, floating, rocking, tilting, walking on an uneven surface, lightheadedness

The duration of the disequilibrium is quite variable.  Neuhauser and colleagues (Neuhauser et al. 2001) list the following:

  • 5 to 60 minutes (33%)
  • 1 to 24 hours (21%)
  • Seconds to 5 minutes (18%)
  • More than 24 hours (2%)

There are also well-documented series of MAV symptoms being chronic (Waterston 2004).

Migraine in general, and MAV, can present with aural symptoms.  Dash and colleagues (Dash et al. 2008)report the following aural symptoms and associated frequencies:

  • 66% describe sonophobia
  • 63% describe tinnitus
  • 32% describe hearing loss
  • 11% report fluctuating hearing loss and aural fullness

These aural symptoms can, of course, can be features of non-migrainous otovestibular diseases, and are thus another reason to keep such pathologies on the differential diagnosis.

For migraine in general, and probably also for MAV, some patients report symptom triggers such as:

  • Weather changes: onset of storm fronts, changes of season
  • Activities and states: physical exertion, dehydration, sleep deprivation, menses, exposure to bright light
  • Dietary factors: caffeine, chocolate, alcohol, aged cheeses, monosodium glutamate, nitrites, artificial sweeteners

Patients with migraines in general, and probably also MAV, often give a history of susceptibility to motion sickness.  This is reported in 45% of pediatric patients (Barabas et al. 1983) and 50% of adult patients (Kayan and Hood 1984).

Physical examination

Unless a patient with MAV has other medical problems, the physical examination is usually normal (but see below regarding the ocular motor examination).

Ocular motor examination

A patient with MAV may have eye movement abnormalities that are intermittent and fluctuating (Kayan and Hood 1984; Polensek and Tusa ; von Brevern et al. 2005); these may be sufficiently subtle that they are only detectable on infrared video oculography.

Testing: auditory

While there are case reports of hearing loss in patients with migraine (Lee et al. 2000; Lee et al. 2003; Lipkin et al. 1987; Viirre and Baloh 1996), our experience is that patients with MAV generally have normal hearing, unless MAV is comorbid with an otologic disorder such as Ménière’s (Battista 2004).

Testing: vestibular

Studies of other otovestibular tests occasionally report abnormalities in patients with migraine, including otoacoustic emissions (Bolay et al. 2008), brainstem auditory evoked responses (Bayazit et al. 2001; Dash et al. 2008), vestibular evoked myogenic potentials (Baier et al. 2009), caloric testing (Celebisoy et al. 2008; Teggi et al. 2009), rotatory chair testing (Arriaga et al. 2006; Cass et al. 1997; Furman et al. 2005; Kim et al. 2023), and computerized dynamic posturography (Celebisoy et al. 2008; Furman et al. 2005; Teggi et al. 2009).  However, none has been rigorously evaluated in patients specifically with MAV.

Testing: imaging

It has been reported that approximately 23% of migraine patients accumulate white matter abnormalities not attributable to other disorders.  Furthermore, migraine patients are at approximately a four-fold higher risk for developing white matter abnormalities than patients without migraine, even after controlling for vascular risk factors (Swartz and Kern 2004).  The imaging findings typically include scattered punctate foci of T2 and FLAIR signal hyperintensity in the deep cerebral white matter.  These imaging findings, which can resemble those of multiple sclerosis, are generally not accompanied by any clinical correlates.  In our experience, these common MRI findings do not appear to be associated with an increased risk of migrainous infarction.

Testing: overall

None of the abnormal findings in the paraclinical tests mentioned above (auditory, vestibular, imaging) comprise proof-positive evidence for MAV.  The main benefit of undertaking these studies is to assess for competing diagnoses — such as otologic disease that could account for auditory and/or vestibular symptoms.

Differential diagnosis

Since patients with migraines can have causes of disequilibrium unrelated to their migraines, and since MAV is a diagnosis of exclusion, it is medically reasonable to undertake a screening otovestibular workup in patients for whom a diagnosis of MAV is being considered.

For a potential MAV patient who only has vestibular symptoms (without any auditory symptoms) it is reasonable to check cervical and ocular vestibular evoked myogenic potentials, video head impulse testing and possibly videonystagmography and computerized dynamic posturography.  If the patient has any auditory symptoms whatsoever, then it is reasonable to check otoacoustic emissions (if under the age of 60 years), audiometry, cervical and ocular vestibular evoked myogenic potentials, and possibly electrocochleography.

Reasons for checking neuroimaging of the brain include:

  • If the headache is new, or if it has developed new associated features, or if there are focal abnormalities on neurological examination, then imaging is recommended by the American Academy of Neurology ([No authors] 1994; Frishberg 1994).
  • Clear lateralizing deficits on otovestibular testing compatible with specific pathologies that could be objectively (e.g., vestibular schwannoma, superior semicircular canal dehiscence).

Given the otologic diseases on the differential diagnosis (at least for MAV), MRI of the brain and internal auditory canals without and with contrast is more likely to be helpful; this images not only the brain, but also structures relevant to vestibular disease (labyrinth, vestibular nerve, brainstem, cerebellum).  CT imaging is generally less helpful, except in the specific circumstance of superior semicircular canal dehiscence, in which case a temporal bone CT without contrast may be considered.

Treatment: overview

The vast majority of research in the treatment of migraine focuses on outcomes in patients whose phenotype meets criteria for migraine headache.  There is relatively sparse research on the treatment of supposed subtypes of migraine, such as migraine presenting exclusively with visual aura (“retinal migraine,” “optical migraine”).  Consequently, clinicians confronted with a case of a subtype of migraine will usually extrapolate from the existing literature on migraine headaches.

Management of MAV suffers from this same problem.  Reviews of literature focused on the treatment of MAV note that the quantity and quality of studies is poor (Almohammed et al. 2025).

A Cochrane Review of pharmacologic prophylaxis for MAV concluded that, “There is very limited evidence from placebo-controlled randomised trials regarding the efficacy and potential harms of pharmacological interventions for prophylaxis of vestibular migraine. We only identified evidence for two of our interventions of interest (beta-blockers and calcium channel blockers) and all evidence was of low or very low certainty. Further research is necessary to identify whether these treatments are effective at improving symptoms and whether there are any harms associated with their use” (Webster et al. 2023a).

A Cochrane Review of non-pharmacologic prophylaxis for MAV concluded that, “There is a paucity of evidence for non-pharmacological interventions that may be used for prophylaxis of vestibular migraine. Only a limited number of interventions have been assessed by comparing them to no intervention or a placebo treatment, and the evidence from these studies is all of low or very low certainty. We are therefore unsure whether any of these interventions may be effective at reducing the symptoms of vestibular migraine and we are also unsure whether they have the potential to cause harm” (Webster et al. 2023b).

A Cochrane Review of pharmacologic abortive treatments for MAV concluded that, “The evidence for interventions used to treat acute attacks of vestibular migraine is very sparse. We identified only two studies, both of which assessed the use of triptans. We rated all the evidence as very low-certainty, meaning that we have little confidence in the effect estimates and cannot be sure if triptans have any effect on the symptoms of vestibular migraine” (Webster et al. 2023c).

Treatment: non-pharmacologic approaches

Absent robust evidence for treatment specifically aimed at MAV, most practitioners simply extrapolate from existing literature regarding treatment of migraine in general.  Since the risks of pharmacologic intervention overall probably exceed those of non-pharmacologic intervention, our usual practice is to consider non-pharmacologic strategies first.

Nutritional supplements

The American Academy of Neurology’s evidence-based guideline on non‑pharmacologic treatments for migraine in general (Holland et al. 2012) found efficacy for riboflavin, coenzyme Q10 and magnesium, which are endogenous substances, and available without a prescription in the United States.

Magnesium is taken at a dose of 300 – 600 mg once per day.  Different formulations have been studied, including magnesium citrate and magnesium oxide.  The efficacy of magnesium becomes apparent within 9 – 12 weeks in adults (Peikert et al. 1996) and within 16 weeks in children (Wang et al. 2003).  Magnesium is currently not recommended during pregnancy because of possible effects on the bone metabolism of the fetus (Yokoyama et al. 2010).

Riboflavin (vitamin B2), is taken at a dose of 400 mg once per day.  The efficacy of riboflavin becomes apparent around 12 weeks (Schoenen et al. 1998).  Riboflavin can be taken during pregnancy and nursing.

Vitamin D has been studied as a migraine prophylactic.  Some studies (Buettner et al. 2015; Cayir et al. 2014; Gazerani et al. 2019; Ghorbani et al. 2020; Ghorbani et al. 2019; Kilic and Kilic 2019; Mottaghi et al. 2015) report that taking vitamin D supplementation improves migraine frequency.  Vitamin D supplementation as a prophylactic treatment for migraine has been studied in both pediatric (Kilic and Kilic 2019) and adult populations (Gazerani et al. 2019).  Recommended doses of vitamin D supplementation vary from 1000 to 4000 international units (I.U.) per day; one study explored 50,000 I.U. per week (Mottaghi et al. 2015) (amounting to about 7000 mg per day).  The time to onset of efficacy remains unclear; observation periods varied from 10 weeks (Mottaghi et al. 2015) to 24 weeks (Gazerani et al. 2019).

Coenzyme Q10 is taken at a dose of 100 mg three times per day.  The efficacy of coenzyme Q10 becomes apparent around 12 weeks (Hershey et al. 2007).  Coenzyme Q10 can be taken during pregnancy and nursing.

Melatonin is taken at a dose of 3 mg once per night (Peres et al. 2004).  Melatonin has been studied in randomized controlled trials versus placebo (Alstadhaug et al. 2010; Ebrahimi-Monfared et al. 2017) and versus other medications (Gonçalves et al. 2016).  While some reviews describe these trials as demonstrating a “positive trend” (Moreno-Ajona et al. 2021), most systematic reviews and meta-analyses conclude that the evidence is still emerging (Leite Pacheco et al. 2018; Liampas et al. 2020; Long et al. 2019; Puliappadamb et al. 2022; Yamanaka et al. 2021).  Melatonin appears to be safe in pregnancy and lactation (Vine et al. 2022).  Melatonin is currently available over-the-counter in the United States.

Herbal supplements

The American Academy of Neurology’s evidence-based guideline on non‑pharmacologic treatments for migraine (Holland et al. 2012) found efficacy for several herbal supplements.  These supplements do not require prescriptions.

Feverfew (also called Tanacetum parthenium) has been studied as a migraine prophylactic.  There are several different extracts of feverfew (Pareek et al. 2011).  The most commonly used extract of feverfew, called parthenolides, is taken at a dose of 100 – 300 mg four times per day.  Another extract of feverfew, called MIG‑99, is taken at a dose of 6.25 mg three times per day (Diener et al. 2005).  Several Cochrane reviews found insufficient evidence to support the use of feverfew for migraine prophylaxis (Pittler and Ernst 2004; Pittler et al. 2000), though the most recent Cochrane review as of this writing concluded, “Since the last version of this review, one larger rigorous study has been included, reporting a difference in effect between feverfew and placebo of 0.6 attacks per month. This adds some positive evidence to the mixed and inconclusive findings of the previous review. However, this constitutes low quality evidence, which needs to be confirmed in larger rigorous trials with stable feverfew extracts and clearly defined migraine populations before firm conclusions can be drawn” (Wider et al. 2015).

A previously popular herbal supplement, Butterbur (also called Petasites hybridus) is taken at a dose of 50 to 75 mg twice per day.  The efficacy of Butterbur becomes apparent around 16 weeks (Lipton et al. 2004). Some, but not all, preparations of Butterbur, contain pyrrolizidine alkaloids, which can damage the liver in humans, and can cause cancer in some animal studies (Aydin et al. 2013).  Since different preparations of Butterbur vary in their content of pyrrolizidine alkaloids (Avula et al. 2012), most patients prefer to avoid this supplement.

Acupuncture

Acupuncture has been applied to an enormous number of illnesses, and in the 1980s researchers began examining this approach systematically through randomized trials for migraines.  As of this writing there is reasonable evidence that acupuncture is effective both for migraine abortive therapy (Wang et al. 2012) and for migraine prophylaxis (Chessman 2016; Linde et al. 2016; Linde et al. 2009).  The frequency and duration of acupuncture treatment as prophylaxis for migraine remain to be clarified, though one review recommended two sessions per week for 10 weeks (Zheng et al. 2010).  Acupuncture usually does not require a referral.  Acupuncture is rarely covered by insurance.

Transcutaneous electrical stimulation

The technology of transcutaneous electrical neurostimulation (TENS) units has long been in use for a variety of musculoskeletal disorders.  Studies of this therapy for migraine prophylaxis have demonstrated it to be both safe (Magis et al. 2013) and effective (Schoenen et al. 2013).  This therapy is currently marketed in the United States as the Cefaly® device (2014) (see http://www.cefaly.com/en, accessed 8/27/23), and requires a prescription.

Behavioral therapy: biofeedback

Biofeedback is a behavioral therapy that has been used in many medical conditions, and has been studied specifically for migraine.  There is an emerging literature about the use of biofeedback for management of migraine (Allen and Shriver 1997; Andrasik 2010; Andreychuk and Skriver 1975; Baumann 2002; Blanchard et al. 1978; Burke and Andrasik 1989; Buse and Andrasik 2009; de Tommaso and Delussi 2017; Drury et al. 1979; Ellertsen et al. 1987; Fahrion 1977; Fentress et al. 1986; Gamble and Elder 1983; Gauthier et al. 1981; Gauthier et al. 1994; Gauthier et al. 1983; Gauthier et al. 1985; Gauthier and Carrier 1991; Gauthier et al. 1991; Grazzi and Bussone 1993; Hermann et al. 1997; Hoffmann 1975; Holmes and Burish 1983; Ingvaldsen et al. 2021; Johansson and Ost 1982, 1987; Kaiser and Primavera 1987; Kaushik et al. 2005; Kewman and Roberts 1980; Lacroix et al. 1983; Lake et al. 1979; Lisspers and Ost 1990; Martic-Biocina et al. 2017; Mathew et al. 1980; McGrady et al. 1994; Medina et al. 1976; Minen et al. 2021; Mullally et al. 2009; Nestoriuc and Martin 2007; Odawara et al. 2015; Pfaller 2010; Prima et al. 1979; Reid and McGrath 1996; Scharff et al. 2002; Silver et al. 1979; Sovak et al. 1981; Stokes and Lappin 2010; Stubberud et al. 2020; Stubberud et al. 2016; Turin and Johnson 1976; Vasudeva et al. 2003; Wauquier et al. 1995).  A variety of biofeedback strategies has been studied.  Patients usually learn biofeedback under the instruction of a specially trained psychologist.  One can search for an appropriately trained psychologist through the website of the Association for Applied Psychophysiology and Biofeedback (http://www.resourcenter.net/scripts/4disapi9.dll/4dcgi/resctr/search.html, accessed 8/27/23).  Biofeedback does not require a referral, and is not covered by insurance in the United States.

Behavioral therapy: relaxation training

Although the biological connection between psychological stress and migraine is uncertain (Rains 2009; Sauro and Becker 2009), it appears that behavioral therapies such as relaxation training and stress management benefit many patients with migraine (Becker and Sauro 2009).  The literature regarding relaxation training is emerging (Butt et al. 2022; D’Souza et al. 2008; Fentress et al. 1986; Fichtel and Larsson 2001; Hay and Madders 1971; Kaushik et al. 2005; Lacroix et al. 1983; McGrady et al. 1994; McGrath et al. 1988; Meyer et al. 2016; Richter et al. 1986; Silver et al. 1979; Sorbi and Tellegen 1986; Vasudeva et al. 2003; Warner 1975; Wauquier et al. 1995).  A variety of relaxation training strategies have been attempted.  Relaxation training does not require a referral, and is not covered by insurance in the United States.

Notes on migraine treatment during pregnancy and nursing

Although more than half of women experience improvement in their migraine patterns (without any treatment) during pregnancy, some women still have migraine symptoms requiring management (Airola et al. 2010).  Unfortunately, most of the drugs commonly used in migraine are relatively contraindicated in pregnancy.  Of the non‑pharmacologic approaches discussed above, those applicable in pregnancy include smoking cessation, maintaining a regular sleep schedule, aerobic exercise, some nutritional supplements (riboflavin, vitamin D, coenzyme Q10 and melatonin), acupuncture, biofeedback, transcutaneous electrical neurostimulation and relaxation training.

Prognosis

The prognosis of MAV is probably similar to that of migraine in general, though this has not been formally assessed in large prospective studies.

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