Vestibular Migraine (VM)

Timothy C. Hain, MD •Page last modified: May 2, 2023

You may also be interested in our many other pages on migraine on this site•Also see our vestibular migraine calculator.

Dizziness and headache are individually very common human conditions and their combination is also a common symptom complex. Diagnostically, one must determine whether the dizziness and headaches are independent or related to each other, and in particular, whether they are a manifestation of migraine. Here we will review the association between vertigo and migraine. This subject has also been reviewed by Reploeg and Goebel (2002) as well as Radke et al (2002). Here we use the acronyms "VM" and MAV" to mean the same thing -- dizziness caused by migraine.

Epidemiology (how many people have VM)

The above reflects population data.

 

Migraine is one of the major causes of vertigo (with BPPV being the only one causing more).

About 14% of the adult population of the United States has migraine. The distribution differs between male and females. At all ages, about 5% of men have migraine (Stewart, 1994; Lipton et al, 2002). Women of childbearing age have a much higher prevalence, jumping up to roughly 10% at the onset of menstruation, and increasing to nearly 30% at the peak age of 35 years. At menopause, rates of migraine abruptly decline in women back to roughly 10%. The genetics of migraine is usually polygenetic with multiple genes contributing a little risk. This implies that perhaps we are dealing with a collection of illnesses, rather than a single one.

The figure above shows the distribution of migraine with dizziness in a subset of patients from the dizziness practice of the author. Although the populations being drawn from is different, and in particular includes very few children, it illustrates that migraine with dizziness is most commonly encountered in persons between 40 and 70, and that the female:male ratio is about 3:1.

Migraine headaches are often misdiagnosed by patients themselves as sinus headaches. Schreiber suggested that 88% of 2991 patients who had diagnosed themselves as having sinus headache, actually had migraine (Schreiber et al, 2004). Eross's study had a similar conclusion (Eross, 2007). Of course this depends on the patient and their medical care, as well as the environment that they live in.

Migraine occurs frequently with several other causes of dizziness. The prevalence of migraine (13-14%), or MAV/VM (1%) is hugely higher than that of Meniere's disease, which occurs in only 0.05% (1/2000) of the US population (Wladislavosky-Waserman et al, 1984).

In a small study of persons with Menieres disease, the prevalence ofMMigraine was about 50%, compared with a figure of about 25% in the non-Meniere's population (Radke et al, 2002). This is shown on the diagram above, where there is an overlap between Meniere's disease and Migraine. Our clinic experience is roughly comparable, and we have seen far more patients than reported in the majority of these studies.

Other studies have shown different results however. There have also been recent studies showing that there is a higher frequency of BPPV in persons with Migraine, as well as vice versa (Ishiyama et al, 2000; Uneri 2004), and about half of persons with BPPV onset before the age of 50 meet criteria for migraine. Occasionally, of course, patients with migraine will have other disorders such as brain tumors. Click HERE to see an example of this rare situation.

In practices focused on treating migraine, 27-42 % of patients report episodic vertigo (See table 1). A large number (about 36%) of these patients experienced vertigo during headache-free periods. The remainder experienced vertigo either just before or during the headache. The incidence of vertigo during the headache period was higher in patients with aura as opposed to in those without aura. Akdal et al (2013) reported on 5000 of his own patients and found that about 25% of migraine patients had vertigo or dizziness, while only about 2.9% of patients that he diagnosed as tension headache, had vertigo or dizziness (Akdal et al, 2013). Although impressive, this is hardly a blinded study and one wonders if perhaps dizziness/vertigo contributed to making a diagnosis of migraine.

In practices focused on treating vertigo, 16-32% of patients have migraine (Savundra et al, 1997). The prevalence of migraine in the general population is roughly 13-14% (Stewart et al, 1994). The pre valance of migraine with vertigo in Germany has recently reported to be 1% (Neuhauser, Radtke et al. 2006). This seems a very low to us, perhaps because of the narrow criteria used in this study -- 3% seems a little more likely. In any case, it seems reasonable to conclude that there is an immense amount of migrainous vertigo, and that migrainous vertigo is among the most common causes of vertigo in the general population (BPPV is also quite common).

Motion sickness is a common migraine accompaniment. Most studies report about 50% of patients with migraine have motion sickness, compared to about 5-20% for control groups.

Syncope can also accompany migraine, and this offers another entirely separate mechanism. In migraine, hypotension is likely hormonal, and is attributed mainly to vasopressin (Gupta, 1997).

What causes the vertigo in MAV ?

There are several theories -- 

• vascular -- patients with migraine sometimes experience spasm of blood vessels, including occasional strokes.  Blood vessel spasm in the ear or brainstem may cause vertigo.
• Neurotransmitter changes -- patients with migraine have irregularities in neurotransmitters, especially serotonin.
• Cerebellar disturbance -- migraine alters metabolism in the cerebellum.
• Sensory exaggerations -- in migraine, all senses can be more acute. This may make patients with migraine more likely to experience motion sickness and amplify the effects of small amounts of vestibular disturbance that other people might not notice.

There has also long been noted a close association between Meniere's disease and Migraine.

How is Migraine associated vertigo (MAV, VM) defined ?

MAV /VM is one of a group of conditions that encompasses many dizzy patients (including Meniere's disease, PPPD, cervical vertigo, MdDS), that are diagnosed from the pattern of symptoms rather than from a "blood test" or "X-ray".  These type of conditions nearly always are at least somewhat controversial, and have proponents as well as detractors.  They always have the clause "not better accounted for by ...", which means that they are "wastebasket" diagnoses. ''

We have calculators that "tick off" the symptoms required for VM, PPPD, and MdDS. Sometimes people meet criteria for several at the same time.

The author of this page, Dr. Hain, based on 1000's of patient care experiences, uses the following simple criteria to assign the diagnosis of VM/MAV.

• Headaches that reduce ability to carry out activities of daily living, either ongoing, or having a past history of migraine headaches (e.g. previous aura)
• Dizziness
• Responds to a migraine medication
• No other reasonable explanation (i.e. wastebasket)

These are a little different than the "official criteria", but are very close. The official VM criteria do not include response to a migraine medication.

The formal criteria for "vestibular migraine"

There are several groups (committees) that have attempted to define vesitbular migraine. The most recent is that of Lempert (2022, which included both the International Headache Society (IHS) and Barany society). Aside from some minor changes in wording, they are identical to the 2013 criteria.

The criteria for vestibular migraine according to the 2022 document are:

A. At least 5 episodes with vestibular symptoms of moderate or severe intensity, lasting 5 min to 72 hours.
B. A current or past history of migraine with or without aura, using the IHS criteria (ICHD-3).
C. At least 50% of episodes are associated with at least one of the following 3 migrainous features:

1. headache with at least two of the following four characteristics:

• a). one-sided location
• b). Pulsating quality. 
• c) Moderate or severe pain intensity.
• d) aggravation by routine physical activity. 

2. Photophobia AND phonophobia.
3. Visual aura.

D. Not better accounted for by another ICHD diagnosis or another vestibular disorder.  

These criteria can be assessed in this calculator.

These criteria likely underdiagnose vestibular migraine. According to Lemos and Manto (2022), "Small observational studies have shown that patients with episodic vestibular syndrome who cannot be diagnosed as definite or probable vestibular migraine, might still improve vestibular symptoms following preventive treatment for migraine. "

Testing for VM/MAV

There is no "test" for VM/MAV that by itself, is specific and diagnostic. MAV, like psychiatric disorders, is usually diagnosed from the clinical pattern and by excluding alternatives. Logically, MAV should be detectable by identifying sensory hypersensitivity, in the context of dizziness and headache. However, so far little has been done to quantify sensory hypersensitivity(such as allodynia) in this population.

For the most part, ENG inner ear testing in MAV is normal, but a low-level positional nystagmus is very common (Polensek and Tusa, 2010).  We agree with this -- especially pure upbeating supine. We also think there is more downbeating upright. Our guess is that these reflect genetic homogeneity in the migraine population.

Migraine

Bilateral low-frequency combined with low thresholds on UDL in patient with very well documented migraine.

 

Hearing testing in MAV is generally normal, but in our large MAV clinic population we sometimes see bilateral reduction of hearing at low frequencies. It resembles early Meniere's disease, but is bilateral. Another finding suggestive of migraine hearing symptoms is low threshold UDLs (as shown above), which suggests phobophobia. Of course, hearing testing is a subjective measurement, and stronger inferences might be possible with an objective measure, but the most accessible option -- OAE's -- do not go down to low frequencies. Still, these obervations are helpful for diagnosis.

On rotational chair testing, some authors report an increased VOR time constant in patients with vestibular migraine (Jeong et al, 2010; Rahman et al, 2022). We have found this in our patients. The same authors also felt that there were higher than normal motion sensitivity susceptibility scores (seems reasonable), and often (21%), perverted head-shaking nystagmus, aka pHSn (we are dubious). As pHSN is unusual in other syndromes, finding it in a patient who otherwise fits the criteria for migraine is helpful.

Panichi et al (2015) suggested that imbalance provoked by optokinetic stimulation was greater in 15 patients with vestibular migraine. This is too low an 'n' to be of much help. It does seem reasonable however, given that patients with migraine complain more strongly about visual motion than non-migraine patients (our observations).

Atilla and Kesici (2022) reported that "Patient with migraine had significant DVA loss as compared with control subjects in four positions (left DVA, right DVA, up DVA, down DVA respectively p < 0.001, <0.001 = 0.001 and <0.001)." We are dubious and would like to see this replicated before adding it to the diagnostic repertoire.

MAV syndromes

Migraine without aura (about 80%) and migraine with aura (about 15-20% -- perhaps less) are the most prevalent forms of migraine and also are the most prevalent types of migraine associated with dizziness and vertigo. Whether or not you designate someone with one of these variants depends largely on how carefully you ask about them and the age of the patient. There is quite a bit of noise related to visual symptoms as people age and they develop retinal disturbances. Symptoms include true vertigo with or without nausea and vomiting, and motion intolerance. Headache is usual but not required (see following). Auditory symptoms are common but usually bilateral (see following).

Sensory amplification is very common in migraine associated vertigo--

Hyperacusis (called phonophobia in this context) is common in migraine, but this may not differentiate it from inner ear disorders where a similar symptom is termed "hyperacusis". Sensitivity to light (photophobia) is also commonly present. Photophobia is not at all specific to migraine however, and can also accompany migraine imitators such as meningitis, and vertigo imitators such as Cogan's syndrome. Other sensory amplifications which are common in persons with migraine include allodynia (pain from stimuli of the head that are not painful in most people), sensitivity to weather changes, motion sensitivity, and medication sensitivity. Commonly persons with vestibular migraine are bothered by visual movement, such as scrolling a computer screen. This is a variant of visual vertigo.

When patients are examined acutely when vertiginous, there is usually minimal or no spontaneous nystagmus. This provides a differential feature from most peripheral vestibular syndromes. When nystagmus is present, it is often directed vertically (e.g. upbeating or downbeating). Vertically directed spontaneous nystagmus is unusual in other contexts, providing another differential point.

Timing. Cutrer and Baloh (1992) found a bimodal distribution of duration of vertigo with 31% of individuals having spells that typically lasted a few minutes to 2 hours and 49% having spells that lasted longer than 24 hours. Symptoms lasting months are possible (Waterson, 2004). Therefore by duration, these episodes could be confused with those due to BPPV, Menieres, or even vestibular neuritis.

Although migraines are usually episodic, they can be chronic too.  Chronic migraine is the most severe of all migraine syndromes, with headaches averaging grater than 15 days/month.  Each year, about 2.5% of those with episodic migraine develop chronic migraine (Manack et al, 2011). In our practice in Chicago, we encounter many persons who are extremely motion sensitive, have visual sensitivity, and sound sensitivity, lasting months ! These persons usually respond to migraine prevention medication. Similar patients with chronic symptoms, even with few headaches, have been reported by others (e.g. Waterson, 2004)

As in migraine, in VM, occasionally aura may occur without headache (acephalgic migraine), it also follows that vertigo may occur without headache. Examples are as follows:

Benign recurrent vertigo of adults (BRV)

Essentially a vertiginous migraine aura without headache, was described first by Slater (1979) but his observations have been confirmed by others (e.g. Lee et al, 2002; Cha et al, 2009). A more detailed discussion of BRV is found here.

Basilar Migraine or Basilar Artery Migraine (BAM )

Basilar Migraine, also known as Bickerstaff ‘s syndrome(1961), consists of two or more symptoms from a rather long list (vertigo, tinnitus, decreased hearing, ataxia, dysarthria, visual symptoms in both hemifields of both eyes, diplopia, bilateral paresthesias or paresis, decreased LOC) followed by a throbbing headache. Vertigo typically lasts between 5 minutes and one hour. In the author’s practice, the typical patient is a woman of about 35 years of age, who attacks of vertigo combined with headache. The family history is often positive. In the differential are TIAs and paroxysmal vestibular disorders accompanied by headache. Some patients become dysarthric during attacks, slur their speech, and even become unconscious. This is extremely impairing.

Patients usually respond to the usual migraine prophylactic drugs. However, BAM can be extremely disabling and in persons who don't respond to the most common suspects, often one ends up trying a large assortment of prophylactics. In our worst patients, we think they do best on dopamine blockers (such as flunarazine). Often we also combine this with venlafaxine, propranolol, topiramate, and sometimes memantine. For abortives, we sometimes use cambia (diclofenac) or haloperidol drops. In other words, everything but the kitchen sink, usually including a dopamine blocker. This is due to the extreme severity of these patient's symptoms, which can resemble seizures or strokes. There is some overlap in these patients with hemiplegic migraine.

Auditory symptoms in BAM are rare compared to vestibular symptoms (Battista, 2004) but nevertheless there is good evidence that hearing loss and tinnitus do occur. Olsson (1991) in a study of 50 patients with basilar migraine (which is rare) documented a fluctuating low-tone sensorineural hearing loss in more than 50% of his patients, and about 50% of his patients noticed a change in hearing immediately prior to their migraine headaches. Virre and Baloh (1996) suggested that sudden hearing loss may also be caused by migraine. Hearing loss in migraine rarely progresses (Battista, 2004).  Only minor changes of no significance are found in formal tests of auditory function in persons with migraine (Hamed et al, 2011).

Tinnitus is also common in migraine (Kayan and Hood, 1984; Olsson, 1991). Because the formal criteria for Menieres disease (audiometrically documented hearing loss (not fluctuation), episodic tinnitus and/or fullness, episodic vertigo) are a subset of the documented spectrum of basilar migraine, there is the possibility for diagnostic ambiguity (Harker, 1996). Boismier and Disher reported that 6% of 770 patients who presented with vertigo fell into an ambiguous diagnostic situation between Meniere's and Migraine (2002). When headache is not prominent, features such as bilateral hearing fluctuation (according to Harker (1996) auditory symptoms are rarely unilateral), family history of migraine and perimenstrual exacerbations are used to decide whether Menieres or migraine is the more likely diagnosis. Sometimes one just has to accept both as reasonable possibilities.

Benign Paroxysmal Vertigo of Childhood

This is a disorder of uncertain origin, possibly migrainous. It's initials (BPV) are easily confused with those of Benign Paroxysmal Positional Vertigo (BPPV), but it is not caused by the same mechanisms. This disorder consists of spells of vertigo and disequlibrium without hearing loss or tinnitus (Basser, 1964). The majority of reported cases occur between 1 and 4 years of age, but this syndrome seems indistinguishable from benign recurrent vertigo (BRV, see following) in adults which is presently attributed to migraine, or so-called "vestibular Menieres", which is also attributed to migraine. The differential diagnosis includes Menieres disease, vestibular epilepsy, perilymphatic fistula, posterior fossa tumors, and psychogenic disorders.

PPPD (Persistent postural-perceptive dizziness)

PPPD is an acronym for a psychiatric diagnosis, "Persistent postural perceptive Dizziness".

Cyclic Vomiting

This is a very disturbing disorder in which persons suddenly develop vomiting, generally without headache or hearing symptoms. It usually responds to migraine prevention medications. Vertigo is common (especially positional resembling lateral canal BPPV). It overlaps with migraine and Meniere's, but pretty much by definition there is no headache or hearing loss (if it did, it wouldn't be called cyclic vomiting -- it would be called migraine or Meniere's). See this page for more.

Familial syndromes:

There has recently been a report of a familial vestibulopathy, confusingly called familial Benign Recurrent Vertigo (BRV) consisting of episodic vertigo with or without migraine headache. Presumably there are both familial and nonfamilial forms -- fBRV and BRV. The non-familial form is sometimes also called recurrent vestibular neuritis as well as vestibular Meniere's. In the current age of VHIT testing, it is easy to tell vestibular neuritis apart from BRV based on objective criteria. Vestibular Meniere's though is still waiting for a diagnostic test (perhaps MRI for hydrops).

Vestibular testing in the familial form can document profound bilateral vestibular loss. The familial syndrome responds to acetazolamide (Baloh et al, 1994). It is not associated with a mutation on the calcium channel gene (Oh et al, 2001). Also reported by Baloh and associates, a form exists with episodic vertigo and essential tremor. This form is also responsive to acetazolamide. (Baloh et al, 1996). Familial hemiplegic migraine has been linked to mutations in the calcium channel gene (Ophoff et al, 1996). French-Canadian intermittent ataxia syndrome also may present similarly. While no mutations have been identified in the common form of migraine, calcium channels could be functionally impaired by subtle gene changes such as polymorphisms.

Antiphospholipid antibodies. There are some reports that individuals with severe migraine headaches are more likely to have antiphospholipid antibodies. In the authors experience, these patients may present with transient monocular visual loss, and some also have fetal wastage and complicated migraines as well as a reticular rash on the legs. (Donders et al, 1998). Recent authors have suggested that the association of migraine with APA is not a valid one.

Treatment of VM/MAV.

For treatment of migraine in general see this page. A flowchart is given here. Because of the possibility for serious injury associated with vertigo, prevention is the advised treatment for most types of MAV. Eliminating dietary triggers and prophylactic medication treatment are the modalities used most frequently. Patients are initially told to abstain from foods such as chocolate, strong cheese, alcohol (especially red wine) and MSG containing preparations (such as oyster sauce). We also suggest magnesium supplements (500 mg/day).

If this is not successful, after a month, patients are started on one of the following -- topiramate, verapamil, a long-acting beta-blocker such as long acting propranolol, or an antidepressant such as amitriptyline or venlafaxine depending on gender and medical situation. Verapamil and amitriptyline are particularly useful because of their anticholinergic properties may help control vertigo independently of whether they are useful for migraine per se. Venlafaxine is a very useful medication for vestibular migraine in particular (Salviz et al, 2015).

 

---

References: are here.