Ann. N.Y. Acad. Sci.

ISSN 0077-8923

A N N A L S O F T H E N E W Y O R K A C A D E M Y O F SC I E N C E S
Issue: Dizziness and Balance Disorders

Vestibular migraine
Joseph M. Furman1 and Carey D. Balaban2
1
Departments of Otolaryngology, Neurology, Bioengineering, and Physical Therapy, University of Pittsburgh, Pittsburgh,
Pennsylvania. 2 Departments of Otolaryngology, Neurobiology, Communication Sciences & Disorders, and Bioengineering,
University of Pittsburgh, Pittsburgh, Pennsylvania

Address for correspondence: Joseph M. Furman, M.D., Ph.D., Departments of Otolaryngology, Neurology, Bioengineering,
and Physical Therapy, University of Pittsburgh, Suite 500, 203 Lothrop Street, Pittsburgh, PA 15213. furmanjm@upmc.edu

Vestibular migraine is now considered a distinct diagnostic entity by both the Barany Society and the International
Headache Society. The recognition of vestibular migraine as a diagnostic entity required decades and was presaged
by several reports indicating that a large proportion of patients with migraine headaches have vestibular symptoms
and that a large proportion of patients with undiagnosed episodic vestibular symptoms have migraine headache.
Despite the availability of diagnostic criteria for vestibular migraine, challenges to diagnosis include variability in
terms of the character of dizziness, the presence or absence of clearly defined attacks, the duration of attacks, and the
temporal association between headache or other migrainous features and vestibular symptoms. Also, symptoms of
vestibular migraine often overlap with symptoms of other causes of dizziness, especially Ménière’s disease and benign
paroxysmal positional vertigo (BPPV). This article will discuss the demographics, epidemiology, clinical manifes-
tations, physical examination findings, laboratory testing, comorbidities, treatment options, and pathophysiology
of vestibular migraine. Future research in the field of vestibular migraine should include both clinical and basic
science efforts to better understand the pathophysiology of this condition. Controlled treatment trials for vestibular
migraine are desperately needed.

Keywords: vestibular; migraine; headache; dizziness; vertigo; imbalance

entity.5 Of note, this single-page editorial with 21

Vestibular migraine
Vestibular migraine is now considered a distinct di-
agnostic entity by both the Barany Society and the
International Headache Society.1 The current view
of vestibular migraine has evolved during the past
approximately 50 years. Before the formulation of
diagnostic criteria for vestibular migraine, there was
a realization that recurrent vertigo in some patients
with migraine could be attributed to migraine it-
self rather than to another neurotologic condition.2
Despite decades of observations and articles regard-
ing the link between vestibular symptoms and mi-
graine headache and the availability of proposed
and validated diagnostic criteria by Neuhauser
et al.,3 as recently as 2010, Phillips et al. published
an article in the journal Headache4 that advocated
the dismissal of vestibular migraine as a diagnostic
entity. Shortly thereafter, in early 2011, a brief edito-
rial in Headache outlined the arguments in support
of recognizing vestibular migraine as a diagnostic
doi: 10.1111/nyas.12645
Ann. N.Y. Acad. Sci. xxxx (2015) 1–7 
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citations was authored by 10 neurologists repre-
senting four countries in Europe and the United
States. Despite some diagnostic uncertainty and un-
resolved issues regarding pathophysiology and treat-
ment, vestibular migraine is generally considered
a bona fide neurotologic disorder. Epidemiologic
data indicate that vestibular migraine is probably the
most common neurotologic condition presenting to
tertiary clinics that care for patients with dizziness
and disequilibrium.6
The recognition of vestibular migraine as a diag-
nostic entity was presaged by several reports that in-
dicated a large proportion of patients with migraine
headaches have vestibular symptoms7–9 and a large
proportion of patients with undiagnosed episodic
vestibular symptoms have migraine headache.10,11
Two well-recognized migraine conditions (i.e., be-
nign recurrent vertigo of childhood12 and basilar-
type migraine13 ) included vestibular symptoms. For
basilar-type migraine, reports of 61%14 and 63%15
1
Vestibular migraine Furman & Balaban

Table 1. Diagnostic criteria for vestibular migraine1

A. At least five episodes with vestibular symptoms of moderate or severe intensity, each lasting 5 min to 72 h
B. Current or previous history of migraine with or without aura according to the International Classification of
Headache Disorders (ICHD)
C. One or more migraine features with at least 50% of the vestibular episodes:
• headache with at least two of the following characteristics: one-sided location, pulsating quality, moderate
or severe pain intensity, or aggravation by routine physical activity
• photophobia and phonophobia
• visual aura
D. Not better accounted for by another vestibular or ICHD diagnosis

of patients having vertigo strongly suggested an
association between vestibular disorders and mi-
graine. However, few patients who meet criteria for
vestibular migraine also meet criteria for basilar-
type migraine, thereby necessitating a separate di-
agnostic category for vestibular migraine.16 Previ-
ous to the 2012 acceptance of vestibular migraine
as the term assigned to this diagnostic entity, var-
ious different terms were used including “benign
recurrent vertigo”2 to denote a condition akin to
vestibular migraine, highlighting the episodic na-
ture of the condition. The earliest use of the term
“vestibular migraine” was in 1917 by Boenheim.17
More recently, Dieterich and Brandt, in 1999,18 rein-
troduced the term “vestibular migraine,” which has
now been selected by the international community.
Importantly, although the term “migrainous ver-
tigo” was used by Neuhauser et al. in their landmark
paper of 2001 that established diagnostic criteria
for this condition,19 their work, and that of others
who used various different terms, can all be consid-
ered studies of the condition we now designate as
vestibular migraine.
Despite the availability of diagnostic criteria for
vestibular migraine, uncertainty remains regarding
neurologic localization, underlying pathophysiol-
ogy, functional balance implications, and manage-
ment. In addition, although diagnostic criteria for
vestibular migraine have been formulated, vestibu-
lar migraine can have various clinical presentations,
both between patients and for individual patients
over time. Variability exists in terms of the character
of dizziness, for example, the presence or absence
of vertigo or imbalance, the presence or absence
of clearly defined attacks, the duration of attacks,
and the temporal association between headache or
other migrainous features and vestibular symptoms.
Symptoms of vestibular migraine often overlap with
symptoms from other causes of dizziness, espe-
cially Ménière’s disease and benign paroxysmal po-
sitional vertigo (BPPV). In fact, some patients with
vestibular migraine have symptoms indistinguish-
able from those of Ménière’s disease, which leads
to diagnostic uncertainty. Vestibular migraine is es-
sentially a diagnosis of exclusion in that there are
no pathognomonic findings on physical examina-
tion or laboratory assessment. The diagnostic cri-
teria for vestibular migraine, shown in Table 1, are
essentially based only on history, although meeting
criterion D—the absence of another diagnosis—is
generally based on the absence of physical examina-
tion or laboratory abnormalities that would suggest
an alternative diagnosis.
As vestibular migraine has only recently been
firmly established as a diagnostic entity, and before
2012 a variety of terms were used to describe what
is probably the same condition, the material in this
review regarding vestibular migraine will be drawn
from articles that may or may not have used the
term “vestibular migraine;” some cited articles used
alternate terms that were previously in favor at var-
ious institutions to describe what is now considered
vestibular migraine.
Regarding demographics and epidemiology, the
female-to-male predominance of vestibular mi-
graine is about 5:1, with a mean age of onset of
37.7 years for women and 42.4 years for men.19
Migraine headache typically predates the onset of
vestibular migraine.18 Neuhauser et al.6 have re-
ported a lifetime prevalence of vestibular migraine
in the German population of approximately 1%.
Thus, relative to other neurotologic disorders, such
as Ménière’s disease, whose incidence is between 7.5
and 160 per 100,000 persons;20 vestibular neuritis,

2 Ann. N.Y. Acad. Sci. xxxx (2015) 1–7 

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Furman & Balaban Vestibular migraine

Table 2. New diagnostic interview for determination of vestibular migraine

1. Does the patient have a lifetime diagnosis of migraine according to IHS criteria?
NO (STOP) YES (proceed to the next question)
2. Have one or more of the following symptoms been experienced with at least five episodes (not necessarily
related to a headache episode) lasting from 5 min to 72 h?
 Spontaneous vertigo
◦ objects in the room seem to spin or turn around the patient
◦ feeling like spinning or turning when stationary
 Positional vertigo
 Head motion–induced vertigo
 Head motion–induced dizziness with nausea
 Visually induced vertigo
 No (STOP)
3. Has one or more of the following symptoms occurred with at least half of the episodes of dizziness?
 Headache with at least two of the following characteristics: one-sided location, pulsating quality, moderate
or severe pain intensity, or aggravation by routine physical activity
 Markedly increased sensitivity to both normal room lighting and normal sounds (the person should
report a need to turn down or turn off lights or close curtains or blinds and a need to turn down or turn
off radio or television, or a need to retreat to a dark, quiet room)
 Visual aura (e.g., visual scotoma or visual hallucination)
 No (STOP)
4. To what degree do the balance symptoms just discussed affect the patient? That is, if not experiencing any
headaches, how much would he/she still be affected by the balance symptoms?
 Vestibular symptoms usually interfere with daily activities (rate as moderate)
 Vestibular symptoms usually prohibit daily activities (rate as severe)
 Vestibular symptoms do not usually interfere with or prohibit daily activities (STOP)
 If symptoms are either moderate or severe, diagnose patient with vestibular migraine. Proceed to the next
question.
5. Is hearing loss or ringing in the ears temporally related to the balance problem?
 YES: A detailed evaluation may be required to determine whether the patient has a nonmigrainous
comorbid otologic disorder.
Note: “STOP” during the interview means that the patient does not have typical vestibular migraine symptoms and
may require additional evaluations for the etiology of vertigo.

whose incidence is 3.5 per 100,000 persons;21 and
BPPV, whose incidence ranges between 0.01% and
0.1% per 100,000,22,23 vestibular migraine is very
common.
The clinical manifestations of vestibular migraine
typically include dizziness, vertigo, imbalance, and
spatial disorientation. Many other symptoms can be
seen, including lightheadedness, a swimming sen-
sation, heavy headedness, a rising sensation, a tin-
gling sensation, a rocking sensation, and excessive
motion-sickness susceptibility. A diagnostic ques-
tionnaire based on the Barany Society criteria1 is
shown in Table 2. The duration of vestibular mi-
graine attacks is highly variable and can range from
seconds to minutes to hours to days (Table 3).
Moreover, some patients complain of nearly con-
stant dizziness with episodic exacerbations. Vestibu-
lar migraine often remits only to return several years
later. In women of childbearing age, there is of-
ten an association with the menstrual cycle. Note
that the currently accepted diagnostic criteria for
vestibular migraine require that half of vestibular
episodes must have associated migrainous features.
Thus, most patients report that some of their at-
tacks of dizziness are not temporally associated with
headache or other migrainous symptoms. Also, the
temporal relationship between dizziness and mi-
grainous symptoms, when present, can vary be-
tween attacks. Some patients never have headache
during attacks of vertigo.24

Ann. N.Y. Acad. Sci. xxxx (2015) 1–7 

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Vestibular migraine
Table 3. Meta-analysis of duration of episodes of vestibular migraine56
Reference Number of Percentage
patients lasting for
seconds
10 84 7.1 (s)
26 100 13 (s)
57 89 20 (1 s to 5 min)
18 90 (rotational 7.8 (s)
vertigo)
19 33 18 (1 s to 5 min)
Total 396 12.6
As noted previously, physical examination and
laboratory testing are often normal between attacks
in vestibular migraine. Neugebauer et al.25 reported
subtle saccadic pursuit in nearly two-thirds of
patients with vestibular migraine between attacks.
Some patients can manifest a persistent positional
nystagmus.26 Others can demonstrate a directional
preponderance on rotational testing.26 Patients with
vestibular migraine have also been found to have
an increased vestibular ocular reflex (VOR) time
constant.27 During attacks, vestibular migraine pa-
tients can present with nystagmus consistent with a
peripheral vestibular abnormality, a central vestibu-
lar abnormality, or a mixture of both central and
peripheral features.28 Although many patients with
vestibular migraine have normal vestibular labora-
tory test results, there are numerous studies that re-
port vestibular laboratory abnormalities in patients
with vestibular migraine.10,18,26 Although there is
no pathognomonic pattern of vestibular laboratory
abnormalities for vestibular migraine, the various
abnormalities that have been reported are of interest
regarding the pathophysiology of the condition.
Unilateral reduction of peripheral vestibular func-
tion occurs in about 25% of patients and vestibulo-
ocular asymmetry has been reported in about
half of patients.29 Recent literature has described
results from vestibular-evoked myogenic potential
(VEMP) testing in patients with vestibular migraine.
Cervical VEMPs, which assess saccular function,
appear to be reduced in patients with vestibular
migraine;30 ocular VEMPs, which presumably assess
utricular function, appear to be normal overall in
patients with vestibular migraine. Thus, peripheral
vestibular abnormalities may involve semicircular
4 Ann. N.Y. Acad. Sci. xxxx (2015) 1–7 
Furman & Balaban
Percentage lasting Percentage lasting Percentage lasting
for minutes for hours for days
31 (1–120 min) 13.1 (2–24 h) 48.8 (>24 h)
38 (min) 43 (h) 25 (>24 h)
13 (5–60 min) 26 (1–24 h) 21 (>24 h)
25.6 (< 5– 30 (1–24 h) 14.4 (>24 h)
60 min)
33 (5–60 min) 21 (1–24 h) 27 (>24 h)
20.2 28 25.8
canal or otolithic function. An interesting line of
research by Lewis et al.31 suggests abnormal vestibu-
lar perceptions in vestibular migraine. Patients
with vestibular migraine have an abnormally high
sensitivity to low-frequency dynamic roll tilting,31
a stimulus that activates both semicircular canal
and otolith organs. Thus, patients with vestibular
migraine may have peripheral or central vestibular
dysfunction between episodes18,29 and, based on
eye-movement recording during acute episodes,
appear to have central, peripheral, or mixed dys-
function during attacks.28 Although vestibular lab-
oratory testing in patients with vestibular migraine
does not at this time influence treatment decisions,
in the future, treatment decisions may benefit from
the results of vestibular laboratory testing.
The genetics of vestibular migraine are heteroge-
neous, uncertain, and complicated.32 Several studies
have sought to evaluate the underlying genetic ab-
normalities in vestibular migraine. Lee et al.33 found
linkage with a region on 11q, and that group also
found an SNP within the PGR-associated region
with vestibular migraine.34 Lee et al.35 found that
familial vestibular migraine may be linked to 22q12.
Bahmad et al.36 reported linkage to 5q35.
A link between Ménière’s disease and vestibular
migraine has been studied by numerous investiga-
tors. Clinically, the diagnosis of both of these dis-
orders primarily relies on history. Unfortunately,
there is much overlap with regard to symptoma-
tology for these two conditions, thus creating di-
agnostic uncertainty.37 Occasionally, patients meet
criteria for both disorders. More frequently, pa-
tients with vestibular migraine have features sugges-
tive, but not diagnostic, of Ménière’s disease, and
C 2015 New York Academy of Sciences.
Furman & Balaban Vestibular migraine

Figure 1. Theoretical pathways in vestibular migraine. Pathways related to sensorimotor performance, interoceptive, and
cognitive-behavioral domains within migraine circuits are shown diagrammatically. The boxes that represent brain stem sensorimo-
tor structures include parallels in peripheral neurochemical organization between vestibular pathways and migraine mechanisms.55

patients with Ménière’s disease have features sug-
gestive, but not diagnostic, of vestibular migraine.
This overlap in presentation presents a diagnostic
challenge. Neff et al.38 studied 147 patients with
vestibular migraine, Ménière’s disease, or both dis-
orders. The lattermost group amounted to about
25% of their sample. Thirty-eight percent of pa-
tients with vestibular migraine had ear complaints
and 49% of patients with Ménière’s had headache.
There is general agreement that vestibular migraine
and Ménière’s disease have some pathophysiological
commonalities. Patients with Ménière’s disease are
twice as likely to have migraine38 and patients with
migraine are more likely to have an earlier onset of
Ménière’s disease.39 Moreover, family history is of-
ten positive for both disorders.40 Cha et al.40 suggest
that an inherited syndrome exists that has a variable
expression of migraine and Ménière’s features.
Another disorder often comorbid with vestibu-
lar migraine is that of anxiety. The conjunction
of migraine, vestibular symptoms, and anxiety
has been termed migraine–anxiety–related dizziness
(MARD).41 Recognizing this condition may have
important treatment implications because such pa-
tients often benefit from treatment for an anxiety
disorder as well as a migrainous disorder in addi-
tion to a balance disorder.
The treatment of vestibular migraine has not
been studied systematically. Rather, retrospective
and anecdotal reports provide most of the infor-
mation regarding treatment. In a recent article,
Strupp et al.42 reviewed pharmacotherapy options
for vestibular migraine and noted that preventative
agents may include ␤-blockers, valproic acid, top-
iramate, tricyclic antidepressants, and lamotrigine.
Other preventative medications for consideration
include zolmitriptan, magnesium oxide, flunar-
izine, butterbur root, and lifestyle changes such as
limiting the intake of foods thought to exacerbate
migraine.43 Selective serotonin reuptake inhibitors,
calcium channel blockers, and acetazolamide
also have been discussed as possible treatments
for vestibular migraine.44,45 Vestibular migraine
is a well-recognized condition in children and
adolescents and is often managed successfully with
migraine prophylactic medication.46 For patients
with interictal symptoms, especially complaints
of imbalance, vestibular rehabilitation therapy
should be considered.47 Acute attacks of vestibular
migraine may respond to antimigrainous treatment
such as triptans.48,49
The pathophysiology of vestibular migraine is
unknown, though several theories have been sug-
gested. The concept of brain stem ischemia, which
was popular several decades ago, as evidenced by the
terms, “vascular headache”7,50 and “basilar artery
migraine,”51 has largely been supplanted by neu-
rochemical theories that may or may not include
a vascular component.52 Cutrer and Baloh pro-
posed that cortical spreading depression may ex-
plain the shorter attacks of vertigo. They also pro-
posed that migraine may lead to damage of the
inner ear secondary to release of neuropeptides
such as calcitonin gene–related peptide. Ishiyama
et al.53 also suggested that vestibular migraine may
cause peripheral vestibular dysfunction. The most

Ann. N.Y. Acad. Sci. xxxx (2015) 1–7 

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Vestibular migraine
current pathophysiologic model of vestibular mi-
graine is summarized in Figure 1. This model is
based upon the overlap in CNS pathways responsible
for pain, equilibrium, and a sense of well-being. This
combined circuitry includes a cognitive–behavioral
component, a sensorineural component, and an in-
teroceptive component. Important modulators of
these circuits include the locus coeruleus and the
dorsal raphe nuclei, their influence mediated largely
by norepinephrine and serotonin, respectively. Con-
sistent with this model of vestibular migraine is a
recent report by Shin et al.54 that showed increased
metabolism in the vestibular cortex and the thalami
during attacks of vestibular migraine.
Future directions in the field of vestibular mi-
graine should include both clinical and basic sci-
ence efforts to understand the pathophysiology of
this condition. Recent articles that probe the overlap
between migraine and central pain mechanisms55
and studies of vestibular psychophysics in vestibu-
lar migraine31 represent important lines of inves-
tigation. Desperately needed are controlled treat-
ment trials for vestibular migraine. The availability
of accepted diagnostic criteria is likely to facilitate
research regarding vestibular migraine.
Conflict of interest
The authors declare no conflicts of interest.
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