1. health and fitness
2. disease
3. headaches and migraines

BASIC AND CLINICAL ASPECTS OF VERTIGO AND DIZZINESS
Vertigo as a Symptom of Migraine
Thomas Lempert,a Hannelore Neuhauser,b
and Robert B. Daroff c
a
b
Department of Neurology, Schlosspark-Klinik, Berlin, Germany; and Vestibular
Research Group, Charit´e, Berlin, Germany
Robert Koch Institut, Department of Epidemiology, Berlin, Germany; and Vestibular
Research Group, Charit´e, Berlin, Germany
c
Department of Neurology, Case Western Reserve University School of Medicine,
Cleveland, Ohio 44106, USA
Migraine and vertigo are common disorders, affecting about 14% and 10%, respectively,
of the general population. If migraine and vertigo were unrelated, the expected comorbidity would be 1%, whereas recent epidemiological studies indicate that 3.2% of the
population have both migraine and vertigo. The excess comorbidity may be attributed
to two factors: 1) vertigo syndromes (including Meni`ere’s disease, benign paroxysmal
positional vertigo, and anxiety-related dizziness) that are more common in migraineurs
than in controls and 2) vestibular migraine (VM) (vertigo as a symptom of migraine.)
VM presents with attacks of spontaneous or positional vertigo lasting seconds to days.
Headaches are often absent during acute attacks, but other migrainous features such as
photophobia or auras, may be present. Like migraine headaches, VM triggers include
stress, sleep deprivation, and hormonal changes. During acute attacks, there may be
central spontaneous or positional nystagmus and, less commonly, unilateral vestibular hypofunction. In the symptom-free interval, vestibular testing shows mostly minor
and nonspecific findings. The pathogenesis of VM is uncertain, but migraine mechanisms may interfere with the vestibular system at the labyrinth, brainstem, and cerebral
cortex. Treatment includes vestibular suppressants for acute attacks and migraine prophylaxis for patients with frequent recurrences. However, treatment efficacy has not
been validated by properly controlled clinical trials. VM does not fit into the 2004 International Headache Society Classification, in which “basilar-type migraine” must have
at least two posterior circulation manifestations; isolated vertigo would not satisfy this
criterion.
Key words: migraine; vestibular; vertigo; dizziness
Introduction
That migraine may commonly cause vertigo is recently achieving greater acceptance.1
A wider recognition of vestibular migraine began with Kayan and Hood’s 1984 paper,2 and
the clinical features have since been delineated
in several case series.3–8 Unfortunately, the terminology has not been uniform, with various
terms (migraine-associated vertigo, migrainerelated vestibulopathy, migrainous vertigo, and
basilar migraine) applied to roughly the same
patient population. We prefer “vestibular migraine” (VM), a term that avoids confusion with
nonvestibular dizziness or motion sickness associated with migraine.9
Epidemiological Links between
Migraine and Vertigo
Address for correspondence: Prof. Thomas Lempert, Neurologische Abteilung, Schlosspark-Klinik, Heubnerweg 2, 14059 Berlin,
Germany. Voice: +0049 30 3264 1152; fax: +049 30 3264 1150.
thomas.lempert@schlosspark-klinik.de
Epidemiological observations indicate a
greater than chance association of migraine
Basic and Clinical Aspects of Vertigo and Dizziness: Ann. N.Y. Acad. Sci. 1164: 242–251 (2009).
C 2009 New York Academy of Sciences.
doi: 10.1111/j.1749-6632.2009.03852.x 242
Lempert et al.: Vertigo as a Symptom of Migraine
243
with vertigo and dizziness. The frequency of
migraine is increased in patients with dizziness and, particularly, those with unclassifiable vertigo.10 Conversely, significantly more
patients with migraine also have vertigo compared with patients with tension headaches2
and headache-free controls.11,12 In the general
population, migraine headaches and vestibular vertigo concur about three times more frequently than would be expected by chance. The
lifetime prevalence of migraine is 14%13 and of
vestibular vertigo is 7%;14 chance concurrence
of the two would be 1%, but a large population
study showed it to be 3.2%.15
Clinicians must attempt to determine
whether individual patients have VM (i.e.,
vestibular vertigo caused by migraine), dizziness/vertigo of an unrelated cause (by chance
occurring in a migraineur), or one of several vestibular and nonvestibular dizziness
syndromes with increased prevalence in migraineurs. The latter group includes Meni`ere’s
disease, benign paroxysmal positional vertigo,
motion sickness, and orthostatic hypotension.
We will now describe the core syndrome of
VM, followed by a discussion of other dizziness syndromes that are statistically associated
with migraine.
TABLE 1. Diagnostic Criteria for Vestibular Migraine7
Diagnostic Criteria
for Vestibular Migraine
The current International Classification of
Headache Disorders (ICHD) of the International Headache Society (IHS) does not include
vertigo as a migrainous symptom in adults,
except in the framework of basilar-type migraine.16 Although more than 60% of basilartype migraine patients have vertigo,17 for a
diagnosis of basilar-type migraine, the ICHD
requires at least two posterior circulation manifestations lasting between 5 and 60 min, followed by a migraine headache. Less than 10%
of patients with VM fulfill these criteria.4–7 Indeed, isolated vertigo is not recognized as a migraine aura in the ICHD, meaning that most
Definite vestibular migraine
A. Episodic vestibular symptoms of at least
moderate severity
B. Current or previous history of migraine
according to the 2004 criteria of the
International Headache Society
C. One of the following migrainous symptoms
during ≥ 2 attacks of vertigo: migrainous
headache, photophobia, phonophobia, visual
or other auras
D. Other causes ruled out by appropriate
investigations
Comment:
Vestibular symptoms are rotational vertigo or
another illusory self or object motion. They
may be spontaneous or positional. Vestibular
symptoms are “moderate” if they interfere
with but do not prohibit daily activities and
“severe” if patients cannot continue daily
activities.
Probable vestibular migraine
A. Episodic vestibular symptoms of at least
moderate severity
B. One of the following:
(a) Current or previous history of migraine
according to the 2004 criteria of the IHS
(b) Migrainous symptoms during vestibular
symptoms
(c) Migraine-precipitants of vertigo in more than
50% of attacks: food triggers, sleep
irregularities, hormonal change
(d) Response to migraine medications in more
than 50% of attacks
C. Other causes ruled out by appropriate
investigations
adult patients with VM cannot be classified
with the current criteria.
Like migraine itself (except for rare forms
such as familial hemiplegic migraine), VM is
not diagnosable by specific biological markers.
A preliminary classification, using operational
clinical criteria modeled on the ICHD,7 proposed two separate diagnostic categories7 : definite, and the more sensitive but less specific,
probable vestibular migraine (Table 1). In accordance with most published reports, the proposed criteria conceptualize VM as an episodic
244
Annals of the New York Academy of Sciences
vestibular disorder. Although several reports included patients with nonspecific dizziness3–5 or
with permanent symptoms, for the sake of simplicity, the core syndrome was defined first,
with exceptions and variations planned to be
included at later date. Furman and colleagues
developed a diagnostic interview applying these
criteria.18
Prevalence and Demographic
Aspects of Vestibular Migraine
According to the above diagnostic criteria,
the frequency of definite VM was 7% in a group
of 200 consecutive dizziness clinic patients, and
9% in a group of 200 migraine patients.7 Using the criteria, a two-stage population-based
study (N = 4869 adults) with screening interviews followed by expert telephone interviews,
estimated the lifetime prevalence of VM to be
0.98% (95% CI 0.7–1.37).15 Of note, definite
VM accounted for only a third of migraineurs
previously diagnosed with “vestibular vertigo,”
which emphasizes the necessity of a thorough
neuro-otological evaluation to exclude other
diagnoses.15
VM may occur at any age,3,4,6 with a reported female-to-male ratio between 1.5- and
5-to-1.4–7 Familial occurrence is not uncommon, probably based on an autosomal dominant pattern of inheritance with decreased penetrance in men.20 In most patients, migraine
headaches begin earlier in life than VM.6,7
Some patients were headache-free for years before VM first manifested.6 VM seems to occur more often in patients with migraine without aura than in those with aura,2,5,6 and the
headaches are often replaced by isolated vertigo
attacks in menopausal women.
Clinical Features
Since migraineurs can present with dizziness or vertigo due to multiple causes, the first
diagnostic step is distinguishing between ver-
tigo (a vestibular symptom) and nonvestibular dizziness. This distinction can usually be
made by a careful history: a sense of rotation
or other illusory sensations of motion indicate
vertigo; whereas sensations of lightheadedness,
dizziness, or impending faint imply nonvestibular dizziness. Nonspinning dizziness occurring
only during standing or walking usually indicates a cause other than VM. A residual area
of uncertainty often remains, either as a semantic problem or because mild vestibular dysfunction may present with dizziness rather than
vertigo.
Patients with VM typically report spontaneous or positional vertigo. Some experience
a sequence of spontaneous vertigo transforming into positional vertigo after several hours
or days.21,22 This positional vertigo is distinct from benign paroxysmal positional vertigo (BPPV) with regard to duration of individual attacks (often as long as the head position
is maintained in VM versus only seconds in
BPPV), duration of individual episodes (minutes to days in VM versus weeks to months
in BPPV), and nystagmus findings (heterogenous in direction and persistent in VM versus
coplanar to the affected canal and transient
in BPPV). Forty to 70% of VM patients experience positional vertigo, but not necessarily with every attack.2,20,23 Head motion intolerance, quite similar to motion sickness (i.e.,
imbalance, illusory motion, and nausea) is a
frequent additional symptom,4,11 as is visual
vertigo (i.e., vertigo provoked by moving visual scenes).4,19,24 Both attack duration and frequency can vary between patients and in individual patients. The duration of vertigo ranges
from seconds (about 10%) and minutes (30%)
to hours (30%) and several days (30%).2,3,5,6,25
Some patients require weeks to recover from an
attack. The attacks may occur days, months, or
even years apart in an irregular fashion. Only
10% to 30% of VM patients have vertigo with
the typical duration of a migraine aura—5 to
60 minutes.6,7
VM, in addition to not often conforming
to the ICHD duration criteria for an aura,
Lempert et al.: Vertigo as a Symptom of Migraine
245
TABLE 2. Clinical Features of Definite Vestibular
Migraine in 33 Patients7
most VM patients neglect to mention accompanying scintillations and photopsias because
these symptoms are not disturbing or for fear
they would be considered as “crazy.” A dizziness diary is useful for prospective recording of
these associated features.
Hearing loss and tinnitus are not prominent
symptoms of VM.2,4,5,26 The hearing loss is
usually mild, transient, and not progressive,5 although some patients do have fluctuating hearing loss, suggestive of Meni`ere’s disease, as well
as migrainous features during attacks of presumed VM.2,5,27
Migraine-specific precipitants of vertigo attacks may provide valuable diagnostic information. These include menstruation, deficient or
irregular sleep, excessive stress, specific foods
(including sharp cheese, red wine, and glutamate) and sensory stimuli such as bright or
scintillating lights, intense odors, or noise.
When migrainous accompaniments and typical precipitants are absent, VM may still be
considered diagnostically after other potential
causes have been eliminated. In such instances,
a favorable response to antimigraine drugs may
support the suspicion of an underlying migraine mechanism. However, the apparent efficacy of a drug cannot be a definite confirmation
of the diagnosis, since spontaneous improvement, placebo response, and additional drug
effects (e.g., anxiolytic or antidepressant) may
be operative.
In summary, the clinical presentation of VM
is quite variable, and its connection to migraine can be subtle. Keys to the diagnosis
are repeated concurrence of migraine symptoms and vertigo, migraine specific precipitants, and the possible response to antimigraine
drugs.
Clinical features
Vestibular symptomsa
Rotational vertigo
Other illusory self or object motion
Positional vertigo
Head motion intoleranceb
Duration of vestibular symptoms
Seconds to 5 min
5 to 60 min
1 hr to 1 day
>1 day
Migrainous symptoms during vertigo
Migrainous headache
Always
Sometimes
No headache
Photophobia
Phonophobia
Visual or other auras
%
70
18
42
48
18
33
21
28
94
46
48
6
70
64
36
a
Several patients had more than one type of vestibular
symptoms.
b
None of the patients had only head-motion
intolerance.
also differs in its relationship to the migraine
headaches. Vertigo may precede headache,
as would be typical for an aura, may begin
with the headache, or may appear late in the
headache phase. Many patients experience attacks both with, and without, headache.3,5,7
Quite frequently, patients have an attenuated
headache with their vertigo as compared to
their usual migraine.5 In some, vertigo and
headache never occur together;3,5,7 here the
diagnosis must be based on migrainous symptoms during the attack, rather than a headache.
These symptoms include photophobia, phonophobia, osmophobia, and visual or other auras.
Such accompaniments are of diagnostic importance, since they may represent the only apparent connection between vertigo and migraine
(Table 2). Patients must be asked specifically
about these migrainous symptoms, as they often fail to mention them. The renowned migraine authority, Neil Raskin (personal communication to Robert Daroff), commented that
Neuro-otologic Findings
In most VM patients, the general neurological and otologic examinations are normal in the symptom-free period,3 but about
20% have unilateral hypo-excitability to caloric
246
stimulation, and about 10% have directional
preponderance of caloric-induced nystagmus.3,6,28 These findings are not specific for
VM and may also occur in other vestibular syndromes, and even in migraine patients without vestibular symptoms.29,30 Neuroophthalmological evaluation may reveal mild
ocular motor abnormalities in the absence of
other brainstem or cerebellar signs.6 Vitkovic
and coworkers found that patients with definite VM became nauseated after caloric testing
four times more often than patients with other
vestibular disorders.31 Von Brevern and colleagues,32 studying 20 patients during the acute
phase of VM, noted that 19 had imbalance with
increased sway on tandem Romberg or tandem walking, or both. Fourteen had pathological nystagmus: three had spontaneous peripheral nystagmus, another three had spontaneous
central nystagmus, five had central positional
nystagmus, and three had both central spontaneous and positional nystagmus. Unlike BPPV,
VM positional nystagmus always persisted as
long as the provoking position was maintained,
and usually did not beat in the plane of positioning. A unilateral deficit of the horizontal
vestibulo-ocular reflex was present in the three
patients with peripheral spontaneous nystagmus, one of whom did not recover peripheral
function when asymptomatic. These authors
concluded that during acute VM episodes, 10
patients (50%) had central vestibular dysfunction, three (15%) peripheral vestibular dysfunction, and seven (35%) could not be classified.32
In clinical practice, history will usually provide more diagnostic clues than vestibular testing, as there are no specific abnormalities for
VM. In patients with clear-cut histories, no additional vestibular tests are required, but testing in symptom-free intervals can reassure patients and physicians as to the absence of an
alternative diagnosis. This is particularly relevant in patients whose studies during, or shortly
after, an attack demonstrated distinct peripheral or central abnormalities, which would
be expected to have improved within a few
weeks.
Annals of the New York Academy of Sciences
Pathophysiology
The pathophysiological mechanisms of VM
are uncertain, but investigators have proffered
several hypotheses.18 Cortical spreading depression, the presumed mechanism of migraine
auras, may be operative in patients with short
attacks.3 Spreading depression could produce
vestibular symptoms by involving the multisensory cortical areas that process vestibular signals, which are mainly located in the
posterior insula and at the temporo-parietal
junctions. However, canal paresis and complex positional nystagmus during the acute
stage of VM cannot be explained by cortical
dysfunction.32
Transmitters, putatively involved in migraine (calcitonin-gene-related peptide, serotonin, norepinephrine, and dopamine), modulate the activities of central and peripheral
vestibular neurons and could contribute to the
pathogenesis of VM.3–5,33 Unilateral release
of these substances—analogous to the usual
unilateral location of migraine headaches—
could cause a static vestibular imbalance leading to rotational vertigo, whereas bilateral release would cause a state of altered vestibular
excitability leading to a motion sickness–type
of dizziness.
Genetic defects of ion channels cause various paroxysmal neurological disorders. The
abnormal voltage-gated calcium-channel gene
CACNA1A in familial hemiplegic migraine
(FHM) and episodic ataxia type 2 (EA-2)34 —
both of which may have vertigo and migraine headache as prominent symptoms—has
prompted the search for a susceptibility gene
for VM in the same region, but no such genetic
defect could be identified.35,36
The only hypothesis that is based on an
experimental model of VM relates to the reciprocal connections between the trigeminal
and vestibular nuclei. Trigeminal activation
by painful electrical stimulation of the forehead produces spontaneous nystagmus in migraine patients but not in controls, indicating
that migraineurs have a lowered threshold for
Lempert et al.: Vertigo as a Symptom of Migraine
247
crosstalk between these neighboring brainstem
structures.37
to 70%) in patients with migraine than in
headache-free controls or patients with tensiontype headaches (20% to 40%).2,11,24 The association is more pronounced in children45 and
in migraine with aura.11 Migraineurs also have
more “visual vertigo” induced by optokinetic
stimuli,11,24 which can be conceptualized as a
decreased threshold for visual–vestibular interaction. In addition, headache, scalp tenderness,
and photophobia can be more easily provoked
by optokinetic stimulation in migraine patients
than in controls.46
Differentiating between episodic motion
sickness and attacks of VM induced by motion stimuli may be difficult, but the distinction
can be made based on the type and duration
of symptoms. Nausea and dizziness improving
after cessation of the motion stimulus suggests
motion sickness, whereas the persistence of rotational or positional vertigo suggests VM triggered by passive motion. Chronic VM19 may
be explained by a constantly lowered threshold
to motion stimuli. Of note is that motion sickness could be prevented by rizatriptan in VM,
but not in patients with migraine alone.47
Treatment
When attacks of VM are severe and frequent, acute or prophylactic treatment is warranted but, apart from one small and inconclusive study on the use of zolmitriptan for acute
VM,38 current treatment recommendations are
based on expert opinion rather than randomized placebo-controlled trials.
A few case reports suggest that medication used for migraine prophylaxis may
be effective. These include propranolol,39
metoprolol,6 tricyclic antidepressants,8 pizotifen,8,19 and flunarizine.6 The carbonic anhydrase inhibitors, acetazolamide40 and dichlorphenamid,41 which are not ordinarily used for
migraine prophylaxis, have also been used successfully, but these studies were not randomized
or controlled.
Treatment of acute VM with acute migraine
medication can be attempted with triptans42,38
and vestibular suppressants such as promethazine, dimenhydrinate, and meclizine.42 A retrospective study found that the effect of triptans on vertigo correlated with its effect on
headache.43 Nonpharmaceutical approaches
may be more efficacious than drugs in individual patients. A thorough explanation of the
migrainous origin of the attacks may relieve
unnecessary fears, and avoidance of identified
triggers and vestibular rehabilitation may also
be helpful.44
Migraine, Motion Sickness, and
Sensitivity to Visual Motion
Discomfort thresholds to sensory stimulation are decreased in migraineurs, both during attacks and in the intervals. Examples include sensitivity to light, sound, and smells.
The vestibular system is no exception. Motion sickness occurs more frequently (30%
Cerebellar Dysfunction
Cerebellar dysfunction causes imbalance
that patients may describe as “dizziness.” Some
families with FHM develop progressive cerebellar ataxia and nystagmus.48 Mutations in the
CACNA1A gene coding for the α 1A subunit
of a neuronal Ca2+ channel, which is heavily
expressed in the cerebellum, occurs in FHM
as well as in EA-249 and spinocerebellar ataxia
type 6.50 EA-2 is characterized by short bouts
of cerebellar ataxia, often with vertigo, interictal nystagmus, and, in approximately 50%, migraine.51 Both FHM and EA-2 have the typical
symptoms of basilar-type migraine.52,51 Cerebellar signs are usually not present in the common types of migraine, but some investigators
found subclinical hypermetria and other subtle cerebellar signs in patients with migraine,
with or without aura.53,30 May and colleagues
248
Annals of the New York Academy of Sciences
suggested dysfunctional Ca2+ channels as a
possible cause, based an involvement of the
CACNA1A gene region in some families with
nonhemiplegic migraine aura.54 Another link
between migraine and cerebellar dysfunction
is the recent observation that migraineurs, particularly when they have migraine with aura,
have a high frequency of subclinical cerebellar
infarctions.55
Meniere’s
Disease
`
An increased frequency of migraine in patients with Meni`ere’s disease (MD) is well documented.56,27 Migraine was twice as high in a
group of 78 patients with unilateral or bilateral MD (based on the American Academy of
Otolaryngology criteria57 ), than in an age- and
sex-matched control group (56% versus 25%,
P < 0.001).27 Migraine leads to a greater susceptibility of developing MD, as suggested by
a study in which MD patients had an earlier
onset of symptoms and a greater susceptibility to bilateral hearing loss when they also had
migraine.58 Vestibular function tests only modestly assist in differentiating between VM and
MD,59 but the distinction can usually be made
based on hearing loss being only occasional,
mild, and nonprogressive in VM,5 while it is
a regular aggressive accompaniment of MD.
Nevertheless, in some patients, the distinction
is not possible.27 A possible explanation might
be that MD and VM are different manifestations of a shared genetic susceptibility that leads
to a spectrum of migrainous, vertiginous, and
cochlear symptoms.60
Benign Paroxysmal Positional
Vertigo
BPPV is the most common cause of recurrent
vestibular symptoms presenting to a dizziness
clinic, both in unselected patients6 and in migraineurs.7 Although BPPV and migraine are
separate entities, there is evidence of a linkage.
Migraine is three times more common in patients with idiopathic BPPV than in those with
BPPV secondary to trauma or surgical procedures,61 and is also twice as common in patients with idiopathic BPPV than in age- and
sex-matched controls.62
Psychiatric Causes of Dizziness
The interrelations of migraine, dizziness,
and certain psychiatric disorders are complex.
There are bidirectional associations of migraine with both major depression and panic
disorder, with migraine being a risk factor for
first-onset major depression and panic disorder,
and vice versa.63,64 After palpitations, dizziness
is the second most common symptom of panic
attacks65 and can also be a symptom of major depression. Patients with panic and anxiety
have an increased rate of vestibular test abnormalities,66 which may reflect an elevated risk
of patients with vestibular disorders developing
an anxiety disorder.67 Compared to other vertigo syndromes, VM patients show the highest
rate of concurrent anxiety or depressive disorders.68 Because of the frequent association
of dizziness, migraine, and anxiety, Furman
and colleagues proposed a new syndrome designated “migraine–anxiety related dizziness”
(MARD).69
Orthostatic Hypotension
Patients with migraine report not only more
vertigo than controls, but also significantly
more “dizzy spells,” which can usually be attributed to nonvestibular causes, (32% versus
13%).11 However, mild vestibular dysfunction
may also present with dizziness rather than vertigo. Syncope during migraine attacks occurred
in 5% of 500 unselected migraineurs.70 A large
population study found an elevated frequency
of syncope (46% versus 31%) and orthostatic
intolerance (32% versus 12%) in migraineurs
compared with controls.71 Of interest is that
Lempert et al.: Vertigo as a Symptom of Migraine
249
orthostatic hypotension can be induced by
small doses of dopamine agonists, and counteracted by dopamine antagonists, in migraineurs
but not in controls, suggesting hypersensitivity
to dopaminergic stimulation as the underlying
mechanism.72
5. Johnson, G.D. 1998. Medical management of
migraine-related dizziness and vertigo. Laryngoscope
108: 1–28.
6. Dieterich, M. & T. Brandt. 1999. Episodic vertigo
related to migraine (90 cases): vestibular migraine? J.
Neurol. 246: 883–892.
7. Neuhauser, H., M. Leopold, et al. 2001. The interrelations of migraine, vertigo, and migrainous vertigo.
Neurology 56: 436–441.
8. Reploeg, M.D. & J. A. Goebel. 2002. Migraineassociated dizziness: patient characteristics and management options. Otol. Neurotol. 23: 364–371.
9. Brandt, T. & M. Strupp. 2006. Migraine and Vertigo:
Classification, clinical features, and special treatment
considerations. Headache Currents 3: 12–19.
10. Lee, H., S.I. Sohn, et al. 2002. Migraine and isolated
recurrent vertigo of unknown cause. Neurol. Res. 24:
663–665.
11. Kuritzky, A., D.K. Ziegler, et al. 1981. Vertigo, motion sickness and migraine. Headache 21: 227–231.
12. Vukovic, V., D. Plavec, et al. 2007. Prevalence of vertigo, dizziness, and migrainous vertigo in patients
with migraine. Headache 47: 1427–1435.
13. Jensen, R. & L.J. Stovner. 2008. Epidemiology and
comorbidity of headache. Lancet Neurol. 7: 354–361.
14. Neuhauser, H.K., M. von Brevern, et al. 2005. Epidemiology of vestibular vertigo: a neurotological survey of the general population. Neurology 65: 898–
904.
15. Neuhauser, H.K., A. Radtke, et al. 2006. Migrainous vertigo. Prevalence and impact on quality of life.
Neurology 67: 1028–1033.
16. International Headache Society Classification
Subcommittee. 2004. International classification
of headache disorders. 2nd edtion. Cephalalgia
24(Suppl 1): 1–160.
17. Sturzenegger, M.H. & O. Meienberg. 1985. Basilar artery migraine: a follow-up study of 82 cases.
Headache 25: 408–415.
18. Furman, J.M. & D.A. Marcus, et al. 2003. Migrainous
vertigo: development of a pathogenetic model and
structured diagnostic interview. Curr. Opin. Neurol. 16:
5–13.
19. Waterston, J. 2004. Chronic migrainous vertigo. J.
Clin. Neurosci. 11: 384–388.
20. Oh, A.K., H. Lee, et al. 2001. Familial benign recurrent vertigo. Am. J. Med. Genet. 100: 287–291.
21. Slater, R. 1979. Benign recurrent vertigo. J. Neurol.
Neurosurg. Psychiatry 42: 363–367.
22. Moretti, G., G.C. Manzoni, et al. 1980. Benign recurrent vertigo and its connection with migraine.
Headache 20: 344–346.
23. von Brevern, M., A. Radtke, et al. 2004. Migrainous vertigo presenting as episodic positional vertigo.
Neurology 62: 469–472.
Dizziness Due to Antimigraine
Medication
Dizziness occurs as a side effect of many
drugs, some of which are used in the treatment of migraine. Therefore, it is useful to elicit
a detailed drug history and ascertain the onset of dizziness in relation to any changes in
medication, such as beta blockers and tricyclic
antidepressants.
Closing Comment
Like migraine itself, VM is usually diagnosed
by a careful history, with laboratory tests having
only minor roles. However, a history of both
migraine and vertigo is insufficient evidence
for VM, as they may represent a concurrence
by chance alone or specific vertigo syndromes
that are epidemiologically associated with
migraine.
Conflicts of Interest
The authors declare no conflicts of interest.
References
1. Stahl, J.S. & R.B. Daroff. 2001. Time for more attention to migrainous vertigo? Neurology 56: 428–429.
2. Kayan, A. & J.D. Hood. 1984. Neuro-otological
manifestations of migraine. Brain 107: 1123–1142.
3. Cutrer, F.M. & R.W. Baloh. 1992. Migraineassociated dizziness. Headache 32: 300–304.
4. Cass, S.P., J.M. Furman, et al. 1997. Migraine-related
vestibulopathy. Ann. Otol. Rhinol. Laryngol. 106: 182–
189.
250
Annals of the New York Academy of Sciences
24. Drummond, P.D. 2005. Triggers of motion sickness
in migraine sufferers. Headache 45: 653–656.
25. Versino, M., G. Sances, et al. 2003. Dizziness and
migraine: a causal relationship? Funct. Neurol. 18: 97–
101.
26. Parker, W. 1991. Migraine and the vestibular system
in adults. Am. J. Otol. 12: 25–34.
27. Radtke, A., T. Lempert, et al. 2002. Migraine and
Meniere’s disease: is there a link? Neurology 59: 1700–
1704.
28. Celebisoy, N., F. G¨okc¸ay, et al. 2008. Migrainous vertigo: clinical, oculographic and posturographic findings. Cephalalgia 28: 72–77.
29. Toglia, J.U., D. Thomas, et al. 1981. Common migraine and vestibular function. Electronystagmographic study and pathogenesis. Ann. Otol. Rhinol.
Laryngol. 90: 267–271.
30. Harno, H., T. Hirvonen, et al. 2003. Subclinical
vestibulocerebellar dysfunction in migraine with and
without aura. Neurology 61: 1748–1752.
31. Vitkovic, J., M. Paine, et al. 2008. Neuro-otological
findings in patients with migraine- and nonmigrainerelated dizziness. Audiol Neurootol. 13: 113–122.
32. von Brevern, M., D. Zeise, et al. 2005. Acute migrainous vertigo: clinical and oculographic findings. Brain
128: 365–374.
33. Babalian, A., N. Vibert, et al. 1997. Central vestibular
networks in the guinea-pig: functional characterization in the isolated whole brain in vitro. Neuroscience
81: 405–426.
34. Ophoff, R.A., G.M. Terwindt, et al. 1996. Familial hemiplegic migraine and episodic ataxia type-2
are caused by mutations in the Ca2+ channel gene
CACNL1A4. Cell 87: 543–552.
35. Kim, J.S., Q. Yue, et al. 1998. Familial migraine with
vertigo: no mutations found in CACNA1A. Am. J.
Med. Genet. 79: 148–151.
36. von Brevern, M., N. Ta, et al. 2006. Migrainous vertigo: mutation analysis of the candidate
genes CACNA1A, ATP1A2, SCN1A, and CACNB4.
Headache 46: 1136–1141.
37. Marano, E., V. Marcelli, et al. 2005. Trigeminal stimulation elicits a peripheral vestibular imbalance in
migraine patients. Headache 45: 325–331.
38. Neuhauser, H., A. Radtke, et al. 2003. Zolmitriptan
for treatment of migrainous vertigo: a pilot randomized placebo-controlled trial. Neurology 60: 882–883.
39. Harker, L.A. & C.H. Rassekh. 1987. Episodic vertigo
in basilar artery migraine. Otolaryngol. Head Neck Surg.
96: 239–250.
40. Baloh, R.W., C.A. Foster, et al. 1996. Familial migraine with vertigo and essential tremor. Neurology
46: 458–460.
41. Asprella Libonati, G. & G. Gagliardi. 2004. La
malattia di Meniere e vertigine emicranica: terapi
intercritica, terapia medica. Otoneurologia 18: 40–
42.
Baloh, R.W. 1997. Neurotology of migraine. Headache
37: 615–621.
Bikhazi, P., C. Jackson, et al. 1997. Efficacy of antimigrainous therapy in the treatment of migraineassociated dizziness. Am. J. Otol. 18: 350–354.
Whitney, S.L., D.M. Wrisley, et al. 2000. Physical therapy for migraine-related vestibulopathy and
vestibular dysfunction with history of migraine. Laryngoscope 110: 1528–1534.
Barabas, G., W.S. Matthews, et al. 1983. Childhood
migraine and motion sickness. Pediatrics 72: 188–190.
Drummond, P.D. 2002. Motion sickness and migraine: optokinetic stimulation increases scalp tenderness, pain sensitivity in the fingers and photophobia. Cephalalgia 22: 117–124.
Marcus, D.A. & J.M. Furman. 2006. Prevention
of motion sickness with rizatriptan: a double-blind,
placebo-controlled pilot study. Med. Sci. Monit. 12:
1–7.
Ophoff, R.A., R. van Eijk, et al. 1994. Genetic heterogeneity of familial hemiplegic migraine. Genomics
22: 21–26.
Denier, C., A. Ducros, et al. 1999. High prevalence
of CACNA1A truncations and broader clinical spectrum in episodic ataxia type 2. Neurology 52: 1816–
1821.
Zhuchenko, O., J. Bailey, et al. 1997. Autosomal dominant cerebellar ataxia (SCA6) associated with small
polyglutamine expansions in the alpha 1A-voltagedependent calcium channel. Nat. Genet. 15: 62–69.
Baloh, R.W., Q. Yue, et al. 1997. Familial episodic
ataxia: clinical heterogeneity in four families linked
to chromosome 19p. Ann. Neurol. 41: 8–16.
Haan, J., G.M. Terwindt, et al. 1995. Is familial
hemiplegic migraine a hereditary form of basilar migraine? Cephalalgia 15: 477–481.
Sandor, P.S., A. Mascia, et al. 2001. Subclinical cerebellar impairment in the common types of migraine:
a three-dimensional analysis of reaching movements.
Ann. Neurol. 49: 668–672.
May, A., R.A. Ophoff, et al. 1995. Familial hemiplegic migraine locus on 19p13 is involved in the
common forms of migraine with and without aura.
Hum. Genet. 96: 604–608.
Kruit, M.C., L.J. Launer, et al. 2005. MRI Infarcts
in the posterior circulation territory in migraine. The
population-based CAMERA study. Brain 128: 2068–
2077.
Rassekh, C.H. & L.A. Harker. 1992. The prevalence
of migraine in Meniere’s disease. Laryngoscope 102:
135–138.
American Academy of Otolaryngology. 1995. Committee on Hearing and Equilibrium guidelines for
42.
43.
44.
45.
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
Lempert et al.: Vertigo as a Symptom of Migraine
251
the diagnosis and evaluation of therapy in Meni`ere’s
disease. Otolaryngol. Head Neck Surg. 113: 181–185.
Cha, Y.H., J. Brodsky, et al. 2007. The relevance of
migraine in patients with M´eni`ere’s disease. Acta OtoLaryngologica 127: 1241–1245.
Shepard, N.T. 2006. Differentiation of M´eni`ere’s disease and migraine-associated dizziness: a review. J.
Am. Acad. Audiol. 17: 69–80.
Cha, Y.H., M. Kane, et al. 2008. Familial clustering
of migraine, episodic vertigo, and M´eni`ere’s disease.
Otol. Neurotol. 29: 93–96.
Ishiyama, A., K.M. Jacobson, et al. 2000. Migraine
and benign positional vertigo. Ann. Otol. Rhinol. Laryngol. 109: 377–380.
Lempert, T., M. Leopold, et al. 2000. Migraine and
benign positional vertigo. Ann. Otol. Rhinol. Laryngol.
109: 1176.
Breslau, N., L.R. Schultz, et al. 2000. Headache and
major depression: is the association specific to migraine? Neurology 54: 308–313.
Breslau, N., L.R. Schultz, et al. 2001. Headache types
and panic disorder: directionality and specificity. Neurology 56: 350–354.
Margraf, J., B. Taylor, et al. 1987. Panic attacks in
the natural environment. J. Nerv. Ment. Dis. 175: 558–
565.
Jacob, R.G., J.M. Furman, et al. 1996. Panic, agoraphobia, and vestibular dysfunction. Am. J. Psychiatry
153: 503–512.
Eagger, S., L.M. Luxon, et al. 1992. Psychiatric morbidity in patients with peripheral vestibular disorder:
a clinical and neuro-otological study. J. Neurol. Neurosurg. Psychiatry 55: 383–387.
Eckhardt-Henn, A., C. Best, et al. 2008. Psychiatric
comorbidity in different organic vertigo syndromes.
J. Neurol. 255: 420–428.
Furman, J.M., C.D. Balaban, et al. 2005. Migraineanxiety related dizziness (MARD): a new disorder? J.
Neurol. Neurosurg. Psychiatry 76: 1–8.
Lance, J.W. & M. Anthony. 1966. Some clinical aspects of migraine. A prospective survey of 500 patients. Arch. Neurol. 15: 356–361.
Thijs, R.D., M.C. Kruit, et al. 2006. Syncope in
migraine: the population-based CAMERA study.
Neurology 66: 1034–1037.
Bes, A., P. Dupui, et al. 1986. Pharmacological exploration of dopamine hypersensitivity in migraine
patients. Int. J. Clin. Pharmacol. Res. 6: 189–192.
58.
59.
60.
61.
62.
63.
64.
65.
66.
67.
68.
69.
70.
71.
72.