Vertigo and migraine: A more than
! International Headache Society 2010
Reprints and permissions:
Andreas Straube1and Steven D Rauch2
Migraine headache is one of the most common symp-
toms in general practice with a 12-month prevalence of
around 10–12% in Western populations (1). Vertigo is
no less often the reason for clinical consultations. In
Germany, about 3.4% of all out-patient consultations
are due to the symptom vertigo/dizziness: the 12-month
prevalence for all types of vertigo is about 23% and for
rotational vertigo about 5% (2). Therefore, a concur-
rence of the two conditions by chance can be expected
in about 1.1%. However, in contrast to this, clinical case
series as well as recent population-based studies showed
a much higher co-occurrence of about 3.2% (3–7). At
this point, all available evidence points to a related
co-morbidity of migraine and some forms of vertigo.
However, in recent years, it has also become clear that
this association between migraine and vertigo is not due
to a single clinical entity but that several clinical vertigo
syndromes are more often seen in migraine patients (8).
It is still unclear what the underlying pathophysio-
logical mechanism is and whether one mechanism or
several mechanisms are involved. Furthermore, how
can the headache specialist differentiate between
migrainous vertigo and migraine-associated vertigo?
The importance of this point is shown by the study
by Bisdorff and colleagues (9), which shows that dizzi-
ness as a symptom during the headache attacks is
reported in 51% of the headache episodes. But this
finding does not differentiate between dizziness due to
the migraine attack per se or due to a co-morbid disor-
der (e.g. Me ´ nie ` re’s disease) which triggers a migraine
attack, as was shown for experimental vestibular stim-
ulation (10). Based on the available data, the life-time
prevalence of migrainous vertigo is about 1%, when the
following criteria were used: (i) recurrent vestibular ver-
tigo (rotational or positional vertigo); (ii) history of
Society criteria, at least two attacks in which migraine
and vertigo occurred together; and (iii) the vertigo was
not explained by other disorders (6). In some of these
attacks, oculographic recordings were made and patho-
logical nystagmus was seen in 70% of the patients; 50%
showed a more central vestibular dysfunction, 15% eye
movements as in a peripheral vestibular lesion and in
the rest no clear pattern could be detected (11). It is not
clear whether some oculomotor deficits can be seen out-
side the attacks (4,11). Patients did not complain of
hearing problems during or outside of the attacks.
The onset of the migraine seems to be years earlier
than the onset of the vertigo and the duration of the
vertigo is between 1–24h in most attacks (8). The
pathophysiological mechanisms responsible for these
findings are still not known; activation of trigeminal
fibres to the inner ear during the trigeminal-vascular
activation (12), which causes a plasma extravasation,
has been discussed as a possible mechanism. Another
explanation is the induction of a spreading depression
in the brainstem (13) or cortical spreading depression in
vestibular or oculomotor areas (e.g. parietal temporal
cortex). A rare cause of such vertiginous migraine
attacks is episodic ataxia type 2 (14).
attacks, other mechanisms may also contribute to the
sensation of dizziness. General increased sensitivity
across all kinds of sensory stimulation (e.g. phonopho-
bia, photophobia, and osmophobia) may be one mech-
anism. Such a general increased sensitivity may also
contribute to the known increased prevalence of
motion sickness in migraineurs (3,15). Otherwise,
panic attacks are sometimes described by the patients
as dizziness as well and are much more prevalent in
migraineurs than in the general population (16).
Most interesting are the findings that some well
known ‘classic’ vertigo syndromes, namely Me ´ nie ` re’s
disease and benign paroxysmal positional vertigo, can
be found more often than expected in patients with
migraine. In the literature, the prevalence of migraine
in patients with Me ´ nie ` re’s disease can be as high as 22–
76% (8,17), but population-based studies are still
1Department of Neurology, University of Munich, Munich, Germany
2Department of Otology and Laryngology, Harvard Medical School,
Boston, Massachusetts, USA.
Prof. Andreas Staube MD, Department of Neurology Ludwig Maximilians
University Munich, Klinikum Grosshadern
at University of Sydney on August 16, 2010 cep.sagepub.comDownloaded from
missing. The reason for such a co-morbidity is not
trigeminal-vascular activation with consecutive plasma
extravasation (18) and, in the long run, development of
an endolymphatic hydrops. Similarly, several case stu-
dies indicate an increased risk of benign paroxysmal
positional vertigo (BPPV) in migraine. A study by
Ishiyama et al. (19) found a history of migraine three
times more often in idiopathic BPPV than in traumatic
BPPV (seealso Cha
population-based study, the prevalence of migraine in
the BPPV group was even 7.5 times higher than in the
controls (20). As in Me ´ nie ` re’s disease, the exact connec-
tion between migraine and BPPV is not known; one
hypothesis is that the repeated trigeminal vascular acti-
vation of the inner ear may also cause an accelerated
degeneration of the membranes of the otoliths which
may be the reason for the shearing-off of otoconia which
then are allocated in the labyrinth. The differentiation
between these syndromes, which are more often present
in migraineurs, and migrainous vertigo in the more
sequences are different. In the case of migrainous ver-
tigo, the treatment is related to the migraine, although
controlled studies have not been published yet. In the
case of BPPV, deliberation manoeuvres which help to
reposition the otoconia are the treatment of choice (21).
Me ´ nie ` re’s disease can be treated with betahistine or gen-
tamycin installation in the inner ear (22).
The consequence of this is that headache specialists
should be able to differentiate vestibular vertigo (e.g.
rotational or positional vertigo) from a more unspecific
dizziness and they should also be familiar with the most
prevalent oculomotor findings in the case of Me ´ nie ` re’s
head-shaking nystagmus) and BPPV (brief attacks of
a crescendo-decrescendo torsional geotropic-beating
nystagmus in the head hanging position) in order to
differentiate correctly between these disorders. The
challenge for science in the coming years will be to
gain more insight into the pathophysiology of migrai-
Historically, migraine has been considered a head-
ache disorder, with a variety of adjunctive symptoms,
including ocular manifestations, allodynia, photopho-
bia and phonophobia, and vertigo/imbalance, to name
a few. This historical fact is reflected in the diagnostic
classifications of the International Headache Society.
What is becoming clearer year by year is that migraine
is a disorder of neurological function that can produce
wide spectrum of changes in sensory perception, usually
an intensification and/or distortion. The conventional,
headache-centric definition of migraine tends to reduce
awareness and importance of the other symptoms and
manifestations of the problem. In the best studies
to-date of the epidemiology of migrainous vertigo, all
patients had to meet International Headache Society
criteria for migraine headache and have vestibular
symptoms (6–8). However, this may well underestimate
the prevalence of migrainous dizziness. Clinicians spe-
cialising in balance disorders will agree that there
are many patients exhibiting all the symptoms and
signs of migrainous dizziness, but no temporally related
headache (or no headache history at all). This is
exactly analogous to ocular migraine, but the ocular
symptoms alone can justify a diagnosis of migraine
even in the absence of headache. It is time to consider
redefining migraine as a global disturbance of sensory
signal processing, in which headache is a common
1. Jensen R, Stovner LJ. Epidemiology and comorbidity of
headache. Lancet Neurol 2008; 7: 354–361.
2. Neuhauser HK. [Epidemiology of dizziness and vertigo].
Nervenarzt 2009; 80: 887–894.
3. Kayan A, Hood JD. Neuro-otological manifestations of
migraine. Brain 1984; 107: 1123–1142.
4. Dieterich M, Brandt T. Episodic vertigo related to
migraine (90 cases): vestibular migraine? J Neurol 1999;
5. Cha YH, Lee H, Santell LS, Baloh RW. Association of
benign recurrent vertigo and migraine in 208 patients.
Cephalalgia 2009; 29: 550–555.
6. Neuhauser HK, Radtke A, von Brevern M, et al. Migrai-
nous vertigo: prevalence and impact on quality of life.
Neurology 2006; 67: 1028–1033.
and vestibular migraine. J Neurol 2009; 256: 333–338.
8. Cha YH, Baloh RW. Migraine associated vertigo. J Clin
Neurol 2007; 3: 121–126.
9. BisdorffA,Andree C,
Headache-associated dizziness in a headache population:
prevalence and impact. Cephalalgia
First 12 March 2010, doi: 10.1177/0333102409353617.
10. Murdin L, Davies RA, Bronstein AM. Vertigo as a
migraine trigger. Neurology 2009; 73: 638–642.
11. von Brevern M, Zeise D, Neuhauser H, Clarke AH,
Lempert T. Acute migrainous vertigo: clinical and oculo-
graphic findings. Brain 2005; 128: 365–374.
12. Koo JW, Balaban CD. Serotonin-induced plasma extra-
vasation in the murine inner ear: possible mechanism of
migraine-associated inner ear dysfunction. Cephalalgia
2006; 26: 1310–1319.
13. Richter F, Bauer R, Lehmenku ¨ hler A, Schaible HG.
Spreading depression in the brainstem of the adult rat:
electrophysiological parameters and influences on regio-
nal brainstem blood flow. J Cereb Blood Flow Metab
2008; 28: 984–994.
14. Robbins MS, Lipton RB, Laureta EC, Grosberg BM.
Headache 2009; 49: 1042–1046.
at University of Sydney on August 16, 2010 cep.sagepub.comDownloaded from
15. Drummond PD. Triggers of motion sickness in migraine Download full-text
sufferers. Headache 2005; 45: 653–656.
16. Hamelsky SW, Lipton RB. Psychiatric comorbidity of
migraine. Headache 2006; 46: 1327–1333.
17. Radtke A, Lempert T, Gresty MA, Brookes GB,
Bronstein AM, Neuhauser H. Migraine and Me ´ nie ` re’s
disease: is there a link? Neurology 2002; 59: 1700–1704.
18. Vass Z, Steyger PS, Hordichok AJ, Trune DR, Jancso ´ G,
Nuttall AL. Capsaicin stimulation of the cochlea and
electric stimulation of the trigeminal ganglion mediate
vascular permeability in cochlear and vertebro-basilar
arteries: a potential cause of inner ear dysfunction in
headache. Neuroscience 2001; 103: 189–201.
19. Ishiyama A, Jacobson KM, Baloh RW. Migraine and
benign positional vertigo. Ann Otol Rhinol Laryngol
2000; 109: 377–380.
benign paroxysmal positional vertigo: a population based
study. J Neurol Neurosurg Psychiatry 2007; 78: 710–715.
21. Bhattacharyya N, Baugh RF, Orvidas L, et al. American
Academy of Otolaryngology-Head and Neck Surgery
Foundation. Clinical practice guideline: benign paroxys-
mal positional vertigo. Otolaryngol Head Neck Surg 2008;
139(Suppl 4): S47–S81.
22. Straube A. Nystagmus: an update on treatment in adults.
Expert Opin Pharmacother 2005; 6: 583–590.
at University of Sydney on August 16, 2010cep.sagepub.comDownloaded from