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2 AUTHORS:
Andreas Straube
Steven D Rauch
Ludwig-Maximilians-University of Munich
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Editorial
Cephalalgia
30(7) 774776
! International Headache Society 2010
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DOI: 10.1177/0333102409355603
cep.sagepub.com
Migraine headache is one of the most common symptoms in general practice with a 12-month prevalence of
around 1012% 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 concurrence 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% (37). 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 pathophysiological 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 dizziness 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 disorder (e.g. Menie`res disease) which triggers a migraine
attack, as was shown for experimental vestibular stimulation (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 vertigo (rotational or positional vertigo); (ii) history of
migraine according the International Headache
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 pathological 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
Corresponding author:
Prof. Andreas Staube MD, Department of Neurology Ludwig Maximilians
University Munich, Klinikum Grosshadern
Email: astraube@nefo.med.uni-muenchen.de
775
Editorial
missing. The reason for such a co-morbidity is not
known; a possible mechanism could be the
trigeminal-vascular activation with consecutive plasma
extravasation (18) and, in the long run, development of
an endolymphatic hydrops. Similarly, several case studies 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 (see also Cha and Baloh (8)). In a
population-based study, the prevalence of migraine in
the BPPV group was even 7.5 times higher than in the
controls (20). As in Menie`res disease, the exact connection between migraine and BPPV is not known; one
hypothesis is that the repeated trigeminal vascular activation 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
narrow sense is important because the therapeutical consequences are different. In the case of migrainous vertigo, 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).
Menie`res disease can be treated with betahistine or gentamycin 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 Menie`res
disease (peripheral spontaneous nystagmus or
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 migrainous vertigo.
Historically, migraine has been considered a headache disorder, with a variety of adjunctive symptoms,
including ocular manifestations, allodynia, photophobia 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
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Cephalalgia 30(7)