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Editorial:Vertigoandmigraine:Amorethantwo-foldconnection

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AndreasStraube

Ludwig-Maximilians-UniversityofMunich

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StevenDRauch

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Editorial

Vertigo and migraine: A more thantwo-fold connection

Cephalalgia

30(7) 774–776

! International Headache Society 2010

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DOI: 10.1177/0333102409355603

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Andreas Straube1 and Steven D Rauch2

Migraine headache is one of the most common symp-toms in general practice with a 12-month prevalence ofaround 10–12% in Western populations (1). Vertigo isno less often the reason for clinical consultations. InGermany, about 3.4% of all out-patient consultationsare due to the symptom vertigo/dizziness: the 12-monthprevalence for all types of vertigo is about 23% and forrotational vertigo about 5% (2). Therefore, a concur-rence of the two conditions by chance can be expectedin about 1.1%. However, in contrast to this, clinical caseseries as well as recent population-based studies showeda much higher co-occurrence of about 3.2% (3–7). Atthis point, all available evidence points to a relatedco-morbidity of migraine and some forms of vertigo.However, in recent years, it has also become clear thatthis association between migraine and vertigo is not dueto a single clinical entity but that several clinical vertigosyndromes are more often seen in migraine patients (8).

It is still unclear what the underlying pathophysio-logical mechanism is and whether one mechanism orseveral mechanisms are involved. Furthermore, howcan the headache specialist di!erentiate betweenmigrainous vertigo and migraine-associated vertigo?

The importance of this point is shown by the studyby Bisdor! and colleagues (9), which shows that dizzi-ness as a symptom during the headache attacks isreported in 51% of the headache episodes. But thisfinding does not di!erentiate between dizziness due tothe migraine attack per se or due to a co-morbid disor-der (e.g. Meniere’s disease) which triggers a migraineattack, as was shown for experimental vestibular stim-ulation (10). Based on the available data, the life-timeprevalence of migrainous vertigo is about 1%, when thefollowing criteria were used: (i) recurrent vestibular ver-tigo (rotational or positional vertigo); (ii) history ofmigraine according the International HeadacheSociety criteria, at least two attacks in which migraineand vertigo occurred together; and (iii) the vertigo wasnot explained by other disorders (6). In some of theseattacks, oculographic recordings were made and patho-logical nystagmus was seen in 70% of the patients; 50%showed a more central vestibular dysfunction, 15% eyemovements as in a peripheral vestibular lesion and in

the rest no clear pattern could be detected (11). It is notclear whether some oculomotor deficits can be seen out-side the attacks (4,11). Patients did not complain ofhearing problems during or outside of the attacks.The onset of the migraine seems to be years earlierthan the onset of the vertigo and the duration of thevertigo is between 1–24 h in most attacks (8). Thepathophysiological mechanisms responsible for thesefindings are still not known; activation of trigeminalfibres to the inner ear during the trigeminal-vascularactivation (12), which causes a plasma extravasation,has been discussed as a possible mechanism. Anotherexplanation is the induction of a spreading depressionin the brainstem (13) or cortical spreading depression investibular or oculomotor areas (e.g. parietal temporalcortex). A rare cause of such vertiginous migraineattacks is episodic ataxia type 2 (14).

Beside the vestibular vertigo during migraineattacks, other mechanisms may also contribute to thesensation of dizziness. General increased sensitivityacross all kinds of sensory stimulation (e.g. phonopho-bia, photophobia, and osmophobia) may be one mech-anism. Such a general increased sensitivity may alsocontribute to the known increased prevalence ofmotion sickness in migraineurs (3,15). Otherwise,panic attacks are sometimes described by the patientsas dizziness as well and are much more prevalent inmigraineurs than in the general population (16).

Most interesting are the findings that some wellknown ‘classic’ vertigo syndromes, namely Meniere’sdisease and benign paroxysmal positional vertigo, canbe found more often than expected in patients withmigraine. In the literature, the prevalence of migrainein patients with Meniere’s disease can be as high as 22–76% (8,17), but population-based studies are still

1Department of Neurology, University of Munich, Munich, Germany2Department of Otology and Laryngology, Harvard Medical School,Boston, Massachusetts, USA.

Corresponding author:

Prof. Andreas Staube MD, Department of Neurology Ludwig MaximiliansUniversity Munich, Klinikum GrosshadernEmail: astraube@nefo.med.uni-muenchen.de

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missing. The reason for such a co-morbidity is notknown; a possible mechanism could be thetrigeminal-vascular activation with consecutive plasmaextravasation (18) and, in the long run, development ofan endolymphatic hydrops. Similarly, several case stu-dies indicate an increased risk of benign paroxysmalpositional vertigo (BPPV) in migraine. A study byIshiyama et al. (19) found a history of migraine threetimes more often in idiopathic BPPV than in traumaticBPPV (see also Cha and Baloh (8)). In apopulation-based study, the prevalence of migraine inthe BPPV group was even 7.5 times higher than in thecontrols (20). As in Meniere’s disease, the exact connec-tion between migraine and BPPV is not known; onehypothesis is that the repeated trigeminal vascular acti-vation of the inner ear may also cause an accelerateddegeneration of the membranes of the otoliths whichmay be the reason for the shearing-o! of otoconia whichthen are allocated in the labyrinth. The di!erentiationbetween these syndromes, which are more often presentin migraineurs, and migrainous vertigo in the morenarrow sense is important because the therapeutical con-sequences are di!erent. In the case of migrainous ver-tigo, the treatment is related to the migraine, althoughcontrolled studies have not been published yet. In thecase of BPPV, deliberation manoeuvres which help toreposition the otoconia are the treatment of choice (21).Meniere’s disease can be treated with betahistine or gen-tamycin installation in the inner ear (22).

The consequence of this is that headache specialistsshould be able to di!erentiate vestibular vertigo (e.g.rotational or positional vertigo) from a more unspecificdizziness and they should also be familiar with the mostprevalent oculomotor findings in the case of Meniere’sdisease (peripheral spontaneous nystagmus orhead-shaking nystagmus) and BPPV (brief attacks ofa crescendo-decrescendo torsional geotropic-beatingnystagmus in the head hanging position) in order todi!erentiate correctly between these disorders. Thechallenge for science in the coming years will be togain more insight into the pathophysiology of migrai-nous vertigo.

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 namea few. This historical fact is reflected in the diagnosticclassifications of the International Headache Society.What is becoming clearer year by year is that migraineis a disorder of neurological function that can producewide spectrum of changes in sensory perception, usuallyan intensification and/or distortion. The conventional,headache-centric definition of migraine tends to reduceawareness and importance of the other symptoms andmanifestations of the problem. In the best studies

to-date of the epidemiology of migrainous vertigo, allpatients had to meet International Headache Societycriteria for migraine headache and have vestibularsymptoms (6–8). However, this may well underestimatethe prevalence of migrainous dizziness. Clinicians spe-cialising in balance disorders will agree that thereare many patients exhibiting all the symptoms andsigns of migrainous dizziness, but no temporally relatedheadache (or no headache history at all). This isexactly analogous to ocular migraine, but the ocularsymptoms alone can justify a diagnosis of migraineeven in the absence of headache. It is time to considerredefining migraine as a global disturbance of sensorysignal processing, in which headache is a commonmanifestation.

References

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2. Neuhauser HK. [Epidemiology of dizziness and vertigo].Nervenarzt 2009; 80: 887–894.

3. Kayan A, Hood JD. Neuro-otological manifestations ofmigraine. Brain 1984; 107: 1123–1142.

4. Dieterich M, Brandt T. Episodic vertigo related tomigraine (90 cases): vestibular migraine? J Neurol 1999;246: 883–892.

5. Cha YH, Lee H, Santell LS, Baloh RW. Association ofbenign 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.

7. Lempert T,NeuhauserH. Epidemiology of vertigo,migraineand vestibular migraine. J Neurol 2009; 256: 333–338.

8. Cha YH, Baloh RW. Migraine associated vertigo. J ClinNeurol 2007; 3: 121–126.

9. Bisdorff A, Andree C, Vaillant M, Sandor PS.Headache-associated dizziness in a headache population:prevalence and impact. Cephalalgia Published OnlineFirst 12 March 2010, doi: 10.1177/0333102409353617.

10. Murdin L, Davies RA, Bronstein AM. Vertigo as amigraine 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 ofmigraine-associated inner ear dysfunction. Cephalalgia2006; 26: 1310–1319.

13. Richter F, Bauer R, Lehmenkuhler 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 Metab2008; 28: 984–994.

14. Robbins MS, Lipton RB, Laureta EC, Grosberg BM.CACNA1A nonsense mutation is associated withbasilar-type migraine and episodic ataxia type 2.Headache 2009; 49: 1042–1046.

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15. Drummond PD. Triggers of motion sickness in migrainesufferers. Headache 2005; 45: 653–656.

16. Hamelsky SW, Lipton RB. Psychiatric comorbidity ofmigraine. Headache 2006; 46: 1327–1333.

17. Radtke A, Lempert T, Gresty MA, Brookes GB,Bronstein AM, Neuhauser H. Migraine and Meniere’sdisease: 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 andelectric stimulation of the trigeminal ganglion mediatevascular permeability in cochlear and vertebro-basilararteries: a potential cause of inner ear dysfunction inheadache. Neuroscience 2001; 103: 189–201.

19. Ishiyama A, Jacobson KM, Baloh RW. Migraine andbenign positional vertigo. Ann Otol Rhinol Laryngol2000; 109: 377–380.

20. Von BrevernM,Radtke A, Lezius F, et al. Epidemiology ofbenign paroxysmal positional vertigo: a population basedstudy. J Neurol Neurosurg Psychiatry 2007; 78: 710–715.

21. Bhattacharyya N, Baugh RF, Orvidas L, et al. AmericanAcademy of Otolaryngology-Head and Neck SurgeryFoundation. 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.

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