Abstract
Migraine headache is one of the most common symptoms 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 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% (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 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. Ménière’s 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 the rest no clear pattern could be detected (11). It is not clear whether some oculomotor deficits can be seen outside 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 1–24 h 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).
Beside the vestibular vertigo during migraine attacks, other mechanisms may also contribute to the sensation of dizziness. General increased sensitivity across all kinds of sensory stimulation (e.g. phonophobia, photophobia, and osmophobia) may be one mechanism. 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 Ménière’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 Ménière’s disease can be as high as 22–76% (8,17), but population-based studies are still 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 Ménière’s 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). Ménière’s 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 Ménière’s 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 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 specialising 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 manifestation.