Vertigo and Dizziness Related to Migraine-A Diagnostic Challenge

8/6/2019 Vertigo and Dizziness Related to Migraine-A Diagnostic Challenge

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Blackwell Publishing Ltd Cephalalgia, 2004, 24, 8391 83

Blackwell Science, LtdOxford, UKCHACephalalgia1468-2982Blackwell Science, 20032428391Original ArticleVertigo and dizziness related to migraineH Neuhauser & T Lempert

REVIEW

Vertigo and dizziness related to migraine: a diagnostic challenge

H Neuhauser1,2 & T Lempert1,31

Neurologische Klinik, Charit, Humboldt-Universitt,

2

Robert Koch-Institut and

3

Abteilung fr Neurologie, Schlosspark-Klinik, Berlin, Germany

Neuhauser H & Lempert T. Vertigo and dizziness related to migraine: a diagnosticchallenge. Cephalalgia 2004; 24:8391. London. ISSN 0333-1024

Vertigo and dizziness can be related to migraine in various ways: causally, statis-tically or, quite frequently, just by chance. Migrainous vertigo (MV) is a vestibularsyndrome caused by migraine and presents with attacks of spontaneous or posi-tional vertigo lasting seconds to days and migrainous symptoms during theattack. MV is the most common cause of spontaneous recurrent vertigo and ispresently not included in the International Headache Society classification ofmigraine. Benign paroxysmal positional vertigo (BPPV) and Mnires disease(MD) are statistically related to migraine, but the possible pathogenetic links havenot been established. Moreover, migraineurs suffer from motion sickness moreoften than controls. Persistent cerebellar symptoms may develop in the course offamilial hemiplegic migraine. Dizziness may also be due to orthostatic hypoten-sion, anxiety disorders or major depression which all have an increased preva-lence in patients with migraine. Cerebellar, dizziness, migraine, motion sickness,vertigo

Dr Hannelore Neuhauser, Robert Koch-Institut, Seestr. 10, D-13353 Berlin, Germany.Tel. +49 30 45 47 34 62, fax +49 30 45 47 35 13, e-mail [email protected] Received 8April 2003, accepted 11 July 2003

Introduction

Dizziness and vertigo rank amongst the most com-mon complaints in the general population and arefrequently reported by patients with migraine. Inindividual migraineurs, the critical question iswhether the dizziness or vertigo is related tomigraine or not.

This review will explore the association ofmigraine with: (i) vestibular vertigo, (ii) motionsickness, (iii) cerebellar symptoms and (iv) non-vestibular dizziness. We thereby distinguishbetween vertigo, which is a vestibular symptom anddizziness, which is not. Patients may report a varietyof different sensations that need to be carefullyinquired about: rotational vertigo or other illusorysensations of motion indicate vertigo, i.e. vestibularsymptoms, while a sensation of lightheadedness, gid-diness, unsteadiness, drowsiness or impending faintimplies dizziness ofnon-vestibular origin. This distinc-tion can be made in most cases. However, a residualgrey area remains, either as a semantic problem or

because mild vestibular dysfunction may presentwith dizziness rather than vertigo. Moreover, in themedical literature, a clear differentiation betweenvertigo and dizziness is sometimes not made. In thefollowing, we will use quotation marks to denote anambiguous use of the term dizziness.

Approximately 16% of the adult population areaffected by migraine at some time in their lives (1)and the lifetime prevalence of dizziness (comprisingboth vertigo and non-vestibular dizziness) has beenfound to be 23% in a large population-based survey(2). Thus, about 34% of the general populationwould be expected to have both migraine and diz-ziness by pure coincidence. However, there is evi-dence that migraine and dizziness actually concurmuch more often. In a recent study, the prevalenceof migraine according to the criteria of the Interna-tional Headache Society (HIS) (3) was 1.6 timeshigher in 200 dizziness clinic patients than in 200 age-and sex-matched controls from an orthopaedic clinic(38% vs 24%, P< 0.01) (4). In particular amongpatients with unclassified or idiopathic vertigo, the


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84 H Neuhauser & T Lempert

Blackwell Publishing Ltd Cephalalgia, 2004, 24, 8391

prevalence of migraine has been shown to be elevated(57). Conversely, 53 out of 200 unselected migrainepatients reported vertigo, compared with nine out of116 patients with tension headache (27% vs 8%,P= 0.01) (8). The association between migraine andvertigo was significant, both for vertigo with head-ache and for vertigo in the headache-free period. Inanother study, migraine patients reported about 2.5times more vertigo and also about 2.5 times moredizzy spells during the headache-free phase thancontrols not suffering from headaches (9). In sum-mary, the available data indicate a more-than-chanceassociation of migraine with vertigo and dizziness.

Migraine and vertigo

Patients with both episodic vertigo and migrainehave been reported from the early days of clinicalneurology (10). However, systematic studies on the

interrelations of migraine and vertigo have beenundertaken in the last two decades only. Both fromthe clinical and from a research point of view, itis useful to assign the association of migraine withvertigo to one of three categories: (i) vertigo that iscausally related to migraine migrainous vertigo, (ii)vertigo syndromes that are not caused by migrainebut show a statistical association with migraine, pos-sibly as a result of an association of both conditionswith a third factor, or (iii) vertigo that co-exists withmigraine in the same patient just by coincidence.

Migrainous vertigo (MV)

In the last decades, a syndrome that causally linksvertigo to migraine has started to take shape frompublished case series. Comprehensive clinical obser-vations suggest that vertigo can be an independentmigrainous symptom which usually does not corre-spond to an aura and which may dissociate fromheadaches.

An early manifestation of migrainous vertigo isbenign paroxysmal vertigo of childhood which is charac-terized by brief attacks of vertigo or disequilibrium,anxiety and often nystagmus or vomiting that occurrecurrently for months or years in otherwise healthyyoung children (11). Many of these children laterdevelop migraine, often years after vertigo attackshave ceased (12). A family history of migraine infirst-degree relatives is twofold increased comparedwith controls (13). In a population-based study, theprevalence of recurrent vertigo probably related tomigraine was estimated at 2.8% in children between6 and 12 years (13).

In adults, the term benign recurrent vertigo has beenused for a vestibular disorder that shows some fea-

tures in common with migraine which include pre-cipitation by alcohol, lack of sleep or emotionalstress, female preponderance, an individual historyor a positive family history of migraine (14, 15). Sub-sequently, various names have been introduced suchas vertigo as a migraine equivalent (16), migraine-associated dizziness (17, 18), migraine-related vestibulop-athy (19, 20), vestibular migraine (21), or migrainousvertigo (4). Case series, which have included up to100 patients, have highlighted additional featuresthat provide evidence for the migrainous origin ofepisodic vertigo even in the absence of headache:the concurrence of visual auras, photophobia andphonophobia, relief by sleep and effectiveness ofanti-migraine therapy (4, 1425, 27). It should benoted that most authors have conceptualized MVas a vestibular disorder, but some have includedunspecific dizziness as well (17, 19, 25).

MV may occur at any age (17, 19, 21). It has a

female preponderance with a reported female-to-male ratio between 1.5 and 5 and 1 (4, 19, 21, 25). Inmost patients, migraine begins earlier in life thanMV (4, 21). Some patients have been free frommigraine attacks for years when MV first manifestsitself (21). MV seems to occur more often in patientswith migraine without aura than in patients withmigraine with aura (8, 18, 21, 25). Population-basedprevalence studies are still lacking.

Clinical presentation of MV

Patients typically report spontaneous or positionalvertigo. Some patients first experience spontaneousvertigo, which transforms into positional vertigolater in the attack (14, 15). Altogether, 4070% ofpatients experience positional vertigo (but notbenign paroxysmal positional vertigo) in the courseof the disease (4, 8, 25). Head motion intolerance, i.e.episodic imbalance and illusory motion aggravatedor provoked by head movements, is a frequent addi-tional symptom suggesting a vestibular problem. Ofnote, migrainous vertigo and non-vestibular dizzi-ness can co-exist in the same patient (17, 18, 25) butcan be well differentiated in most cases. Nausea andimbalance are frequent but unspecific accompani-ments of acute MV. Both duration and frequency ofattacks can vary between patients and in individualpatients over time. The duration of vertigo rangesfrom seconds to several hours and, sometimes, up toseveral days. For some patients, it may take severalweeks to fully recover from an attack. The attacksmay occur days, months or even years apart in anirregular fashion. Some patients experience clustersof short attacks of vertigo, lasting seconds to a few


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Vertigo and dizziness related to migraine 85


minutes. Such clusters can last for hours to days andpatients may experience head motion intolerancebetween the short attacks. Overall, between 10 and30% of patients have vertigo with the typical dura-tion of a migraine aura, i.e. 560 min (4, 21). Attacksshorter than a migraine aura are not unusual andhave been reported in 2030% of patients whileattacks lasting hours or days occur in 2050% ofpatients (4, 17, 19, 21). MV often misses not only theduration criterion for an aura as defined by the IHS,but also the temporal relationship to migraine head-aches: vertigo can precede headache as would betypical for an aura, may begin with headache orappear late in the headache phase. Many patientsexperience both attacks with and without headache(4, 17, 25). Quite frequently, patients have an atten-uated headache with their vertigo as compared withtheir usual migraine (22, 25). In some patients, ver-tigo and headache never occur together (4, 17, 25).

Absence or attenuation of migrainous headache dur-ing MV attacks may be due to an interaction of ves-tibular and trigeminal mechanisms as suggested bya study showing disappearance of headache or adecrease in headache intensity after caloric activa-tion of the vestibular system during migraine attacks(26).

Along with the vertigo, patients may experiencephotophobia, phonophobia and visual or otherauras. These phenomena are of diagnostic impor-tance, as they may represent the only apparent con-nection of vertigo and migraine. They need to be

specifically inquired about as patients often do notvolunteer them.Hearing loss and tinnitus are not prominent

symptoms of MV but have been reported in individ-ual patients with MV (19, 23, 25). Hearing loss isusually mild and transient, without progression inthe course of the disorder. The frequency of cochlearsymptoms and their temporal association with thevertiginous attacks has not been studied systemati-cally. Cochlear symptoms have also been found invertigo-free migraine patients (8).

In summary, the clinical presentation of MV isvariable in many respects and the connection tomigraine can be subtle. The repeated presence ofmigrainous symptoms along with the vertigo(migrainous headache, photophobia, phonophobia,auras) points to the correct diagnosis.

Clinical and neurotologic findings in patientswith MV

The general neurologic and otologic examinationand tests in the symptom-free period are unremark-

able in most cases (17, 24). About 1020% of MVpatients have unilateral hypoexcitability to caloricstimulation and about 10% have directional prepon-derance of nystagmus responses (17, 21). Such find-ings, however, are not specific for MV, as they can befound also in migraine patients without vestibularsymptoms (28) and in many other vestibular syn-dromes. Neuro-ophthalmological evaluation mayreveal mild central oculomotor deficits in theabsence of other brainstem or cerebellar signs (21).

A neurotologic study of 15 patients during theacute phase of MV showed imbalance in all patients but one, a peripheral type of spontaneous nystag-mus in three, a central type of spontaneous nystag-mus in four and a central positional nystagmus infour patients. A unilateral deficit of the horizontalvestibulo-ocular reflex was observed in threepatients and saccadic pursuit in two (29). Overall,findings during acute MV pointed to central vestib-

ular dysfunction in eight patients (53%), to periph-eral vestibular dysfunction in three patients (20%),and were inconclusive with regard to the involvedstructures in four patients (27%).

Diagnostic criteria of MV

Like migraine itself, MV cannot be diagnosed byspecific biological markers but only on the basisof history. To date, there are no internationallyapproved criteria for the diagnosis of MV. A recentproposal from our group uses operational clinical

criteria modelled on the IHS classification of head-aches (4). Operational diagnostic criteria, however,are a trade-off between sensitivity and specificity.Therefore, two separate diagnostic categories appearto be useful: definite and probable migrainous ver-tigo (Table 1). A diagnostic interview applying thesecriteria has been proposed recently (30).

The criteria for definite MV are stricter than theinclusion criteria of most MV case series publishedso far. The prevalence of definite migrainous vertigoaccording to these criteria was 7% in a group of 200consecutive dizziness clinic patients and 9% in agroup of 200 migraine clinic patients (4). The clinicalfeatures of MV in 33 patients from our dizzinessclinic fulfilling the criteria for definite MV are sum-marized in Table 2.

Migrainous vertigo and the IHS classification ofmigraine

Vertigo is not included in the IHS classification as amigrainous symptom in adults except in the frame-work of basilar migraine (3), which involves ver-


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tigo in more than 60% of the patients (31). As anaura symptom of basilar migraine, vertigo shouldlast between 5 and 60 min and should be followed by migrainous headache. In addition, in order tofulfil the IHS criteria for basilar migraine, a secondaura symptom from the posterior circulation

should be reported (e.g. dysarthria, double visionor bilateral paresthesias). In fact, less than 10% ofMV patients in published case series fulfil the crite-ria for basilar migraine (4, 19, 21, 25), which makes basilar migraine an inappropriate category forthese patients. As a consequence, most patientswith MV cannot be classified with the current IHScriteria.

Differential diagnosis of MV

Differential diagnosis of MV should be guided bydistinction of vestibular symptoms and non-vestibular dizziness and should consider thecommon causes of recurrent vertigo (Table 3). Ofnote, among 75 patients with migraine presenting toa neurological dizziness clinic, MV was only thethird most common diagnosis after benign posi-tional vertigo and psychiatric dizziness (e.g. due topanic disorder or depression) (4). MV of recent onsetmay be difficult to differentiate from early Mniresdisease, where cochlear symptoms may be lacking.

Pathophysiology of MV

The pathophysiology of MV is unclear. Spreadingdepression may play a role (17) when cortical areasare involved that process vestibular information.Several neurotransmitters which are involved in thepathogenesis of migraine (calcitonin-gene relatedpeptide, serotonin, noradrenaline, dopamine), arealso known to modulate the activity of vestibular

Table 1 Diagnostic criteria for definite migrainous vertigo

Definite migrainous vertigo

A Recurrent episodic vestibular symptoms of at least moderate severity

B Current or previous history of migraine according to the criteria of the International Headache Society

C One of the following migrainous symptoms during at least two vertiginous attacks: 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, or may be provoked or aggravated by head motion (head motion intolerance). Vestibular symptoms are moderate

if they interfere with but do not prohibit daily activities and severe if patients cannot continue daily activities.

Probable migrainous vertigo

A Recurrent episodic vestibular symptoms of at least moderate severity

B One of the following:

a) Current or previous history of migraine according to the criteria of the International Headache Society

b) Migrainous symptoms during 2 attacks of vertigo

c) Migraine-precipitants before vertigo in more than 50% of attacks: food triggers, sleep irregularities, hormonal changes

d) Response to migraine medications in more than 50% of attacks

C Other causes ruled out by appropriate investigations

Table 2 Clinical features of definite migrainous vertigo in 33patients

Clinical features %

Vestibular symptoms *

Rotational vertigo 70

Other illusiory self or object motion 18

Positional vertigo 42

Head motion intolerance** 48

Duration of vestibular symptoms

Seconds to 5 min 18

560 min 33

1 h to 1 d 21

>1 d 27

Migrainous symptoms during vertigo

Migrainous headache 94

always 45

sometimes 48

No headache 6

Photophobia 70

Phonophobia 64

Visual or other auras 36

*Several patients had more than one type of vestibular

symptoms, **none of the patients had head motion intoler-

ance only.


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neurones and could contribute to the pathogenesisof MV (17, 19, 25, 32). Recently, a synopsis of poten-tial pathophysiological links between migrainousand vestibular mechanisms has been presented(30). Such interactions may involve the vestibularnuclei, the trigeminal system and thalamocortical

pathways.In the last decade, genetic defects of ion channelshave been identified as the cause of various parox-ysmal neurologic disorders. The finding of an abnor-mal voltage-gated calcium-channel gene in familialhemiplegic migraine (FHM) and episodic ataxiatype 2 (EA-2) (33) both of which can have vertigoand migraine headache as prominent symptoms has prompted the search for a susceptibility genefor MV in the same region. So far, however, no suchgenetic defect could be identified (27, 34). Insummary, none of the potential pathophysiologicalmechanisms for MV has been experimentally inves-tigated. Therefore, they are all still highly speculative.

Treatment of MV

In many patients, MV attacks are severe, long andfrequent enough to warrant acute or prophylactictreatment. However, evidence for effective treatmentis scarce.

A few case reports suggest that medication usedfor migraine prophylaxis may be effective: propra-

nolol (35), metoprolol (21), pizotifen (22), or flunariz-ine (21). Acetazolamide, which is not normally usedfor migraine prophylaxis (36), has also been appliedsuccessfully. A recent retrospective study reported aprophylactic effect of a stepwise treatment consist-ing of avoidance of food triggers, low-dose tricyclic

antidepressants and a beta-blocker in more than 50%of patients (18). However, these findings are difficultto interpret in the absence of a control group and awell-documented pre-treatment period, as both fre-quency and duration of attacks vary considerably inthe natural course of the disorder (17).

Treatment ofacute MV with acute migraine medi-cation can be attempted with ergotamine (21),sumatriptan (37, 38) and vestibular suppressantssuch as promethazine, dimenhydrinate and mecliz-ine (37). A pilot randomised placebo-controlled trialof oral zolmitriptan for acute MV according to theabove criteria showed inconclusive results due tolow power (39). Multicentre trials with triptansadministered subcutaneously or nasally for fastrelief of migrainous vertigo are clearly needed.

Migraine and Mnires disease

An association between Mnires disease (MD) andmigraine has been considered already by ProsperMnire in 1861 (40). Sporadic accounts of headachesas an additional symptom in typical Mnire attacks

Table 3 Recurrent vertigo in patients with migraine: differential diagnoses for migrainous vertigo

Disorder Key features

Benign paroxysmal positional vertigo

(BPPV)

Vertigo lasting seconds to 1 min provoked by changes in head position. Positive

positional test with typical torsional nystagmus.

Mnires disease Vertigo lasting 20 min to 3 h with concurrent hearing loss, tinnitus and aural

fullness. Progressive hearing loss over years is a diagnostic criterion (46)Central positional vertigo History similar to BPPV but latency, duration and direction of positional nystagmus

not typical for BPPV. Frequently additional neurological or neurotological signs.

Vertebrobasilar TIA Attacks lasting mostly minutes, with brainstem symptoms including vertigo, ataxia,

dysarthria, diplopia or visual field defects (not longstanding recurrent vertigo

alone). Usually elderly patients with vascular risk factors.

Vascular compression of the 8th nerve Brief attacks of vertigo (seconds) several times per day with or without cochlear

symptoms, response to carbamazepine.

Perilymph fistula Vertigo after head trauma, barotrauma, stapedectomy of provoked by coughing,

sneezing, straining or loud sounds.

Autoimmune inner ear disease Frequent attacks of variable duration, often bilateral with rapidly progressing

hearing loss.

Insufficient compensation of unilateralvestibular loss

Brief and mild spells of vertigo during rapid head movements, oscillopsia with headturns to affected ear. Positive head thrust test to affected side.

Schwannoma of the 8th nerve Rarely presents with attacks of vertigo. Key symptoms are slowly progressive

unilateral hearing loss and tinnitus. Abnormal BAER.


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have provided further reason to suspect a linkbetween MD and migraine (41, 42). Subsequent stud-ies of the prevalence of migraine in MD producedconflicting results (43, 44,) but a recent controlledstudy has provided well-documented evidence forsuch an association (45). The study compared 78patients with idiopathic unilateral or bilateral MDaccording to the criteria of the American Academyof Otolaryngology (AAO) (46) with age- and sex-

matched controls. The prevalence of migraineaccording to the IHS criteria was almost twice as highin the MD group than in the control group (56% vs25%, P< 0.001). Furthermore, 35 (45%) of the patientswith MD always experienced at least one migrainoussymptom (migrainous headache, photophobia, aurasymptoms) along with their MD attacks. Twenty-eight (36%) of MD patients had IHS migraine andalways experienced at least one migrainous symp-tom (migrainous headache, photophobia, aurasymptoms) along with their MD attacks (Table 4, A.Radtke, personal communication). The study illus-

trates that there are migraine patients with recurrentvertigo for whom it is not possible to differentiatewith certainty whether they have migrainous vertigoor MD. The two conditions may share pathophysio-logical mechanisms such as neurotransmitter imbal-ances or ion-channel-dysfunction that lead to aspectrum of migrainous, vertiginous and cochlearsymptoms. Of note, this diagnostic ambiguitybetween migrainous vertigo and MD will only rarelyoccur in unselected patients with migraine and ver-tigo, considering the rarity of MD compared withmigrainous vertigo. As a rule of thumb, hearing lossis an occasional, mild and non-progressive feature inMV, while it is a regular accompaniment of MD pro-gressing to severe hearing loss within a few years.

Migraine and benign paroxysmal positional vertigo

Benign paroxysmal positional vertigo (BPPV) is themost common cause of recurrent vestibular symp-toms both in unselected patients (21, 47) and inmigraineurs (4) presenting at a dizziness clinic. Thediagnosis of BPPV is straightforward. Patients give

a very typical account of recurrent short (1020 s,maximum 1 min) attacks of rotational vertigo, whichare provoked by certain changes in head position,like turning over in bed, lying down or sitting up,looking up or bending down. A positive positionaltest as described by Dix and Hallpike with a typicaltorsional nystagmus beating towards the undermostear frequently with an upbeating vertical compo-nent confirms the diagnosis (48). Patients can be

treated effectively with the Epley or Semont canalithrepositioning manoeuvre (4951). When the nystag-mus is atypical, variants such as horizontal canalBPPV and central positional nystagmus should beconsidered.

Although clinically two separate entities, there isevidence for a link between migraine and BPPV.Migraine has been found to be three times morecommon in patients with idiopathic BPPV than inpatients with BPPV secondary to trauma or surgicalprocedures (52). Moreover, migraine was two timesmore common in patients with idiopathic BPPV than

in age and sex-matched controls (53). Genetic factorsand vascular damage to the labyrinth have been dis-cussed as pathogenetic mechanisms linking the twoconditions (52).

Vertigo as a symptom of migrainous infarction

Migraine is associated with an incresed risk forstroke (54). Migrainous infarctions are rare and occurpredominatly in the territory of the posterior cerebral artery (55, 56). Vertigo accompanied by otherbrainstem symptoms has been reported in individ-ual patients with migrainous stroke (7, 57).

Migraine and motion sickness

Motion sickness occurs more frequently in patientswith migraine (30 to 50%) than in controls with ten-sion headache or in headache-free controls (about20%) (8, 9). The association is more pronounced inchildren (58) and in migraine with aura (9). Findingsfrom a study in crew members of a yacht race sug-gest an influence of the menstrual cycle on the occur-

Table 4 Migrainous symptoms during Mnire attacks in 44 patients with MD and IHS-migraine (%)

Frequency

Migrainous

headache Photophobia

Aura

symptoms

At least one

of the three

Always 25 61 2 64

Sometimes 23 9 14 23

Never 52 30 84 18


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rence of both motion sickness and headache (59).Migraineurs also report more visual vertigo whilelooking at spinning objects (9). Headache, scalptenderness and photophobia could be provoked by optokinetic stimulation in a recent study.Migraineurs were more nauseated and had longer-lasting headache and photophobia than controls(60). In an individual patient, it may be difficult todifferentiate between episodic motion sickness andattacks of MV induced by motion stimuli. Thisshould be decided by taking into account the typeand duration of symptoms. Nausea and dizzinessimproving after cessation of the motion stimuluspoint to a diagnosis of motion sickness, while rota-tional or positional vertigo persisting after themotion stimulus has disappeared, suggest MV.

Migraine and cerebellar symptoms

Cerebellar dysfunction causes imbalance whichpatients may experience as dizziness. Some familieswith familial hemiplegic migraine (FHM), a rare sub-type of migraine, develop progressive cerebellarataxia and nystagmus (61). Interestingly, mutationsin the CACNA1A gene coding for the a1A subunit ofa neuronal Ca2+ channel, which is heavily expressedin the cerebellum, have been identified not only inFHM but also in episodic ataxia type 2 (EA-2) andspinocerebellar ataxia type 6. EA-2 is characterizedby short bouts of cerebellar ataxia, often with ver-tigo, and interictal nystagmus. Approximately half

of the patients with EA-2 have migraine (62). BothFHM and EA-2 are associated with typical symp-toms of basilar migraine (62, 63).

In more common types of migraine, cerebellarsymptoms are not usually present, but subclinicalhypermetria and other subtle subclinical cerebellarsigns in patients with migraine with or without aurahave been reported recently (64). The authors sug-gested dysfunctional Ca2+ channels as a possiblecause. This hypothesis relies on findings of aninvolvement of the CACNA1A gene region in somefamilies with non-hemiplegic migraine with andwithout aura (65). Another possible link betweenmigraine and cerebellar dysfunction is the mild ocu-lomotor deficits of cerebellar origin observed inpatients with migrainous vertigo (21).

Migraine and non-vestibular dizziness

Migraine patients report not only more vertigo butalso significantly more dizzy spells than controls (32%vs 13%) (9). These can usually be attributed to non-vestibular causes. However, mild vestibular dys-

function may also present with dizziness rather thanvertigo.

Migraine, orthostatic hypotension and syncope

Among 500 unselected migraineurs, syncope duringmigraine attacks has been reported in 5% (66).Orthostatic symptoms have been found to be morefrequent in students with frequent headaches thanin controls with rare or no headaches (67) and alsomore common in patients with migraine than in con-trols (68% vs 8%) (68). Orthostatic hypotension can be induced by small doses of dopamine agonistssuch as bromocriptine and piribedil and counter-acted by dopamine antagonist domperidone inmigraineurs, but not in controls, suggesting hyper-sensitivity to dopaminergic stimulation as theunderlying mechanism (69, 70).

Migraine and dizziness due to a comorbidpsychiatric disorder

The interrelations of migraine, dizziness and certainpsychiatric disorders are intricate. There are bi-directional associations of migraine with both majordepression and panic disorder, with migraine beinga risk factor for first-onset major depression andpanic disorder and vice versa (71, 72). Dizziness isthe second most common symptom of panic attacksafter palpitations (73) and can be a symptom ofmajor depression as well. To complicate things fur-

ther, patients with panic and anxiety have an incre-sed rate of vestibular test abnormalities (74), whichmay reflect an elevated risk of patients with vestib-ular disorders to develop an anxiety disorder (75).Likewise, anxiety or panic disorder was reported by14 out of 100 patients with migrainous vertigo (19).

Dizziness due to anti-migraine medication

Dizziness is listed as a side-effect of many medica-tions, some of which are used in the treatment ofmigraine. Therefore, it is useful to elicit a detaileddrug history and ascertain the onset of dizziness inrelation to changes in medication. Beta-blockers andcalcium-channel blockers, like most anti-hyperten-sive agents, can cause orthostatic hypotension, par-ticularly at the beginning of treatment. Long-termtreatment with beta-blockers can also cause light-headedness and fatigue. Antidepressants, particu-larly tricyclic antidepressants, which are used in theprophylactic therapy of migraine, can cause sleepi-ness, blurred vision, lightheadedness and posturalhypotension.


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Conclusions

The associations of vertigo and dizziness withmigraine are complex and can be subdivided intocausal, statistical and coincidental relationships.There is emerging clinical evidence that recurrent

vertigo is often causally related to migraine and thatMV can be diagnosed by operational diagnostic cri-teria. The syndrome of MV deserves further researchactivity as it is common and clinically relevant. Inaddition, it may help to clarify the pathomechanismsof migraine itself. However, the current IHS classifi-cation of migraine does not reflect vertigo as a symp-tom of migraine and may thus hinder therecognition of MV. We would therefore advocate theinclusion of MV in a future revision of the IHS clas-sification of migraine.

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Vertigo and Dizziness Related to Migraine-A Diagnostic Challenge