Vestibular migraine treatment and

prevention

A. Lapira

HNO
Deutsche Gesellschaft für Hals-Nasen-
Ohren-Heilkunde, Kopf- und Hals-
Chirurgie

ISSN 0017-6192
Volume 67
Number 6

HNO (2019) 67:425-428

DOI 10.1007/s00106-019-0661-3

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Leitthema

HNO 2019 · 67:425–428 A. Lapira1,2,3

https://doi.org/10.1007/s00106-019-0661-3 1
St James & Capua Hospitals, Sliema, Malta
Published online: 8 April 2019 2
University of Malta, Msida, Malta
© Springer Medizin Verlag GmbH, ein Teil von
3
Springer Nature 2019 Nova Southeastern University, Fort Lauderdale, USA

Vestibular migraine treatment

and prevention

Background The development of clinical criteria Asymmetric neuropeptide release results

for migrainous vertigo was an impor- in vertigo and increased motion sensitiv-
Vestibular migraine (VM) is considered tant step in defining diagnostic markers ity. Similarly, serotonin (5-HT) has been
to be the commonest cause of sponta- for VM [10]. The presentation of VM found to be an important substrate in the
neous episodic vertigo and the second varies with symptoms of spontaneous and pathogenesis of migraine with therapeu-
most common cause of vertigo [1, 2]. positional vertigo, head motion vertigo/ tic implications. Interestingly the sero-
The association between cochleovestibu- dizziness, and ataxia of variable duration, tonergic pathways directly influence the
lar dysfunction and migraine has been ranging from a few seconds to days. Most firing rate of vestibular nucleus neurons
recognized since 1861 when Prosper episodes have no temporal relationship [11, 13–17].
Ménière described Ménière syndrome with the headaches [8, 12]. For VM the concept of an ion chan-
in migraine patients [3]. Other authors nelopathy is relevant because mutations
highlighted the concept that vertigo, Pathophysiology of the CACNA1A gene coding for a trans-
hearing loss, and tinnitus were part membrane component of a neuronal cal-
of the symptoms that some migraine The pathophysiology of VM has not been cium channel can provoke familial hemi-
patients presented [4, 5]. established. Interictal observations sug- plegic migraine or episodic ataxia type 2
gest that it is a central vestibular disorder, [17]. In a large study, familial vestibular

»the Vestibular migraine is

commonest cause of
but peripheral vestibular causes cannot
be excluded [12, 13]. Cortical spreading
migraine was found to be genetically het-
erogeneous with a subgroup linking to
depression is assumed to be the mecha- chromosome 22q12 [18]. Lee et al. have
spontaneous episodic vertigo nism for migraine aura and for symptoms also proposed a positive association of
originating in the cerebellum [13]. Mi- progesterone receptor factor (PGR) and
Terms used to describe recurring vestibu- graine is considered to be a brain disorder, migraine-associated vertigo [19].
lar symptoms in migraine, such as “mi- invalidating the vascular mechanism of Furman et al. proposed a pathophys-
graine-associated dizziness,” “migrain- migraine [14]. iological model (. Fig. 1) to explain the
ous vertigo,” and “vestibular migraine,” thalomocortical network disruption in
imply a causal link between migraine
and the vestibular symptoms [5, 6]. »vestibular
The pathophysiology of
migraine has not been
vestibular migraine [20].

These are based on epidemiology and on Diagnostic approach

abnormalities in vestibular tests during established
and between vertigo episodes [6–8]. Patients with migraine vestibulopathy
Significantly more patients with mi- Russo et al. explored the role of the exhibit episodic symptoms that may be
graine have vertigo than do patients with mediodorsal thalamus in pain process- solitary or a combination of vertigo,
tension-type headache [8] and headache- ing and cortical excitability with over- headache, or imbalance [8]. Many pa-
free controls [9]. In a German study the lap in the migraine circuit. This creates tients are unaware that their dizziness/
lifetime prevalence of migraine in the a dysfunctional thalamocortical network headaches originate from migraine [9].
general population was found to be about disrupting vestibular, visual, propriocep- Neuhauser and Lempert proposed cri-
14% and the lifetime prevalence of ver- tive, and somatosensory afferent inputs teria for the diagnosis of probable mi-
tigo 7%, resulting in a chance coincidence [15]. Cutrer and Baloh suggested that grainous vertigo [21]. A probable diag-
of 1%. The co-occurrence of vertigo and the dizziness unrelated to headaches oc- nosis of VM is made when patients ex-
migraine, however, was found to be 3.2% curs from the release of neuropeptides perience recurrent dizzy spells or vertigo
[7]. (substance P, neurokinin A, and calci- in the absence of neurologic symptoms,
tonin gene-related peptide [CGRP]) [8]. when the vertigo is temporally unrelated

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Medulla and pons Midbrain, thalamus, and forebrain

Trigeminovascular reflex Cognition,

Trigeminal pain pathways behaviours
Thalamocortical
processing
Meningeal, brain, and Sensorimotor
labyrinthine vasculature Visceral pathways
integration

Amygdala

Vestibular apparatus Vestibular pathways Interoception

Insula Migraine features

Perceptions and sensations
Sensorimotor responses Parabrachial nucleus Premonitory symptoms
• Eye movement
• Head movement
• Posturalchanges
Autonomic responses Locus coeruleus Dorsal raphe nucleus
Endocrine responses (norepinephrine) (5-hydroxytryptamine)

Fig. 1 8 A pathophysiological model for vestibular migraine. (Adapted from [20])

to headache, and when a past or fam- Ménière disease vs. vestibular Diagnostic tests
ily history of migraine exists. In all these migraine
patients, migraine therapy can be started 1. High-frequency headshake test: VM is
both for diagnostic and therapeutic pur- Both Ménière disease (MD) and VM characterized by dynamically induced
poses [21]. present with episodic vertigo, sen- motion sensitivity, exhibiting nys-
The International Headache Society sorineural hearing loss, and tinnitus. tagmus enhanced by high-frequency
(IHS) and the Barany Society created One distinguishing feature is that ver- headshake testing [8, 21].
a consensus document with diagnostic tigo in VM may last longer than 24 h and 2. Video-oculography (VOG) positioning
criteria for vestibular migraine, added to that a persistent imbalance lasts for many testing: 24% of migrainous vertigo
the ICHD-3 (2013; [22]): weeks. In MD by contrast, vertigo usu- patients exhibit positive positional
A. At least five episodes fulfilling crite- ally does not last longer than 1 day [21]. deficits in vertical or horizontal canals
ria C and D Other symptoms pointing toward VM [10].
B. A current or past history of 1.1 mi- would include photo- or phonophobia, 3. Videonystagmography (VNG)/
graine without aura or 1.2 migraine nonprogressive sensorineural hearing electronystagmography (ENG)
with aura loss (SNHL), as well as history of motion calorics: 20–25% of patients with VM
C. Vestibular symptoms of moderate intolerance and/or of dizziness around were determined to have permanent
or severe intensity, lasting between the menstrual cycle. Childhood benign reduced caloric weakness due to the
5 min and 72 h positional vertigo also supports a diag- recurrent channelopathies causing
D. At least half of episodes are associated nosis of VM. Furthermore, migraine and peripheral vestibular dysfunction
with at least one of the following three vestibular disease can coexist. Patients [11, 23].
migrainous features: who fit the criteria for MD should be 4. Electrocochleography (ECoG): helps to
j headache with at least two of the managed accordingly for MD, even if differentiate MD from VM. In active
following four characteristics: a history of migraine headache exists MS, the ratio of the summating po-
a) unilateral location [21]. tential and the nerve action potential
b) pulsating quality Nonprogressive sensorineural hear- is greater than 35% [10, 11].
c) moderate or severe intensity ing loss is rarely a significant feature 5. Magnetic resonance imaging (MRI):
d) aggravation by routine physical of VM and thus helps to differentiates MRI to exclude acoustic or cerebel-
activity it from MD. However, up to 80% of lopontine angle tumors is necessary
j photophobia and phonophobia patients with basilar migraine have been if patients present with unilateral
j visual aura reported to have SNHL, affecting the cochleovestibular symptoms or re-
E. Not better accounted for by another low frequencies and often being bilateral fractory to treatment [10, 12].
ICH-3 diagnosis or other vestibular [23]. Fluctuation is also possible, but
diagnosis. unlike MD, the SNHL in basilar migraine Treatment of vestibular migraine
rarely progresses.
Behavioral
Neuhauser et al. advise that it is impor-
tant to establish regular sleep patterns,

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Abstract · Zusammenfassung

stress reduction, a migraine diet (avoid- HNO 2019 · 67:425–428 https://doi.org/10.1007/s00106-019-0661-3

ing chocolate; aged cheeses; red wine © Springer Medizin Verlag GmbH, ein Teil von Springer Nature 2019
and port; monosodium glutamate [MSG]
found in fast food, soy sauce, yeast, and A. Lapira
meat tenderizers), and eliminate caffeine Vestibular migraine treatment and prevention
or habitual analgesic use (rebound; [7,
10]). Abstract
Vestibular migraine probably represents Some authors recommend treating vestibular
migraine using multiple drugs; others have
Pharmacologic the second most common cause of vertigo
focused on using only one drug. Although
after benign positional vertigo, by far
Abortive attempts—combinations of caf- exceeding Ménière disease. There are still at present it is not possible to quantify the
feine, aspirin, and acetaminophen with relatively few published reports on vestibular effects of the treatments proposed, some
anti-emetics—may be effective. Use of migraine management, despite its enormous recommendations can be made.
newer antagonists (triptan derivatives) importance in daily practice. In 2003 the first
clinical definition of vestibular migraine was Keywords
of the serotonin receptors involved in
proposed. Studies published before 2003 Migraine disorders · Vertigo · Episodic vertigo ·
migraine pathophysiology (5HT1 sub- used variable terms for vestibular migraine. Pharmacotherapy · Vestibular apparatus
types) has provided partial benefit to pa-
tients studied in trials [24–28]. These
are mainly effective if taken in the early Behandlung und Prävention von vestibulärer Migräne
phase of VM attack [28].
Prophylactic pharmacotherapy Zusammenfassung
(. Table 1) is indicated when attacks Die vestibuläre Migräne ist wahrscheinlich die der vestibulären Migräne mit mehreren
zweithäufigste Ursache für Schwindel nach Medikamenten, andere haben sich auf
of VM occur several times monthly, are die Verwendung nur eines Medikaments
dem gutartigen positionellen Schwindel,
continuous over several weeks, or have der die Menière-Krankheit bei Weitem konzentriert. Derzeit ist es zwar nicht möglich,
severely impacted a patient’s lifestyle. übersteigt. Es gibt bisher nur wenige die Auswirkungen der vorgeschlagenen
A stepped approach starting with a beta- veröffentlichte Berichte über die Behandlung Behandlungen zu quantifizieren, aber es
blocker (propranolol or metoprolol) or der vestibulären Migräne, trotz ihrer enormen können einige Empfehlungen ausgesprochen
Bedeutung für die tägliche Praxis. Im Jahr werden.
calcium-channel blocker (verapamil or
2003 wurde die erste klinische Definition der
diltiazem) is often effective [26]. If the vestibulären Migräne vorgeschlagen. Vor Schlüsselwörter
patient does not tolerate verapamil, a trial 2003 veröffentlichte Studien verwendeten Migräneerkrankungen · Schwindel ·
of amitriptyline can be made. variable Begriffe für vestibuläre Migräne. Episodischer Schwindel · Pharmakotherapie ·
Topiramate, an anticonvulsant with Einige Autoren empfehlen die Behandlung Vestibularapparat
GABA-α agonistic properties, is proving
to be an effective prophylactic treatment
for VM migraine [24, 28]. It is thought Vestibular rehabilitation therapy ety symptoms predominate, a selective
to act via central modulation of GABA The diagnostic workup should determine serotonin reuptake inhibitor, such as
and glutamate levels, which in turn in- whether the migraine has resulted in pe- paroxetine or sertraline, is preferred.
hibit release of c-GRP and substance P. ripheral vestibular dysfunction with mo- VRT might be beneficial, particularly
Acetazolamide has also been reported to tion provoked disequilibrium. Vestibular in patients with additional space and
be an effective prophylactic agent [33]. rehabilitation therapy (VRT) may then be motion discomfort [30].
If dizziness is not controlled by one indicated to resolve persistent imbalance
class of medication, another class should despite vertigo control with prophylactic Summary
be used. Effective control should be medication [26].
maintained for at least 1 year and Vestibular migraine, despite being the
restarted if dizziness recurs on stop- Psychiatric comorbidity commonest cause of episodic vertigo,
ping medication. Vestibular migraine and MD seem to be is still an underdiagnosed and under-
Controlled studies have investigated the vestibular disorders with the highest treated condition [1]. The impact that it
betahistine, a histamine analogue, and risk of secondary psychiatric complica- can have on the individual’s quality of
flunarizine, a calcium antagonist, to treat tions, mainly anxiety. Along this line, life can be huge [7]. Important data on
recurrent vestibular vertigo [31, 32]. The the term “MARD” (migraine–anxiety-re- VM management revealed that over 72%
findings from studies of flunarizine are lated dizziness) was proposed [30]. of patients improved or had complete
consistent in showing it reduces episodes In patients with MARD where bal- remission of symptoms with a staggered
of VM, whereas betahistine, a classic drug ance symptoms predominate, a com- approach [28]. This consists of diet and
for MD, might also relieve the vestibular bination of an antidepressant, such as behavior modification, followed by mi-
symptoms of migraine [32]. imipramine, and a benzodiazepine, such graine-suppressing drugs such as low-
as clonazepam, is recommended. For dose tricyclic antidepressants, calcium
patients with MARD in whom anxi- channel blockers, or beta-blockers. Rare

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12. Baloh RW (1997) Neurotology of migraine.

Table 1 Medication used in vestibular migraine prophylaxis
Headache 37:615–621
Drug Side effects 13. Vincent M, Hadjikhani N (2007) The cerebellum
Propranolol 40–240 mg Postural hypotension, falls; bradycardia and migraine. Headache 47:820–833
14. Goadsby PJ (2009) The vascular theory of
Metoprolol 50–200 mg Postural hypotension, falls; bradycardia migraine—a great story wrecked by the facts.
Topiramate 50–100 mg Sedation, appetite disturbances, depression Brain 132:6–7
15. RussoA, Marcelli V, EspositoFetal(2014)Abnormal
Amitriptyline 75–150 mg 25–75 Weight gain; dry mouth, urinary retention thalamic function in patients with vestibular
Flunarizine 5–10 mg Weight gain, depression migraine. Baillieres Clin Neurol 82(23):2120–2126
16. Goadsby PJ, Charbit AR, Andreou AP, Akerman
S, Holland PR (2009) Neurobiology of migraine.
and long vestibular attacks would call Neuroscience 161:327–341
Corresponding address 17. Jen J, Kim GW, Baloh RW (2004) Clinical spectrum
for rescue medication only; frequent of episodic ataxia type 2. Baillieres Clin Neurol
episodes would require a prophylaxis Dr. A. Lapira, MD, MA, MSc, DLORCS, AuD, 62:17–22
with topiramate. Acetazolamide is a po- FAAA 18. Lee H, Jen JC, Wang H et al (2006) A genome-wide
St James & Capua Hospitals linkage scan of familial benign recurrent vertigo:
tentially interesting drug for vestibular linkage to 22q12 with evidence of heterogeneity.
George Borg Olivier St, SLM 1807 Sliema, Malta
migraine [33]. aleclapira@gmail.com Hum Mol Genet 15(2):251–258
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Vestibular rehabilitation therapy competing interests. vertigo, and migrainous vertigo. Baillieres Clin
Neurol 56:436–441
should be considered for all patients, 22. International Headache Soxiety (2018) The
For this article no studies with human participants
particularly if secondary complications or animals were performed by any of the authors. All
international classification of headache disorders,
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