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Actualidad
Médica
SUPLEMENTO
Otoneurología 2014:
comprendiendomejor lostrastornosvestibulares
ACTUAL IDAD
M É D I C A
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SUPLEMENTO
Actual.Med.
2014; 99: (791). Supl. 33-60
Vestibularmigraine:apractical approach
Abstract
Vestibular migraine (VM) is one of themost common causes of the episodic vestibular syndrome. It occurs in
patientswithprevious or current historyofmigrainewhoexperience recurrent episodes of vestibular symptoms
with migrainous features during the attacks. The pathophysiology of VM is poorly understood and several
hypotheses have been proposed. Probably various mechanisms are involved resulting in both peripheral and
central vestibular dysfunctionparticipate.
A smart clinical characterizationof the attacks is essential to establish aproper diagnosis andplanning a correct
approach. The diagnosis should bemade on the basis of the clinical history. Now, diagnostic criteria of VM are
well defined.Occasionally, diagnosisofVMcannotbeeasybecauseof varietyof confusingclinicalmanifestations,
suchaspositional nystagmusor hearing loss causingmisdiagnosis.
There is not awell-established therapy for VM. It is assumed thatmanagement of VM is similar tomigraine, in
both acute crisis and preventive therapy. The role of neuroleptics, H1 receptor antagonists, benzodiazepines,
steroids and triptans in the acute attacks, and dietary changes and lifestyle modifications, anticonvulsants,
antidepressants, beta-blocking drugs, and calcium antagonists, as well as vestibular rehabilitation, in VM
preventionhavebeen revised.
Preventive treatment for VM is not well supported by prospective, randomized, placebo-controlled clinical
trials. Several drugs have been shown to be effective in some studies, but the clinical evidence is limited. Large
randomized clinical trials areneeded.
JuanManuel Espinosa-Sánchez
1,2
,Ángel Batuecas-Caletrio
3
1
Otology & Neurotology Group CTS495, GENYO, - Centro de Genómica e Investigación Oncológica – Pfizer/
UniversidaddeGranada/ JuntadeAndalucía, PTSGranada, Spain
2
OtolaryngologyUnit, Hospital SanAgustín, Linares (Jaén), Spain
3
Department of Otorhinolaryngology, Otoneurology Unit, University Hospital of Salamanca, University of
Salamanca
Vestibularmigraine (VM) is a disorder that occurs inpatients
with previous or current history of migraine who experience
recurrentepisodesofvestibularsymptomswithmigrainous features
during theattacks. AlthoughVM isunderdiagnosed, it is considered
the second most common cause of episodic vertigo after benign
paroxysmal positional vertigo (BPPV), with a lifetime prevalence of
about1% (1).
Various terms have been previously used to mention this
clinical entity: migrainous vertigo, migraine-associated vertigo or
dizziness, migraine-related or migraine-induced vestibulopathy.
Nowadays, there is universal agreement that the correct term is
VM.Manypatientsdiagnosedashavingbenign recurrent vertigoor
whatused tobecalled in thepastvestibularMeniere´sdisease (MD)
probably also correspond to this same entity, particularly if they
suffer frommigraine.
There isnobiologicalmarker forVM, so thediagnosis ismade
on the basis of the clinical history. It is remarkable that themere
concurrenceof vertigoandmigraine is not enough for diagnosis. In
fact,most patientswithmigraine and episodic vertigodonot have
VM. Diagnostic criteria developed by the Bárány Society and the
International Headache Society (IHS) are nowwidely accepted and
haveprovenahighvalidity (2,3). Thedisseminationof thesecriteria
and the inclusion in thebeta versionof the3rdeditionof the ICHD
has renewed the intereston thisdisorder (4,5,6,7,8).
Neuro-otological examination between episodes is usually
normal, although during crisis spontaneous and positional
nystagmus,mostlyof central type, canbe found.Vestibular function
tests may reveal subtle oculomotor disturbances and a mild
unilateral canal paresis.
The pathophysiology of VM is poorly understood and several
hypotheses have been proposed. Probably various mechanisms
are involvedandbothperipheral and central vestibular dysfunction
participate.Theinteractionandoverlapbetweenvestibularpathways
and migraine circuits can provide a framework for understanding
VM pathophysiology (6). The connections between the vestibular
nuclei and the spinal trigeminal nucleus caudalis could explain the
activationof trigemino-vascular systemand the subsequent release
of neuropeptides (substance P, calcitonin gene-related peptide or
CGRP) from perivascular axons. For the purposes of this review, it
should be noted the diversity of neurotransmitters and receptors
involved in thedifferent suggestedmechanisms. Thiswouldexplain
thewidevarietyof pharmacological groups than canbeeffective in
the treatmentofVM.
Familial occurrence of VM supports the hypothesis of a
genetic basis with an autosomal dominant inheritance pattern
with incomplete penetrance. Nevertheless, although genome-
Keywords: Vestibular, migraine,
prophylaxis, vertigo, dizziness,
treatment.
Abordajeprácticode lamigrañavestibular
Dr. JuanM. Espinosa
UnidaddeORL.Hospital SanAgustín
Avda. deSanCristóbal s/n · 23700Linares (Jaén)
e-mail:
Tlf.: +34953024200
