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JOURNAL OF NEUROLOGY AND NEUROSCIENCE
associated with migraine without aura (1). MARV not only di-ers rom BTM in the clinical spectrum but also in the longerduration o the vertigo attacks.Assuming the relevance o cortical spreading depression, andtrigeminal nociception in the pathophysiology o migraine, it’swell known the trigeminal innervations o the crista ampulla-ris, and there are cortical regions that projects to the brainstemvestibular complex (9-10). The release o neuropeptides intothe vestibular peripheral cells or in the vestibular nucleus couldprecipitate and maintain the vertigo. Even this neuropeptidescould sensitized the vestibular system and justiy the subclini-cal vestibular alteration shown in migraine patients (11). Otherexplanation o vertigo in migraine patients is the cortical sprea-ding depression. It has been described vertigo episodes as anepileptic symptom and vertigo is one o the eatures o BTM(1, 12). And nally both syndromes share some eatures: Are re-current and chronic, the episodes last rom hours to days, andboth could be the result o peripheral or/and central neuronalmechanisms.Neurons in lateral and medial vestibular nucleus respond to se-rotonin increasing the ring rate and autoradiographic studiesconrm the presence o 5-HT 1 and 5-HT2 receptors in the ratvestibular nucleus (13, 14). There are evidences about the par-ticipation o glutamate and calcitonin gene-related peptide inthe vestibular nerve bres (15). The presence o those receptorsand neurotransmitters bring nearer again migraine and MARV. There is some controversy about the peripheral or central ori-gin o MARV. The duration o the episodes lasting even dayswithout compensation, the lack o hypoacusia, ullness or tinni-tus and the improvement with triptans or migraine-preventivedrugs uphold the central-origin hypothesis.MARV responds to several migraine-preventive drugs (16-20). Topiramate seems to be an option reducing the requency o the vertigo attacks (18). Flunarizine has shown to be an eec-tive treatment or MARV (16-17). As a personal communicationvalproic acid also works well in these patients. Acetazolamidea drug eective in amilial hemiplegic migraine and episodicataxia type 2 may be also a useul option in both MARV and mi-graine with aura (11, 21). The vertigo attacks seem to respondto triptans (22).
Waking through the diagnostic criteria.
Tables 2, 3 and 4 show the proposed diagnosis criteria dividedby denitive, probable and possible.
MARV is an entity that has its own clinical pattern, pathophysio-logy and treatment. Dierential diagnosis should be make withbenign positional vertigo, Meniere disease and basilar type mi-graine. Specic diagnosis criteria could help in its recognitionand management.
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