Neuro-Otological Findings in Patients with Migraine- and Nonmigraine-Related Dizziness

Department of Otolaryngology, The University of Melbourne, East Melbourne, Australia.
Audiology and Neurotology (Impact Factor: 1.71). 02/2008; 13(2):113-22. DOI: 10.1159/000111783
Source: PubMed


This study presents the neuro-otological findings of 523 patients attending a tertiary vestibular clinic with migraine- and nonmigraine-related dizziness. Subjects were categorized into one of 4 groups, definite migrainous vertigo, probable migrainous vertigo, vestibular disorder coexisting with migraine and nonmigraine-related dizziness. No notable relationship was found between the numbers of abnormal findings between the groups for the majority of the neuro-otological tests. However, there was a significant trend in emetic response to caloric testing. The definite migrainous vertigo group were at least 4 times more likely to be nauseous to caloric testing than any other migraine category. This difference was independent of the magnitude of caloric responses between the emetic migraine groups. While further investigation is required, this study has potentially identified that nauseous/emetic response to caloric stimulation may be a distinguishing factor between migrainous vertigo and other vestibular disorders including those with a coexisting history of migraine.

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    • "Vestibular abnormalities have been identified in migraineurs when asymptomatic between headache episodes. A small study comparing interictal vestibular function in individuals with migraine with and without vertigo and controls (N=15) showed reduction in mean gain of the semicircular canal-ocular reflex, a larger modulation component of the otolith-ocular reflex, and increased postural sway during optic flow testing among individuals with migrainous vertigo 3. Recently, a larger study similarly testing vestibular function in patients with migraine or controls (N=75) identified saccadic pursuit, unilateral caloric hypofunction, and increased sway velocity on posturography in individuals with migrainous vertigo 4. Others have failed to differentiate migraineurs with and without vertigo, based on specialized vestibular testing 5, 6. "
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    ABSTRACT: Limited evidence suggests that rizatriptan given before vestibular stimulation reduces motion sickness in persons with migraine-related dizziness. The present study was designed to test whether rizatriptan is also effective in protecting against visually-induced motion sickness and to test whether rizatriptan blocks the augmentation of motion sickness by head pain. Using randomized double-blind, placebo-controlled methodology, 10 females, 6 with migrainous vertigo (V+) and four without vertigo (V-) received 10 mg rizatriptan or placebo two hours prior to being stimulated by optokinetic stripes. Visual stimulation was coupled with three pain conditions: no pain (N), thermally-induced hand pain (H) and temple pain (T). Motion sickness and subjective discomfort were measured. Motion sickness was less after pre-treatment with rizatriptan for 4 of 10 subjects and more for 5 of 10 subjects. Augmentation of motion sickness by head pain was seen in 6 of 10 subjects; this effect was blunted by rizatriptan in 4 of these 6 subjects. Subjective discomfort was significantly more noticeable in V+ subjects as compared with V- subjects. These pilot data suggest that rizatriptan does not consistently reduce visually-induced motion sickness in migraineurs. Rizatriptan may diminish motion sickness potentiation by cranial pain.
    International journal of medical sciences 02/2009; 6(4):212-7. · 2.00 Impact Factor
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    ABSTRACT: The goal of this project is to identify what effect vestibular stimulation has on the reaction of the autonomic nervous system, as measured by blood pressure, blood-oxygen saturation levels, and heart rate monitoring, on subjects with migraine associated dizziness (MAD) as compared to healthy non-MAD subjects.
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    ABSTRACT: Epidemiology: Since both migraine and vertigo are common complaints in clinical practice they may coincide in an individual patient just by chance. There are, however, numerous patients with vestibular symptoms caused by migraine, accounting for 6-8% of diagnoses in specialized dizziness clinics. CLINICAL MANIFESTATION: Migraine-associated vertigo is a vestibular disorder which manifests itself with spontaneous or positional rotational vertigo or dizziness induced by head motion. The vertigo may occur without accompanying headache and may last from seconds to several weeks. Diagnosis: Migraine-associated vertigo can be diagnosed according to the following criteria: 1. recurrent vestibular symptoms, 2. migraine according to the criteria of the International Headache Society, 3. migrainous symptoms during the vertigo such as headache, photophobia, phonophobia, scintillating scotoma or other auras, 4. exclusion of other causes. Pathophysiology: The mechanism of migraine-associated vertigo is still obscure. Several hypotheses relating to the pathophysiology of migraine have been proposed: cortical spreading depression, regional changes in brain perfusion, release of neurotransmitters and paroxysmal dysfunction of ion channels. Clinical findings suggest both central and peripheral vestibular involvement. Therapy: Treatment is based on the repertoire of acute and prophylactic medications that are used for migrainous headaches. Controlled studies on the treatment of migraine-associated vertigo are still lacking.
    Annals of the New York Academy of Sciences 06/2009; 1164(1):242-51. DOI:10.1111/j.1749-6632.2009.03852.x · 4.38 Impact Factor
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