Article

Neuro-otological findings in patients with migraine- and nonmigraine-related dizziness. Audiol Neurootol

Department of Otolaryngology, The University of Melbourne, East Melbourne, Australia.
Audiology and Neurotology (Impact Factor: 1.85). 02/2008; 13(2):113-22. DOI: 10.1159/000111783
Source: PubMed

ABSTRACT 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.

0 Followers
 · 
317 Views
  • Source
    [Show abstract] [Hide abstract]
    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.
  • Source
    [Show abstract] [Hide abstract]
    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. · 1.55 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Migraine and vertigo are common disorders, affecting about 14% and 10%, respectively, of the general population. If migraine and vertigo were unrelated, the expected comorbidity would be 1%, whereas recent epidemiological studies indicate that 3.2% of the population have both migraine and vertigo. The excess comorbidity may be attributed to two factors: 1) vertigo syndromes (including Menière's disease, benign paroxysmal positional vertigo, and anxiety-related dizziness) that are more common in migraineurs than in controls and 2) vestibular migraine (VM) (vertigo as a symptom of migraine.) VM presents with attacks of spontaneous or positional vertigo lasting seconds to days. Headaches are often absent during acute attacks, but other migrainous features such as photophobia or auras, may be present. Like migraine headaches, VM triggers include stress, sleep deprivation, and hormonal changes. During acute attacks, there may be central spontaneous or positional nystagmus and, less commonly, unilateral vestibular hypofunction. In the symptom-free interval, vestibular testing shows mostly minor and nonspecific findings. The pathogenesis of VM is uncertain, but migraine mechanisms may interfere with the vestibular system at the labyrinth, brainstem, and cerebral cortex. Treatment includes vestibular suppressants for acute attacks and migraine prophylaxis for patients with frequent recurrences. However, treatment efficacy has not been validated by properly controlled clinical trials. VM does not fit into the 2004 International Headache Society Classification, in which "basilar-type migraine" must have at least two posterior circulation manifestations; isolated vertigo would not satisfy this criterion.
    Annals of the New York Academy of Sciences 06/2009; 1164(1):242-51. DOI:10.1111/j.1749-6632.2009.03852.x · 4.31 Impact Factor
Show more