Recovery of the Vestibular Function after Vestibular Neuronitis

Ohbayashi, Satoko; Oda, Makoto; Yamamoto, Masahiko; Urano, Mari; Harada, Kensuke; Horikoshi, Hidenori; Orihara, Hiromi; Kitsuda, Chiaki

doi:10.3109/00016489309128067

Cited by 53 publications

(49 citation statements)

References 6 publications

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“…Concurring with the literature, which indicates that 20 to 30% of the subjects involved can present at least one relapse (9), this study also confirms the high probability of recurrent vertigo (30% of the patients examined). In our study, the presence of several episodes of vertigo corresponding to AV parameters in the patient's medical history seems to be related mainly to persistent canal dysfunction.…”

Section: Discussionsupporting

confidence: 86%

Study of Vestibular Evoked Myogenic Potentials in Unilateral Vestibulopathy

Faralli

Molini

Ricci

et al. 2006

Otology &Amp; Neurotology

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The combined VEMPs-canal test study shows predictive value regarding certain evolving clinical pictures of vestibulopathy. The absence of VEMPs confirms the role of otolithic dysfunction in the onset of dizziness. Likewise, it suggests that a vestibular origin of these disorders should be considered in cases that have shown aspecific symptoms since onset, without frank vertigo and with normal vestibular response to canal function testing.

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Section: Discussionsupporting

confidence: 86%

Study of Vestibular Evoked Myogenic Potentials in Unilateral Vestibulopathy

Faralli

Molini

Ricci

et al. 2006

Otology &Amp; Neurotology

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“…Also in labyrinthine-defective subjects, the COR is substantially higher than in normal controls [Bronstein and Hood, 1986;Huygen et al, 1991]. A gradual recovery of vestibular functions, centrally or peripherally after onset of VN was also reported [Bergenius and Perols, 1999;Strupp et al, 2004;Ohbayashi et al, 1993]. Wide distribution of directional preponderance in the patient group compared to the normal group can represent the changes of somatosensory input, although they are not statistically different in this study.…”

Section: Vin In Patients With Unilateral Vnmentioning

confidence: 45%

Mechanisms of Vibration-Induced Nystagmus in Normal Subjects and Patients with Vestibular Neuritis

Park¹,

Shin²,

Shim³

2007

Audiol Neurotol

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It has been reported that vibration applied either on the mastoid or on the sternocleidomastoid (SCM) muscles induces nystagmus in normal subjects or patients after unilateral vestibular neuritis (VN). The aims of the study were to characterize vibration-induced nystagmus (VIN) in normal and patient groups and to propose the mechanism of VIN. We recorded eye movements during unilateral 100-Hz vibration on the mastoid bone and SCM muscles in 22 normal subjects and 19 patients with unilateral VN. In normal subjects, the direction of slow-phase velocity (SPV) tended to be toward the vibrated side. Vibration on the right/left SCM muscles induced mean SPV of 1.7°/s, –1.9°/s toward the stimulated side in all normal subjects. Vibration on the right/left mastoid bone induced mean SPV of 1.5°/s, –0.4°/s toward the stimulated side in most of the normal subjects. Positive value means SPV to the right side. This directional preponderance to the vibrated side was statistically significant. Among the patients with VN, the slow phase of the VIN was directed towards the lesioned side, irrespective of whether vibration was applied on the lesioned or intact side. Vibration on the right/left mastoid bone induced mean SPV of –10.4°/s, –10.8°/s toward the lesioned side. Vibration on the right/left SCM induced mean SPV of –7.9°/s, –10.5°/s toward the lesioned side. The amplitude of SPV showed a significant correlation with the unilateral weakness of caloric test. Our results suggest that the proprioceptive stimulation plays a major role in producing VIN in normal subjects, while VIN is generated mostly by the vestibular stimulation in patients with unilateral VN, which helps us localize the lesion side. Vibration tests on the SCM muscles as well as on the mastoid are recommended and our hypothetic mechanisms of VIN are presented.

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“…Electronystagmographic follow-up at 1 month revealed that caloric testing lateralization returned to normal in all 16 patients treated by the corticosteroid and in only 2 of the 4 patients in the placebo group. In a retrospective study, the outcome of 34 patients who had VN and were treated by intravenous hydrocortisone and oral prednisone was compared with that of 77 patients not treated by corticosteroids (25). The follow-up period in this study ranged from 1 week to 9 years, with a mean of approximately 7 months.…”

Section: Discussionmentioning

confidence: 99%