Adolfo M Bronstein1, Marianne Dieterich2,3,4. 1. Neuro-otology Unit, Division of Brain Sciences, Imperial College London, London, UK. 2. German Center for Vertigo and Balance Disorders. 3. Department of Neurology, University Hospital, Ludwig-Maximilians-University. 4. SyNergy - Munich Cluster for Systems Neurology, Munich, Germany.
Abstract
PURPOSE OF REVIEW: To review recent work on clinical and imaging aspects of vestibular neuritis (or acute vestibular syndrome), in particular with a view to identifying factors predicting long-term clinical outcome. RECENT FINDINGS: Evidence for a role of inflammation in the vestibular nerve, and the presence of Gadolinium enhancement acutely in vestibular neuritis, is accruing. Visual dependence, anxiety and somatization traits predict the development of chronic dizziness after acute vestibular neuritis. Adaptation to asymmetric rotation is impaired in vestibular neuritis and this may indicate insufficient central compensation in chronic dizzy patients. Corticosteroids appear ineffective at improving long-term clinical outcome. Functional imaging changes during the central compensation period lead to structural brain changes; both processes correlate with clinical recovery. SUMMARY: Vestibular neuritis appears to be the result of postviral neuroinflammation of the vestibular nerve. However, long-term prognosis is not dependent on the magnitude of the peripheral residual damage (as measured with caloric and video head-impulse test). Instead, a combination of visuovestibular psychophysical factors (visual dependence), psychological traits and dysfunctional vestibular perception are relevant. Several functional and structural neuroimaging changes develop after vestibular neuritis, which reflect and underlie the aforementioned psychophysiological and psychological features.
PURPOSE OF REVIEW: To review recent work on clinical and imaging aspects of vestibular neuritis (or acute vestibular syndrome), in particular with a view to identifying factors predicting long-term clinical outcome. RECENT FINDINGS: Evidence for a role of inflammation in the vestibular nerve, and the presence of Gadolinium enhancement acutely in vestibular neuritis, is accruing. Visual dependence, anxiety and somatization traits predict the development of chronic dizziness after acute vestibular neuritis. Adaptation to asymmetric rotation is impaired in vestibular neuritis and this may indicate insufficient central compensation in chronic dizzypatients. Corticosteroids appear ineffective at improving long-term clinical outcome. Functional imaging changes during the central compensation period lead to structural brain changes; both processes correlate with clinical recovery. SUMMARY:Vestibular neuritis appears to be the result of postviral neuroinflammation of the vestibular nerve. However, long-term prognosis is not dependent on the magnitude of the peripheral residual damage (as measured with caloric and video head-impulse test). Instead, a combination of visuovestibular psychophysical factors (visual dependence), psychological traits and dysfunctional vestibular perception are relevant. Several functional and structural neuroimaging changes develop after vestibular neuritis, which reflect and underlie the aforementioned psychophysiological and psychological features.
Authors: Sergio Martínez-Gallardo; José A Miguel-Puga; Davis Cooper-Bribiesca; Adolfo M Bronstein; Kathrine Jáuregui-Renaud Journal: J Vestib Res Date: 2021 Impact factor: 2.354