Abstract

Vestibular syndromes are one of the commonest paroxysmal disorders in our clinical practice. These consist of vertigo, oculomotor abnormalities (nystagmus), postural changes and nausea/vomiting. Vertigo can be classified as real vertigo and dizziness, based upon the presence of clinical rotatory perception. In order to diagnose a responsible lesion for various central and peripheral vestibular syndromes, we have to carefully observe nystagmus in patients with acute vertigo. Gaze-evoked nystagmus is the most important nystagmus in patients with the central vestibular syndromes. The finding is easily found at the bed side examination. In order to keep a velocity-position neural signal such as gaze holding, the neural structure to hold and maintain the neural command for a saccade is hypothesized and this has been called as the brainstem neural integrator, which sends tonic-step commands for eccentric gaze. If this fails then the integrator becomes leaky and the eyes drift back to the central position. This movement necessitates corrective saccades, hence gaze-evoked nystagmus will ensue. Vertical nystagmus such as primary position upbeat or downbeat nystagmus is also seen only in the central vestibular syndromes. The detection and diagnosis of these characteristic nystagmus are essential for primary clinicians who care patients with acute vertigo.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.