Abstract
Various drugs are known to be toxic to the vestibular endorgan. Aminoglycosides are the best known among those. The action of aminoglycosides are two fold; one is direct inhibition of the ion channels on the cell surface, and the other is metabolic inhibition of phosphatidylinositol in the cell. The patterns of morphological damage have been well documented. The central portions of the crista ampullaris and the striola are more vulnerable to ototoxicity than other portions. Physiological effects of ototoxic drugs were studied using an isolated semicircular canal model. Injection of the drugs into the perilymphatic space resulted in marked inhibition of the ampullary nerve potential, indicating that the drug acts on the basal membrane rather than inhibiting the ion channels of the cell surface. Dizziness induced by ototoxic drugs is characterized by various symptoms, such as persistent dizziness, the jumbling phenomenon, and disturbance of the righting reflex. Since medication has very little effect on dizziness, prevention should be given the top priority. Regular follow-up of hearing as well as vestibular function is mandatory for preventing future ototoxic side effects.
