Experimental study on mechanism of positional vertigo using the non-otolithic vestibular organ.

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Mechanism of positional vertigo was studied using isolated labyrinth of the bull frog. Canalolithiasis and cupulolithiasis models were established using the saccular otoconia as responsible debris inside of the canal and on the cupula respectively. The action potentials of the ampullary nerve were recorded using glass suction electrode. The latency and time course of the responses were comparable to those of clinical course of positional nystagmus. Thus, canalolithiasis is a potential mechanism of positional vertigo. Vertigo as a primary symptom increases according to the speed of head changing. This phenomenon was studied using canalolithiasis model. The faster the change of canal position, the greater the action potentials, indicating the hair cells respond to acceleration of the moving debris. Elastase was injected into the inner ear of the guinea pigs in order to dislodge the otoconia from the macula. The animals showed positional nystgmus after surgery. Vibration was given to the bony bulla of the guinea pigs in order to establish a model of positional vertigo after middle ear surgery. The saccular otoconia were dislodged from the macula, thus indicating surgical drilling being a possible cause of positional vertigo.