Abstract
Patients with superior canal dehiscence syndrome may experience vertigo and nystagmus when pressure changes occur in the external auditory canal, the middle ear, or the intracranial space. The cause is a defect in the bone of the superior canal. To study the mechanisms of pressure sensitivity of the labyrinth in superior canal dehiscence syndrome and its surgical repair in a chinchilla model. We investigated the changes in firing rates of vestibular nerve afferents in the chinchilla in response to changes in external auditory canal pressure before and after fenestration of the superior canal, and after repair of the fenestra. Before superior canal fenestration, external auditory canal pressure changes caused no responses in horizontal canal or otolith afferents, and only 1 of 9 superior canal afferents responded to pressure. After fenestration, all superior canal afferents were excited by positive pressure and inhibited by negative pressure. Half of 18 otolith and most (21 of 33) horizontal canal afferents were unaffected by pressure. The superior canal afferents had higher pressure gain than the horizontal canal afferents (P =.03). Pressure responses could be abolished only by applying a rigid seal to the fenestra. Fenestration of the superior canal rendered all superior canal afferents sensitive to pressure, whereas less than half of the other afferents became pressure sensitive. The direction of the superior canal afferent responses agreed with the predictions of our model of endolymph flow within the superior canal. A rigid seal applied to the fenestra abolished pressure sensitivity while maintaining physiologic rotational sensitivity.
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