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Otol Neurotol. 2012 Sep;33(7):1151-5.

Vestibular system changes in sudden deafness with and without vertigo: a human temporal bone study.

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Department of Otolaryngology, University of Minnesota, Minneapolis, Minnesota 55455, USA.



To investigate the vestibular system changes in sudden deafness with vertigo (SDwV) and sudden deafness without vertigo (SDwoV) and the cause of persistent canal paresis (CP) in SDwV patients.


Retrospective study.


Four temporal bones from the affected ear in 4 patients with unilateral sudden deafness (SD), 2 SDwV and 2 SDwoV, were selected. Four contralateral temporal bones with normal-hearing ears were defined as the control. Morphologic findings of the labyrinth, the number of Scarpa's ganglion cells, and the density of vestibular hair cells were investigated in all temporal bones. Clinical data and the results of vestibular tests of 11 patients with unilateral SD, as a separate group, also were investigated.


Atrophic change of the organ of Corti, tectorial membrane, and stria vascularis in cochlea, and deposits and atrophic otoconial membrane in vestibular sense organs were seen on affected ears more than control ears. The density of Type I hair cells seemed to decrease on the saccular macula and the posterior semicircular canal crista on affected ears, and there was no remarkable difference between SDwV and SDwoV. In 1 patient with SDwoV who died 10 months after the onset of SD, there were large amount of deposits on the cupula, the atrophied otoconial membrane was peeling off from the saccular macula, and the saccular membrane collapsed to the saccular macula in the affected ear. In the clinical data, all SDwV who were examined within 2 years from the onset had CP, and all SDwV had profound hearing loss.


There is no remarkable difference between SDwV and SDwoV in the number of Scarpa's ganglion cells and the density of vestibular hair cells. The damage of the extracellular superstructure is seen in SD with or without vertigo. The damage of extracellular superstructure is potentially one of the causes of persistent CP in patients with SD.

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