Bone-conduction hyperacusis induced by superior canal dehiscence in human: the underlying mechanism

Xiying Guan,Deepa J Galaiya,John J Rosowski,Y Song Cheng,Daniel J Lee,Hideko Heidi Nakajima

doi:10.1038/s41598-020-73565-4

Abstract

Our ability to hear through bone conduction (BC) has long been recognized, but the underlying mechanism is poorly understood. Why certain perturbations affect BC hearing is also unclear. An example is BC hyperacusis (hypersensitive BC hearing)—an unnerving symptom experienced by patients with superior canal dehiscence (SCD). We measured BC-evoked sound pressures in scala vestibuli (PSV) and scala tympani (PST) at the basal cochlea in cadaveric human ears, and estimated hearing by the cochlear input drive (PDIFF = PSV – PST) before and after creating an SCD. Consistent with clinical audiograms, SCD increased BC-driven PDIFF below 1 kHz. However, SCD affected the individual scalae pressures in unexpected ways: SCD increased PSV below 1 kHz, but had little effect on PST. These new findings are inconsistent with the inner-ear compression mechanism that some have used to explain BC hyperacusis. We developed a computational BC model based on the inner-ear fluid-inertia mechanism, and the simulated effects of SCD were similar to the experimental findings. This experimental-modeling study suggests that (1) inner-ear fluid inertia is an important mechanism for BC hearing, and (2) SCD facilitates the flow of sound volume velocity through the cochlear partition at low frequencies, resulting in BC hyperacusis.

Highlights

Initial assessment of the specimen included using Laser-Doppler measurements to check for inner-ear air or leak by ensuring that AC-evoked velocity of the stapes (VSTAP) and round window (VRW) had 1⁄2 cycle phase difference below 500 Hz, and that middle-ear velocities were normal[4]
To monitor the sensor sensitivity during the experiment, we developed a new intracochlear monitoring method described in detail in Stieger et al.[4]
If sequential calibrations were stable within 0.2 dB across all frequencies, sensors were inserted into the cochlea and sealed with only alginate

Summary

Introduction

Initial assessment of the specimen included using Laser-Doppler measurements to check for inner-ear air or leak by ensuring that AC-evoked velocity of the stapes (VSTAP) and round window (VRW) had 1⁄2 cycle phase difference below 500 Hz, and that middle-ear velocities were normal[4]. The fiberoptic pressure sensors were calibrated (C1) in a water vial attached to a shaker (4290, Bruel and Kjaer, Denmark). If sequential calibrations were stable within 0.2 dB across all frequencies, sensors were inserted into the cochlea and sealed with only alginate. Imperfect seals or introduction of air could occur, altering velocities of the stapes and RW and their phase relationship. The velocity responses were confirmed to be stable before and after insertion of sensor, which ensured that air did not enter the cochlea and there was no leak at the seal. Thereby, the first intracochlear pressure measurements (AC1) were made in the condition equivalent to a normal intact inner e

Methods

Results

Discussion

Conclusion