Finite-element Modeling of the Effect of Superior Canal Dehiscence on Intracochlear Pressures in Bone Conduction

Superior canal dehiscence (SCD) is a pathological opening of the bone encapsulating the superior semicircular canal, causing various vestibular and auditory symptoms. One of the most debilitating symptoms associated with SCD is bone conduction (BC) hyperacusis, manifested as awareness of self-generated sounds (one's own heartbeat, voices, joint movements, eye movements) and increased sensitivity to certain external sounds and vibrations (machinery, noise experienced inside an automobile) that can be heard via BC. While BC hyperacusis is increasingly recognized by clinicians and researchers, how SCD enhances BC sensitivity is unclear, mainly because the mechanisms underlying BC are not well understood Recently, we developed a finite element (FE) human ear model to elucidate the inertial BC mechanism and gain insights into the cause of BC hyperacusis. The goal of the present study is to compare the FE-model simulated SCD effects on air conduction (AC) and BC with our previous intracochlear pressure measurements from human temporal bones. In the model, the SCD was simulated by creating an opening in the bony wall in the middle of the superior canal arch. The AC excitation was simulated by applying sound pressure into the ear canal. The BC excitation was simulated by applying rigid-body vibrations to the model along the stapes piston-motion direction and the other two orthogonal directions. The AC- and BC-evoked intracochlear sound pressures in scala vestibuli (P-SV) and scala tympani (P-ST) at the basal cochlea and the pressure difference (P-DIFF=P-SV-P-ST) were simulated under normal and SCD conditions. The comparison between the simulated and measured intracochlear pressures in AC suggests that the damping of the cochlear channels (scala vestibuli and scala tympani) in the current model is lower than that of a real ear. In BC, the model predicts that SCD increases P-DIFF - the cochlear input drive - for all three excitation directions, indicating an increase in BC sensitivity. However, the simulated changes in P-SV and P-ST due to SCD in BC are inconsistent with our previous measurements and are highly dependent on the excitation direction. The discrepancy between the simulated results and the experimental data may stem from the direction-dependent nature of the SCD effect and insufficient damping of the cochlear fluid channels.