Anti-symmetric inputs at the cochlear windows drive bone-and air-conduction hearing [electronic resource] : finite element analysis
Keywords: Mechanical Engineering

Of the two pathways through which we hear, air conduction (AC) and bone conduction (BC), the fundamental mechanisms of the BC pathway remains to be poorly understood, despite its clinical significance. In the first study, a finite-element (FE) model of a human middle ear and cochlea was developed to gain insight into the mechanisms of BC hearing. BC excitations were simulated in the form of rigid-body vibrations of the surrounding bony structures in the x, y, and z orthogonal directions. The results show that the BM vibration characteristics are essentially invariant regardless of whether the excitation is BC, independent of excitation directions, or for AC. Analysis reveals that this is because the BM vibration apparently responds only to the anti-symmetric slow wave cochlea fluid pressure component and not the symmetric fast wave pressure component. In the second study, an improved three-dimensional FE model of a human middle ear coupled to a cochlea was formulated. The geometry of both the middle ear and cochlea, including semicircular canals, was obtained from micro-computed tomography ([mu]CT) images. In the study, BC and AC excitations were simulated as the same way as the previous simulation in the first study. After testing a range of vibrational directions, it was found that the vibrational direction normal to the BM surface at the base of the cochlea caused the highest BM velocity response across all tested frequencies—higher even than an excitation direction normal to the BM surface at the (non-basal) best-frequency locations corresponding to the other stimulus frequencies. The basal part of the human cochlea features a well-developed hook region, in which the BM undergoes a sudden curvature that produces the largest difference in fluid volume between the scala vestibuli (SV) and scala tympani (ST) found throughout the whole cochlea, and due to the sudden curvature of the hook region, the normal direction to the BM surface in this region differs significantly from the normal directions to the BM along the rest of the length of the cochlea. In the third study, the effects of otosclerosis and superior semicircular canal (SSC) dehiscence (SSCD) on hearing sensitivity were investigated via AC and BC pathways, using the FE model developed in the second study. Otosclerosis conditions were simulated by stiffing stapes annular ligament and removing the middle-ear inertia through removing stapedius tendon and incudostapedial joint. Dehiscences were modeled by removing a section of the outer bony wall of the SSC and applying a zero-pressure condition to the fluid surface thus exposed. In the results, otosclerosis condition caused the biggest bone-conduction hearing loss around 1.5 kHz, which is called 'Carhart notch'. In addition, dehiscence caused decreasing of the basilar membrane velocity, VBM(x), and fluid pressure in the cochlea in air conduction whereas increasing in bone conduction at low frequencies. Furthermore, the location and size of dehiscence affected the BC hearing threshold. Not previously shown is that the initial width (defined as the edge of dehiscence at which the flowing energy from the oval window meets for the first time) on the vestibular side of the dehiscence has more effect than the area of the dehiscence. The analyses of the FE model further predict that the ABG due to a dehiscence should converge to 0 dB at 10 kHz.