Article thumbnail

Inertial Bone Conduction: Symmetric and Anti-Symmetric Components

By Namkeun Kim, Kenji Homma and Sunil Puria

Abstract

Of the two pathways through which we hear, air conduction (AC) and bone conduction (BC), the fundamental mechanisms of the BC pathway remain poorly understood, despite their clinical significance. A finite element model of a human middle ear and cochlea was developed to gain insight into the mechanisms of BC hearing. The characteristics of various cochlear response quantities, including the basilar membrane (BM) vibration, oval-window (OW) and round-window (RW) volume velocities, and cochlear fluid pressures were examined for BC as well as AC excitations. These responses were tuned and validated against available experimental data from the literature. 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 via BC, independent of excitation direction, or via AC. This at first appeared surprising because the cochlear fluid pressures differ considerably depending on the excitation mode. Analysis reveals that the BM vibration responds only to the lower-magnitude anti-symmetric slow-wave cochlear fluid pressure component and not to the symmetric fast-wave pressure component, which dominates the magnitude of the total pressure field. This anti-symmetric fluid pressure is produced by the anti-symmetric component of the window volume velocities. As a result, the BM is effectively driven by the anti-symmetric component of the OW and RW volume velocities, irrespective of the type of excitation. Middle ear modifications that alter the anti-symmetric component of the OW and RW volume velocities corroborate this assertion. The current results provide further clarification of the mechanisms underlying Békésy’s “paradoxical motion” concept

Topics: Article
Publisher: Springer-Verlag
OAI identifier: oai:pubmedcentral.nih.gov:3085688
Provided by: PubMed Central
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • http://www.pubmedcentral.nih.g... (external link)

  • To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.

    Suggested articles