Inner Ear Excitation in Normal and Postmastoidectomy Participants by Fluid Stimulation in the Absence of Air- and Bone-Conduction Mechanisms.

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Inner Ear Excitation in Normal and Postmastoidectomy Participants by Fluid Stimulation in the Absence of Air- and Bone-Conduction Mechanisms.

J Am Acad Audiol. 2017 Feb;28(2):152-160

Authors: Ronen O, Geal-Dor M, Kaufmann-Yehezkely M, Perez R, Chordekar S, Adelman C, Sohmer H

Abstract
BACKGROUND: Hearing can be induced not only by airborne sounds (air conduction [AC]) and by the induction of skull vibrations by a bone vibrator (osseous bone conduction [BC]), but also by inducing vibrations of the soft tissues of the head, neck, and thorax. This hearing mode is called soft tissue conduction (STC) or nonosseous BC.
PURPOSE: This study was designed to gain insight into the mechanism of STC auditory stimulation.
RESEARCH DESIGN: Fluid was applied to the external auditory canal in normal participants and to the mastoidectomy common cavity in post-radical mastoidectomy patients. A rod coupled to a clinical bone vibrator, immersed in the fluid, delivered auditory frequency vibratory stimuli to the fluid. The stimulating rod was in contact with the fluid only. Thresholds were assessed in response to the fluid stimulation.
STUDY SAMPLE: Eight ears in eight normal participants and eight ears in seven post-radical mastoidectomy patients were studied.
DATA COLLECTION AND ANALYSIS: Thresholds to AC, BC, and fluid stimulation were assessed. The postmastoidectomy patients were older than the normal participants, with underlying sensorineural hearing loss (SNHL). Therefore, the thresholds to the fluid stimulation in each participant were corrected by subtracting his BC threshold, which expresses any underlying SNHL.
RESULTS: Hearing thresholds were obtained in each participant, in both groups in response to the fluid stimulation at 1.0 and 2.0 kHz. The fluid thresholds, corrected by subtracting the BC thresholds, did not differ between the groups at 1.0 kHz. However, at 2.0 kHz the corrected fluid thresholds in the mastoidectomy patients were 10 dB lower (better) than in the normal participants.
CONCLUSIONS: Since the corrected fluid thresholds at 1.0 kHz did not differ between the groups, the response to fluid stimulation in the normal participants at least at 1.0 kHz was probably not due to vibrations of the tympanic membrane and of the ossicular chain induced by the fluid stimulation, since these structures were absent in the mastoidectomy patients. In addition, the fluid in the external canal (normal participants) and the absence of the tympanic membrane and the ossicular chain (mastoidectomy patients) induced a conductive hearing loss (threshold elevation to air-conducted sounds coming from the bone vibrator), so that AC mechanisms were probably not involved in the thresholds to the fluid stimulation. In addition, as a result of the acoustic impedance mismatch between the fluid and skull bone, the audio-frequency vibrations induced in the fluid at threshold would probably not lead to vibrations of the bony wall of the meatus, so that hearing by osseous BC is not likely. Therefore, it seems that the thresholds to the fluid stimulation, in the absence of AC and of osseous BC, represent an example of STC, which is an additional mode of auditory stimulation in which the cochlea is activated by fluid pressures transmitted along a series of soft tissues, reaching and exciting the inner ear directly. STC can explain the mechanism of several auditory phenomena.

PMID: 28240982 [PubMed - in process]

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