2026-09-24T03:45:41Zhttps://dspace.mit.edu/server/oai/requestoai:dspace.mit.edu:1721.1/978222026-06-16T18:51:47Zcom_1721.1_7582com_1721.1_7581col_1721.1_131022
John. J. Guinan Jr.
Berezina, Maria Andrey
Harvard--MIT Program in Health Sciences and Technology.
Harvard University--MIT Division of Health Sciences and Technology
2015-07-17T19:50:08Z
2015-07-17T19:50:08Z
2014
2015
http://hdl.handle.net/1721.1/97822
913224960
Thesis: Ph. D., Harvard-MIT Program in Health Sciences and Technology, February 2015.
Cataloged from PDF version of thesis. "February 2015."
Includes bibliographical references.
In humans, SFOAEs can non-invasively assess MOC strength and, may predict the MOC reduction of damage from traumatic sounds. However, the functionally important MOC effect is inhibition of auditory-nerve (AN) responses. Understanding the relationship between MOC effects on SFOAEs and AN CAPs is important for understanding SFOAE generation and for development of clinical tools that use these measures. This thesis presents several novel data sets that address MOC effects on SFOAEs, CAPs and the relationship between them in guinea pigs. Classic theory indicates that SFOAEs come from cochlear irregularities that coherently reflect energy at the peak of the traveling wave (TW), and that reflected energy arrives in the ear canal as a single wave at certain delay. Contrary to theory, in humans and chinchillas there have been reports of SFOAEs having multiple components with different delays, and that lowfrequency SFOAE delays are too short. The first thesis aim used time-frequency analysis to show that guinea pigs have frequency regions over which SFOAEs appear to have multiple components. However, we argue that the multiple components can be a simple result of variations in the patters of irregularities near the TW peak and are not necessarily indicative of multiple SFAOE sources. From comparison of our SFOAE delays with previously reported neural delays, we hypothesize that short SFOAE delays at low frequencies arise from a cochlear motion with a group delay shorter than the TW group delay. Aim 2 investigated how SFOAEs are affected by brainstem electrical stimulation of MOC fibers and found that MOC activation sometimes inhibited and sometimes enhanced SFOAEs. MOC stimulation always decreased CAP sensitivity which rules out SFOAE enhancement from increased cochlear amplification. We propose that shock-evoked MOC activity increases cochlear irregularity which results in increased SFOAE amplitudes. Aim 3 investigated the relationship between MOC effects on SFOAEs and tone-pip-evoked AN CAPs at same frequency and sound level. The ratio of the MOC effect on the SFOAE to the MOC effect on the CAP showed a highly-significant decrease (p<0.001) as the strength of MOC stimulation was increased. Although this observation was unexpected, several hypothesis to explain it are presented.
by Maria Andrey Berezina.
Ph.D.
101 pages
eng
Massachusetts Institute of Technology
M.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission.
http://dspace.mit.edu/handle/1721.1/7582
Harvard--MIT Program in Health Sciences and Technology.
Medial olivocochlear efferent (MOC) effects on stimulus frequency otoacoustic emissions (SFOAEs) and auditory-nerve compound action potentials (CAP) in guinea pigs
Thesis
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<Abstract>In humans, SFOAEs can non-invasively assess MOC strength and, may predict the MOC reduction of damage from traumatic sounds. However, the functionally important MOC effect is inhibition of auditory-nerve (AN) responses. Understanding the relationship between MOC effects on SFOAEs and AN CAPs is important for understanding SFOAE generation and for development of clinical tools that use these measures. This thesis presents several novel data sets that address MOC effects on SFOAEs, CAPs and the relationship between them in guinea pigs. Classic theory indicates that SFOAEs come from cochlear irregularities that coherently reflect energy at the peak of the traveling wave (TW), and that reflected energy arrives in the ear canal as a single wave at certain delay. Contrary to theory, in humans and chinchillas there have been reports of SFOAEs having multiple components with different delays, and that lowfrequency SFOAE delays are too short. The first thesis aim used time-frequency analysis to show that guinea pigs have frequency regions over which SFOAEs appear to have multiple components. However, we argue that the multiple components can be a simple result of variations in the patters of irregularities near the TW peak and are not necessarily indicative of multiple SFAOE sources. From comparison of our SFOAE delays with previously reported neural delays, we hypothesize that short SFOAE delays at low frequencies arise from a cochlear motion with a group delay shorter than the TW group delay. Aim 2 investigated how SFOAEs are affected by brainstem electrical stimulation of MOC fibers and found that MOC activation sometimes inhibited and sometimes enhanced SFOAEs. MOC stimulation always decreased CAP sensitivity which rules out SFOAE enhancement from increased cochlear amplification. We propose that shock-evoked MOC activity increases cochlear irregularity which results in increased SFOAE amplitudes. Aim 3 investigated the relationship between MOC effects on SFOAEs and tone-pip-evoked AN CAPs at same frequency and sound level. The ratio of the MOC effect on the SFOAE to the MOC effect on the CAP showed a highly-significant decrease (p<0.001) as the strength of MOC stimulation was increased. Although this observation was unexpected, several hypothesis to explain it are presented.</Abstract>
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