Using otoacoustic emissions to evaluate efferent auditory function in humans

The auditory system continually adapts to changes in the acoustic environment over short periods of time. This fine-tuning of its dynamics is mediated in part by the medial olivocochlear (MOC) bundle, a neural feedback loop which aids in the regulation of cochlear micro-mechanics. The ability to measure the response of the MOC system in humans may provide significant insight into unique cochlear functions, such as its sharp frequency selectivity and wide dynamic range. In humans the efferent system can be investigated non-invasively using otoacoustic emissions (OAEs). However, how OAEs can best be used to evaluate efferent function, the pitfalls associated with such measurements, as well as the relationship between OAEs and perception are not fully understood. This dissertation presents three experiments that explore the use of OAEs to assess efferent function in humans. The first study examined the advantages of separating the major components of distortion product otoacoustic emissions (DPOAEs) when evaluating efferent function using contralateral acoustic stimulation (CAS). CAS-induced activation of the medial olivocochlear reflex (MOCR) was found to produce both reductions and enhancements of total DPOAE level. Analysis of the separated components of the DPOAE revealed that these changes could be accounted for by the contribution of an efferent-induced phase change in the reflection component of the DPOAE. In the second, analysis of DPOAE primary level and phase changes over a wide range of CAS levels used to induce MOCR revealed that middle ear muscle reflex (MEMR) activation could be simultaneously monitored. CAS levels commonly used to elicit MOCR could also elicit MEMR responses, which results in contamination of MOCR estimates. Finally, a novel technique to measure simultaneous OAEs and masked behavioral thresholds is presented and used to investigate a perceptual phenomenon thought to be associated with an efferent activation. While a direct association between physiological and behavioral masked thresholds was not observed, a strong relationship was found between the physiological measure of masked thresholds and a measure of CAS-induced efferent suppression, suggesting that although efferent-mediated suppression of basilar membrane mechanics is related to the phenomenon, more central mechanisms may be required to modulate the perceptual response

The Medial Olivocochlear Reflex Is Unlikely to Play a Role in Listening Difficulties in Children

The medial olivocochlear reflex (MOCR) has been implicated in several auditory processes. The putative role of the MOCR in improving speech perception in noise is particularly relevant for children who complain of listening difficulties (LiD). The hypothesis that the MOCR may be impaired in individuals with LiD or auditory processing disorder has led to several investigations but without consensus. In two related studies, we compared the MOCR functioning of children with LiD and typically developing (TD) children in the same age range (7–17 years). In Study 1, we investigated ipsilateral, contralateral, and bilateral MOCR using forward-masked click-evoked otoacoustic emissions (CEOAEs; n = 17 TD, 17 LiD). In Study 2, we employed three OAE types: CEOAEs (n = 16 TD, 21 LiD), stimulus frequency OAEs (n = 21 TD, 30 LiD), and distortion product OAEs (n = 17 TD, 22 LiD) in a contralateral noise paradigm. Results from both studies suggest that the MOCR functioning is not significantly different between the two groups. Some likely reasons for differences in findings among published studies could stem from the lack of strict data quality measures (e.g., high signal-to-noise ratio, control for the middle ear muscle reflex) that were enforced in the present study. The inherent variability of the MOCR, the subpar reliability of current MOCR methods, and the heterogeneity in auditory processing deficits that underlie auditory processing disorder make detecting clinically relevant differences in MOCR function impractical using current methods

Mechanisms of otoacoustic emissions

Otoacoustic emissions (OAE) are sounds which are emitted by the ear in response to acoustic stimulation as a byproduct of normal mammalian auditory function. Published research into OAEs leaves many of their detailed characteristics unreported or of uncertain explanation. For example, the mechanisms by which the emissions occur and how many emission mechanisms or categories there are have not yet been clearly established. The purpose of this study was to obtain comprehensive OAE data in a format which would permit specific questions regarding the mechanism of their generation and emission to be answered. Both distortion and transient evoked OAEs responses (DPOAE and TEOAE) were obtained from healthy human ears. It was found these two responses can have similar characteristics but only if a restricted set of DPOAE stimulus parameters are employed, implying that under these conditions the underlying emission mechanisms are closely related. Another significant finding is that lower sideband DPOAE (e.g. 2f1-f2) obtained with stimuli f2/f1>1.1 has fundamentally different phase characteristics (and hence origins) to all other DPOAEs. A new frequency/area representation of detailed DPOAE intensity and phase data has been developed. This revealed that lower and upper DPOAE sidebands are a continuation of each other for f1~=f2, implying a continuity of emission mechanism. This and the transition of behaviour pattern in lower sideband DPOAE for f2/f1>1.1 supports a one source/two emission routes model for DPOAE. DPOAEs arriving in the ear canal by these two routes have been successfully separated and analysed and inferences are drawn regarding the location of DP generation. Amplitude fine structure was demonstrated to be partly due to interference between the two components but also an additional mechanism is involved, perhaps interference within emission generation regions or internal reflections. A simple transmission line model demonstrated that the hypothesis can explain the results seen to a good approximation

Noise-induced cochlear neuronal degeneration and its role in hyperacusis -- and tinnitus-like behavior

Thesis (Ph. D. in Speech and Hearing Bioscience and Technology)--Harvard-MIT Program in Health Sciences and Technology, 2013.Cataloged from PDF version of thesis.Includes bibliographical references (p. 46-57).Perceptual abnormalities such as hyperacusis and tinnitus often occur following acoustic overexposure. Although such exposure can also result in permanent threshold elevation, some individuals with noise-induced hyperacusis or tinnitus show clinically normal thresholds. Recent work in animals has shown that noise exposure can cause permanent degeneration of the cochlear nerve despite complete threshold recovery and lack of hair cell damage (Kujawa and Liberman, J Neurosci 29:14077-14085, 2009). Here we ask whether this noise-induced primary neuronal degeneration results in abnormal auditory behavior, indexed by the acoustic startle response and prepulse inhibition (PPI) of startle. Responses to tones and to broadband noise were measured in mice exposed either to a neuropathic exposure causing primary neuronal degeneration, or to a lower intensity, nonneuropathic noise, and in unexposed controls. Mice with cochlear neuronal loss displayed hyper-responsivity to sound, as evidenced by lower startle thresholds and enhanced PPI, while exposed mice without neuronal loss showed control-like responses. Gap PPI tests, often used to assess tinnitus, revealed spectrally restricted, as well as broadband, gap-detection deficits in mice with primary neuronal degeneration, but not in exposed mice without neuropathy. Crossmodal PPI tests and behavioral assays of anxiety revealed no significant differences among groups, suggesting that the changes in startle-based auditory behavior reflect a neuropathyrelated alteration specifically of auditory neural pathways. Despite significantly reduced cochlear nerve response, seen as reduced wave 1 of the auditory brainstem response, later peaks were unchanged or enhanced, suggesting neural hyperactivity in the auditory brainstem that could underlie the abnormal behavior on the startle tests. Taken together, the results suggest a role for cochlear primary neuronal degeneration in central neural excitability and, by extension, in the generation of tinnitus and hyperacusis.by Ann E. Hickox.Ph.D.in Speech and Hearing Bioscience and Technolog