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at that time as research models of hearing impairments such as noise-induced hearing loss and drug-induced ototoxicity in common laboratory animals including Old World mon- keys, gerbils, guinea pigs, chinchillas, and rabbits.
As discussed in greater detail below, within a decade or so after their original discovery, both hearing scientists and audiology-trained practitioners recognized the remarkable potential utility of evoked OAEs as a test of the status of co- chlear function based on their objective, efficient, quantita- tive, and, particularly, noninvasive properties. The purpose of this review is to summarize the current status of OAEs with respect to both the research and clinical fields and to deduce from these analyses what the future holds for the ap- plication of emission measures in these specialized arenas.
Significant Theoretical Issues
The presence of cochlear emissions was hypothesized in the late 1940s based on mathematical models of cochlear nonlin- earity (Gold, 1948). However, OAEs could not be measured until the late 1970s when technology enabled the development of the extremely sensitive low-noise microphones needed to record these responses. Exactly how OAEs arise and how they are propagated in and out of the cochlea, through the middle ear, and to the acoustic probe consisting of a sound emitter and pickup sensor seated in the outer ear canal is still being debated (e.g., He and Ren, 2013). Both experimental find- ings and related theoretical notions suggest that there are two fundamental mechanisms of OAE generation as proposed by Shera and Guinan (1999). In the nomenclature established by Shera and Guinan (1999), SOAEs, TEOAEs, and SFOAEs are considered to arise mostly from coherent linear reflections produced by impedance discontinuities such as differences in the strengths of outer hair cell (OHC) micromechanical forces or possibly structural microirregularities such as out-of-place OHCs or disarranged hair bundles (i.e., stereocilia) that are distributed along the cochlear partition (e.g., Lonsbury- Martin et al., 1988), whereas DPOAEs result from nonlinear distortion processes secondary to but inherent to normal cochlear function (for examples of the four OAE types, see Whitehead et al., 1994). Thus, the prevailing view is that the sources of OAE generation are reflection- (SOAEs, TEOAEs, and SFOAEs) or a combination of reflection and distortion- (DPOAEs) generating processes.
A current understanding about the microprocesses that underlie the generation of OAEs is that the electromotility of the OHC receptors is due to receptor potential-initiated movements of prestin “motor” molecules that are embed-
ded in the lateral membrane of the OHCs (see the discussion about electromotility and its discovery in Brownell, 2017). Indeed, further reasoning presumes that OAEs are in some way generated as a by-product of a combination of these electromotile-based vibrations of the OHCs, such as short- ening/lengthening, along with the stimulation-induced non- linear openings and closings of the ion-based transduction channels at the tips of OHC stereocilia. As noted above, the existence of OAEs provides solid evidence that the cochlea is an active participant in the processing of acoustic signals in that the miniscule movements of the subcomponents of the OHCs act to enhance the sensitivity and frequency tuning of the vibrations of the cochlear partition.
In the current theories of cochlear function, the OHCs act as a “cochlear amplifier” in the form of a biological micro- mechanical feedback system that enhances and sharpens the peak of the broader Békésy traveling wave (TW; von Békésy, 1960). With OHC damage, the sensitivity and sharp tuning of basilar membrane (BM) vibrations are greatly reduced, and the passive mechanical analysis and poor tuning of the Békésy TW predominate. It is well established that when the OHCs are damaged or eliminated through degeneration processes, the sharp tuning and sensitivity of the cochlea are greatly compromised and OAEs are reduced or absent.
In the case of reflection emissions, the peak of the TW likely plays an important role as a source of reflection and filtering for TEOAEs, SFOAEs, and SOAEs. Hence, OHC damage greatly affects these types of OAEs. In contrast, DPOAEs appear to be generated mainly in the nonlinear “distortion” aspects of the OHC transduction process that probably involves the stereocilia of the OHCs. This explains why DPOAEs evoked by high-level primaries persist after the administration of certain ototoxins (drugs that damage the sensory cells of the ear) such as various diuretics. In this instance, the BM vibrations are absent due to the reduction in the driving voltage across the OHC to stimulate the hair bundle nonlinearities. However, for high-level stimuli, this lack of gain is overcome and DPOAEs can again be observed at such suprathreshold levels of stimulation.
Middle Ear Influences on Measures of Otoacoustic Emissions
Before proceeding with a review of the status of OAEs in today’s audiology clinic, it is important to address how the middle ear transmission pathway affects the measured fea- tures of emissions. Because both the stimulus and the OAEs pass through the middle ear, they are modified in cases of
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