By Carolina Abdala
This article is a part of the January/February 2018, Volume 30, Number 1, Audiology Today issue.
Otoacoustic emissions (OAEs), low-level sounds produced by the healthy cochlea, require normal or near-normal outer hair cells (OHCs) to provide amplification of the backward traveling waves so the outgoing energy can be detected in the ear canal and, for some types of OAEs, to produce the nonlinearities that give rise to the emission itself. As most audiologists know, these low-level acoustic by-products provide an invaluable window into the otherwise inaccessible cochlea and a useful gauge of OHC health and hearing.
When OAEs were first discovered (Kemp, 1978), it was thought that each type of emission was basically a duplicate of the other; that is, although some were evoked with clicks and others with tones, we assumed that they all came about the same way and provided redundant information about the cochlea. However, in the last decade or so, we have come to understand that not all OAEs are alike (Shera and Guinan, 1999). There are two basic types of OAEs: nonlinear distortion and linear reflection. The familiar OAEs that audiologists use in the clinic generally fall into one or the other of these two categories, or include a mix of the two.
Distortion-type emissions are created by nonlinearities in OHC transduction. Nonlinearity in the cochlea likely originates at the ion channels found on the tips of OHC stereocilia. A stimulus vibrates the basilar membrane within the cochlea and in doing so, displaces the OHC and stereocilia atop these specialized cells. The thin filaments attached to the tips of the stereocilia sway with the motion and pull open ion channels like trap doors, near the ciliary tip. Opening the ion channels [mechanoelectric transduction (MET) channels] allows current to flow into the cell and change the intracellular voltage, initiating OHC motility which powers the “cochlear amplifier.” Because there are only a limited number of MET channels, the intracellular voltage and resulting OHC force cannot increase in direct proportion to an increasing stimulus, but grows more slowly (i.e., compressively). As a result, the cochlear response to sound slows and saturates. We believe this cochlear compression is the principal nonlinearity gauged by distortion-type OAEs.
Reflection-type emissions are another animal. Reflection OAEs arise through a linear reflection process: that is, the back-scattering of incoming waves, much as waves might bounce back off of pier pilings in a large body of water. No biological membrane or array of cells can be perfectly smooth and uniform along its length—the cochlea is no exception. When a sound is presented to the ear, traveling waves are launched down the cochlear spiral on the basilar membrane. As they propagate, they encounter irregularities that disrupt the smooth forward flow of energy and give rise to back-scattered wavelets that turn energy around. This reflected energy travels back toward the base of the cochlea and some of it makes its way into the ear canal. The physics of this scattering process indicates that the strongest reflection occurs near the peak of the traveling wave (Zweig and Shera, 1995). When enough of these back-scattered wavelets sum in a coherent way, they produce an emission that is large enough to be recorded in the ear canal as a reflection OAE.
How do familiar clinical OAEs fit into this taxonomy? As you might have suspected, the DPOAEs, which are evoked by two tones presented simultaneously near the overlap of the two traveling waves elicited by these two primary tones, are nonlinear distortion emissions, though they also include a small reflection component. (The DPOAE is really a mixed OAE but the distortion part is dominant under most clinical protocols.) Click-evoked or transient-evoked OAEs, stimulus-frequency OAEs (OAEs generated with one low level pure tone), and spontaneous OAEs are all reflection emissions.
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