A pervasive theme in the literature for the transient evoked otoacoustic emission (TEOAE) measured from the human ear canal has been one of the emission arising solely (or largely) from a single, place-fixed mechanism. Here TEOAEs are reported measured in the absence of significant stimulus contamination at stimulus onset, providing for the identification of a TEOAE response beginning within the time window that is typically removed by windowing. Contrary to previous studies, it was found that in humans, as has previously been found in guinea pig, the TEOAE appears to arise from two generation mechanisms, the relative contributions of these two mechanisms being time and stimulus-level dependent. The method of windowing the earliest part of the ear canal measurement to remove stimulus artifact removes part of the TEOAE i.e., much of the component arising from a nonlinear generation mechanism. This reconciliation of TEOAE origin is consistent with all OAEs in mammals arising in a stimulus-level dependent manner from two mechanisms of generation, one linear, one nonlinear, as suggested by Shera and Guinan [J. Acoust. Soc. Am. 105, 782-798 (1999)].

The extra-cellular cochlear microphonic is believed to be generated predominantly by outer hair cells and therefore it would seem reasonable to assume that the presence of a cochlear microphonic excludes outer hair cell dysfunction. Indeed, a diagnosis of auditory neuropathy might be, and has been, made on the basis of a cochlear microphonic present with an abnormal auditory brainstem response. Animal studies, however, have shown that the cochlear microphonic recorded from the round window is dominated by cellular generators located in the base of the cochlea. Primarily on this basis, it is argued that the presence of a cochlear microphonic does not exclude outer hair cell pathology and so outer hair cell integrity should not necessarily be inferred from the presence of the cochlear microphonic alone. In contrast, the absence of an otoacoustic emission in such cases is consistent with outer hair cell dysfunction.

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Quantifying how the sound delivered to the ear canal relates to hearing threshold has historically relied on acoustic calibration in physical assemblies with an input impedance intended to match the human ear (e.g., a Zwislocki coupler). The variation in the input impedance of the human ear makes such a method of calibration questionable. It is preferable to calibrate the acoustic signal in each ear individually. By using a calibrated sound source and microphone, the acoustic input impedance of the ear can be determined, and the sound delivered to the ear calibrated in terms of either (i) the incident sound pressure wave or (ii) that portion of the incident sound pressure wave transmitted to the middle ear and cochlea. Hearing thresholds expressed in terms of these quantities are reported, these in situ calibrations not being confounded by ear canal standing waves. Either would serve as a suitable replacement for the current practice of hearing thresholds expressed in terms of sound pressure level calibrated in a 6cc or 2cc coupler.

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Otoacoustic emissions (OAEs) have become a commonly used clinical tool for assessing cochlear health status, in particular, the integrity of the cochlear amplifier or motor component of cochlear function. Predicting hearing thresholds from OAEs, however, remains a research challenge. Models and experimental data suggest that there are two mechanisms involved in the generation of OAEs. For distortion product, transient, and high-level stimulus frequency emissions, the interaction of multiple sources of emissions in the cochlea leads to amplitude variation in the composite ear canal signal. Multiple sources of emissions complicate simple correlations between audiometric test frequencies and otoacoustic emission frequencies. Current research offers new methods for estimating the individual components of OAE generation. Input-output functions and DP-grams of the nonlinear component of the 2f2-f2 DPOAE may ultimately show better correlations with hearing thresholds. This paper reviews models of OAE generation and methods for estimating the contribution of source components to the composite emission that is recorded in the ear canal. The clinical implications of multiple source components are discussed.

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In the guinea pig it has been shown that the nonlinear derived transient evoked otoacoustic emission (TEOAEnl) is comprised of significant amounts of intermodulation distortion energy. It is expected that intermodulation distortion arising from a nonlinear distortion mechanism will contribute to the overall TEOAE in a stimulus-level-dependent manner, being greatest when basilar-membrane vibration in response to a click stimulus is greatest; with decay of vibration of the basilar membrane subsequent to stimulation by a click, nonlinear interaction along the cochlear partition should reduce and so provide for a linear mechanism to dominate TEOAEnl generation, i.e., the contributions of each of these mechanisms should be delay dependent. To examine this delay dependence, TEOAEnl evoked by acoustic clicks of varying bandwidth were time-domain windowed using a recursive exponential filter in an attempt to separate two components with amplitude and phase properties consistent with different mechanisms of OAE generation. It was found that the part of the TEOAEnl occurring first in time can have a relatively constant amplitude and shallow phase slope, consistent with a nonlinear distortion mechanism. The latter part of the TEOAEnl has an amplitude microstructure and a phase response more consistent with a place-fixed mechanism.