Robert H. Withnell

Sources and mechanisms of DPOAE generation: Implications for the prediction of auditory sensitivity

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.

The role of intermodulation distortion in transient-evoked otoacoustic emissions.

Transient-evoked otoacoustic emissions (TEOAEs) are low-intensity sounds recorded in the external ear canal immediately following stimulation by a transient stimulus, typically a click. While the details of their production is unknown, there is evidence to suggest that the amplitude of each component frequency reflects the physiological condition of the corresponding region of the cochlea. Certain observations are at variance with this assumption, however, suggesting that pathology at a basal site within the cochlea might affect the production of emissions at frequencies which are not characteristic for that site. We have recorded click-evoked emissions in guinea pigs using high-pass clicks and found emissions at frequencies which are not present in the stimulus and which could not, therefore, have originated from the characteristic place for those emission frequencies. These new frequencies are, by definition, intermodulation distortion frequencies and must have been generated from combinations of frequencies in the stimulus by non-linear processes within the cochlea. Further processing of the emissions by Kemps technique of non-linear recovery showed that the magnitude of emissions at frequencies within the stimulus frequency pass-band was approximately the same as that of frequencies not present in the stimulus. We propose that, in guinea pigs at least, most of the click-evoked emission energy is generated as intermodulation distortion, produced by non-linear intermodulation between various frequency components of the stimulus. If this result is confirmed in humans, many of the anomalies in the literature may be resolved.

Generation of DPOAEs in the guinea pig

In humans, distortion product otoacoustic emissions (DPOAEs) at frequencies lower than the f(2) stimulus frequency are a composite of two separate sources, these two sources involving two distinctly different mechanisms for their production: non-linear distortion and linear coherent reflection [Talmadge et al., J. Acoust. Soc. Am. 104 (1998) 1517-1543; Talmadge et al., J. Acoust. Soc. Am. 105 (1999) 275-292; Shera and Guinan, J. Acoust. Soc. Am. 105 (1999) 332-348; Kalluri and Shera, J. Acoust. Soc. Am. 109 (2001) 662-637]. In rodents, DPOAEs are larger, consistent with broader filters; however the evidence for two separate mechanisms of DPOAE production as seen in humans is limited. In this study, we report DPOAE amplitude and phase fine structure from the guinea pig with f(2)/f(1) held constant at 1.2 and f(2) swept over a range of frequencies. Inverse Fast Fourier Transform analysis and time-domain windowing were used to separate the two components. Both the 2f(1)-f(2) DPOAE and the 2f(2)-f(1) DPOAE were examined. It was found that, commensurate with human data, the guinea pig DPOAE is a composite of two components arising from different mechanisms. It would appear that the 2f(1)-f(2) emission measured in the ear canal is usually dominated by non-linear distortion, at least for a stimulus frequency ratio of 1.2. The 2f(2)-f(1) DPOAE exhibits amplitude fine structure that, for the animals examined, is predominantly due to the variation in amplitude of the place-fixed component. Cochlear delay times appear consistent with a linear coherent reflection mechanism from the distortion product place for both the 2f(1)-f(2) and 2f(2)-f(1) place-fixed components.

The origin of SFOAE microstructure in the guinea pig

Human stimulus-frequency otoacoustic emissions (SFOAEs) evoked by low-level stimuli have previously been shown to have properties consistent with such emissions arising from a linear place-fixed reflection mechanism with SFOAE microstructure thought to be due to a variation in the effective reflectance with position along the cochlea [Zweig and Shera, J. Acoust. Soc. Am. 98 (1995) 2018-2047]. Here we report SFOAEs in the guinea pig obtained using a nonlinear extraction paradigm from the ear-canal recording that show amplitude and phase microstructure akin to that seen in human SFOAEs. Inverse Fourier analysis of the SFOAE spectrum indicates that SFOAEs in the guinea pig are a stimulus level-dependent mix of OAEs arising from linear-reflection and nonlinear-distortion mechanisms. Although the SFOAEs are dominated by OAE generated by a linear-reflection mechanism at low and moderate stimulus levels, nonlinear distortion can dominate some part of, or all of, the emission spectrum at high levels. Amplitude and phase microstructure in the guinea pig SFOAE is evidently a construct of (i). the complex addition of nonlinear-distortion and linear-reflection components; (ii). variation in the effective reflectance with position along the cochlea; and perhaps (iii). the complex addition of multiple intra-cochlear reflections.

Brief report: the cochlear microphonic as an indication of outer hair cell function.

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.

Changes to low-frequency components of the TEOAE following acoustic trauma to the base of the cochlea

Several studies have shown that acoustic trauma to the base of the cochlea can result in loss of transient-evoked otoacoustic emission (TEOAE) energy at frequencies much lower than those affected in the audiogram. We have extended these studies to show that the low-frequency emission energy was substantially affected if the transient stimulus included frequencies within the range affected by the trauma, otherwise the change observed was small. In keeping with the suggestion that TEOAEs are predominantly comprised of intermodulation distortion energy (Yates and Withnell, Hear. Res. 136 (1999) 49-64), trauma to the basal region of the cochlea was found to affect emission energy across a broad frequency range in response to a wide-band acoustic stimulus. Further, group delay measurements demonstrated that the dominant contribution to the TEOAE originated from the basal region of the cochlea.

Reconciling the origin of the transient evoked ototacoustic emission in humans

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)].

An in situ calibration for hearing thresholds

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.

Enhancement of the transient-evoked otoacoustic emission produced by the addition of a pure tone in the guinea pig.

This study examined the transient-evoked otoacoustic emission obtained in response to a click stimulus presented in combination with a pure tone in the guinea pig. Low-pass filtered click waveforms were digitally generated using a sin(t)/t function windowed over 3 ms with an elevated cosine envelope. Transient-evoked otoacoustic emissions were obtained using the nonlinear derived response technique. Phase locked pure tones of various frequencies at approximately 70 dB SPL were electrically mixed with electrical clicks, with the pure tone present only for the three lower level stimuli in the train of four stimuli. Enhancement in the amplitude of the response spectrum at frequencies which corresponded to regions of the basilar membrane apical to the tone was observed with the addition of the tone. This finding is inconsistent with the transient-evoked otoacoustic emission being the result of independent generators. It suggests that intermodulation distortion energy may contribute to the transient-evoked otoacoustic emission, the enhancement in the emission response spectrum at frequencies below the pure tone being a result of a complex interaction on the basilar membrane of intermodulation distortion products.

Onset of basilar membrane non-linearity reflected in cubic distortion tone input-output functions

The basilar membrane (BM) input output (I/O) function is a non-linear compressive function over much of its operating range. A low level non-compressive region with a break-point or compression threshold between 20 and 40 dB SPL has been identified. To date, no similar compression threshold in cubic distortion tone otoacoustic emission (CDT) data, which would illustrate the dependence of the CDT on BM growth, has been demonstrated. A Taylor series expansion of the outer hair cell gating function yields an amplitude term for 2f1-f2 of p.A1(2).A2, where A1 and A2 are the displacement amplitudes of the BM for two pure tone input stimuli of levels L1 and L2, p a constant. By selectively varying either L1 or L2 with f2/f1 appropriately chosen to reduce suppression effects, the CDT I/O function can be examined for deviation from the power law. In particular, if the amplitude of the CDT were dependent on BM displacement amplitude, then it should be possible by an appropriate choice of parameters to measure compression threshold. We have examined CDT I/O functions for an f2 of 8 kHz in the guinea pig and found them to be consistent with the expected power law. With L1 held constant, L2 varied and f2/f1 = 1.6, a low level region with a slope of one and a compressive region with a slope of 0.14-0.27 corresponding to the analogous regions of the BM I/O function was identified, with a break-point or compression threshold of 22-33 dB SPL.