Modifications of a single saturating non-linearity account for post-onset changes in 2f1-f2 distortion product otoacoustic emission

2f1-f2 distortion product otoacoustic emissions (DPOAEs) were recorded from guinea pigs. DPOAEs showed complex time dependence at the onset of stimulation. The DPOAE, measured during the first 500 ms, can either decrease or increase at the onset depending on both the frequencies and levels of the primary tones. These changes are closely associated with amplitude minima (notches) of the DPOAE I/O functions. These notches are characteristic of DPOAE growth functions measured from guinea pigs for primary tones of 50-60-dB sound-pressure level (SPL). Apparent changes in the DPOAE amplitude occur because the notch shifts to higher levels of the primaries during the onset of stimulation. This shift of the notch to higher levels increases for lower f2/f1 ratios but does not exceed about 2 dB. DPOAE amplitude increases for a constant level of the primaries if the onset emission is situated at the low-level, falling slope of the notch. If the onset DPOAE is located on the high-level, rising slope of the notch, then the upward shift of the notch causes the emission either to decrease monotonically, or to decrease initially and then increase. By establishing that the 2f1-f2 onset changes reflect a shift in the growth-function notch, it is possible to predict the temporal behavior of DPOAEs in the two-dimensional space of the amplitude of the primaries and for their different frequency ratios.     

Physiopathological significance of distortion-product otoacoustic emissions at 2f1-f2 produced by high- versus low-level stimuli

Distortion product otoacoustic emissions emitted by the cochlea at 2f1-f2 in response to pairs of pure tones at f1 and f2 (DPOAE) form a class of otoacoustic emissions and as such, are viewed as a reliable tool for screening outer hair cell (OHC) dysfunctions on a pass/fail basis. However, the persistence of residual DPOAEs from impaired cochleae at high stimulus levels has suggested that above 60-70 dB SPL, instead of reflecting "active" cochlear motion, DPOAEs might represent another "passive" modality: they would thus become unsuitable for analyzing cochlear function. The present work reports the consequences on high- vs low-level DPOAEs of three types of cochlear impairments involving OHCs: progressive OHC degeneration of genetic origin in CD1 mice, complete cochlear ischemia in gerbils, and furosemide injection vs ischemia-reperfusion in gerbils. An alternative to the "active-passive" model was used wherein regardless of stimulus level, cubic DPOAEs are produced by N (probably OHC-borne) nonlinear elements driven by input I and modulated by a function F3 of their operating point o; thus, DPOAE proportional to NI3F3(o). When OHCs degenerated, thereby implying a decrease of N, DPOAE levels also decreased regardless of the stimulus level up to 80 dB SPL, in line with the previous formula but at variance with the prediction of the active-passive concept. Instead of affecting N, the other two experiments impaired the efficiency of the cochlear feedback loop as a result of its electrical drive being decreased by strial dysfunction. As it is well accepted that the impaired basilar-membrane motion, although greatly reduced at low levels, tends to catch up with a normal one at higher levels, it was assumed the same was true with I so that DPOAE levels had to be, and indeed were little affected at high levels while plummeting at low levels, without any need for invoking two modalities for DPOAE generation. Finally, comparisons of furosemide vs ischemia effects revealed additional influences on DPOAEs, possibly accounted for by function F3(o). These results lead to the proposal that although high-level DPOAEs are expected to be poor audiometric indicators, they seem well adapted to assessing the functional integrity of nonlinear elements in OHCs, i.e., presumably their mechanoelectrical transduction channels.     

One source for distortion product otoacoustic emissions generated by low- and high-level primaries

Distortion product otoacoustic emissions (DPOAE) elicited by tones below 60-70 dB sound pressure level (SPL) are significantly more sensitive to cochlear insults. The vulnerable, low-level DPOAE have been associated with the postulated active cochlear process, whereas the relatively robust high-level DPOAE component has been attributed to the passive, nonlinear macromechanical properties of the cochlea. However, it is proposed that the differences in the vulnerability of DPOAEs to high and low SPLs is a natural consequence of the way the cochlea responds to high and low SPLs. An active process boosts the basilar membrane (BM) vibrations, which are attenuated when the active process is impaired. However, at high SPLs the contribution of the active process to BM vibration is small compared with the dominating passive mechanical properties of the BM. Consequently, reduction of active cochlear amplification will have greatest effect on BM vibrations and DPOAEs at low SPLs. To distinguish between the "two sources" and the "single source" hypotheses we analyzed the level dependence of the notch and corresponding phase discontinuity in plots of DPOAE magnitude and phase as functions of the level of the primaries. In experiments where furosemide was used to reduce cochlear amplification, an upward shift of the notch supports the conclusion that both the low- and high-level DPOAEs are generated by a single source, namely a nonlinear amplifier with saturating I/O characteristic.     

Evidence for two discrete sources of 2f1-f2 distortion-product otoacoustic emission in rabbit: I. Differential dependence on stimulus parameters.

The results of studies of the physiological vulnerability of distortion-product otoacoustic emissions (DPOAEs) suggest that the DPOAE at 2f1-f2 in vertebrate ears is generated by more than one source. The principal aims of the present study were to provide independent evidence for the existence of more than one DPOAE source, and to determine the contributions of each to the ear-canal 2f1-f2 signal. To accomplish these aims, specific stimulus parameters were separately and systematically varied to provide detailed parametric information regarding 2f1-f2 DPOAE amplitude and phase in normal ears of awake rabbits. The findings indicate that two discrete sources, demonstrating differential dependence on stimulus parameters, dominate the generation of the 2f1-f2 DPOAE. One source of distortion is dominant above 60-70 dB SPL at moderate primary-frequency separations, and at all stimulus levels when the primary tones are closely spaced. The other source is dominant below 60-70 dB SPL at moderate primary-frequency separations, and may be dominant at all stimulus levels when the primary tones are widely separated in frequency. The results suggest that by varying stimulus parameters, it may be possible to independently study the two generator mechanisms.     

Influence of primary frequencies ratio on distortion product otoacoustic emissions amplitude. II. Interrelations between multicomponent DPOAEs, tone-burst-evoked OAEs, and spontaneous OAEs

Distortion product otoacoustic emissions (DPOAEs) are used widely in humans to assess cochlear function. It is well known that 2f1-f2 DPOAE amplitude increases as the f2/f1 ratio increases from 1.0 to about 1.20, and then decreases as the f2/f1 ratio increases above 1.20, showing an amplitude ratio function, which is thought to be related to cochlear filtering properties. Different lower sideband DPOAEs are believed to show the same amplitude ratio functions as the 2f1-f2 DPOAE, with a magnitude peak situated at a constant DPOAE frequency relative to f2. More recently, several studies have suggested the involvement of a DPOAE component coming from its own distortion product place as well as the DPOAE component coming from the f2 place. To investigate DPOAE generation sites and the importance of the DPOAE frequency place, amplitude ratio functions of 2f1-f2, 3f1-2f2, 4f1-3f2 and 2f2-f1, 3f2-2f1, 4f2-3f1 DPOAE components have been systematically studied in 18 normally hearing subjects, using an f2 fixed, f1 sweep method, and an f1 fixed, f2 sweep method, at ten different f2 frequencies. Results show a dependency of the distortion magnitude peak on f2 frequency for each lower sideband DPOAE, and a small frequency shift of the distortion peak for the high order lower sideband DPOAE components. Strong correlation between the different lower sideband DPOAE amplitude were obtained, whether they were recorded with the same f1 (and a different f2) or with the same f2 (and a different f1), suggesting that lower side-band DPOAE amplitude does not depend on small variations in the f2 frequency. Moreover, correlations between DPOAE amplitude and tone-burst evoked otoacoustic emissions (TBOAEs) are highly significant for TBOAEs centered at the f2 frequency and at 1/2 octave below the f2 frequency, suggesting some degree of importance of the cochlear status at frequencies below f2 in DPOAE amplitude. Subjects presenting spontaneous otoacoustic emissions showed a greater lower sideband DPOAE amplitude recorded for low f2/f1 ratios, and a distortion magnitude peak shifted towards higher frequencies. The best correlation between upper sideband DPOAE amplitude and lower sideband DPOAE amplitude occurred for lower sideband DPOAEs generated by an f2 frequency 1/2 octave to 1 octave below the primaries used to generate upper sideband DPOAEs, suggesting a site of generation basal to f2 for the upper sideband DPOAEs. Correlations between TBOAE amplitude and upper sideband DPOAE amplitude agreed with a site of upper sideband DPOAE generation basal to f2, and which would move with the DPOAE frequency itself.     

Otoacoustic emissions without somatic motility: can stereocilia mechanics drive the mammalian cochlea?

Distortion product otoacoustic emissions (DPOAEs) evoked by low-level tones are a sensitive indicator of outer hair cell (OHC) function. High-level DPOAEs are less vulnerable to cochlear insult, and their dependence on the OHC function is more controversial. Here, the mechanism underlying high-level DPOAE generation is addressed using a mutant mouse line lacking prestin, the molecular motor driving OHC somatic motility, required for cochlear amplification. With prestin deletion, attenuated DPOAEs were measurable at high sound levels. DPOAE thresholds were shifted by approximately 50 dB, matching the loss of cochlear amplifier gain measured in compound action potentials. In contrast, at high sound levels, distortion products in the cochlear microphonic (CM) of mutants were not decreased re wildtypes (expressed re CM at the primaries). Distortion products in both CM and otoacoustic emissions disappeared rapidly after death. The results show that OHC somatic motility is not necessary for the production of DPOAEs at high SPLs. They also suggest that the small, physiologically vulnerable DPOAE that remains without prestin-based motility is due directly to the mechanical nonlinearity associated with stereociliary transduction, and that this stereocilia mechanical nonlinearity is robustly coupled to the motion of the cochlear partition to the extent that it can drive the middle ear.     

The influence of systematic primary-tone level variation L2-L1 on the acoustic distortion product emission 2f1-f2 in normal human ears

The purpose of the present study was to determine the effect of primary-tone level variation, L2--L1, on the amplitude of distortion-product otoacoustic emissions (DPOAEs). The DPOAE at the frequency 2f1--f2 (f2 greater than f1) was measured in 20 ears of ten normally hearing subjects. Acoustic distortion products were generated by primaries f1 and f2 with geometric mean frequencies of 1, 2, and 4 kHz. The f2/f1 ratios were 1.25 (1 kHz), 1.23 (2 kHz), and 1.21 (4 kHz). The primary-tone level L1 was kept constant at either 65 or 75 dB SPL while the second primary-tone level L2 was varied between 20 and 90 dB SPL in 5-dB steps. The level differences L2--L1 generating maximal DPOAE amplitudes depended on L1 and on the geometric mean frequency of f1 and f2. There were large interindividual differences. Overall, the L2--L1 evoking maximal mean DPOAE amplitudes was --10 dB for geometric mean frequencies of 1 and 2 kHz with both L1 = 65 dB SPL and L1 = 75 dB SPL. For 4 kHz, L2-L1 was --5 dB with L1 = 65 dB SPL and 0 dB with L1 = 75 dB SPL. The mean slopes of the DPOAE growth functions in the initial linearly increasing portions were steeper at higher stimulus frequencies, increasing from 0.52 at 1 kHz to 0.72 at 4 kHz for L1 = 65 dB SPL and from 0.48 at 1 kHz to 0.72 at 4 kHz for L1 = 75 dB SPL.     

Level dependence of distortion-product otoacoustic emissions measured at high frequencies in humans

Given that high-frequency hearing is most vulnerable to cochlear pathology, it is important to characterize distortion-product otoacoustic emissions (DPOAEs) measured with higher-frequency stimuli in order to utilize these measures in clinical applications. The purpose of this study was to explore the dependence of DPOAE amplitude on the levels of the evoking stimuli at frequencies greater than 8 kHz, and make comparisons with those data that have been extensively measured with lower-frequency stimuli. To accomplish this, DPOAE amplitudes were measured at six different f2 frequencies (2, 5, 10, 12, 14, and 16 kHz), with a frequency ratio (f2/f1) of 1.2, at five fixed levels (30 to 70 dB SPL) of one primary (either f1 or f2), while the other primary was varied in level (30 to 70 dB SPL). Generally, the level separation between the two primary tones (L1 > L2) generating the largest DPOAE amplitude (referred to as the "optimal level separation") decreased as the level of the fixed primary increased. Additionally, the optimal level separation was frequency dependent, especially at the lower fixed primary tone levels ( < or = 50 dB SPL). In agreement with previous studies, the DPOAE level exhibited greater dependence on L1 than on L2.     

Pure-tone threshold estimation from extrapolated distortion product otoacoustic emission I/O-functions in normal and cochlear hearing loss ears

A new method for direct pure-tone threshold estimation from input/output functions of distortion product otoacoustic emissions (DPOAEs) in humans is presented. Previous methods use statistical models relating DPOAE level to hearing threshold including additional parameters e.g., age or slope of DPOAE I/O-function. Here we derive a DPOAE threshold from extrapolated DPOAE I/O-functions directly. Cubic 2 f1-f2 distortion products and pure-tone threshold at f2 were measured at 51 frequencies between f2=500 Hz and 8 kHz at up to ten primary tone levels between L2=65 and 20 dB SPL in 30 normally hearing and 119 sensorineural hearing loss ears. Using an optimized primary tone level setting (L1 = 0.4L2 + 39 dB) that accounts for the nonlinear interaction of the two primaries at the DPOAE generation site at f2, the pressure of the 2 f1-f2 distortion product pDP is a linear function of the primary tone level L2. Linear regression yields correlation coefficients higher than 0.8 in the majority of the DPOAE I/O-functions. The linear behavior is sufficiently fulfilled for all frequencies in normal and impaired hearing. This suggests that the observed linear functional dependency is quite general. Extrapolating towards pDP=0 yields the DPOAE threshold for L2. There is a significant correlation between DPOAE threshold and pure-tone threshold (r=0.65, p<0.001). Thus, the DPOAEs that reflect the functioning of an essential element of peripheral sound processing enable a reliable estimation of cochlear hearing threshold up to hearing losses of 50 dBHL without any statistical data.     

Distortion product otoacoustic emissions and basilar membrane vibration in the 6-9 kHz region of sensitive chinchilla cochleae

Distortion product otoacoustic emissions (DPOAEs) and basilar membrane (BM) vibration were measured simultaneously in the 6-9 kHz region of chinchilla cochleae. BM-Input-Output functions in a two-tone paradigm behaved similarly to DPOAEs for the 2f1-f2 component, nonmonotonic growth with the intensity of the lower frequency primary and a notch in the functions around 60 dB SPL. Ripples in frequency functions occur in both BM and OAE curves as a function of the distortion frequency. Optimum f2/f1 ratios for DPOAE generation are near 1.2. The slope of phase curves indicates that for low f2f1(<1.1) the emission source is the place location while for f2f1>1.1 the relative constancy of the phase function suggests that the place is the nonlinear region of f2, i.e., the wave location. Magnitudes of the DPOAEs increase rapidly above 60 dB SPL suggesting a different source or mechanism at high levels. This is supported by the observation that the high level DPOAE and BM-DP responses remain for a considerable period postmortem.     

Influence of primary frequencies ratio on distortion product otoacoustic emissions amplitude. I. Intersubject variability and consequences on the DPOAE-gram

Distortion product otoacoustic emissions (DPOAEs) are used widely in humans to assess cochlear function. The standard procedure consists of recording the 2f1-f2 DPOAE amplitude as a function of the f2 frequency, using a fixed f2/f1 ratio (DPOAE-gram), close to 1.20. DPOAE amplitude, as recorded in the DPOAE-gram, shows a wide range of values in normal-hearing subjects, which can impair the predictive value of the DPOAE-gram for hearing thresholds. This study is aimed at comparing intersubject variability in 2f1-f2 DPOAE amplitude according to three paradigms: a fixed f2/f1 ratio, such as the DPOAE-gram, a variable ratio DPOAE-gram (f2/f1 adapted to frequency) and an "optimum" DPOAE-gram, where the f2/f1 is adapted both to subject and frequency. The 2f1-f2 DPOAE amplitude has been investigated on 18 normally hearing subjects at ten different f2 frequencies (from 0.75 to 6 kHz), using an f2 fixed, f1 sweep paradigm, and allowed to define, for each frequency, the f2/f1 ratio giving the greatest 2f1-f2 DPOAE amplitude (or optimum ratio). Results showed a large intersubject variability of the optimum ratio, especially at frequencies below 1.5 kHz, and a significant decrease of the optimum ratio with frequency. The optimum DPOAE-gram was underestimated by up to 5.8 dB on average (up to 14.9 dB for an individual subject) by the fixed ratio DPOAE-gram, and by up to 3 dB on average (up to 10.6 dB for an individual subject) by the variable ratio DPOAE-gram. Intersubject variability was slightly but significantly reduced in the optimum DPOAE-gram versus the fixed-ratio DPOAE-gram. Lastly, correlations between tone-burst evoked otoacoustic emission (TBOAE) amplitudes and maximum DPOAE amplitudes were significantly greater than correlations between TBOAE amplitudes and fixed-ratio DPOAE amplitudes.     

DPOAE group delays versus electrophysiological measures of cochlear delay in normal human ears

Group delays of 2 f1-f2 distortion product otoacoustic emissions (DPOAEs) were determined using both f1- and f2-sweep paradigms in 24 normal-hearing subjects. These DPOAE group delays were studied in comparison with cochlear delays estimated from derived band VIIIth nerve compound action potentials (CAPs) and auditory brainstem responses (ABRs) in the same subjects. The center frequencies of the derived bands in the electrophysiological experiment were matched with the f2-frequencies in the DPOAE recording to ensure that DPOAEs and derived CAPs and ABRs were generated at the same places along the cochlear partition, thus allowing for a direct comparison. The degree to which DPOAE group delays are larger in the f2- than in the f1-sweep paradigm is consistent with a theoretical analysis of the so-called wave-fixed model. Both DPOAE group delays are highly correlated with CAP- and ABR-derived measures of cochlear delay. The principal result of this study is that "roundtrip" DPOAE group delay in the f1-sweep paradigm is exactly twice as large as the neural estimate of the "forward" cochlear delay. The interpretation of this notion in the context of cochlear wave propagation properties and DPOAE-generating mechanisms is discussed.     

Input-output functions for stimulus-frequency otoacoustic emissions in normal-hearing adult ears

Input-output (I/O) functions for stimulus-frequency (SFOAE) and distortion-product (DPOAE) otoacoustic emissions were recorded in 30 normal-hearing adult ears using a nonlinear residual method. SFOAEs were recorded at half octaves from 500-8000 Hz in an L1=L2 paradigm with L2=0 to 85 dB SPL, and in a paradigm with L1 fixed and L2 varied. DPOAEs were elicited with primary levels of Kummer et al. [J. Acoust. Soc. Am. 103, 3431-3444 (1998)] at f2 frequencies of 2000 and 4000 Hz. Interpretable SFOAE responses were obtained from 1000-6000 Hz in the equal-level paradigm. SFOAE levels were larger than DPOAEs levels, signal-to-noise ratios were smaller, and I/O functions were less compressive. A two-slope model of SFOAE I/O functions predicted the low-level round-trip attenuation, the breakpoint between linearity and compression, and compressive slope. In ear but not coupler recordings, the noise at the SFOAE frequency increased with increasing level (above 60 dB SPL), whereas noise at adjacent frequencies did not. This suggests the existence of a source of signal-dependent noise producing cochlear variability, which is predicted to influence basilar-membrane motion and neural responses. A repeatable pattern of notched SFOAE I/O functions was present in some ears, and explained using a two-source mechanism of SFOAE generation.     

Group delays of distortion product otoacoustic emissions in the guinea pig.

This paper presents a comprehensive set of experimental data on group delays of distortion product otoacoustic emissions (DPOAEs) in the guinea pig. Group delays of the DPOAEs with frequencies 2f1-f2, 3f1-2f2, 4f1-3f2, and 2f2-f1 were measured with the phase gradient method. Both the f1- and the f2-sweep paradigm were used. Differences between the two sweep paradigms were investigated for the four DPOAEs, as well as the group delay differences between the DPOAEs. Analysis revealed larger group delays with the f2-sweep paradigm, but only for the lower sideband DPOAEs (with fdp < f1,f2). For the lower sideband cubic distortion product 2f1-f2, the f2-sweep delays were a factor of 1.17-1.54 larger than the f1-sweep delays, depending on frequency. The upper sideband DPOAE 2f2-f1 showed no significant difference between f1- and f2-sweep group delays, except for the highest and lowest f2 frequencies. Comparing the group delays of the DPOAEs for each sweep paradigm separately, equal group delays were found for all four DPOAEs measured with the f1-sweep. With the f2-sweep paradigm on the other hand, the group delays of the three lower sideband DPOAEs occurred to be larger than the group delays of the upper sideband DPOAE 2f2-f1. A tentative interpretation of the data in the context of proposed explanatory hypotheses on DPOAE group delays is given.     

Frequency specificity of distortion-product otoacoustic emissions produced by high-level tones despite inefficient cochlear electromechanical feedback

Distortion product otoacoustic emissions (DPOAEs) are thought to stem from the outer hair cells (OHCs) around the normally narrow place tuned to the primary tone stimuli. They are thus said to be frequency-specific: their local absence should accurately pinpoint local OHC damage. Yet the influence of impaired tuning on DPOAE frequency specificity is poorly documented. Mice with local damage to OHCs were examined. Their DPOAEs were frequency-specific in that audiometric notches were accurately tracked. The same cochleae were further impaired by ischemia or furosemide injection inducing strial dysfunction with flat loss of sensitivity and tuning, while the preexisting pattern of damaged OHCs remained unaltered. Despite the loss of cochlear activity, DPOAEs produced by high-level (> or =70 dB SPL) primaries remained large in about the same interval where they had been initially normal, i.e., that with nondamaged OHCs, albeit with a slight frequency shift, of -1.1 kHz on average. Thus, the ability of DPOAEs to map structurally intact OHCs cannot be a mere consequence of cochlear tuning as it largely persists in its absence. The key element for this correct mapping is likely part of intact OHC structures (e.g., stereocilia bundles) and must have some tuning of its own.     

Modeling the growth rate of distortion product otoacoustic emissions by active nonlinear oscillators

In this work, growth-rate curves of the 2 f1-f2 distortion product otoacoustic emission (DPOAE) are analyzed in a population of 30 noise exposed subjects, including both normal-hearing and hearing impaired subjects. A particular embedded limit-cycle oscillator equation is used to model the cochlear resonant response at the cochlear places of the primary and secondary tone frequencies (f2 and 2 f1-f2). The parameters of the oscillator equation can be directly interpreted in terms of effectiveness of the cochlear feedback mechanisms associated with the active filter amplification. A two-sources paradigm is included in the model, in agreement with experimental evidence and with the assumptions of more detailed full cochlear models based on the transmission line formalism. According to this paradigm, DPOAEs are nonlinearly generated at the cochlear place that is resonant at frequency f2, and coherently reflected at the 2 f1-f2 place. The analysis shows that the model, which had been previously used to describe the relaxation dynamics of transient evoked otoacoustic emissions (TEOAEs), also correctly predicts the observed growth rate of the DPOAE response as a function of the primary tones amplitude. A significant difference is observed between normal and impaired ears. The comparison between the growth rate curves at different frequencies provides information about the dependence of cochlear tuning on frequency.     

Characteristics of distortion product otoacoustic emissions in the frog from L1,L2 maps

For a given set of stimulus frequencies (f1 ,f2), the level of distortion product otoacoustic emissions (DPOAEs) varies with the levels of the stimulus tones. By variation of the stimulus levels, L1,L2-maps for DPOAEs can be constructed. Here, we report on L1 ,L2-maps for DPOAEs from the frog ear. In general, these maps were similar to those obtained from the mammalian cochlea. We found a conspicuous difference between the equal-level contour lines for low-level and high-level DPOAEs, which could be modeled by a saturating and an expansive nonlinearity, respectively. The transition from the high-level to the low-level response was accompanied by a DPOAE phase-change, which increased from 0 to pi rad with increasing frequency. These results suggest that in the frog low-level and high-level DPOAEs are generated by separate nonlinear mechanisms. Also, there was a conspicuous difference in the growth of the low-level emissions from the two anuran auditory papillae. In the basilar papilla, this growth was expansive for the lowest stimulus levels and saturated for intermediate levels. This is consistent with the behavior of a Boltzman nonlinearity. In the amphibian papilla this growth was compressive, suggesting the additional effect of a compressive amplification mechanism on the generation of DPOAEs.     

Group delays of distortion product otoacoustic emissions: relating delays measured with f1- and f2-sweep paradigms

A theoretical analysis is presented of group delays of distortion product otoacoustic emissions (DPOAEs) measured with the phase-gradient method. The aim of the analysis is to clarify the differences in group delays D1 and D2, obtained using the f1- and the f2-sweep paradigms, respectively, and the dependence of group delays on the order of the DPOAE. Two models are considered, the place-fixed and the wave-fixed models. While in the former model the generation place is assumed to be invariant with both f1- and f2-sweeps, in the latter model the shift of generation place is fully accounted for. By making a simple local approximation of the cochlear scale invariance, a mathematical conversion from phase-place to phase-frequency gradients is incorporated in the wave-fixed model. Under the assumption that the DPOAE (as recorded at the best f2/f1 ratio) is dominated by the contribution from the generation site and not by, e.g., reflection components, the analysis leads to simple expressions for the ratio and difference between D1 and D2. Validation of the models against experimental data indicates that lower sideband DPOAEs (2f1-f2, 3f1-2f2, 4f1-3f2) are most consistent with the wave-fixed model. Upper sideband components (2f2-f1), in contrast, are not properly described by either the place-fixed or the wave-fixed model, independent whether DPOAE generation is assumed to originate at the f2 or at the more basally located f(dp) characteristic place.     

Distortion-product source unmixing: a test of the two-mechanism model for DPOAE generation

This paper tests key predictions of the "two-mechanism model" for the generation of distortion-product otoacoustic emissions (DPOAEs). The two-mechanism model asserts that lower-sideband DPOAEs constitute a mixture of emissions arising not simply from two distinct cochlear locations (as is now well established) but, more importantly, by two fundamentally different mechanisms: nonlinear distortion induced by the traveling wave and linear coherent reflection off pre-existing micromechanical impedance perturbations. The model predicts that (1) DPOAEs evoked by frequency-scaled stimuli (e.g., at fixed f2/f1) can be unmixed into putative distortion- and reflection-source components with the frequency dependence of their phases consistent with the presumed mechanisms of generation; (2) The putative reflection-source component of the total DPOAE closely matches the reflection-source emission (e.g., low level stimulus-frequency emission) measured at the same frequency under similar conditions. These predictions were tested by unmixing DPOAEs into components using two completely different methods: (a) selective suppression of the putative reflection source using a third tone near the distortion-product frequency and (b) spectral smoothing (or, equivalently, time-domain windowing). Although the two methods unmix in very different ways, they yield similar DPOAE components. The properties of the two DPOAE components are consistent with the predictions of the two-mechanism model.