Mechanisms of generation of the 2f2-f1 distortion product otoacoustic emission in humans

The 2f1-f2 distortion product otoacoustic emission (DPOAE) is considered to consist of two components in normally hearing ears, one having constant phase with changing DP frequency (wave fixed) and one having an increasing phase lag with increasing frequency (place fixed). The aim was to identify the wave-fixed and place-fixed components of both 2f1-f2 and 2f2-f1 DPs, and, in particular, to show whether a wave-fixed 2f2-f1 DP exists in normally hearing adults. DPOAE recordings were made in 20 ears of normally hearing young adults. Four frequency ratios were used and recording entailed fixed frequency-ratio sweeps. A separation into wave-fixed and place-fixed components was carried out using a time-window separation method. A method for estimating the noise floor after data processing was developed. Results confirmed the presence of wave-fixed and place-fixed components for 2f1-f2, consistent with previous studies. Both components were also present for 2f2-f1 in virtually all subjects. This latter finding conflicts with current models of DPOAE generation, and so a modified model is proposed. Unlike the 2f1-f2 emission, which has a wave-fixed component that is strongly dependent on the frequency ratio, neither component of the 2f2-f1 emission showed such a dependence. The proposed model explains these findings in terms of the overlap of the primary frequency traveling waves.     

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.     

Evidence for the distortion product frequency place as a source of distortion product otoacoustic emission (DPOAE) fine structure in humans. I. Fine structure and higher-order DPOAE as a function of the frequency ratio f2/f1

Critical experiments were performed in order to validate the two-source hypothesis of distortion product otoacoustic emissions (DPOAE) generation. Measurements of the spectral fine structure of DPOAE in response to stimulation with two sinusoids have been performed with normal-hearing subjects. The dependence of fine-structure patterns on the frequency ratio f2/f1 was investigated by changing f1 or f2 only (fixed f2 or fixed f1 paradigm, respectively), and by changing both primaries at a fixed ratio and looking at different order DPOAE. When f2/f1 is varied in the fixed ratio paradigm, the patterns of 2 f1-f2 fine structure vary considerably more if plotted as a function of f2 than as a function of fDP. Different order distortion products located at the same characteristic place on the basilar membrane (BM) show similar patterns for both, the fixed-f2 and fDP paradigms. Fluctuations in DPOAE level up to 20 dB can be observed. In contrast, the results from a fixed-fDP paradigm do not show any fine structure but only an overall dependence of DP level on the frequency ratio, with a maximum for 2f1-f2 at f2/f1 close to 1.2. Similar stimulus configurations used in the experiments have also been used for computer simulations of DPOAE in a nonlinear and active model of the cochlea. Experimental results and model simulations give strong evidence for a two-source model of DPOAE generation: The first source is the initial nonlinear interaction of the primaries close to the f2 place. The second source is caused by coherent reflection from a re-emission site at the characteristic place of the distortion product frequency. The spectral fine structure of DPOAE observed in the ear canal reflects the interaction of both these sources.     

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.     

Amplitude and phase of distortion product otoacoustic emissions in the guinea pig in an (f1 ,f2) area study

Lower sideband distortion product otoacoustic emissions (DPOAEs), measured in the ear canal upon stimulation with two continuous pure tones, are the result of interfering contributions from two different mechanisms, the nonlinear distortion component and the linear reflection component. The two contributors have been shown to have a different amplitude and, in particular, a different phase behavior as a function of the stimulus frequencies. The dominance of either component was investigated in an extensive (f1 ,f2) area study of DPOAE amplitude and phase in the guinea pig, which allows for both qualitative and quantitative analysis of isophase contours. Making a minimum of additional assumptions, simple relations between the direction of constant phase in the (f ,f2) plane and the group delays in f1-sweep, f2-sweep, and fixed f2/f1 paradigms can be derived, both for distortion (wave-fixed) and reflection (place-fixed) components. The experimental data indicate the presence of both components in the lower sideband DPOAEs, with the reflection component as the dominant contributor for low f2/f1 ratios and the distortion component for intermediate ratios. At high ratios the behavior cannot be explained by dominance of either component.     

In search of basal distortion product generators

The 2f1-f2 distortion product otoacoustic emission (DPOAE) is thought to arise primarily from the complex interaction of components that come from two different cochlear locations. Such distortion has its origin in the nonlinear interaction on the basilar membrane of the excitation patterns resulting from the two stimulus tones, f1 and f2. Here we examine the spatial extent of initial generation of the 2f1-f2 OAE by acoustically traumatizing the base of the cochlea and so eliminating the contribution of the basal region of the cochlea to the generation of 2f1-f2. Explicitly, amplitude-modulated, or continuously varying in level, stimulus tones with f2/f1= 1.2 and f2 =8000-8940 Hz were used to generate the 2f1-f2 DPOAE in guinea pig before and after acoustically traumatizing the basal region of the cochlea (the origin of any basal-to-f2 distortion product generators). It was found, based on correlation analysis, that there does not appear to be a basal-to-f2 distortion product generation mechanism contributing significantly to the guinea pig 2f1-f2 OAE up to L1 = 80 dB sound pressure level (SPL).     

Evidence for two discrete sources of 2f1-f2 distortion-product otoacoustic emission in rabbit. II: Differential physiological vulnerability.

In a previous report, it was shown that, in normal rabbit ears, the amplitude and phase of 2f1-f2 distortion-product otoacoustic emissions (DPOAEs) elicited by low-level (< 60-70 dB SPL) stimuli display a differential dependence on stimulus parameters to those evoked by high-level (> 60-70 dB SPL) stimuli, indicating differences in the underlying generation mechanisms. In the present study, the physiological vulnerability of DPOAEs in each of the two 2f1-f2 DPOAE-response regions identified on the basis of differential parametric properties, was characterized. Thus emissions evoked using stimulus levels from 45-75 dB SPL were measured over time upon: (1) induction of lethal anoxia, (2) acute injection of ethacrynic acid, and (3) acute injection of ethacrynic acid 2 h after a single administration of gentamicin. The DPOAEs evoked by low-level stimuli (45 dB SPL) were abolished within 3-4 min of induction of anoxia, whereas DPOAEs evoked by high-level stimuli (75 dB SPL) were unchanged in this period. The high-level emissions decreased with a complex time course postmortem, and demonstrated behaviors, including evidence of susceptibility to fatigue, suggesting a dependence upon a cochlear energy supply. Low-level DPOAEs could be temporarily abolished, with complete recovery, by an acute administration of ethacrynic acid that had little effect on high-level DPOAEs. Treatment with the gentamicin and ethacrynic-acid combination, which would be expected to produce widespread hair-cell damage, eliminated low-level DPOAEs, and greatly reduced high-level emissions. In combination with previously published data, these findings strongly suggest that low- and high-level 2f1-f2 DPOAEs arise from discrete sources. The data are consistent with the proposal that the low-level DPOAE source is an active, micromechanical process, but suggest that the proposed origin of high-level DPOAEs exclusively in the passive macromechanics of the cochlear partition may be incorrect. The elimination of both low- and high-level DPOAEs revealed the presence of a third, residual 2f1-f2 DPOAE component, approximately 75-80 dB below the stimulus-tone levels, that may reflect the true passive-distortion response of the cochlea.     

Distortion product otoacoustic emissions provide clues hearing mechanisms in the frog ear

2f1-f2 and 2 f2-f1 distortion product otoacoustic emissions (DPOAEs) were recorded from both ears of male and female Rana pipiens pipiens and Rana catesbeiana. The input-output (I/O) curves obtained from the amphibian papilla (AP) of both frog species are analogous to I/O curves recorded from mammals suggesting that, similarly to the mammalian cochlea, there may be an amplification process present in the frog AP. DPOAE level dependence on L1-L2 is different from that in mammals and consistent with intermodulation distortion expectations. Therefore, if a mechanical structure in the frog inner ear is functioning analogously to the mammalian basilar membrane, it must be more broadly tuned. DPOAE audiograms were obtained for primary frequencies spanning the animals' hearing range and selected stimulus levels. The results confirm that DPOAEs are produced in both papillae, with R. catesbeiana producing stronger emissions than R. p. pipiens. Consistent with previously reported sexual dimorphism in the mammalian and anuran auditory systems, females of both species produce stronger emissions than males. Moreover, it appears that 2 f1-f2 in the frog is generated primarily at the DPOAE frequency place, while 2 f2-f1 is generated primarily at a frequency place around the primaries. Regardless of generation place, both emissions within the AP may be subject to the same filtering mechanism, possibly the tectorial membrane.     

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.     

Cortical responses to the 2f1-f2 combination tone measured indirectly using magnetoencephalography

The simultaneous presentation of two tones with frequencies f(1) and f(2) causes the perception of several combination tones in addition to the original tones. The most prominent of these are at frequencies f(2)-f(1) and 2f(1)-f(2). This study measured human physiological responses to the 2f(1)-f(2) combination tone at 500 Hz caused by tones of 750 and 1000 Hz with intensities of 65 and 55 dB SPL, respectively. Responses were measured from the cochlea using the distortion product otoacoustic emission (DPOAE), and from the auditory cortex using the 40-Hz steady-state magnetoencephalographic (MEG) response. The perceptual response was assessed by having the participant adjust a probe tone to cause maximal beating ("best-beats") with the perceived combination tone. The cortical response to the combination tone was evaluated in two ways: first by presenting a probe tone with a frequency of 460 Hz at the perceptual best-beats level, resulting in a 40-Hz response because of interaction with the combination tone at 500 Hz, and second by simultaneously presenting two f(1) and f(2) pairs that caused combination tones that would themselves beat at 40 Hz. The 2f(1)-f(2) DPOAE in the external auditory canal had a level of 2.6 (s.d. 12.1) dB SPL. The 40-Hz MEG response in the contralateral cortex had a magnitude of 0.39 (s.d. 0.1) nA m. The perceived level of the combination tone was 44.8 (s.d. 11.3) dB SPL. There were no significant correlations between these measurements. These results indicate that physiological responses to the 2f(1)-f(2) combination tone occur in the human auditory system all the way from the cochlea to the primary auditory cortex. The perceived magnitude of the combination tone is not determined by the measured physiological response at either the cochlea or the cortex.     

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.     

Evidence for the distortion product frequency place as a source of distortion product otoacoustic emission (DPOAE) fine structure in humans. II. Fine structure for different shapes of cochlear hearing loss

Distortion product otoacoustic emissions (DPOAE) were recorded from eight human subjects with mild to moderate cochlear hearing loss, using a frequency spacing of 48 primary pairs per octave and at a level L1 = L2 = 60 dBSPL and with a fixed ratio f2/f1. Subjects with different shapes of hearing thresholds were selected. They included subjects with near-normal hearing within only a limited frequency range, subjects with a notch in the audiogram, and subjects with a mild to moderate high-frequency loss. If the primaries were located in a region of normal or near-normal hearing, but DP frequencies were located in a region of raised thresholds, the distortion product 2 f1-f2 was still observable, but the DP fine structure disappeared. If the DP frequencies fell into a region of normal thresholds, fine structure was preserved as long as DPOAE were generated, even in cases of mild hearing loss in the region of the primaries. These experimental results give further strong evidence that, in addition to the initial source in the primary region, there is a second source at the characteristic place of fDP. Simulations in a nonlinear and active computer model for DPOAE generation indicate different generation mechanisms for the two components. The disappearance of DPOAE fine structure might serve as a more sensitive indicator of hearing impairment than the consideration of DP level alone.     

Distortion product otoacoustic emission (2f1-f2) amplitude growth in human adults and neonates

Distortion product otoacoustic emissions (DPOAEs) are thought to be by-products of an active amplification process in the cochlea and thus serve as a metric for evaluating the integrity of this process. Because the cochlear amplifier functions in a level-dependent fashion, DPOAEs recorded as a function of stimulus level (i.e., a DPOAE growth function) may provide important information about the range and operational characteristics of the cochlear amplifier. The DPOAE growth functions recorded in human adults and neonates may provide information about the maturation of these active cochlear processes. Two experiments were conducted. Experiment I included normal-hearing adults and term-born neonates. The 2f1-f2 DPOAE growth functions were recorded for both age groups at three f2 frequencies. Experiment II was an extension of the first experiment but added a subject group of premature neonates. The results of these studies indicate that DPOAE growth functions most often show amplitude saturation and nonmonotonic growth for all age groups. However, premature neonates show monotonic growth and the absence of amplitude saturation more often than adults. Those premature neonates who do show saturation also show an elevated threshold for amplitude saturation relative to adults. In contrast, term neonates are adultlike for most measures except that they show a larger percentage of nonsaturating growth functions than adults. These results may indicate immaturity in cochlear amplifier function prior to term birth in humans. Outer hair cell function and/or efferent regulation of outer hair cell function are hypothesized sources of this immaturity, although some contribution from the immature middle ear cannot be ruled out.     

On the relationships between the fixed-f1, fixed-f2, and fixed-ratio phase derivatives of the 2f1-f2 distortion product otoacoustic emission

For primary frequency ratios, f2/f1, in the range 1.1-1.3, the fixed-f1 ("f2-sweep") phase derivative of the 2f1-f2 distortion product otoacoustic emission (DPOAE) is larger than the fixed-f2("f1-sweep") one. It has been proposed by some researchers that part or all of the difference between these delays may be attributed to the so-called cochlear filter "build-up" or response time in the DPOAE generation region around the f2 tonotopic site. The analysis of an approximate theoretical expression for the DPOAE signal [Talmadge et al., J. Acoust. Soc. Am. 104, 1517-1543 (1998)] shows that the contributions to the phase derivatives associated with the cochlear filter response is small. It is also shown that the difference between the phase derivatives can be qualitatively accounted for by assuming the approximate scale invariance of cochlear mechanics. The effects of DPOAE fine structure on the phase derivative are also explored, and it is found that the interpretation of the phase derivative in terms of the phase variation of a single DPOAE component can be quite problematic.     

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.     

Sources of distortion product otoacoustic emissions revealed by suppression experiments and inverse fast Fourier transforms in normal ears.

Primary and secondary sources combine to produce the 2f1-f2 distortion product otoacoustic emission (DPOAE) measured in the ear canals of humans. DPOAEs were obtained in nine normal-hearing subjects using a fixed-f2 paradigm in which f1 was varied. The f2 was 2 or 4 kHz, and absolute and relative primary levels were varied. Data were obtained with and without a third tone (f3) placed 15.6 Hz below 2f1-f2. The level of f3 was varied in order to suppress the stimulus frequency otoacoustic emission (SFOAE) coming from the 2f1-f2 place. These data were converted from the complex frequency domain into an equivalent time representation using an inverse fast Fourier transform (IFFT). IFFTs of unsuppressed DPOAE data were characterized by two or more peaks. Relative amplitudes of these peaks depended on overall primary level and on primary-level differences. The suppressor eliminated later peaks, but early peaks remained relatively unaltered. Results are interpreted to mean that the DPOAE measured in humans includes components from the f2 place (intermodulation distortion) and DP place (in the form of a SFOAE). These findings build on previous work by providing evidence that multiple peaks in the IFFT are due to a secondary source at the DP place.     

Multiple internal reflections in the cochlea and their effect on DPOAE fine structure

In recent years, evidence has accumulated in support of a two-source model of distortion product otoacoustic emissions (DPOAEs). According to such models DPOAEs recorded in the ear canal are associated with two separate sources of cochlear origin. It is the interference between the contributions from the two sources that gives rise to the DPOAE fine structure (a pseudoperiodic change in DPOAE level or group delay with frequency). Multiple internal reflections between the base of the cochlea (oval window) and the DP tonotopic place can add additional significant components for certain stimulus conditions and thus modify the DPOAE fine structure. DPOAEs, at frequency increments between 4 and 8 Hz, were recorded at fixed f2/f1 ratios of 1.053, 1.065, 1.08, 1.11, 1.14, 1.18, 1.22, 1.26, 1.30, 1.32, 1.34, and 1.36 from four subjects. The resulting patterns of DPOAE amplitude and group delay (the negative of the slope of phase) revealed several previously unreported patterns in addition to the commonly reported log sine variation with frequency. These observed "exotic" patterns are predicted in computational simulations when multiple internal reflections are included. An inverse FFT algorithm was used to convert DPOAE data from the frequency to the "time" domain. Comparison of data in the time and frequency domains confirmed the occurrence of these "exotic" patterns in conjunction with the presence of multiple internal reflections. Multiple internal reflections were observed more commonly for high primary ratios (f2/f1 > or = 1.3). These results indicate that a full interpretation of the DPOAE level and phase (group delay) must include not only the two generation sources, but also multiple internal reflections.     

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.