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.     

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.     

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.     

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.     

Characterizing distortion-product otoacoustic emission components across four species

Distortion-product otoacoustic emissions (DPOAEs) were measured as level/phase (L/P) maps in humans, rabbits, chinchillas, and rats with and without an interference tone (IT) placed either near the 2f(1)-f(2) DPOAE frequency place (f(dp)) or at one-third of an octave above the f(2) primary tone (1/3-oct IT). Vector differences between with and without IT conditions were computed to derive a residual composed of the DPOAE components removed by the IT. In humans, a DPOAE component could be extracted with the expected steep phase gradient indicative of reflection emissions by ITs near f(dp). In the laboratory species, ITs near f(dp) failed to produce any conclusive evidence for reflection components. For all species, 1/3-oct ITs extracted large DPOAE components presumably generated at or basal to the IT-frequency place that exhibited both distortion- and reflection-like phase properties. Together, these findings suggested that basal distortion components could assume reflection-like phase behavior when the assumptions of cochlear-scaling symmetry, the basis for shallow phase gradients for constant f(2)/f(1) ratio sweeps, are violated. The present results contradict the common belief that DPOAE components associated with steep or shallow phase slopes are unique signatures for reflection emissions arising from f(dp) or distortion emissions generated near f(2), respectively.     

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.     

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.     

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.     

Mechanism for bandpass frequency characteristic in distortion product otoacoustic emission generation

It is commonly observed that the levels of the 2f1-f2 and the other mf1-nf2 (m = n + 1 = integer) distortion product otoacoustic emissions (DPOAEs) initially increase in level for fixed f2 as fl -->f2, starting at f1 相似文献   

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.     

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.     

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.     

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.     

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.     

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.     

Origin of the bell-like dependence of the DPOAE amplitude on primary frequency ratio.

For low and medium sound pressure levels (SPLs), the amplitude of the distortion product otoacoustic emission (DPOAE) recorded from guinea pigs at the 2f1-f2 frequency is maximal when f2/f1 approximately 1.23 and decreases for lower and higher f2/f1 ratios. The high-ratio slope of the DPOAE dependence on the ratio of the primary frequencies might be anticipated since the f1 amplitude at the f2 place is expected to decrease for higher f2/f1 ratios. The low-ratio slope of the dependence at low and medium SPLs of the primaries is actually one slope of a notch. The DPOAE amplitude recovers from the notch when the f2/f1 ratio is further reduced. In two-dimensional space formed by the f2/f1 ratio, and the levels of the primaries, the notch is continuous and has a level-dependent phase transition. The notch is identical to that seen in DPOAE growth functions. Similar notches and phase transitions were observed for high-order and high-frequency DPOAEs. Theoretical analysis reveals that a single saturating nonlinearity is capable of generating similar amplitude notch and phase transition when the f2/f1 ratio is decreased because of the increase in f1 amplitude at the DPOAE generation place (f2 place). The difference between the DPOAE recorded from guinea pigs and humans is discussed in terms of different position of the operating point of the DPOAE generating nonlinearity.     

Auditory efferent activation in CBA mice exceeds that of C57s for varying levels of noise

The medial olivocochlear efferent (MOC) system enhances signals in noise and helps mediate auditory attention. Contralateral suppression (CS) of distortion product otoacoustic emissions (DPOAEs) has revealed age-related MOC declines. Here, differences in CS as a function of contralateral noise intensity (43-67 dB sound pressure level) were measured; 2f1-f2 DPOAE grams were recorded for young adult CBA and C57 mice. In CBAs, CS was a monotonic function of contralateral noise level. The C57s showed normal hearing, measured with DPOAE amplitudes and auditory brainstem response thresholds, but showed little CS, suggesting a loss of efferent dynamics preceding any deficiencies of the afferent auditory system.     

Wave and place fixed DPOAE maps of the human ear

Human intermodulation distortion product otoacoustic emissions (DPOAE) can be a mixture of low and high latency components. They have different level, phase, and suppression characteristics, which indicate that emissions arise both from the frequency region of the primary tones directly and indirectly via the DP frequency place. Which component dominates the measured DPOAE in the ear canal depends on the stimulus parameters, especially the frequency ratio, f2/f1. Interference between the two emissions adds complexity to measurements of DPOAE. The behavior and even existence of whichever emission route is lower in level often cannot directly be deduced from the raw DPOAE data because the other emission covers it. It is therefore not known whether both emissions are present for all stimulus parameters or whether the trends seen in each emission when they are the dominant emission route continue under stimulus conditions when they are not dominant. In this study, the two DPOAE components are separated by a post-processing method. Previously, maps of raw DPOAE data against f2/f1 and DP frequency have been obtained. To separate the components, sets of data consisting of f2/f1 sweeps were transformed by an inverse Fourier transform into the time domain. The low and high latency components appeared as two distinct peaks because of their different phase gradients. These peaks were separated by windowing in the time domain and two frequency domain maps were reconstructed, representing the low and high latency DPOAEs. It was found that the low latency component of the 2 f1-f2 DP was only emitted strongly with f2/f1 between approximately 1.1 and 1.3. The removal of the high latency component revealed the low ratio edge of this region, at which the level falls sharply. However, the low latency emission has been traced at reduced amplitude over a wide range of stimulus parameters. Although previously only observed at small frequency ratios, the high latency component was found to be present widely in the lower sideband, its level reducing slowly at larger f2/f1. Its phase behavior changes in the lower sideband, being approximately constant with DP frequency at small ratios of f2/f1, but deviating from this at wider ratios. These results support the hypothesis that a DPOAE component which propagates to and is re-emitted from the DP frequency place (place fixed emission) is present across a wide parameter range. However, for all but the close primary condition the lower sideband DPOAE is dominated by direct emission from the region of f2 and f1 wave interaction (wave fixed emission). A simple transmission line model is presented to illustrate how the observed DPOAE maps can arise on the basis of this hypothesis.     

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.