Distortion Product Otoacoustic Emissions Components Research Articles

Loss and Recovery of Sound-Evoked Otoacoustic Emissions in Young Chicks following Acoustic Trauma

Young and adult chickens exhibit substantial inner-ear damage and post-exposure deterioration in cochlear nerve activity following exposure to intense sound. Both the structural and functional losses largely recover in both age groups within 2–4 weeks after exposure. However, some aspects of acoustic trauma differ between the young and adult chicken ear. Overstimulation in the young chick causes considerable post-exposure loss and then recovery of the steady-state endocochlear potential, while in the adult animal there is little post-exposure effect on this potential. Moreover, in adults there is post-exposure loss but little recovery in the distortion product otoacoustic emission (DPOAE). The present study explores the possibility of an age difference in the effects of overstimulation on the DPOAE by examining these emissions in young chicks following exposure to an intense pure tone. Chicks exposed to intense sound were formed into groups at 0 and 12 days of recovery, and these were complemented by two additional groups of age-matched controls. The cubic difference tone emission (the 2f₁–f₂ DPOAE component) was measured at 9 levels for 13 frequencies in all groups. Shortly after the exposure, the DPOAE reliably declined with the maximum loss at or above the exposure tone frequency. The exposed chicks examined 12 days after exposure showed complete recovery of the DPOAE. It would appear that 12 days of recovery sufficiently repaired inner ear damage to completely restore DPOAE production. This result is different from that in adult chicken and may be related to the greater severity of acoustic damage in the adult ear, a reduced susceptibility of the young ear to acoustic trauma, or the ability of the young animal to more successfully repair the inner ear.

The effect of stimulus-frequency ratio on distortion product otoacoustic emission components

A detailed measurement of distortion product otoacoustic emission (DPOAE) fine structure was used to extract estimates of the two major components believed to contribute to the overall DPOAE level in the ear canal. A fixed-ratio paradigm was used to record DPOAE fine structure from three normal-hearing ears over a range of 400 Hz for 12 different stimulus-frequency ratios between 1.053 and 1.36 and stimulus levels between 45 and 75 dB SPL. Inverse Fourier transforms of the amplitude and phase data were filtered to extract the early component from the generator region of maximum stimulus overlap and the later component reflected from the characteristic frequency region of the DPOAE. After filtering, the data were returned to the frequency domain to evaluate the impact of the stimulus-frequency ratio and stimulus level on the relative levels of the components. Although there were significant differences between data from different ears some consistent patterns could be detected. The component from the overlap region of the stimulus tones exhibits a bandpass shape, with the maximum occurring at a ratio of 1.2. The mean data from the DPOAE characteristic frequency region also exhibits a bandpass shape but is less sharply tuned and exhibits greater variety across ears and stimulus levels. The component from the DPOAE characteristic frequency region is dominant at ratios narrower than approximately 1.1 (the transition varies between ears). The relative levels of the two components are highly variable at ratios greater than 1.3 and highly dependent on the stimulus level. The reflection component is larger at all ratios at the lowest stimulus level tested (45/45 dB SPL). We discuss the factors shaping DPOAE-component behavior and some cursory implications for the choice of stimulus parameters to be used in clinical protocols.

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.

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.

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.

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.

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.

Evidence for multiple DPOAE components based upon group delay of the 2 f1− f2 distortion in the gerbil

The cochlear delay of the 2 f 1− f 2 distortion product otoacoustic emission (DPOAE) was measured using the phase gradient method. With a constant f 2 and swept f 1, the resulting phase change of 2 f 1− f 2 was used to calculate the group delay for f 2 frequencies from 1 to 60 kHz. For f 2 frequencies between 2 and 60 kHz, the group delays were between 2.2 and 0.11 ms and continuously decreased for increasing f 2 and for increasing primary stimulus levels. For f 2 frequencies below 2 kHz, the group delay decreased to around 1 ms and was largely independent of stimulus level. The ratio curves resulting from the f 1 sweeps for high frequencies ( f 2>16 kHz) displayed the typical mammalian shape with a peak in the level of 2 f 1− f 2 for a larger primary frequency separation ( f 2/ f 1>1.15) and decreasing 2 f 1− f 2 level for smaller primary separation. In addition to this typical level maximum, for f 2 frequencies from about 1.8 to 16 kHz, the ratio curves displayed a second component in the form of an increase in the level of 2 f 1− f 2 for small primary separation at higher primary levels (level of f 2>30 dB SPL). For f 2 frequencies below 1.8 kHz, only the second component and no typical ratio peak as for higher f 2 could be observed and the associated group delay was always close to 0.8 ms. Several possible causes for this behavior are discussed, including different modes of DPOAE generation and modulation as well as changes in the nature of mechanical processing from base to apex in the gerbil cochlea. To evaluate the relative sensitivity of non-linear cochlear mechanics, an iso-distortion threshold curve was constructed from acoustical growth functions of the 2 f 1− f 2 DPOAE at optimum primary separation, by plotting the level of f 2 sufficient to evoke a distortion of −10 dB SPL as a function of f 2. This distortion audiogram resembled the neuronal and behavioral audiogram for frequencies >2.5 kHz but failed to reflect the sensitivity for lower frequencies. This may be a consequence of more linear frequency processing in the apex.

Multicomponent acoustic distortion product otoacoustic emission phase in humans. II. Implications for distortion product otoacoustic emissions generation

Phase characteristics and latency of 2f1-f2, 3f1-2f2, and 2f2-f1 acoustic distortion product otoacoustic emissions (DPOAEs) recorded in normally hearing adults have been described in a companion paper [Moulin and Kemp, "Multicomponent acoustic distortion product otoacoustic emission phase in humans. I. General characteristics," J. Acoust. Soc. Am. 100, 1617-1639 (1996)]. Phase-versus-frequency functions (PFF) have been recorded using two methods, depending whether f1 or f2 was swept in frequency, defining, respectively, an "f1 sweep" and an "f2 sweep" method. The present study compares 2f1-f2, 3f1-2f2, 4f1-3f2, and 2f2-f1 DPOAEs phase characteristics, and latencies obtained by these two methods. For lower sideband DPOAEs, the f2 sweep gave consistently longer latencies than the f1 sweep method, whereas no difference was obtained for the 2f2-f1 DPOAE. This suggests that the lower sideband DPOAEs and the 2f2-f1 DPOAE do not come from the same aspect of the traveling wave. The longer delay obtained with an f2 sweep is suggested to be due to an additional delay added by the proximity of the peak of the f2 traveling wave. The place-fixed and the wave-fixed models of DPOAE generation are discussed, and an "intermediate" model of DPOAE generation is introduced to explain such additional delay and the existence of phase irregularities which were observed in the PFF. The ratio of the latencies obtained by the two sweep methods is frequency dependent and a relation to cochlear frequency selectivity is suggested. Finally, analysis of the differences in latency of the different lower sideband DPOAE components allowed an estimation of the return latency of DPOAEs.

Multicomponent acoustic distortion product otoacoustic emission phase in humans. I. General characteristics.

Phase characteristics and latency of 2f1-f2, 3f1-2f2, and 2f2-f1 acoustic distortion product otoacoustic emissions (DPOAEs) have been analyzed in 12 adults with normal hearing. Phase-versus-frequency functions (PFF) have been recorded at each of ten pairs of primary frequencies, by two methods, depending on which one of the primary frequencies f1 or f2 was swept in frequency. Whichever sweep method was used, local phase irregularities were found in the PFF and were shown to be independent of the phase variability due to the measured noise, to be reproducible and frequency specific. Phase irregularities were significantly greater in subjects exhibiting spontaneous otoacoustic emissions. The latency calculation was unaffected by phase irregularities provided that a suitably large range of f2/f1 ratio was used. The DPOAE latencies that were obtained at low ratios of primaries were significantly longer than those obtained at higher ratios. For all DPOAE components and sweep methods used, the latency decreased as frequency increased from 750 Hz to 6 kHz. Substantial intersubject differences were found. They might be due to two main factors: differences in middle ear acoustic properties and in cochlea mechanical characteristics. The influence of pressure in the outer ear canal increased the DPOAE latencies recorded with both the f1 and f2 sweep methods at low frequencies. Men showed significantly longer 2f2-f1 DPOAE latencies than women, especially at low frequencies, which can be attributed to the difference in length of the cochlea according to gender. Lastly, the latencies measured using the f2 sweep were consistently longer than the latencies obtained using an f1 sweep for lower sideband DPOAEs, but no difference was observed for upper sideband DPOAEs.

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.