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.     

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.     

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.     

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.     

L1,L2 maps of distortion-product otoacoustic emissions from a moth ear with only two auditory receptor neurons

The tympanal organ of the moth Empyreuma affinis emits physiologically vulnerable distortion-product otoacoustic emissions. To assess the nature of underlying mechanical nonlinearities, we measured L1,L2 maps by varying both stimulus levels. Two types of maps were found: (1) Maps containing dominant islands centered at the L1=L2 diagonal as it is typical for saturating nonlinearities that can be described by Boltzmann functions. In contrast to maps published for mammals and frogs, the shape of such islands includes sharp ridges at L1 or L2 levels close to 70 dB sound pressure level. This could be produced by a strongly asymmetric operating point of the respective transfer functions, consistent with the fact that the auditory sensory cells are not hair cells but primary mechanoreceptors with a single cilium. The saturating map components could be selectively reduced by acoustic suppression. (2) Maps where separated islands were less conspicuous but in which the dominant feature consisted of contour lines which were orthogonal to the L1=2L2 diagonal and could be generated by an expansive nonlinearity. Maps showing strong islands were found for f2 frequencies between 26.7 and 45 kHz, maps without strong islands for f2 between 42 and 57.5 kHz. This suggests a frequency-dependent change regarding the involved mechanical nonlinearities.     

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.     

Influence of primary-level and primary-frequency ratios on human distortion product otoacoustic emissions

The combined influence of primary-level differences (L1-L2) and primary-frequency ratio (f2/f1) on distortion product otoacoustic emission (DPOAE) level was investigated in 20 normal-hearing subjects. DPOAEs were recorded with continuously varying stimulus levels [Neely et al. J. Acoust. Soc. Am. 117, 1248-1259 (2005)] for the following stimulus conditions: f2= 1, 2, 4, and 8 kHz and f2/f1=1.05 to 1.4; various L1-L2, including one individually optimized to produce the largest DPOAE. For broadly spaced primary frequencies at low L2 levels, the largest DPOAEs were recorded when L1 was much higher than L2, with L1 remaining relatively constant as L2 increased. As f2/fl decreased, the largest DPOAEs were observed when L1 was closer to L2 and increased as L2 increased. Optimal values for L1-L2 and f2 f1 were derived from these data. In general, average DPOAE levels for the new L1-L2 and f2/f1 were equivalent to or larger than those observed for other stimulus combinations, including the L1-L2 described by Kummer et al. [J. Acoust. Soc. Am. 103, 3431-3444 (1998)] and those defined by Neely et al. in which L1-L2 was evaluated, but f2/f1 was fixed at 1.2.     

Suppression of distortion product otoacoustic emissions in the anuran ear

When a two-tone stimulus is presented to the ear, so-called distortion product otoacoustic emissions (DPOAEs) are evoked. Adding an interference tone (IT) to these two DPOAE-evoking primaries affects normal DPOAE generation. The "effectiveness" of interference depends on the frequency of the IT in relation to the primary frequencies and this provides clues about the locus of emission generation within the inner ear. Here results are presented on the effects of ITs on DPOAEs thought to originate from the basilar papilla (BP) of a frog species. It is found that the IT always resulted in a reduction of the recorded DPOAE amplitude: DPOAE enhancement was not observed. Furthermore, iso-suppression curves (ISCs) exhibited two relative minima suggesting that the DPOAEs arise at different loci in the inner ear. These minima occurred at fixed frequencies, which coincided with those primary frequencies that resulted in maxima in DPOAE audiograms. The occurrence of two minima suggests that DPOAEs, which are presumed to originate exclusively from the BP, partially arise from the amphibian papilla as well. Finally, the finding that the minima in the ISCs are independent of the primary or DPOAE frequencies provides support for the notion that the BP functions as a single auditory filter.     

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.     

Cochlear compression estimates from measurements of distortion-product otoacoustic emissions

Evidence of the compressive growth of basilar-membrane displacement can be seen in distortion-product otoacoustic emission (DPOAE) levels measured as a function of stimulus level. When the levels of the two stimulus tones (f1 and f2) are related by the formula L1 = 39 dB + 0.4 x L2 [Kummer et al., J. Acoust. Soc. Am. 103, 3431-3444 (1998)] the shape of the function relating DPOAE level to L2 is similar (up to an L2 of 70 dB SPL) to the classic Fletcher and Munson [J. Acoust. Soc. Am. 9, 1-10 (1933)] loudness function when plotted on a logarithmic scale. Explicit estimates of compression have been derived based on recent DPOAE measurements from the laboratory. If DPOAE growth rate is defined as the slope of the DPOAE I/O function (in dB/dB), then a cogent definition of compression is the reciprocal of the growth rate. In humans with normal hearing, compression varies from about 1 at threshold to about 4 at 70 dB SPL. With hearing loss, compression is still about 1 at threshold, but grows more slowly above threshold. Median DPOAE I/O data from ears with normal hearing, mild loss, and moderate loss are each well fit by log functions. When the I/O function is logarithmic, then the corresponding compression is a linear function of stimulus level. Evidence of cochlear compression also exists in DPOAE suppression tuning curves, which indicate the level of a third stimulus tone (f3) that reduces DPOAE level by 3 dB. All three stimulus tones generate compressive growth within the cochlea; however, only the relative compression (RC) of the primary and suppressor responses is observable in DPOAE suppression data. An RC value of 1 indicates that the cochlear responses to the primary and suppressor components grow at the same rate. In normal ears, RC rises to 4, when f3 is an octave below f2. The similarities between DPOAE and loudness compression estimates suggest the possibility of predicting loudness growth from DPOAEs; however, intersubject variability makes such predictions difficult at this time.     

Differential responses to acoustic damage and furosemide in auditory brainstem and otoacoustic emission measures

Characteristics of distortion product otoacoustic emissions (DPOAEs) and auditory brainstem responses (ABRs) were measured in Mongolian gerbil before and after the introduction of two different auditory dysfunctions: (1) acoustic damage with a high-intensity tone, or (2) furosemide intoxication. The goal was to find emission parameters and measures that best differentiated between the two dysfunctions, e.g., at a given ABR threshold elevation. Emission input-output or "growth" functions were used (frequencies f1 and f2, f2/f1 = 1.21) with equal levels, L1 = L2, and unequal levels, with L1 = L2 + 20 dB. The best parametric choice was found to be unequal stimulus levels, and the best measure was found to be the change in the emission threshold level, delta x. The emission threshold was defined as the stimulus level required to reach a criterion emission amplitude, in this case -10 dB SPL. (The next best measure was the change in emission amplitude at high stimulus levels, specifically that measured at L1 x L2 = 90 x 70 dB SPL.) For an ABR threshold shift of 20 dB or more, there was essentially no overlap in the emission threshold measures for the two conditions, sound damage or furosemide. The dividing line between the two distributions increased slowly with the change in ABR threshold, delta ABR, and was given by delta x(t) = 0.6 delta ABR + 8 dB. For a given delta ABR, if the shift in emission threshold was more than the calculated dividing line value, delta x(t), the auditory dysfunction was due to acoustic damage, if less, it was due to furosemide.     

Growth of suppression in humans based on distortion-product otoacoustic emission measurements

Distortion-product otoacoustic emissions (DPOAEs) were used to describe suppression growth in normal-hearing humans. Data were collected at eight f(2) frequencies ranging from 0.5 to 8 kHz for L(2) levels ranging from 10 to 60 dB sensation level. For each f(2) and L(2) combination, suppression was measured for nine or eleven suppressor frequencies (f(3)) whose levels varied from -20 to 85 dB sound pressure level (SPL). Suppression grew nearly linearly when f(3) ≈ f(2), grew more rapidly for f(3)?< f(2), and grew more slowly for f(3)?> f(2). These results are consistent with physiological and mechanical data from lower animals, as well as previous DPOAE data from humans, although no previous DPOAE study has described suppression growth for as wide a range of frequencies and levels. These trends were evident for all f(2) and L(2) combinations; however, some exceptions were noted. Specifically, suppression growth rate was less steep as a function of f(3) for f(2) frequencies ≤ 1 kHz. Thus, despite the qualitative similarities across frequency, there were quantitative differences related to f(2), suggesting that there may be subtle differences in suppression for frequencies above 1 kHz compared to frequencies below 1 kHz.     

Is it necessary to penalize impulsive noise +5 dB due to higher risk of hearing damage?

It is studied whether the +5 dB penalty for impulsiveness established by ISO 1999:1990 accounts for a higher risk of noise-induced hearing loss. A total of 16 normal-hearing human subjects were exposed for 10 min to two types of binaural industrial-recordings: (1) a continuous broad-band noise normalized to L(EX,8 h)=80 dBA and (2) the combination of the previous stimulus with an impulsive noise normalized to L(EX,8 h)=75+5(db penalty)=80 dBA (peak level 117 dBC and repetition rate of 0.5 impacts per second). Distortion product otoacoustic emissions (DPOAEs) were measured in a broad frequency range before and in the following 90 min after the exposure. The group results show that the continuous exposure had a bigger impact on DPOAE levels, with a maximum DPOAE shift of approximately 5 dB in the frequency range of 2-3.15 kHz during the first 10 min of the recovery. No evident DPOAE shift is seen for the impulsive + continuous stimulus. The results indicate that the penalty overestimated the effects on DPOAE levels and support the concept that the risk of hearing loss from low-level impulses may be predicted on an equal-energy basis.     

Hearing threshold estimation using concurrent measurement of distortion product otoacoustic emissions and auditory steady-state responses

Both distortion product otoacoustic emissions (DPOAEs) and auditory steady-state responses (ASSRs) provide frequency-specific assessment of hearing. However, each method suffers from some restrictions. Hearing losses above 50 dB HL are not quantifiable using DPOAEs and their performance at frequencies below 1 kHz is limited, but their recording time is short. In contrast, ASSRs are a time-consuming method but have the ability to determine hearing thresholds in a wider range of frequencies and hearing losses. Thus, recording DPOAEs and ASSRs simultaneously at their adequate frequencies and levels could decrease the overall test time considerably. The goal of the present study was to develop a parameter-setting and test-protocol to measure DPOAEs and ASSRs binaurally and simultaneously at multiple frequencies. Ten normal-hearing and 23 hearing-impaired subjects participated in the study. The interaction of both responses when stimulated simultaneously at frequencies between 0.25 and 6 kHz was examined. Two limiting factors need to be kept. Frequency distance between ASSR carrier frequency f(c) and DPOAE primary tone f(2) needs to be at least 1.5 octaves, and DPOAEs may not be measured if the ASSR stimulus level is 70 dB SPL or above. There was a significant correlation between pure-tone and DPOAE/ASSR-thresholds in sensorineural hearing loss ears.     

Evidence for basal distortion-product otoacoustic emission components

Distortion-product otoacoustic emissions (DPOAEs) were measured with traditional DP-grams and level/phase (L/P) maps in rabbits with either normal cochlear function or unique sound-induced cochlear losses that were characterized as either low-frequency or notched configurations. To demonstrate that emission generators distributed basal to the f(2) primary-tone contribute, in general, to DPOAE levels and phases, a high-frequency interference tone (IT) was presented at 1/3 of an octave (oct) above the f(2) primary-tone, and DPOAEs were re-measured as "augmented" DP-grams (ADP-grams) and L/P maps. The vector difference between the control and augmented functions was then computed to derive residual DP-grams (RDP-grams) and L/P maps. The resulting RDP-grams and L/P maps, which described the DPOAEs removed by the IT, supported the notion that basal DPOAE components routinely contribute to the generation of standard measures of DPOAEs. Separate experiments demonstrated that these components could not be attributed to the effects of the 1/3-oct IT on f(2), or DPOAEs generated by the addition of a third interfering tone. These basal components can "fill in" the lesion estimated by the commonly employed DP-gram. Thus, ADP-grams more accurately reveal the pattern of cochlear damage and may eventually lead to an improved DP-gram procedure.     

Impact of three hours of discotheque music on pure-tone thresholds and distortion product otoacoustic emissions

The aim of this study was to investigate whether distortion product otoacoustic emissions (DPOAEs) are a suitable means for detecting changes in outer hair cell (OHC) functionality due to exposure to three hours of discotheque music and whether efferent reflex strength of the medial olivocochlear bundle is able to predict the ear's susceptibility to high-level noise. High-resolution DPOAEs (Δf(2)=47 Hz) were recorded between 3.5 and 4.5 kHz at close-to-threshold primary tone levels. For comparison, high-resolution pure-tone audiometry was conducted in the same frequency range. Efferent reflex strength was measured by means of DPOAEs at a specific frequency with and without contralateral acoustic stimulation. A significant deterioration of more than 10 dB was found for pure-tone thresholds and DPOAE levels indicating that three hours of high-level noise exert a considerable influence on hearing capability and OHC functionality. A significant correlation between shifts in pure-tone threshold and shifts in DPOAE level occurred when removing data with differing calibration across measurements. There was no clear correlation between efferent reflex strength and shifts in pure-tone threshold or shifts in DPOAE level suggesting that the applied measures of efferent reflex strength may not be suitable for quantifying individual vulnerability to noise.     

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.     

Temporal aspects of suppression in distortion-product otoacoustic emissions

This study examined the time course of cochlear suppression using a tone-burst suppressor to measure decrement of distortion-product otoacoustic emissions (DPOAEs). Seven normal-hearing subjects with ages ranging from 19 to 28 yr participated in the study. Each subject had audiometric thresholds ≤ 15 dB HL [re ANSI (2004) Specifications for Audiometers] for standard octave and inter-octave frequencies from 0.25 to 8 kHz. DPOAEs were elicited by primary tones with f(2)?= 4.0 kHz and f(1)?= 3.333 kHz (f(2)/f(1)?= 1.2). For the f(2), L(2) combination, suppression was measured for three suppressor frequencies: One suppressor below f(2) (3.834 kHz) and two above f(2) (4.166 and 4.282 kHz) at three levels (55, 60, and 65 dB SPL). DPOAE decrement as a function of L(3) for the tone-burst suppressor was similar to decrements obtained with longer duration suppressors. Onset- and setoff- latencies were ≤ 4 ms, in agreement with previous physiological findings in auditory-nerve fiber studies that suggest suppression results from a nearly instantaneous compression of the waveform. Persistence of suppression was absent for the below-frequency suppressor (f(3)?= 3.834 kHz) and was ≤ 3 ms for the two above-frequency suppressors (f(3)?= 4.166 and 4.282 kHz).