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).     

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.     

Transient-evoked stimulus-frequency and distortion-product otoacoustic emissions in normal and impaired ears

Transient-evoked stimulus-frequency otoacoustic emissions (SFOAEs), recorded using a nonlinear differential technique, and distortion-product otoacoustic emissions (DPOAEs) were measured in 17 normal-hearing and 10 hearing-impaired subjects using pairs of tone pips (pp), gated tones (gg), and for DPOAEs, continuous and gated tones (cg). Temporal envelopes of stimulus and OAE waveforms were obtained by narrow-band filtering at the stimulus or DP frequency. Mean SFOAE latencies in normal ears at 2.7 and 4.0 kHz decreased with increasing stimulus level and were larger at 4.0 kHz than latencies in impaired ears. Equivalent auditory filter bandwidths were calculated as a function of stimulus level from SFOAE latencies by assuming that cochlear transmission is minimum phase. DPOAE latencies varied less with level than SFOAE latencies. The ppDPOAEs often had two (or more) peaks separated in time with latencies consistent with model predictions for distortion and reflection components. Changes in ppDPOAE latency with level were sometimes explained by a shift in relative amplitudes of distortion and reflection components. The pp SFOAE SPL within the main spectral lobe of the pip stimulus was higher for normal ears in the higher-frequency half of the pip than the lower-frequency half, which is likely an effect of basilar membrane two-tone suppression.     

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

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

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

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

Recovery of distortion-product otoacoustic emissions after a 2-kHz monaural sound-exposure in humans: effects on fine structures

A better understanding of the vulnerability of the fine structures of distortion-product otoacoustic emissions (DPOAEs) after acoustic overexposure may improve the knowledge about DPOAE generation, cochlear damage, and lead to more efficient diagnostic tools. It is studied whether the DPOAE fine structures of 16 normal-hearing human subjects are systematically affected after a moderate monaural sound-exposure of 10 min to a 2-kHz tone normalized to an exposure level L(EX,8h) of 80 dBA. DPOAEs were measured before and in the following 70 min after the exposure. The experimental protocol allowed measurements with high time and frequency resolution in a 1/3-octave band centered at 3 kHz. On average, DPOAE levels were reduced approximately 5 dB in the entire measured frequency-range. Statistically significant differences in pre- and post-exposure DPOAE levels were observed up to 70 min after the end of the sound exposure. The results show that the effects on fine structures are highly individual and no systematic change was observed.     

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.     

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.     

Comparison of distortion-product otoacoustic emission growth rates and slopes of forward-masked psychometric functions

Slopes of forward-masked psychometric functions (FM PFs) were compared with distortion-product otoacoustic emission (DPOAE) input/output (I/O) parameters at 1 and 6 kHz to test the hypothesis that these measures provide similar estimates of cochlear compression. Implicit in this hypothesis is the assumption that both DPOAE I/O and FM PF slopes are functionally related to basilar-membrane (BM) response growth. FM PF-slope decreased with signal level, but this effect was reduced or reversed with increasing hearing loss; there was a trend of decreasing psychometric function (PF) slope with increasing frequency, consistent with greater compression at higher frequencies. DPOAE I/O functions at 6 kHz exhibited an increase in the breakpoint of a two-segment slope as a function of hearing loss with a concomitant decrease in the level of the distortion product (L(d)). Results of the comparison between FM PF and DPOAE I/O parameters revealed only a weak correlation, suggesting that one or both of these measures may provide unreliable information about BM compression.     

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.     

纯音信号的响度与响度差阈的关系

关于响度与响度差阈关系的己有假设总是不能很好地解释心理声学的实验结果,这些假设也不曾对响度的编码和判断的物理过程以及物理过程与心理反映间的联系作过明确的描述。本文基于信号检测理论和关于响度编码的两个假设:响度是一定时间T内的听神经电冲动的记数、稳态纯音激励的神经电冲动速率的时间分布是一个平稳的正态随机分布,得出纯音信号的响度差阈与响度的比与强度无关。这一关系很好地解释了纯音信号强度差阈测试的实验结果,尤其是以前难以解释的Weber比的中部突起、near miss to Weber's law。     

A review of otoacoustic emissions

Otoacoustic emissions measured in the external ear canal describe responses that the cochlea generates in the form of acoustic energy. For the convenience of discussing their principal features, emitted responses can be classified into several categories according to the type of stimulation used to evoke them. On this basis, four distinct but interrelated classes can be distinguished including spontaneous, transiently evoked, stimulus-frequency, and distortion-product otoacoustic emissions. The present review details the findings that have been described for each emission type according to this classification schema. Additionally, the known features of emitted responses are discussed for both normally hearing and hearing-impaired humans and experimental animals, and with respect to their potential clinical applications. The findings reviewed here clearly indicate that future studies of otoacoustic emissions will significantly increase our understanding of the basic mechanisms of cochlear function while, at the same time, provide a new and important clinical tool.     

Simultaneous recording of stimulus-frequency and distortion-product otoacoustic emission input-output functions in human ears

Stimulus frequency otoacoustic emission (SFOAE) input-output (I/O) functions were elicited in normal-hearing adults using unequal-frequency primaries in equal-level and fixed-suppressor level (Ls) conditions. Responses were repeatable and similar across a range of primary frequency ratios in the fixed-Ls condition. In comparison to equal-frequency primary conditions [Schairer, Fitzpatrick, and Keefe, J. Acoust. Soc. Am. 114, 944-966 (2003)], the unequal-frequency, fixed-Ls condition appears to be more useful for characterizing SFOAE response growth and relating it to basilar-membrane response growth, and for testing the ability to predict audiometric thresholds. Simultaneously recorded distortion-product OAE (DPOAE) I/O functions had higher thresholds than SFOAE I/O functions, and they identified the onset of the nonlinear-distortion mechanism in SFOAEs. DPOAE threshold often corresponded to nonmonotonicities in SFOAE I/O functions. This suggests that the level-dependent nonmonotonicities and associated phase shifts in SFOAE I/O functions were due to varying degrees of cancellation of two sources of SFOAE, such as coherent reflection and distortion mechanisms. Level-dependent noise was observed on-band (at the frequencies of the stimuli) but not off-band, or in the DPOAEs. The variability was observed in ears with normal hearing and ears with cochlear implants. In general, these results indicate the source of the variability is biological, possibly from within the middle ear.     

Influence of in situ, sound-level calibration on distortion-product otoacoustic emission variability

Standing waves can cause errors during in-the-ear calibration of sound pressure level (SPL), affecting both stimulus magnitude and distortion-product otoacoustic emission (DPOAE) level. Sound intensity level (SIL) and forward pressure level (FPL) are two measurements theoretically unaffected by standing waves. SPL, SIL, and FPL in situ calibrations were compared by determining sensitivity of DPOAE level to probe-insertion depth (deep and "shallow") for a range of stimulus frequencies (1-8 kHz) and levels (20-60 dB). Probe-insertion depth was manipulated with the intent to shift the frequencies with standing-wave minima at the emission probe, introducing variability during SPL calibration. The absolute difference in DPOAE level between insertions was evaluated after correcting for an incidental change caused by the effect of ear-canal impedance on the emission traveling from the cochlea. A three-way analysis of variance found significant main effects for stimulus level, stimulus frequency, and calibration method, as well as significant interactions involving calibration method. All calibration methods exhibited changes in DPOAE level due to the insertion depth, especially above 4 kHz. However, SPL demonstrated the greatest changes across all stimulus levels for frequencies above 2 kHz, suggesting that SIL and FPL provide more consistent measurements of DPOAEs for frequencies susceptible to standing-wave calibration errors.     

Amplitude and frequency fluctuations of spontaneous otoacoustic emissions

Amplitude and frequency fluctuations of spontaneous otoacoustic emissions have been studied. Spontaneous otoacoustic emissions were recorded from eight human ears and two frog ears (Rana esculenta). Record length typically was 80 s. For a recorded emission signal, the amplitude signal A(t) (average A0) and time intervals T(ti) between successive positive-going zero crossings (i counts zero crossings) were determined. Emission amplitude and period both showed small fluctuations: delta Arms/A0 ranged from 0.7 X 10(-2) to 6.3 X 10(-2) for human emissions and was 24 X 10(-2) for both frog emissions; delta Trms ranged from 1.4 to 6.9 X 10(-7) s for human emission and was 50.0 and 55.0 X 10(-7) s for the two frog emissions. There was a positive correlation between delta Arms/A0 and delta Trms as determined for different emissions (R = 0.9). Spectra of A(t) and T(ti) revealed that amplitude and period were slowly fluctuating functions: cutoff frequency delta f delta A of the amplitude spectrum ranged from 3 to 18 Hz; delta f delta T ranged from 7 to 32 Hz. Results have been compared to amplitude and frequency fluctuations of a second-order oscillator, that interacts with a noise source. It has been concluded that an oscillator with linear stiffness (for example a Van der Pol oscillator) driven by white Gaussian noise, cannot account for all experimental results. Other possible oscillators (e.g., nonlinear stiffness) and noise sources (e.g., narrow-band noise), that may account for the observed phenomena, are discussed.     

Temperature dependence of frog spontaneous otoacoustic emissions

Spontaneous otoacoustic emissions are recorded from frog ears at various body temperatures. Frequency spectra and amplitude distributions of emissions are determined. Both power and frequency of emission signals show a strong temperature dependence.     

Two-tone suppression of stimulus frequency otoacoustic emissions

Stimulus frequency otoacoustic emissions (SFOAEs) measured using a suppressor tone in human ears are analogous to two-tone suppression responses measured mechanically and neurally in mammalian cochleae. SFOAE suppression was measured in 24 normal-hearing adults at octave frequencies (f(p)=0.5-8.0 kHz) over a 40 dB range of probe levels (L(p)). Suppressor frequencies (f(s)) ranged from -2.0 to 0.7 octaves re: f(p), and suppressor levels ranged from just detectable suppression to full suppression. The lowest suppression thresholds occurred for "best" f(s) slightly higher than f(p). SFOAE growth of suppression (GOS) had slopes close to one at frequencies much lower than best f(s), and shallow slopes near best f(s), which indicated compressive growth close to 0.3 dBdB. Suppression tuning curves constructed from GOS functions were well defined at 1, 2, and 4 kHz, but less so at 0.5 and 8.0 kHz. Tuning was sharper at lower L(p) with an equivalent rectangular bandwidth similar to that reported behaviorally for simultaneous masking. The tip-to-tail difference assessed cochlear gain, increasing with decreasing L(p) and increasing f(p) at the lowest L(p) from 32 to 45 dB for f(p) from 1 to 4 kHz. SFOAE suppression provides a noninvasive measure of the saturating nonlinearities associated with cochlear amplification on the basilar membrane.     

Low-level otoacoustic emissions may predict susceptibility to noise-induced hearing loss

In a longitudinal study with 338 volunteers, audiometric thresholds and otoacoustic emissions were measured before and after 6 months of noise exposure on an aircraft carrier. While the average amplitudes of the otoacoustic emissions decreased significantly, the average audiometric thresholds did not change. Furthermore, there were no significant correlations between changes in audiometric thresholds and changes in otoacoustic emissions. Changes in transient-evoked otoacoustic emissions and distortion-product otoacoustic emissions were moderately correlated. Eighteen ears acquired permanent audiometric threshold shifts. Only one-third of those ears showed significant otoacoustic emission shifts that mirrored their permanent threshold shifts. A Bayesian analysis indicated that permanent threshold shift status following a deployment was predicted by baseline low-level or absent otoacoustic emissions. The best predictor was transient-evoked otoacoustic emission amplitude in the 4-kHz half-octave frequency band, with risk increasing more than sixfold from approximately 3% to 20% as the emission amplitude decreased. It is possible that the otoacoustic emissions indicated noise-induced changes in the inner ear, undetected by audiometric tests. Otoacoustic emissions may therefore be a diagnostic predictor for noise-induced-hearing-loss risk.     

Changes in amplitude and phase of distortion-product otoacoustic emission fine-structure and separated components during efferent activation

Medial olivocochlear (MOC) efferent fibers synapse directly on the outer hair cells (OHCs). Efferent activation evoked by contralateral acoustic stimulation (CAS) will affect OHC amplification and subsequent measures of distortion-product otoacoustic emissions (DPOAEs). The aim of this study was to investigate measures of total and separated DPOAEs during efferent activation. Efferent activation produces both suppression and enhancement of the total DPOAE level. Level enhancements occurred near fine-structure minima and were associated with consistent MOC evoked upward shifts in DPOAE fine-structure frequency. Examination of the phase of the separated components revealed that frequency shifts stemmed from increasing phase leads of the reflection component during CAS, while the generator component phase was nearly invariant. Separation of the two DPOAE components responsible for the fine-structure revealed more consistent reduction of the levels of both components. Using vector subtraction (which takes into account both level and phase) to estimate the changes in the unseparated DPOAE provided consistent evidence of DPOAE suppression. Including phase information provided a more sensitive, valid and consistent estimate of CAS function even if one does not know the position of the DPOAE in the fine-structure.     

Near equivalence of human click-evoked and stimulus-frequency otoacoustic emissions

Otoacoustic emissions (OAEs) evoked by broadband clicks and by single tones are widely regarded as originating via different mechanisms within the cochlea. Whereas the properties of stimulus-frequency OAEs (SFOAEs) evoked by tones are consistent with an origin via linear mechanisms involving coherent wave scattering by preexisting perturbations in the mechanics, OAEs evoked by broadband clicks (CEOAEs) have been suggested to originate via nonlinear interactions among the different frequency components of the stimulus (e.g., intermodulation distortion). The experiments reported here test for bandwidth-dependent differences in mechanisms of OAE generation. Click-evoked and stimulus-frequency OAE input/output transfer functions were obtained and compared as a function of stimulus frequency and intensity. At low and moderate intensities human CEOAE and SFOAE transfer functions are nearly identical. When stimulus intensity is measured in "bandwidth-compensated" sound-pressure level (cSPL), CEOAE and SFOAE transfer functions have equivalent growth functions at fixed frequency and equivalent spectral characteristics at fixed intensity. This equivalence suggests that CEOAEs and SFOAEs are generated by the same mechanism. Although CEOAEs and SFOAEs are known by different names because of the different stimuli used to evoke them, the two OAE "types" are evidently best understood as members of the same emission family.