Maturation of medial efferent system function in humans

Otoacoustic emissions are typically reduced in amplitude when broadband noise is presented to the contralateral ear. This contralateral suppression is attributed to activation of the medial olivocochlear system, which has an inhibitory effect on outer hair-cell activity. By studying the effects of contralateral noise on cochlear output at different stages of auditory maturation in human neonates, it is possible to describe the timecourse for development of medial efferent system function in humans. The present study recorded 2 f1-f2 distortion product otoacoustic emissions (DPOAE) in human adults, term and premature neonates at three f2 frequencies: 1500, 3000, and 6000 Hz, using fixed primary tone frequency ratio (f2/f1 = 1.2) and level separation (10 dB, L1 > L2). Average DPOAE growth functions were recorded with and without contralateral broadband noise. Results indicate that contralateral suppression of DPOAEs is absent at 6000 Hz, but present at 1500 and 3000 Hz for all ages. However, DPOAE amplitude from premature neonates was not altered by noise in an adult-like manner; in this age group, DPOAE amplitude was equally likely to by suppressed or enhanced by noise presented contralaterally. Contralateral enhancement may reflect a temporary stage of immaturity in outer hair cell-medial efferent fiber synapses just prior to term birth.     

DPOAE suppression tuning: cochlear immaturity in premature neonates or auditory aging in normal-hearing adults?

Previous work has shown that distortion product otoacoustic emission (DPOAE) suppression tuning curves (STCs) recorded from premature neonates are narrower than adult STCs at both low and high frequencies. This has been interpreted to indicate an immaturity in cochlear function prior to term birth. However, an alternative explanation for this finding is that adult DPOAE STCs are broadened and reflect cochlear hair cell loss in normal-hearing adults due to aging, and natural exposure to noise and ototoxins. This alternative hypothesis can be tested by studying suppression tuning in normal-hearing school-aged children. If normal-hearing children, who have not aged significantly or been exposed to noise/ototoxins, have DPOAE suppression tuning similar to adults, the auditory aging hypothesis can be ruled out. However, if children have tuning similar to premature neonates and dissimilar from adults, it implicates aging or other factors intrinsic to the adult cochlea. DPOAE STCs were recorded at 1500, 3000, and 6000 Hz using optimal parameters in normal-hearing children and adults. DPOAE STCs collected previously from premature neonates were used for age comparisons. In general, results indicate that tuning curves from children are comparable to adult STCs and significantly different from neonatal STCS at 1500 and 6000 Hz. Only the growth of suppression was not adultlike in children and only at 6000 Hz. These findings do not strongly support the auditory aging hypothesis as a primary explanation for previously observed neonatal-adult differences in DPOAE suppression tuning. It suggests that these age differences are most likely due to immaturities in the neonatal cochlea. However, nonadultlike suppression growth observed in children at 6000 Hz warrants further attention and may be indicative of subtle alternations in the adult cochlea at high frequencies.     

Effects of middle-ear immaturity on distortion product otoacoustic emission suppression tuning in infant ears

Distortion product otoacoustic emission (DPOAE) measures of cochlear function, including DPOAE suppression tuning curves and input/output (I/O) functions, are not adultlike in human infants. These findings suggest the cochlear amplifier might be functionally immature in newborns. However, many noncochlear factors influence DPOAEs and must be considered. This study examines whether age differences in DPOAE I/O functions recorded from infant and adult ears reflect maturation of ear-canal/middle-ear function or cochlear mechanics. A model based on linear middle-ear transmission and nonlinear cochlear generation was developed to fit the adult DPOAE I/O data. By varying only those model parameters related to middle-ear transmission (and holding cochlear parameters at adult values), the model successfully fitted I/O data from infants at birth through age 6 months. This suggests that cochlear mechanics are mature at birth. The model predicted an attenuation of stimulus energy through the immature ear canal and middle ear, and evaluated whether immaturities in forward transmission could explain the differences consistently observed between infant and adult DPOAE suppression. Results show that once the immaturity was compensated for by providing infants with a relative increase in primary tone level, DPOAE suppression tuning at f2= 6000 Hz was similar in adults and infants.     

Distortion product otoacoustic emission (2f1-f2) suppression in 3-month-old infants: evidence for postnatal maturation of human cochlear function?

The complete timeline for maturation of human cochlear function has not been defined. Distortion product otoacoustic emission (DPOAE)-based measures of cochlear function show non-adult-like responses from premature and term-born neonates at high f2 frequencies; however, older infants were not included in these studies. In the present experiment, previously collected DPOAE ipsilateral suppression data from premature neonates were combined with new data collected from adults, term-born neonates, and 3-month-old infants to further examine the time course for maturation of cochlear function. DPOAE suppression tuning curves (STC) and suppression growth patterns were measured in the three age groups at f2 = 6000 Hz, L1 = 65, L2 = 55 dB SPL, with an f2/f1 of 1.2. Results indicate that term-born neonates and 3-month-old infants have non-adult-like STC width, slope on the low-frequency flank, and tip features. However, the two infant groups are not significantly different from one another. Suppression growth patterns for low-frequency suppressor tones show a clear developmental progression. In general, the younger the infant, the more shallow and compressive the suppression growth for the lowest suppressor frequencies. These findings suggest a high-frequency postnatal immaturity in cochlear function as measured by DPOAE suppression. Results may have been influenced by noncochlear factors, such as middle-ear immaturity. These factors are reviewed and considered.     

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.     

Maturation of cochlear nonlinearity as measured by distortion product otoacoustic emission suppression growth in humans

The growth of distortion product otoacoustic emission (DPOAE) suppression follows a systematic, frequency-dependent pattern. The pattern is consistent with direct measures of basilar-membrane response growth, psychoacoustic measures of masking growth, and measures of neural rate growth. This pattern has its basis in the recognized nonlinear properties of basilar-membrane motion and, as such, the DPOAE suppression growth paradigm can be applied to human neonates to study the maturation of cochlear nonlinearity. The objective of this experiment was to investigate the maturation of human cochlear nonlinearity and define the time course for this maturational process. Normal-hearing adults, children, term-born neonates, and premature neonates, plus a small number of children with sensorineural hearing loss, were included in this experiment. DPOAE suppression growth was measured at two f2 frequencies (1500 and 6000 Hz) and three primary tone levels (55-45, 65-55, and 75-65 dB SPL). Slope of DPOAE suppression growth, as well as an asymmetry ratio (to compare slope for suppressor tones below and above f2 frequency), were generated. Suppression threshold was also measured in all subjects. Findings indicate that both term-born neonates and premature neonates who have attained term-like age, show non-adult-like DPOAE suppression growth for low-frequency suppressor tones. These age effects are most evident at f2 = 6000 Hz. In neonates, suppression growth is shallower and suppression thresholds are elevated for suppressor tones lower in frequency than f2. Additionally, the asymmetry ratio is smaller in neonates, indicating that the typical frequency-dependent pattern of suppression growth is not present. These findings suggest that an immaturity of cochlear nonlinearity persists into the first months of postnatal life. DPOAE suppression growth examined for a small group of hearing-impaired children also showed abnormalities.     

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.     

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.     

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.     

Ipsilateral distortion product otoacoustic emission (2f1-f2) suppression in children with sensorineural hearing loss

Distortion product otoacoustic emission (DPOAE) ipsilateral suppression has been applied to study cochlear function and maturation in laboratory animals and humans. Although DPOAE suppression appears to be sensitive to regions of specialized cochlear function and to cochlear immaturity, it is not known whether it reflects permanent cochlear damage, i.e., sensorineural hearing loss (SNHL), in a reliable and systematic manner in humans. Eight school-aged children with mild-moderate SNHL and 20 normal-hearing children served as subjects in this study. DPOAE (2f1-f2) suppression data were collected at four f2 frequencies (1500, 3000, 4000, and 6000 Hz) using moderate-level primary tones. Features of the DPOAE iso-suppression tuning curves and suppression growth were analyzed for both subject groups. Results show that DPOAE suppression tuning curves from hearing-impaired subjects can be reliably recorded. DPOAE suppression tuning curves were generally normal in appearance and shape for six out of eight hearing-impaired subjects but showed subtle abnormalities in at least one feature. There was not one single trend or pattern of abnormality that characterized all hearing-impaired subjects. The most prominent patterns of abnormality included: broadened tuning, elevated tip, and downward shift of tip frequency. The unique patterns of atypical DPOAE suppression in subjects with similar audiograms may suggest different patterns of underlying sensory cell damage. This speculation warrants further investigation.     

Distortion product otoacoustic emissions for hearing threshold estimation and differentiation between middle-ear and cochlear disorders in neonates

Our aim in the present study was to apply extrapolated DPOAE I/O-functions [J. Acoust. Soc. Am. 111, 1810-1818 (2002); 113, 3275-3284 (2003)] in neonates in order to investigate their ability to estimate hearing thresholds and to differentiate between middle-ear and cochlear disorders. DPOAEs were measured in neonates after birth (mean age = 3.2 days) and 4 weeks later (follow-up) at 11 test frequencies between f2 = 1.5 and 8 kHz and compared to that found in normal hearing subjects and cochlear hearing loss patients. On average, in a single ear hearing threshold estimation was possible at about 2/3 of the test frequencies. A sufficient test performance of the approach is therefore suggested. Thresholds were higher at the first measurement compared to that found at the follow-up measurement. Since thresholds varied with frequency, transitory middle ear dysfunction due to amniotic fluid instead of cochlear immaturity is suggested to be the cause for the change in thresholds. DPOAE behavior in the neonate ears differed from that found in the cochlear hearing loss ears. From a simple model it was concluded that the difference between the estimated DPOAE threshold and the DPOAE detection threshold is able to differentiate between sound conductive and cochlear hearing loss.     

Spectral fine-structures of low-frequency modulated distortion product otoacoustic emissions

Biasing of the cochlear partition with a low-frequency tone can produce an amplitude modulation of distortion product otoacoustic emissions (DPOAEs) in gerbils. In the time domain, odd- versus even-order DPOAEs demonstrated different modulation patterns depending on the bias tone phase. In the frequency domain, multiple sidebands are presented on either side of each DPOAE component. These sidebands were located at harmonic multiples of the biasing frequency from the DPOAE component. For odd-order DPOAEs, sidebands at the even-multiples of the biasing frequency were enhanced, while for even-order DPOAEs, the sidebands at the odd-multiples were elevated. When a modulation in DPOAE magnitude was presented, the magnitudes of the sidebands were enhanced and even greater than the DPOAEs. The amplitudes of these sidebands varied with the levels of the bias tone and two primary tones. The results indicate that the maximal amplitude modulations of DPOAEs occur at a confined bias and primary level space. This can provide a guide for optimal selections of signal conditions for better recordings of low-frequency modulated DPOAEs in future research and applications. Spectral fine-structure and its unique relation to the DPOAE modulation pattern may be useful for direct acquisition of cochlear transducer nonlinearity from a simple spectral analysis.     

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.     

Similarity in loudness and distortion product otoacoustic emission input/output functions: implications for an objective hearing aid adjustment

The aim of the present study was to compare distortion product otoacoustic emissions (DPOAEs) to loudness with regard to the potentiality of DPOAEs to determine characteristic quantities of the cochlear-impaired ear and to derive objective hearing aid parameters. Recently, Neely et al. [J. Acoust. Soc. Am. 114, 1499-1507 (2003)] compared DPOAE input/output functions to the Fletcher and Munson [J. Acoust. Soc. Am. 5, 82-108 (1933)] loudness function finding a close resemblance in the slope characteristics of both measures. The present study extended their work by performing both loudness and DPOAE measurements in the same subject sample, and by developing a method for the estimation of gain needed to compensate for loss of cochlear sensitivity and compression. DPOAEs and loudness exhibited similar behavior when plotted on a logarithmic scale and slope increased with increasing hearing loss, confirming the findings of Neely et al. To compensate for undesired nonpathological impacts on the magnitude of DPOAE level, normalization of DPOAE data was implemented. A close resemblance between gain functions based on loudness and normalized DPOAE data was achieved. These findings suggest that DPOAEs are able to quantify the loss of cochlear sensitivity and compression and thus might provide parameters for a noncooperative hearing aid adjustment.     

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.     

Distortion product otoacoustic emission suppression tuning and acoustic admittance in human infants: birth through 6 months

Previous work has reported non-adultlike distortion product otoacoustic emission (DPOAE) suppression in human newborns at f2=6000 Hz, indicating an immaturity in peripheral auditory function. In this study, DPOAE suppression tuning curves (STCs) were recorded as a measure of cochlear function and acoustic admittance/reflectance (YR) in the ear canal recorded as a measure of middle-ear function, in the same 20 infants at birth and through 6 months of age. DPOAE STCs changed little from birth through 6 months, showing excessively narrow and sharp tuning throughout the test period. In contrast, several middle-ear indices at corresponding frequencies shifted systematically with increasing age, although they also remained non-adultlike at 6 months. Linear correlations were conducted between YR and DPOAE suppression features. Only two correlations out of 76 were significant, and all but three YR variables accounted for <10% of the variance in DPOAE suppression tuning. The strongest correlation was noted between admittance phase at 5700 Hz and STC tip-to-tail (R=0.49). The association between middle-ear variables and DPOAE suppression may be stronger during other developmental time periods. Study of older infants and children is needed to fully define postnatal immaturity of human peripheral auditory function.     

Suppression tuning in noise-exposed rabbits

Psychophysical, basilar-membrane (BM), and single nerve-fiber tuning curves, as well as suppression of distortion-product otoacoustic emissions (DPOAEs), all give rise to frequency tuning patterns with stereotypical features. Similarities and differences between the behaviors of these tuning functions, both in normal conditions and following various cochlear insults, have been documented. While neural tuning curves (NTCs) and BM tuning curves behave similarly both before and after cochlear insults known to disrupt frequency selectivity, DPOAE suppression tuning curves (STCs) do not necessarily mirror these responses following either administration of ototoxins [Martin et al., J. Acoust. Soc. Am. 104, 972-983 (1998)] or exposure to temporarily damaging noise [Howard et al., J. Acoust. Soc. Am. 111, 285-296 (2002)]. However, changes in STC parameters may be predictive of other changes in cochlear function such as cochlear immaturity in neonatal humans [Abdala, Hear. Res. 121, 125-138 (1998)]. To determine the effects of noise-induced permanent auditory dysfunction on STC parameters, rabbits were exposed to high-level noise that led to permanent reductions in DPOAE level, and comparisons between pre- and postexposure DPOAE levels and STCs were made. Statistical comparisons of pre- and postexposure STC values at CF revealed consistent basal shifts in the frequency region of greatest cochlear damage, whereas thresholds, Q10dB, and tip-to-tail gain values were not reliably altered. Additionally, a large percentage of high-frequency lobes associated with third tone interference phenomena, that were exhibited in some data sets, were dramatically reduced following noise exposure. Thus, previously described areas of DPOAE interference above f2 may also be studied using this type of experimental manipulation [Martin et al., Hear. Res. 136, 105-123 (1999); Mills, J. Acoust. Soc. Am. 107, 2586-2602 (2002)].     

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.     

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.     

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.