Distortion Product Otoacoustic Emissions Magnitude Research Articles

Metabolic and Sensory Components of Age-Related Hearing Loss: Associations With Distortion- and Reflection-Based Otoacoustic Emissions.

Age-related hearing loss is difficult to study in humans because multiple genetic and environmental risk factors may contribute to pathology and cochlear function declines in older adults. These pathologies, including degeneration of the stria vascularis, are hypothesized to affect outer hair cells responsible for active cochlear amplification of low-level sounds. Otoacoustic emission (OAE) measures are used to quantify the energy added to the traveling wave in cochlear amplification, which typically weakens with increased pure-tone thresholds and for older individuals. Thus, the current study evaluated two OAE measures for individuals with different components of age-related hearing loss. We examined two retrospective adult lifespan datasets (18 to 89+ years of age) from independent sites (Medical University of South Carolina and Boys Town National Research Hospital), which included demographics, noise history questionnaires, distortion-product otoacoustic emissions (DPOAE), and cochlear reflectance (CR). Metabolic and sensory estimates of age-related hearing loss were derived from the audiograms in each dataset, and then tested for associations with DPOAE and CR. The results showed that metabolic estimates increased for older participants and were associated with lower overall DPOAE and CR magnitudes across frequency (i.e., lower fitted intercepts). Sensory estimates were significantly higher for males, who reported more positive noise histories compared to females and were associated with steeper negative across-frequency slopes for DPOAEs. Although significant associations were observed between OAE configurations, DPOAEs appeared uniquely sensitive to metabolic estimates. The current findings suggest that distortion-based measures may provide greater sensitivity than reflection-based measures to the components of age-related hearing loss.

Accelerated Age-Related Degradation of the Tectorial Membrane in the Ceacam16βgal/βgal Null Mutant Mouse, a Model for Late-Onset Human Hereditary Deafness DFNB113.

CEACAM16 is a non-collagenous protein of the tectorial membrane, an extracellular structure of the cochlea essential for normal hearing. Dominant and recessive mutations in CEACAM16 have been reported to cause postlingual and progressive forms of deafness in humans. In a previous study of young Ceacam16βgal/βgal null mutant mice on a C57Bl/6J background, the incidence of spontaneous otoacoustic emissions (SOAEs) was greatly increased relative to Ceacam16+/+ and Ceacam16+/βgal mice, but auditory brain-stem responses (ABRs) and distortion product otoacoustic emissions (DPOAEs) were near normal, indicating auditory thresholds were not significantly affected. To determine if the loss of CEACAM16 leads to hearing loss at later ages in this mouse line, cochlear structure and auditory function were examined in Ceacam16+/+, Ceacam16+/βgal and Ceacam16βgal/βgal mice at 6 and 12 months of age and compared to that previously described at 1 month. Analysis of older Ceacam16βgal/βgal mice reveals a progressive loss of matrix from the core of the tectorial membrane that is more extensive in the apical, low-frequency regions of the cochlea. In Ceacam16βgal/βgal mice at 6–7 months, the DPOAE magnitude at 2f1-f2 and the incidence of SOAEs both decrease relative to young animals. By ∼12 months, SOAEs and DPOAEs are not detected in Ceacam16βgal/βgal mice and ABR thresholds are increased by up to ∼40 dB across frequency, despite a complement of hair cells similar to that present in Ceacam16+/+ mice. Although SOAE incidence decreases with age in Ceacam16βgal/βgal mice, it increases in aging heterozygous Ceacam16+/βgal mice and is accompanied by a reduction in the accumulation of CEACAM16 in the tectorial membrane relative to controls. An apically-biased loss of matrix from the core of the tectorial membrane, similar to that observed in young Ceacam16βgal/βgal mice, is also seen in Ceacam16+/+ and Ceacam16+/βgal mice, and other strains of wild-type mice, but at much later ages. The loss of Ceacam16 therefore accelerates age-related degeneration of the tectorial membrane leading, as in humans with mutations in CEACAM16, to a late-onset progressive form of hearing loss.

Slow oscillatory changes of DPOAE magnitude and phase after exposure to intense low-frequency sounds.

Sensitive sound detection within the mammalian cochlea is performed by hair cells surrounded by cochlear fluids. Maintenance of cochlear fluid homeostasis and tight regulation of intracellular conditions in hair cells are crucial for the auditory transduction process but can be impaired by intense sound stimulation. After a short, intense low-frequency sound, the cochlea shows the previously described "bounce phenomenon," which manifests itself as slow oscillatory changes of hearing thresholds and otoacoustic emissions. In this study, distortion product otoacoustic emissions (DPOAEs) were recorded after Mongolian gerbils were exposed to intense low-frequency sounds (200 Hz, 100 dB SPL) with different exposure times up to 1 h. After all sound exposure durations, a certain percentage of recordings (up to 80% after 1.5-min-long exposure) showed oscillatory DPOAE changes, similar to the bounce phenomenon in humans. Changes were quite uniform with respect to size and time course, and they were independent from sound exposure duration. Changes showed states of hypo- and hyperactivity with either state preceding the other. The direction of changes was suggested to depend on the static position of the cochlear operating point. As assessed with DPOAEs, no indication for a permanent damage after several or long exposure times was detected. We propose that sensitivity changes occur due to alterations of the mechanoelectrical transduction process of outer hair cells. Those alterations could be induced by different challenged homeostatic processes with slow electromotility of outer hair cells being the most plausible source of the bounce phenomenon. NEW & NOTEWORTHY Low-frequency, high-intensity sound can cause slowly cycling activity changes in the mammalian cochlea. We examined the effect of low-frequency sound duration on the degree of these alterations. We found that cochlear changes showed a stereotypical biphasic pattern independent of sound exposure duration, but the probability that significant changes occurred decreased with increasing sound duration. Despite exposure durations of up to 1 h, no permanent or transient impairments of the cochlea were detected.

Auditory Impairments in HIV-Infected Children.

In a cross-sectional study of human immunodeficiency virus (HIV)-infected adults, the authors showed lower distortion product otoacoustic emissions (DPOAEs) in HIV+ individuals compared with controls as well as findings consistent with a central auditory processing deficit in HIV+ adults on antiretroviral therapy. The authors hypothesized that HIV+ children would also have a higher prevalence of abnormal central and peripheral hearing test results compared with HIV- controls. Pure-tone thresholds, DPOAEs, and tympanometry were performed on 244 subjects (131 HIV+ and 113 HIV- subjects). Thirty-five of the HIV+, and 3 of the HIV- subjects had a history of tuberculosis treatment. Gap detection results were available for 18 HIV- and 44 HIV+ children. Auditory brainstem response results were available for 72 HIV- and 72 HIV+ children. Data from ears with abnormal tympanograms were excluded. HIV+ subjects were significantly more likely to have abnormal tympanograms, histories of ear drainage, tuberculosis, or dizziness. All audiometric results were compared between groups using a two-way ANOVA with HIV status and ear drainage history as grouping variables. Mean audiometric thresholds, gap detection thresholds, and auditory brainstem response latencies did not differ between groups, although the HIV+ group had a higher proportion of individuals with a hearing loss >25 dB HL in the better ear. The HIV+ group had reduced DPOAE levels (p < 0.05) at multiple frequencies compared with HIV- subjects. No relationships were found between treatment regimens or delay in starting treatment and audiological parameters. As expected, children with HIV+ were more likely to have a history of ear drainage, and to have abnormal tympanograms. Similar to the adult findings, the HIV+ group did not show significantly reduced audiometric thresholds, but did have significantly lower DPOAE magnitudes. These data suggest that (1) HIV+ children often have middle ear damage which complicates understanding the direct effects of HIV on the hearing system, and (2) even when corrected for confounders DPOAEs were lower in the HIV+ group. Previous studies suggest ototoxicity from antiretroviral drugs is an unlikely cause of the reduced DPOAE magnitudes. Other possibilities include effects on efferent pathways connecting to outer hair cells or a direct effect of HIV on the cochlea.

Distortion Product Otoacoustic Emissions and Intracranial Pressure During CSF Infusion Testing.

A noninvasive method to monitor changes in intracranial pressure (ICP) is required for astronauts on long-duration spaceflight who are at risk of developing the Visual Impairment/Intracranial Pressure syndrome that has some, but not all of the features of idiopathic intracranial hypertension. We assessed the validity of distortion product otoacoustic emissions (DPOAEs) to detect changes in ICP. Subjects were eight patients undergoing medically necessary diagnostic cerebrospinal fluid (CSF) infusion testing for hydrocephalus. DPOAE measurements were obtained with an FDA-approved system at baseline and six controlled ICP levels in ∼3 mmHg increments in random order, with a range from 10.8 ± 2.9 mmHg (SD) at baseline to 32.3 ± 4.1 mmHg (SD) at level 6. For f2 frequencies between 800 and 1700 Hz, when ICP was ≥ 12 mmHg above baseline ICP, DPOAE angles increased significantly and DPOAE magnitudes decreased significantly, but less robustly. Significant changes in DPOAE angle and magnitude are seen when ICP is ≥ 12 mmHg above a subject's supine baseline ICP during CSF infusion testing. These results suggest that the changes in DPOAE angle and magnitude seen with change in ICP are physiologically based, and suggest that it should be possible to detect pathological ICP elevation using DPOAE measurements. To use DPOAE for noninvasive estimation of ICP during spaceflight will require baseline measurements in the head-up, supine, and head-down positions to obtain baseline DPOAE values at different ICP ranges. Williams MA, Malm J, Eklund A, Horton NJ, Voss SE. Distortion product otoacoustic emissions and intracranial pressure during CSF infusion testing. Aerosp Med Hum Perform. 2016; 87(10):844-851.

Negative Middle Ear Pressure and Composite and Component Distortion Product Otoacoustic Emissions.

Distortion product otoacoustic emissions (DPOAEs), a by-product of normal outer hair cell function, are used in research and clinical settings to noninvasively test cochlear health. The composite DPOAE recorded in the ear canal is the result of interactions of at least two components: a nonlinear distortion component (the generator component) and a linear reflection component. Negative middle ear pressure (NMEP) results in the tympanic membrane being pulled inward and increases middle ear impedance. This influences both the forward travel of stimuli used to induce distortion products and the reverse travel of the emissions back to the ear canal. NMEP may therefore limit the effectiveness of DPOAEs in clinical settings. Twenty-six normal-hearing subjects were recruited, and eight were able to reliably and consistently induce NMEP using the Toynbee maneuver. Eight interleaved measures of tympanic peak pressure (TPP) were collected for each subject at normal pressure and NMEP. DPOAEs were then collected both when middle ear pressure was normal and during subject-induced NMEP. All measures were interleaved. Two primary tones were swept logarithmically across frequency (1 second per octave) from f1 = 410 to 6560 Hz and f2 = 500 to 8000 Hz (f1/f2 = 1.22), producing 2f1 - f2 DPOAEs from 320 to 5120 Hz. DPOAEs were collected at three equal-level primary level combinations (L65, L70, L75 dB SPL). Before composite and component DPOAE analysis, analysis of the f1 DPOAE primary confirmed that subjects had successfully induced NMEP. DPOAE and component magnitudes were separately analyzed using repeated measures analysis of variances with three factors, primary level (L65, L70, L75 dB SPL), middle ear pressure (normal pressure versus NMEP), and frequency (500 to 4000 Hz). Mean subject-induced NMEP ranged from -65 to -324 daPa. Changes in the magnitude (dB) of the primary tones used to induce the DPOAE provided a reliable indicator of subject-induced NMEP. Composite DPOAE and component levels were significantly affected by NMEP for all the frequencies tested. Changes were most clearly observed for the generator component with one subject demonstrating a mean decrease of 12 dB in magnitude during NMEP. Results were subject-specific, and there was a correlation between the degree of negative TPP induced and the amount of change in DPOAE level. Mean TPPs collected during NMEP ranged from -65 to -324 daPa and significantly affected composite DPOAE, generator, and reflection component levels. Changes in the magnitude of the swept-primaries as a function of frequency were used to confirm that NMEP had been successfully induced. The patterns of change in the composite DPOAEs were clearer and easier to interpret when the components of the DPOAE were separated with evaluation of the generator component alone.

Increased contralateral suppression of otoacoustic emissions indicates a hyperresponsive medial olivocochlear system in humans with tinnitus and hyperacusis.

Atypical medial olivocochlear (MOC) feedback from brain stem to cochlea has been proposed to play a role in tinnitus, but even well-constructed tests of this idea have yielded inconsistent results. In the present study, it was hypothesized that low sound tolerance (mild to moderate hyperacusis), which can accompany tinnitus or occur on its own, might contribute to the inconsistency. Sound-level tolerance (SLT) was assessed in subjects (all men) with clinically normal or near-normal thresholds to form threshold-, age-, and sex-matched groups: 1) no tinnitus/high SLT, 2) no tinnitus/low SLT, 3) tinnitus/high SLT, and 4) tinnitus/low SLT. MOC function was measured from the ear canal as the change in magnitude of distortion-product otoacoustic emissions (DPOAE) elicited by broadband noise presented to the contralateral ear. The noise reduced DPOAE magnitude in all groups ("contralateral suppression"), but significantly more reduction occurred in groups with tinnitus and/or low SLT, indicating hyperresponsiveness of the MOC system compared with the group with no tinnitus/high SLT. The results suggest hyperresponsiveness of the interneurons of the MOC system residing in the cochlear nucleus and/or MOC neurons themselves. The present data, combined with previous human and animal data, indicate that neural pathways involving every major division of the cochlear nucleus manifest hyperactivity and/or hyperresponsiveness in tinnitus and/or low SLT. The overactivation may develop in each pathway separately. However, a more parsimonious hypothesis is that top-down neuromodulation is the driving force behind ubiquitous overactivation of the auditory brain stem and may correspond to attentional spotlighting on the auditory domain in tinnitus and hyperacusis.

Intracranial pressure modulates distortion product otoacoustic emissions: a proof-of-principle study.

There is an important need to develop a noninvasive method for assessing intracranial pressure (ICP). We report a novel approach for monitoring ICP using cochlear-derived distortion product otoacoustic emissions (DPOAEs), which are affected by ICP. We hypothesized that changes in ICP may be reflected by altered DPOAE responses via an associated change in perilymphatic pressure. We measured the ICP and DPOAEs (magnitude and phase angle) during opening and closing in 20 patients undergoing lumbar puncture. We collected data on 18 patients and grouped them based on small (<4 mm Hg), medium (5-11 mm Hg), or large (≥15 mm Hg) ICP changes. A permutation test was applied in each group to determine whether changes in DPOAEs differed from zero when ICP changed. We report significant changes in the DPOAE magnitudes and angles, respectively, for the group with the largest ICP changes and no changes for the group with the smallest changes; the group with medium changes had variable DPOAE changes. We report, for the first time, systematic changes in DPOAE magnitudes and phase in response to acute ICP changes. Future studies are warranted to further develop this new approach. DPOAE, distortion product otoacoustic emissionICP, intracranial pressureIIH, idiopathic intracranial hypertensionLP, lumbar punctureTBI, traumatic brain injury.

Test/retest repeatability of effect contralateral acoustic stimulation on the magnitudes of distortion product ototacoustic emissions

Contralateral inhibition of distortion product otoacoustic emissions (DPOAE) has become an important tool to assess the functioning of the medial olivocochlear efferents in humans. However, before this measurement can be applied clinically, the test/retest repeatability needs to be established. Therefore, the current study aimed at evaluating intra- and intersession test/retest repeatability of contralateral inhibition of DPOAE at 2f(1) -f(2) . Prospective Test/Retest Reliability Study. Contralateral inhibition of DPOAE magnitudes were measured in the right ear of 24 adult male participants. To assess the intrasession repeatability, measurements were repeated without altering the position of the DPOAE probe (single-probe-fit). To assess intersession reliability, measurements were repeated on 8 different days (multiple-probe-fit). Repeatability of inhibition of DPOAE magnitudes was evaluated by Cronbach's alpha, interclass correlations, standard error of measurement, and its 95% confidence interval and smallest detectable difference. DPOAE magnitudes were highly stable and repeatable across different recording sessions. However, test/retest reliability coefficients of DPOAE inhibition magnitudes were less than satisfactory for all the frequencies, in both single-probe-fit and multiple-probe-fit modes. Results of the present study showed that contralateral inhibition magnitudes of DPOAEs varied considerably, even though DPOAEs magnitudes remained essentially the same across different recording sessions. As reliability is an essential aspect of any clinical procedure, it is suggested that at present contralateral inhibition of DPOAEs should not be used clinically to evaluate the medial efferent system. Laryngoscope, 2012.

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.

Posture-Induced Changes in Distortion-Product Otoacoustic Emissions and the Potential for Noninvasive Monitoring of Changes in Intracranial Pressure

Intracranial pressure (ICP) monitoring is currently an invasive procedure that requires access to the intracranial space through an opening in the skull. Noninvasive monitoring of ICP via the auditory system is theoretically possible because changes in ICP transfer to the inner ear through connections between the cerebral spinal fluid and the cochlear fluids. In particular, low-frequency distortion-product otoacoustic emissions (DPOAEs), measured noninvasively in the external ear canal, have magnitudes that depend on ICP. Postural changes in healthy humans cause systematic changes in ICP. Here, we quantify the effects of postural changes, and presumably ICP changes, on DPOAE magnitudes. DPOAE magnitudes were measured on seven normal-hearing, healthy subjects at four postural positions on a tilting table (angles 90 degrees , 0 degrees , - 30 degrees , and - 45 degrees to the horizontal). At these positions, it is expected that ICP varied from about 0 (90 degrees ) to 22 mm Hg ( - 45 degrees ). DPOAE magnitudes were measured for a set of frequencies 750 < f2 < 4000, with f2/f1 = 1.2. For the low-frequency range of 750 <or=f2<or= 1500, the differences in DPOAE magnitude between upright and - 45 degrees were highly significant (all p < 0.01), and above 1500 Hz there were minimal differences between magnitudes at 90 degrees versus - 45 degrees. There were no significant differences in the DPOAE magnitudes with subjects at 90 degrees and 0 degrees postures. Changes in ICP can be detected using the auditory-based measurement of DPOAEs. In particular, changes are largest at low frequencies. Although this approach does not allow for absolute measurement of ICP, it appears that measurement of DPOAEs may be a useful means of noninvasively monitoring ICP.

Dyslipidemia and cochlear function

Problem: The relationship between dyslipidemia and hearing is unclear. This study was conducted to investigate whether elevated serum lipid levels impact cochlear function. Methods: Two animal models (human and guinea pig) were used. In the human model, a cross-sectional study of 40 volunteers with dyslipidemia was conducted. Total cholesterol, high density lipoprotein (HDL), low density lipoprotein (LDL), triglycerides, pure tone thresholds, and distortion product otoacoustic emissions (DPOAEs) were measured. In the guinea pig model, a prospective study over 14 weeks was conducted. A control group of 7 males were fed a normal diet. The experimental groups of 9 males and 8 females were fed a high fat diet. Weight, total cholesterol, and DPOAE magnitude were measured for each group. Results: For the human study, multiple linear regression analysis was performed in order to identify an effect of triglycerides, HDL, or LDL on pure tone thresholds and DPOAEs. When controlled for patient age, there was no statistically significant effect of any of the independent variables on cochlear function. For the guinea pig study, the paired students’ t test was performed in order to identify an effect of diet on DPOAEs. While the high fat diet led to a dramatic elevation in the average total cholesterol in all animals (from 61 to 589 mg/dL), there were no meaningful changes in DPOAE magnitudes. This was similar for the males as well as the females. Conclusion: These results suggest that dyslipidemia has no significant effect on cochlear function. Significance: Assessment of a patient’s lipid levels when determining a possible cause of his or her hearing loss may not be warranted. Support: None reported.

Concurrent measurement of distortion product otoacoustic emissions and auditory steady state evoked potentials

Distortion product otoacoustic emissions (DPOAEs) and auditory steady state evoked response potentials (ASSRs) can both be evoked by tone pairs with frequencies f 1 and f 2. The DPOAE is maximal at 2 f 1− f 2 and the ASSR is maximal at f 2− f 1. Since DPOAE magnitude depends on the ratio f 2/ f 1, but ASSR amplitude depends on the beat frequency f 2− f 1, compromises are necessary when recording both responses concurrently. Tone pairs with f 2 of 900, 1800 and 3600 Hz were presented simultaneously at either 40 or 50 dB sound pressure level (SPL). The f 1 frequency of each pair was approximately 85 or 180 Hz lower than f 2. Phase measurements were used to calculate apparent latencies at 40 dB SPL. For increasing f 2, DPOAE latencies were 14.5, 9.7 and 6.3 ms for 85 Hz beats, and 11.5, 9.0 and 4.3 ms for 180 Hz beats. ASSR latencies were 22.0, 15.7 and 17.8 ms at 85 Hz, and 17.7, 11.3 and 9.6 ms at 180 Hz. From a model of the mechanical transmission in the cochlea, delays between the basilar membrane and the generator of the ASSR were estimated as 15.4, 12.2 and 15.3 ms at 85 Hz and 8.6, 7.6 and 8.0 ms at 180 Hz.

Effects of gap junction uncoupling in the gerbil cochlea.

To gain insight into molecular and cellular mechanisms regulating cochlear potassium (K+) recycling, including the possible effects of mutations in the gene, which encodes the gap junction protein connexin 26. Intercellular K+ flux was manipulated in vivo by infusion of the gap junction uncoupler proadifen (SKF-525A) into perilymph. Functional and structural alterations induced by gap junction blockade were assessed by electrophysiological and morphologic analysis. Laboratory study using an animal model. Physiological effects of acute and chronic uncoupling of gap junctions in the Mongolian gerbil inner ear were evaluated by measurement of compound action potential (CAP) thresholds and input-output (I/O) functions, distortion product otoacoustic emissions (DPOAE), and the endocochlear potential (EP). Morphologic changes were assessed by electron microscopy. Acute exposures to proadifen resulted in large decreases in EP values, DPOAE magnitudes, and CAP I/O maximum amplitudes and an increase in high-frequency CAP thresholds. These physiological changes were accompanied by vacuolization of type II and type V fibrocytes in the lateral wall of the cochlea. Chronic treatments revealed some recovery in EP values and CAP thresholds, which showed a relatively flat 15- to 20-dB elevation across frequencies. Gap junctions play a significant role in normal cochlear function. In particular they appear to be essential for maintaining the EP, an activity that could be related to their participation in K+ recycling. Thus, hearing losses associated with mutations in the gene that alter the expression or function of connexin 26 may result from a diminished capacity to recycle K+ from perilymph back to the stria vascularis and a consequent decline in the EP.

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.

Magnitudes and phases of human distortion-product otoacoustic emissions at 2 f1− f2 against f2/ f1: effects of an audiometric notch

The influence of the frequency ratio f 2/ f 1 of two pure-tone stimuli on the distortion-product otoacoustic emissions (DPOAEs) at 2 f 1− f 2 was assessed in 14 hearing-impaired human ears exhibiting a narrow audiometric notch at 4 kHz, whereas 11 normally hearing ears served as controls. A fixed- f 2 paradigm was used, with f 2 values varying from 2 to 8 kHz in 1-kHz steps. The intensities of the two stimuli were either 60 or 70 dB SPL. The magnitudes and phases of DPOAEs were extracted so that the bandpass filter-like profile of DPOAE magnitude against f 2/ f 1 ( f 2/ f 1 magnitude function) could be characterized by the presence and position of its maximum, and DPOAE group delays were derived from the phase gradient of the DPOAE when f 1 varied. The main difference between normal and impaired ears occurred at 4 kHz in that, in contrast with normal ears, nine impaired ears out of 14 did not present any peak in their f 2/ f 1 magnitude function, while the remaining five ears only differed from normal ones by a slightly shifted maximum toward larger f 2/ f 1s. Group delays were significantly shortened in all impaired ears, with a tendency to be shorter in the subset of ears with flat DPOAE magnitude profiles with f 2/ f 1. No clear effect of notch depth was observed, and with the chosen stimulus characteristics, no abnormal DPOAE result was observed whenever f 2 fell outside the audiometric notch. It is concluded that DPOAE group delays apparently provide useful objective clues of cochlear dysfunction, more sensitive than DPOAE magnitudes inasmuch as many of them remained near the normal range. Although a majority of f 2/ f 1 magnitude functions were clearly flattened when f 2 was impaired, this feature was less systematic.

Effects of sample size on the noise floor and distortion product otoacoustic emissions.

This study investigated the effects of sample size on the noise floor and distortion product otoacoustic emissions (DPOAEs) in 55 normal-hearing subjects as a function of intensity. More specifically, we investigated the effects of sample size (12-400 sweeps) as a function of intensity (L1 = L2 = 35, 45 and 55 dB SPL), firstly, on the identifiability of DPOAEs (2F1-F2), secondly, on the noise floor adjacent to DPOAEs, and thirdly, on the magnitude of DPOAEs centred around geometric means of 531 Hz, 1,000 Hz, 2,000 Hz and 4,000 Hz. Testing was conducted with a commercially available system for measuring DPOAEs (Grason-Stadler, GSI-60). A constant F2:F1 ratio of 1.21 was used. As sample size increased from 12 to 400 sweeps, the noise floors decreased by about 13 dB; this closely corresponds to the expected 15 dB reduction based on the square root rule of noise reduction. The highest noise floors were measured at 531 Hz and the lowest noise floors at 2,000 Hz and 4,000 Hz. Identifiability increased as intensity increased from 35 to 55 dB SPL and as sample size increased from 12 to 400 sweeps for all stimulus conditions. Mean DPOAEs for all frequencies (531-4,000 Hz) appeared to decrease as sample size increased, particularly at stimulus levels of 35 dB and 45 dB SPL. These results may be explained by a reduction in the noise levels within the bandwidth of the DPOAE bin. That is, the DPOAE bin is comprised of the DPOAE plus background noise and these two quantities are not separated within the measured bin. Because the magnitude of bin containing DPOAEs is critically dependent on sample size, clinicians should carefully document this variable when collecting normative data. Similarly, clinicians who compare the magnitude of their DPOAEs to published data should note the sample size employed.

Long-term sound conditioning enhances cochlear sensitivity.

Sound conditioning, by chronic exposure to moderate-level sound, can protect the inner ear (reduce threshold shifts and hair cell damage) from subsequent high-level sound exposure. To investigate the mechanisms underlying this protective effect, the present study focuses on the physiological changes brought on by the conditioning exposure itself. In our guinea-pig model, 6-h daily conditioning exposure to an octave-band noise at 85 dB SPL reduces the permanent threshold shifts (PTSs) from a subsequent 4-h traumatic exposure to the same noise band at 109 dB SPL, as assessed by both compound action potentials (CAPs) and distortion product otoacoustic emissions (DPOAEs). The frequency region of maximum threshold protection is approximately one-half octave above the upper frequency cutoff of the exposure band. Protection is also evident in the magnitude of suprathreshold CAPs and DPOAEs, where effects are more robust and extend to higher frequencies than those evident at or near threshold. The conditioning exposure also enhanced cochlear sensitivity, when evaluated at the same postconditioning time at which the traumatic exposure would be delivered in a protection study. Response enhancements were seen in both threshold and suprathreshold CAPs and DPOAEs. The frequency dependence of the enhancement effects differed, however, by these two metrics. For CAPs, effects were maximum in the same frequency region as those most protected by the conditioning. For DPOAEs, enhancements were shifted to lower frequencies. The conditioning exposure also enhanced both ipsilaterally and contralaterally evoked olivocochlear (OC) reflex strength, as assessed using DPOAEs. The frequency and level dependence of the reflex enhancements were consistent with changes seen in sound-evoked discharge rates in OC fibers after conditioning. However, comparison with the frequency range and magnitude of conditioning-related protection suggests that the protection cannot be completely explained by amplification of the OC reflex and the known protective effects of OC feedback. Rather, the present results suggest that sound conditioning leads to changes in the physiology of the outer hair cells themselves, the peripheral targets of the OC reflex.