Search

Cochlear implantation leads to many structural changes within the cochlea which can impair residual hearing. In patients with preserved low-frequency hearing, a delayed hearing loss can occur weeks-to-years post-implantation. We explore whether stiffening of the basilar membrane (BM) may be a contributory factor in an animal model. Our objective is to map changes in morphology and Young's modulus of basal and apical areas of the BM after cochlear implantation, using quantitative nanomechanical atomic force microscopy (QNM-AFM) after cochlear implant surgery. Cochlear implantation was undertaken in the guinea pig, and the BM was harvested at four time-points: 1 day, 14 days, 28 days and 84 days post-implantation for QNM-AFM analysis. Auditory brainstem response thresholds were determined prior to implantation and termination. BM tissue showed altered morphology and a progressive increase in Young's modulus, mainly in the apex, over time after implantation. BM tissue from the cochlear base demonstrated areas of extreme stiffness which are likely due to micro-calcification on the BM. In conclusion, stiffening of the BM after cochlear implantation occurs over time, even at sites far apical to a cochlear implant., (Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.)

Many users of bilateral cochlear implants (BiCIs) localize sound sources less accurately than do people with normal hearing. This may be partly due to using two independently functioning CIs with fixed compression, which distorts and/or reduces interaural level differences (ILDs). Here, we investigate the potential benefits of using binaurally coupled, dynamic compression inspired by the medial olivocochlear reflex; an approach termed "the MOC strategy" (Lopez-Poveda et al., 2016, Ear Hear 37:e138-e148). Twelve BiCI users were asked to localize wideband (125-6000 Hz) noise tokens in a virtual horizontal plane. Stimuli were processed through a standard (STD) sound processing strategy (i.e., involving two independently functioning sound processors with fixed compression) and three different implementations of the MOC strategy: one with fast (MOC1) and two with slower contralateral control of compression (MOC2 and MOC3). The MOC1 and MOC2 strategies had effectively greater inhibition in the higher than in the lower frequency channels, while the MOC3 strategy had slightly greater inhibition in the lower than in the higher frequency channels. Localization was most accurate with the MOC1 strategy, presumably because it provided the largest and less ambiguous ILDs. The angle error improved slightly from 25.3° with the STD strategy to 22.7° with the MOC1 strategy. The improvement in localization ability over the STD strategy disappeared when the contralateral control of compression was made slower, presumably because stimuli were too short (200 ms) for the slower contralateral inhibition to enhance ILDs. Results suggest that some MOC implementations hold promise for improving not only speech-in-noise intelligibility, as shown elsewhere, but also sound source lateralization., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Residual hearing loss in cochlear implant users is investigated using the mechanical-human-cochlear model. Hearing loss due to stiffening of the round window increases significantly as input frequencies decrease from 3 kHz to 1 kHz but remains constant at lower frequencies, whereas loss due to the presence of an electrode insert becomes significantly higher at lower frequencies ([Formula: see text] kHz). The latter also shifts the characteristic frequency map toward the basal end of the cochlea. In the region away from the end of the electrode insert, cochlear function recovers, but the user still suffers from hearing loss caused by round window stiffening.

Cochlear implantation can restore a certain degree of auditory impression of patients suffering from profound hearing loss or deafness. Furthermore, studies have shown that in case of residual hearing, patients benefit from the use of a hearing aid in addition to the cochlear implant. The presented studies aim at the improvement of this electromechanical stimulation (EMS) approach by substituting the external hearing aid by an internal stimulus provided by miniaturized piezoelectric actuators. Finite element analyses are performed in order to derive fundamental guidelines for the actuator layout aiming at maximal mechanical stimuli. Further analyses aim at investigating how the actuator position inside the cochlea influences the basilar membrane oscillation profile. While actuator layout guidelines leading to maximized acoustic stimuli could be derived, some of these guidelines are of complementary nature suggesting that further studies under realistic boundary conditions must be performed. Actuator positioning inside the cochlea is shown to have a significant influence on the resulting auditory impression of the patient. Based on the results, the main differences of external and internal stimulation of the cochlea mechanism are identified. It is shown that if the cochlea tonotopy is considered, the frequency selectivity resulting from the mechanical cochlea stimulus may be improved.

It is well known that pure-tone audiometry does not sufficiently describe individual hearing loss (HL) and that additional measures beyond pure-tone sensitivity might improve the diagnostics of hearing deficits. Specifically, forward masking experiments to estimate basilar-membrane (BM) input-output (I/O) function have been proposed. However, such measures are very time consuming. The present study investigated possible modifications of the temporal masking curve (TMC) paradigm to improve time and measurement efficiency. In experiment 1, estimates of knee point (KP) and compression ratio (CR) of individual BM I/Os were derived without considering the corresponding individual "off-frequency" TMC. While accurate estimation of KPs was possible, it is difficult to ensure that the tested dynamic range is sufficient. Therefore, in experiment 2, a TMC-based paradigm, referred to as the "gap method", was tested. In contrast to the standard TMC paradigm, the maker level was kept fixed and the "gap threshold" was obtained, such that the masker just masks a low-level (12 dB sensation level) signal. It is argued that this modification allows for better control of the tested stimulus level range, which appears to be the main drawback of the conventional TMC method. The results from the present study were consistent with the literature when estimating KP levels, but showed some limitations regarding the estimation of the CR values. Perspectives and limitations of both approaches are discussed.

Hypothesis: Cochlear implant (CI) electrode insertion into the round window induces pressure transients in the cochlear fluid comparable to high-intensity sound transients., Background: Many patients receiving a CI have some remaining functional hearing at low frequencies; thus, devices and surgical techniques have been developed to use this residual hearing. To maintain functional acoustic hearing, it is important to retain function of any hair cells and auditory nerve fibers innervating the basilar membrane; however, in a subset of patients, residual low-frequency hearing is lost after CI insertion. Here, we test the hypothesis that transient intracochlear pressure spikes are generated during CI electrode insertion, which could cause damage and compromise residual hearing., Methods: Human cadaveric temporal bones were prepared with an extended facial recess. Pressures in the scala vestibuli and tympani were measured with fiber-optic pressure sensors inserted into the cochlea near the oval and round windows, whereas CI electrodes (five styles from two manufacturers) were inserted into the cochlea via a round window approach., Results: Pressures in the scala tympani tended to be larger in magnitude than pressures in the scala vestibuli, consistent with electrode insertion into the scala tympani. CI electrode insertion produced a range of pressure transients in the cochlea that could occur alone or as part of a train of spikes with equivalent peak sound pressure levels in excess of 170 dB sound pressure level. Instances of pressure transients varied with electrode styles., Conclusion: Results suggest electrode design, insertion mechanism, and surgical technique affect the magnitude and rate of intracochlear pressure transients during CI electrode insertion. Pressure transients showed intensities similar to those elicited by high-level sounds and thus could cause damage to the basilar membrane and/or hair cells., Competing Interests: Stephen P. Cass is a consultant on the Surgical Advisory Board for Cochlear Corporation.

A triboelectric-based artificial basilar membrane (TEABM) can mimic cochlear tonotopy by triboelectrification between Kapton film and aluminum foil. The two films are stacked and clamped to form a beam structure. The TEABM tonotopy is tested using an animal model to verify the feasibility of a self-powered acoustic sensor for a prototype cochlear implant., (© 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Some listeners with hearing loss show poor speech recognition scores in spite of using amplification that optimizes audibility. Beyond audibility, studies have suggested that suprathreshold abilities such as spectral and temporal processing may explain differences in amplified speech recognition scores. A variety of different methods has been used to measure spectral processing. However, the relationship between spectral processing and speech recognition is still inconclusive. This study evaluated the relationship between spectral processing and speech recognition in listeners with normal hearing and with hearing loss. Narrowband spectral resolution was assessed using auditory filter bandwidths estimated from simultaneous notched-noise masking. Broadband spectral processing was measured using the spectral ripple discrimination (SRD) task and the spectral ripple depth detection (SMD) task. Three different measures were used to assess unamplified and amplified speech recognition in quiet and noise. Stepwise multiple linear regression revealed that SMD at 2.0 cycles per octave (cpo) significantly predicted speech scores for amplified and unamplified speech in quiet and noise. Commonality analyses revealed that SMD at 2.0 cpo combined with SRD and equivalent rectangular bandwidth measures to explain most of the variance captured by the regression model. Results suggest that SMD and SRD may be promising clinical tools for diagnostic evaluation and predicting amplification outcomes.

Clinical conditions have been described in which one of the two cochlear windows is immobile (otosclerosis) or absent (round window atresia), but nevertheless bone conduction (BC) thresholds are relatively unaffected. To clarify this apparent paradox, experimental manipulations which would severely impede several of the classical osseous mechanisms of BC were induced in fat sand rats, including discontinuity or immobilization of the ossicular chain, coupled with window fixation. Effects of these manipulations were assessed by recording auditory nerve brainstem evoked response (ABR) thresholds to stimulation by air conduction (AC), by osseous BC and by non-osseous BC (also called soft tissue conduction-STC) in which the BC bone vibrator is applied to skin sites. Following the immobilization, discontinuity and window fixation, auditory stimulation was also delivered to cerebro-spinal fluid (CSF) and to saline applied to the middle ear cavity. While the manipulations (immobilization, discontinuity, window fixation) led to an elevation of AC thresholds, nevertheless, there was no change in osseous and non-osseous BC thresholds. On the other hand, ABR could be elicited in response to fluid pressure stimulation to CSF and middle ear saline, even in the presence of the severe restriction of ossicular chain and window mobility. The results of these experiments in which osseous and non-osseous BC thresholds remained unchanged in the presence of severe restriction of the classical middle ear mechanisms and in the absence of an efficient release window, while ABR could be recorded in response to fluid pressure auditory stimulation to fluid sites, indicate that it is possible that the inner ear may be activated at low sound intensities by fast fluid pressure stimulation. At higher sound intensities, a slower passive basilar membrane traveling wave may serve to excite the inner ear.

Tone burst-evoked otoacoustic emission (TBOAE) components measured in response to a 1 kHz tone burst (TB1) are suppressed by the simultaneous presence of an additional tone burst (TB2). This "simultaneous suppression of TBOAEs" has been explained in terms of a mechanism based on local nonlinear interactions between the basilar membrane (BM) travelling waves caused by TB1 and TB2. A test of this local nonlinear interaction (LNI)-based mechanism, as a function of the frequency separation (Δf, expressed in kHz) between TB1 and TB2, has previously been reported by Killan et al. (2012) using a simple mathematical model [Killan et al., Hear. Res. 285, 58-64 (2012)]. The two experiments described in this paper add additional data on the extent to which the LNI-based mechanism can account for simultaneous suppression, by testing two further hypotheses derived from the model predictions. Experiment I tested the hypothesis that TBOAE suppression is directly linked to TBOAE amplitude nonlinearity where ears that exhibit a higher degree of amplitude nonlinearity yield greater suppression than more linear ears, and this relationship varies systematically as a function of Δf. In order to test this hypothesis simultaneous suppression at a range of values of Δf at 60 dB peak-equivalent sound pressure level (p.e. SPL) and TBOAE amplitude nonlinearity from normal human ears was measured. In Experiment II the hypothesis that suppression will also increase progressively as a function of increasing tone burst level was tested by measuring suppression for a range of Δf and tone burst levels at 40, 50, 60 and 70 dB p.e. SPL. The majority of the findings from both experiments provide support for the LNI-based mechanism being primarily responsible for simultaneous suppression. However, some data were inconsistent with this view. Specifically, a breakdown in the relationship between suppression and TBOAE amplitude nonlinearity at Δf = 1 (i.e. when TB2 was reasonably well separated from, and had a higher frequency than TB1) and unexpected level-dependence, most notably at Δf = 1, but also where Δf = -0.5, was observed. Either the LNI model is too simple or an alternative explanation, involving response components generated at basal regions of the basilar membrane, is required to account for these findings., (Copyright © 2014 Elsevier B.V. All rights reserved.)

In the mammalian auditory system, the three rows of outer hair cells (OHCs) located in the cochlea are thought to increase the displacement amplitude of the organ of Corti. This cochlear amplification is thought to contribute to the high sensitivity, wide dynamic range, and sharp frequency selectivity of the hearing system. Recent studies have shown that traumatic stimuli, such as noise exposure and ototoxic acid, cause functional loss of OHCs in one, two, or all three rows. However, the degree of decrease in cochlear amplification caused by such functional losses remains unclear. In the present study, a finite element model of a cross section of the gerbil cochlea was constructed. Then, to determine effects of the functional losses of OHCs on the cochlear amplification, changes in the displacement amplitude of the basilar membrane (BM) due to the functional losses of OHCs were calculated. Results showed that the displacement amplitude of the BM decreases significantly when a single row of OHCs lost its function, suggesting that all three rows of OHCs are required for cochlear amplification.

Noise induced hearing loss (NIHL) remains as a severe health problem worldwide. Existing noise metrics and modeling for evaluation of NIHL are limited on prediction of gradually developing NIHL (GDHL) caused by high-level occupational noise. In this study, we proposed two auditory fatigue based models, including equal velocity level (EVL) and complex velocity level (CVL), which combine the high-cycle fatigue theory with the mammalian auditory model, to predict GDHL. The mammalian auditory model is introduced by combining the transfer function of the external-middle ear and the triple-path nonlinear (TRNL) filter to obtain velocities of basilar membrane (BM) in cochlea. The high-cycle fatigue theory is based on the assumption that GDHL can be considered as a process of long-cycle mechanical fatigue failure of organ of Corti. Furthermore, a series of chinchilla experimental data are used to validate the effectiveness of the proposed fatigue models. The regression analysis results show that both proposed fatigue models have high corrections with four hearing loss indices. It indicates that the proposed models can accurately predict hearing loss in chinchilla. Results suggest that the CVL model is more accurate compared to the EVL model on prediction of the auditory risk of exposure to hazardous occupational noise.

Cochlea devices are powered up with the help of batteries and they should possess long working life to avoid replacing of devices at regular interval of years. Hence the devices with low power consumptions are required. In cochlea devices there are numerous filters, each responsible for frequency variant signals, which helps in identifying speech signals of different audible range. In this paper, multiplierless lookup table (LUT) based auditory filter is implemented. Power aware adder architectures are utilized to add the output samples of the LUT, available at every clock cycle. The design is developed and modeled using Verilog HDL, simulated using Mentor Graphics Model-Sim Simulator, and synthesized using Synopsys Design Compiler tool. The design was mapped to TSMC 65 nm technological node. The standard ASIC design methodology has been adapted to carry out the power analysis. The proposed FIR filter architecture has reduced the leakage power by 15% and increased its performance by 2.76%.

The gene causative for the human nonsyndromic recessive form of deafness DFNB22 encodes otoancorin, a 120-kDa inner ear-specific protein that is expressed on the surface of the spiral limbus in the cochlea. Gene targeting in ES cells was used to create an EGFP knock-in, otoancorin KO (Otoa(EGFP/EGFP)) mouse. In the Otoa(EGFP/EGFP) mouse, the tectorial membrane (TM), a ribbon-like strip of ECM that is normally anchored by one edge to the spiral limbus and lies over the organ of Corti, retains its general form, and remains in close proximity to the organ of Corti, but is detached from the limbal surface. Measurements of cochlear microphonic potentials, distortion product otoacoustic emissions, and basilar membrane motion indicate that the TM remains functionally attached to the electromotile, sensorimotor outer hair cells of the organ of Corti, and that the amplification and frequency tuning of the basilar membrane responses to sounds are almost normal. The compound action potential masker tuning curves, a measure of the tuning of the sensory inner hair cells, are also sharply tuned, but the thresholds of the compound action potentials, a measure of inner hair cell sensitivity, are significantly elevated. These results indicate that the hearing loss in patients with Otoa mutations is caused by a defect in inner hair cell stimulation, and reveal the limbal attachment of the TM plays a critical role in this process.

Background: Exposure to intense noise causes the excessive movement of the organ of Corti, stretching the organ and compromising sensory cell functions. We recently revealed changes in the transcriptional expression of multiple adhesion-related genes during the acute phases of cochlear damage, suggesting that the disruption of cell-cell junctions is an early event in the process of cochlear pathogenesis. However, the functional state of cell junctions in the sensory epithelium is not clear. Here, we employed graded dextran-FITC, a macromolecule tracer that is impermeable to the organ of Corti under physiological conditions, to evaluate the barrier function of cell junctions in normal and noise-traumatized cochlear sensory epithelia., Results: Exposure to an impulse noise of 155 dB (peak sound pressure level) caused a site-specific disruption in the intercellular junctions within the sensory epithelium of the chinchilla cochlea. The most vulnerable sites were the junctions among the Hensen cells and between the Hensen and Deiters cells within the outer zone of the sensory epithelium. The junction clefts that formed in the reticular lamina were permeable to 40 and 500 but not 2,000 kDa dextran-FITC macromolecules. Moreover, this study showed that the interruption of junction integrity occurred in the reticular lamina and also in the basilar membrane, a site that had been considered to be resistant to acoustic injury. Finally, our study revealed a general spatial correlation between the site of sensory cell damage and the site of junction disruption. However, the two events lacked a strict one-to-one correlation, suggesting that the disruption of cell-cell junctions is a contributing, but not the sole, factor for initiating acute sensory cell death., Conclusions: Impulse noise causes the functional disruption of intercellular junctions in the sensory epithelium of the chinchilla cochlea. This disruption occurs at an early phase of cochlear damage. Understanding the role of this disruption in cochlear pathogenesis will require future study.

In this study, a three-dimensional finite-element model of the passive human cochlea was created. Dynamic behavior of the basilar membrane caused by the vibration of the stapes footplate was analyzed considering a fluid-structure interaction with the cochlear fluid. Next, the effects of a perilymphatic fistula (PLF) on the vibration of the cochlea were examined by making a small hole on the wall of the cochlea model. Even if a PLF existed in the scala vestibuli, a traveling wave was generated on the basilar membrane. When a PLF existed at the basal end of the cochlea, the shape of the traveling wave envelope showed no remarkable change, but the maximum amplitude became smaller at the entire frequency range from 0.5 to 5kHz and decreased with decreasing frequency. In contrast, when a PLF existed at the second turn of the cochlea, the traveling wave envelope showed a notch at the position of the PLF and the maximum amplitude also became smaller. This model assists in elucidating the mechanisms of hearing loss due to a PLF from the view of dynamics., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Background: To identify a parameter to distinguish normal hearing from hearing impairment in the early stages. The parameter was obtained from transient-evoked otoacoustic emissions (TEOAEs), overcoming the limitations of the usually adopted waveform descriptive parameters which may fail in standard clinical screenings., Material/methods: Audiometric examinations and TEOAE analysis were conducted on 15 normal ears and on 14 hearing-impaired ears that exhibited an audiometric notch around 4 kHz. TEOAE signals were analyzed through a multivariate technique to filter out the individual variability and to highlight the dynamic structure of the signals. The new parameter (named radius 2-dimension--RAD2D) was defined and evaluated for simulated TEOAE signals modeling a different amount of hearing impairment., Results: Audiometric examinations indicated 14 ears as impaired-hearing (IH), while the TEOAE ILO92 whole reproducibility parameter (WWR) indicated as IH 7 signals out of 14 (50%). The proposed new parameter indicated as IH 9 signals out of 14 (64%), reducing the number of false negative cases of WWR., Conclusions: In this preliminary study there is evidence that the new parameter RAD2D defines the topology and the quantification of the damage in the inner ear. The proposed protocol can be useful in hearing screenings to identify hearing impairments much earlier than conventional pure tone audiometry and TEOAE pass/fail test.

Many cochlear models assign zero longitudinal coupling in the cochlea. Although this is consistent with the transverse basilar membrane (BM) fibers, the cochlear partition contains cellular longitudinal coupling. In cochlear models, longitudinal coupling diminishes passive BM tuning; however, it has recently been employed in theories of active mechanics to enhance tuning. Our goal in this study was to probe passive longitudinal coupling by comparing BM responses in damaged cochleae with passive responses in normal cochleae. The cochleae of gerbils were damaged with intratympanic neomycin followed by a waiting period to ensure that all of the cells of the partition were missing or severely disrupted. We then measured BM motion and examined the cochleae histologically. In comparison with passive responses in normal cochleae, we observed a downward shift in characteristic frequency, an expected consequence of reduced stiffness from cellular damage. However, we did not observe enhanced passive tuning in the damaged cochleae, as would be expected if longitudinal coupling were substantially greater in the normal cochleae. Thus, we conclude that cell-based longitudinal coupling is not large enough to influence passive cochlear mechanics. This finding constrains theories of active mechanics., (Copyright © 2011 Biophysical Society. Published by Elsevier Inc. All rights reserved.)

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.

An SCD is a pathologic hole (or dehiscence) in the bone separating the superior semicircular canal from the cranial cavity that has been associated with a conductive hearing loss in patients with SCD syndrome. The conductive loss is defined by an audiometrically determined air-bone gap that results from the combination of a decrease in sensitivity to air-conducted sound and an increase in sensitivity to bone-conducted sound. Our goal is to demonstrate, through physiological measurements in an animal model, that mechanically altering the superior semicircular canal (SC) by introducing a hole (dehiscence) is sufficient to cause such an air-bone gap. We surgically introduced holes into the SC of chinchilla ears and evaluated auditory sensitivity (cochlear potential) in response to both air- and bone-conducted stimuli. The introduction of the SC hole led to a low-frequency (<2000 Hz) decrease in sensitivity to air-conducted stimuli and a low-frequency (<1000 Hz) increase in sensitivity to bone-conducted stimuli resulting in an air-bone gap. This result was consistent and reversible. The air-bone gaps in the animal results are qualitatively consistent with findings in patients with SCD syndrome.

Recent publications show that DPOAE measurements can generate a more accurate diagnosis, if (1) their fine structure is suppressed, and (2) if the calibration of the sound field is improved. Reduction of the fine structure is particularly important in the frequency range below 4 kHz in subjects with intact cochlear amplifier and can reduce the standard deviation of threshold estimations based on DPOAE-input/output functions from 11 dB to 6 dB. Improving the sound-field calibration has most impact in the frequency range above 4 kHz. Threshold estimations based on laserinterferometrically measured DPOAE input-output functions where the sound field was calibrated close to the tympanic membrane have been shown to reduce the standard deviation down to 8.6 dB in humans and 6.5 dB in guinea pigs. Compared with conventional DPOAE measures, such as amplitude or signal-to-noise ratio, threshold estimation based on DPOAE-I/O functions has the advantage that its slope provides additional information about the middle-ear; however, its specificity is limited. In the future, combined methods such as acoustic reflectance or laser vibrometry on the umbo promise a reliable assessment of the middle-ear contribution to DPOAE.

Objective: A dead region (DR) is defined as a region in the cochlea where inner hair cells and/or neurons are functioning so poorly that a tone producing peak vibration in this region is detected by off-frequency listening, i.e., via a place on the basilar membrane with a characteristic frequency different from that of the tone. The presence of a DR can have a significant effect on the perception of speech. People with and without DRs may differ in the benefit obtained from amplification and require different hearing aid settings. The Threshold Equalizing Noise (TEN) test and psychophysical tuning curves (PTCs) are two procedures used to identify a DR in adults. Because diagnosing a DR involves measuring masked thresholds, and there are reports in the literature that young children perform poorly compared with adults in background noise, it may be possible that the criteria used with adults may not be appropriate when testing children. Therefore, the aim of this study was to evaluate the consistency of the fast-PTC and TEN tests in diagnosing a DR in hearing-impaired children. In addition, the masked thresholds for normal-hearing children were measured with different TEN levels to assess whether any age-related effect in children compared with adults may occur., Design: Participants were divided into two groups: eight normal-hearing children (16 ears) and 12 hearing-impaired children (21 ears), aged 7 to 13 yr. TEN is based on measuring masked threshold in TEN. For normal-hearing participants, the masked thresholds were measured for five levels of noise (30, 40, 50, 60, and 70 dB per averaged equivalent rectangular bandwidth). For hearing-impaired participants, the level of the TEN was selected separately for each ear based on the highest acceptable level minus 5 dB. The TEN test results in hearing-impaired children were further validated by measuring fast-PTCs. The fast-PTC technique involves measuring the level of the narrowband noise masker needed to mask the signal. The center frequency of the masker sweeps across the required frequency range., Results: The masked thresholds in TEN measured for normal-hearing children were usually below and never higher than 5 dB above TEN level per averaged equivalent rectangular bandwidth. This suggests that no age-related effect on masked threshold in children compared with adults was observed. All hearing-impaired children were able to perform the TEN test and fast-PTCs. The results of the two tests were consistent in 17 of 21 ears (81%): eight ears did not show evidence of a DR and nine ears did. In three ears, the criteria for a DR were met on the TEN test, but there was no evidence of a DR on the fast-PTC test. In one ear, the TEN test did not show evidence of DRs at two frequencies, whereas fast-PTCs did., Conclusions: The results of this study suggest that DRs can be detected in children using the fast-PTC technique and the TEN test interpreted with the adult criteria, which are the most appropriate in terms of specificity and sensitivity. However, in cases in which the masked threshold is 10 to 15 dB above the TEN level, it is recommended to confirm DR diagnosis with fast-PTC measurement.

Objective: To evaluate the clinical conditions causing an elevation in the click-evoked summation potential (SP)/action potential (AP) amplitude ratio (SP/AP ratio), the cause of the SP enhancement in Ménière's disease (MD) and the diagnostic efficacy of electrocochleography (ECoG) were discussed., Study Design: Retrospective case review., Setting: An outpatient clinic of the Otolaryngology Department of Kochi Medical School., Patients: ECoG testing was performed in 632 patients (727 ears) with vertigo/dizziness and/or deafness over a 10-year period (1995-2005). Among them, 334 patients had diagnoses of definite MD, including 95 cases of bilateral involvement., Main Outcome Measures: Audiological thresholds and SP/AP ratio., Results: An enhanced SP was observed in 56.3% of patients with MD. The incidence of an enhanced SP was low in patients for whom the disease duration was 2 years or less and the frequency of attacks was once a year or less, but was significantly higher in cases where the disease duration was 2 years or longer and/or the frequency of attacks was several times a year (Games-Howell test, p < 0.05). The incidence of an enhanced SP was significantly elevated in cases with pure-tone average exceeding 31 dB (Kendall's rank correlation test, p < 0.001). However, the enhanced SP, once it appeared, did not always disappear in spite of hearing improvement. Hearing improvement induced by the glycerol test also produced no alteration in an SP/AP ratio, and there was no significant difference between the glycerol test results and the incidence of an enhanced SP (chi2 goodness-of-fit test)., Conclusions: The longer the patients were symptomatic or the severer the ear symptoms, the more likely the ECoG was to be positive. The abnormally elevated SP, once it had appeared, persisted for long periods. Spontaneous and glycerol-induced hearing gains did not result in a decrease in SP/AP ratio. These clinical characteristics of ECoG seem to indicate that the enhanced SP in MD might be caused by the malfunction of hair cells, not by the displacement of the basilar membrane toward the scala tympani., (Copyright 2010 S. Karger AG, Basel.)

Tone complexes with positive (m+) and negative (m-) Schroeder phase show large differences in masking efficiency. This study investigated whether the different phase characteristics also affect loudness. Loudness matches between m+ and m- complexes were measured as a function of (1) the fundamental frequency (f0) for different frequency bands in normal-hearing and hearing-impaired subjects, and (2) intensity level in normal-hearing subjects. In normal-hearing subjects, the level of the m+ stimulus was up to 10 dB higher than that of the corresponding m- stimulus at the point of equal loudness. The largest differences in loudness were found for levels between 20 and 60 dB SL. In hearing-impaired listeners, the difference was reduced, indicating the relevance of active cochlear mechanisms. Loudness matches of m+ and m- stimuli to a common noise reference (experiment 3) showed differences as a function of f0 that were in line with direct comparisons from experiment 1 and indicated additionally that the effect is mainly due to the specific internal processing of m+. The findings are roughly consistent with studies pertaining to masking efficiency and can probably not be explained by current loudness models, supporting the need for incorporating more realistic cochlea simulations in future loudness models.

Intense airborne ultrasound has been associated with hearing loss, tinnitus, and various nonauditory subjective effects, such as headaches, dizziness, and fullness in the ear. Yet, when people detect ultrasonic components in music, ultrasound adds to the pleasantness of the perception and evokes changes in the brain as measured in electroencephalograms, behavior, and imaging. How does the airborne ultrasound get into the ear to create such polar-opposite human effects? Surprisingly, ultrasound passes first through the eyes; thus, the eye becomes but another window into the inner ear.

Since 1958, stapedotomy has been the method of choice for middle ear surgeons who operate on patients suffering from otosclerosis, especially stiffening of the interface between the stapes footplate of the middle ear and the oval window, which is a part of the cochlea of the inner ear. Later, many surgeons started to use the Schuknecht prosthesis, which consists of cartilage and is inserted into the complete opened oval window during stapedectomy. Our study shows that basilar membrane (BM) displacement is increased with an increasing stapes footplate area by a numerical simulation including the different geometries. An increase in the footplate area leads to an increase in BM displacement equivalent to 13 dB. Therefore, we recommend prostheses with areas as big as the normal stapes footplate area.

Previous experimental studies of insertion of the Nucleus standard straight and the Contour arrays into the scala tympani have reported that the electrode arrays cause damage to various cochlear structures. However, the level of insertion-induced damage by these electrode arrays to cochlear structures (the spiral ligament, the basilar membrane and the osseous spiral lamina) has not been quantified. Although it has been suggested that rotation can overcome this resistance and prevent the basilar membrane from being pierced by the tip of the Nucleus standard straight array, there has not been any attempt to study the relationship between the rotation and the reduction of damage to the basilar membrane. In this study, 3D finite element analyses of insertions of the Nucleus standard straight array and the Contour array into the scala tympani have been undertaken. The perforation of the basilar membrane by the tip of the Nucleus standard straight array at the region of 11-14 mm from the round window appears to be compounded by the geometry of the spiral passage of the scala tympani. Anti-clockwise rotations between 25 degrees and 90 degrees applied at the basal end of the electrode array (for the right cochlea) were shown to significantly reduce the contact stresses exerted by the tip on the basilar membrane which support the practice of applying small rotation partway through insertion of electrode array to minimize damage to the basilar membrane. Although the Contour array (with its stylet intact) is stiffer than the Nucleus standard straight array, a slight withdrawal of the stylet from the Contour array before insertion was found to significantly reduce damage by the electrode array to the spiral ligament and the basilar membrane.

The decay of forward masking was investigated for three subjects with moderate sensorineural hearing loss. For such subjects, compression on the basilar membrane (BM) is thought to be largely absent, enabling one to determine the decay of masking without the influence of compression. Temporal masking curves (TMCs), plots of the masker level at threshold against delay between masker offset and signal onset, were measured for delays of 0, 15, 30, 45, 60, and 75 ms, for signal frequencies, fs, of 500, 1000, 2000, 4000, and 6000 Hz. Masker frequencies were 0.5, 0.8, 1.0, 1.15, and 1.3 times fs. Most of the TMCs were well fitted with single-segment straight lines, which, except for high masker levels, were roughly parallel for each fs, supporting the belief that BM compression was largely absent in these subjects. However, the slopes of the TMCs were greater for fs = 500 and 1000 Hz than for higher frequencies, which may indicate that the decay of forward masking is not the same for all signal frequencies. The results suggest that it may not be valid to infer BM compression at low signal frequencies by using a reference TMC for a high fs.

Objective: The fact that vibration of the skull causes a hearing sensation has been known since the 19th century. This mode of hearing was termed hearing by bone conduction. Although there has been more than a century of research on hearing by bone conduction, its physiology is not completely understood. Lately, new insights into the physiology of hearing by bone conduction have been reported. Knowledge of the physiology, clinical aspects, and limitations of bone conduction sound is important for clinicians dealing with hearing loss and is the purpose of this review., Data Sources: The data were compiled from the published literature in the areas of clinical bone conduction hearing, bone conduction hearing aids, basic research on bone conduction physiology, and recent research on bone conduction hearing from our laboratory., Conclusion: Five factors contributing to bone conduction hearing have been identified: 1) sound radiated into the external ear canal, 2) middle ear ossicle inertia, 3) inertia of the cochlear fluids, 4) compression of the cochlear walls, and 5) pressure transmission from the cerebrospinal fluid. Of these five, inertia of the cochlear fluid seems most important. Bone conduction sound is believed to reflect the true cochlear function; however, certain conditions such as middle ear diseases can affect bone conduction sensitivity, but less than for air conduction. The bone conduction route can also be used for hearing aids; since the bone conduction route is less efficient than the air conduction route, bone conduction hearing aids are primarily used for hearing losses where air conduction hearing aids are contraindicated.

Psychophysical estimates of basilar membrane (BM) responses suggest that normal-hearing (NH) listeners exhibit constant compression for tones at the characteristic frequency (CF) across the CF range from 250 to 8000 Hz. The frequency region over which compression occurs is broadest for low CFs. This study investigates the extent that these results differ for three hearing-impaired (HI) listeners with sensorineural hearing loss. Temporal masking curves (TMCs) were measured over a wide range of probe (500-8000 Hz) and masker frequencies (0.5-1.2 times the probe frequency). From these, estimated BM response functions were derived and compared with corresponding functions for NH listeners. Compressive responses for tones both at and below CF occur for the three HI ears across the CF range tested. The maximum amount of compression was uncorrelated with absolute threshold. It was close to normal for two of the three HI ears, but was either slightly (at CFs < or =1000 Hz) or considerably (at CFs > or =4000 Hz) reduced for the third ear. Results are interpreted in terms of the relative damage to inner and outer hair cells affecting each of the HI ears. Alternative interpretations for the results are also discussed, some of which cast doubts on the assumptions of the TMC-based method and other behavioral methods for estimating human BM compression.

Background: The low frequency modulation of distortion product otoacoustic emissions (DPOAEs) is an objective audiometric method that appears to be a useful tool for the diagnosis of endolymphatic hydrops (EH), e.g. in patients with Menière's disease, or in those who present only some of the symptoms of the disease., Method: Low-frequency modulated DPOAEs were registered in 20 patients with unilateral Menière's disease (13 women and 7 men, aged 40-66 years) and were compared to a control group matched in age and gender. As a diagnostic parameter, the 'modulation index' MI=1/2 MS/DM was used (MS or modulation span, being the difference between the maximal and the minimal DPOAE-amplitude, and DM, being the mean of the suppressed stationary DPOAE-amplitude)., Results: In the patients with unilateral Menière's disease, MI was lower than in the control group. This difference was highly significant. In 56% of the patients' contralateral ears MI was lower than the cut off-value and significantly lower than in the control group, but did not differ significantly from the patients' ipsilateral ears., Conclusion: The registration of low-frequency modulated DPOAEs is comparable to the generally applied transtympanic electrocochleography in its diagnostic validity. The method is fast and non-invasive and could be applied to monitor the course of the disease.

A number of perceptual phenomena related to normal and impaired level coding can be accounted for by the degree of compression in the basilar-membrane (BM) magnitude response. However, the narrow dynamic ranges of auditory-nerve (AN) fibers complicate these arguments. Because the AN serves as an information bottleneck, an improved understanding of the neural coding of level may clarify some of the limitations of current hearing aids. Here three hypotheses for the neural correlate of loudness recruitment were evaluated based on AN responses from normal-hearing cats and from cats with a noise-induced hearing loss (NIHL). Auditory-nerve fiber rate-level functions for tones were analyzed to test the following hypotheses: Loudness recruitment results from steeper AN rate functions after impairment. This hypothesis was not supported; AN rate functions were not steeper than normal following NIHL, despite steeper estimated BM responses based on the AN data. Loudness is based on the total AN discharge count, and recruitment results from an abnormally rapid spread of excitation after impairment. Whereas abnormal spread of excitation can be observed, steeper growth of total AN rate is not seen over the range of sound levels where recruitment is observed in human listeners. Loudness of a narrowband stimulus is based on AN responses in a narrow BF region, and recruitment results from compression of the AN-fiber threshold distribution after impairment. This hypothesis was not supported because there was no evidence that impaired AN threshold distributions were compressed and the growth of AN activity summed across BFs near the stimulus frequency was shallower than normal.Overall, these results suggest that loudness recruitment cannot be accounted for based on summed AN rate responses and may depend on neural mechanisms involved in the central representation of intensity.

This study investigates the acoustic reflex threshold (ART) dependency on stimulus phase utilizing low-level reflex audiometry [Neumann et al., Audiol. Neuro-Otol. 1, 359-369 (1996)]. The goal is to obtain optimal broadband stimuli for elicitation of the acoustic reflex and to obtain objective determinations of cochlear hearing loss. Three types of tone complexes with different phase characteristics were investigated: A stimulus that compensates for basilar-membrane dispersion, thus causing a large overall neural synchrony (basilar-membrane tone complex-BMTC), the temporally inversed stimulus (iBMTC), and random-phase tone complexes (rTC). The ARTs were measured in eight normal-hearing and six hearing-impaired subjects. Five different conditions of peak amplitude and stimulus repetition rate were used for each stimulus type. The results of the present study suggest that the ART is influenced by at least two different factors: (a) the degree of synchrony of neural activity across frequency, and (b) the fast-acting compression mechanism in the cochlea that is reduced in the case of a sensorineural hearing loss. The results allow a clear distinction of the two subjects groups based on the different ART for the utilized types and conditions of the stimuli. These differences might be useful for objective recruitment detection in clinical diagnostics.

A loss of cochlear compression may underlie many of the difficulties experienced by hearing-impaired listeners. Two behavioral forward-masking paradigms that have been used to estimate the magnitude of cochlear compression are growth of masking (GOM) and temporal masking (TM). The aim of this study was to determine whether these two measures produce within-subjects results that are consistent across a range of signal frequencies and, if so, to compare them in terms of reliability or efficiency. GOM and TM functions were measured in a group of five normal-hearing and five hearing-impaired listeners at signal frequencies of 1000, 2000, and 4000 Hz. Compression values were derived from the masking data and confidence intervals were constructed around these estimates. Both measures produced comparable estimates of compression, but both measures have distinct advantages and disadvantages, so that the more appropriate measure depends on factors such as the frequency region of interest and the degree of hearing loss. Because of the long testing times needed, neither measure is suitable for clinical use in its current form.

The presence of cochlear-based compression at low frequencies was investigated by measuring phase effects in harmonic maskers. In normal-hearing listeners, the amount of masking produced depends strongly on the phase relationships between the individual masker components. This effect is thought to be determined primarily by properties of the cochlea, including the phase dispersion and compressive input-output function of the basilar membrane. Thresholds for signals of 250 and 1000 Hz were measured in harmonic maskers with fundamental frequencies of 12.5 and 100 Hz as a function of the masker phase curvature. Results from 12 listeners with sensorineural hearing loss showed reduced masker phase effects, when compared with data from normal-hearing listeners, at both 250- and 1000-Hz signal frequencies. The effects of hearing impairment on phase-related masking differences were not well simulated in normal-hearing listeners by an additive white noise, suggesting that the effects of hearing impairment are not simply due to reduced sensation level. Maximum differences in masked threshold were correlated with auditory filter bandwidths at the respective frequencies, suggesting that both measures are affected by a common underlying mechanism, presumably related to cochlear outer hair cell function. The results also suggest that normal peripheral compression remains strong even at 250 Hz.

During and after microinjection of artificial endolymph into scala media of the guinea pig, the 2f1- f2 -DPOAE at 4.5 kHz generated by low-level primaries was recorded. Reproducible changes were measured when 1.1 microl of artificial endolymph was injected at a rate of 1.65 nl/s (1.53-1.83). This volume corresponds with an acute endolymphatic hydrops of 23%. After the onset of injection the inner ear pressure immediately increased to a mean higher level of 22 Pa, whereas the 2f1- f2 -amplitude and -phase did not change for about 1 min. Thereafter, the amplitude decreased 2.6 dB (+/- 0.7) on average and slowly regained almost its initial value, with recovery frequently starting within the period of injection. In an attempt to explain the observed changes in 2f1- f2 -amplitude the basilar membrane displacement towards scala tympani at the 2f1- f2 generation site is estimated to be 19 nm for a 1.1 microl increase of endolymph volume. A small deflection of the outer hair cell stereocilia and as a consequence a change in cell conductance may explain the 2f1- f2 -amplitude changes. However, the precise mechanism of cochlear function change caused by endolymph volume increase (hydrops) remains to be elucidated.

The physiological vulnerability of distortion product otoacoustic emissions (DPOAEs) was investigated in the leopard frog, Rana pipiens pipiens. For each frog, DPOAEs were recorded from the amphibian and the basilar papillae. Measurements were taken before and after either the arrest of oxygen supply due to cardioectomy, or the destruction of the central nervous system (CNS). DPOAEs in response to high-level stimuli (> 75 dB SPL) were rather robust to these insults during the first two hours post surgery. In contrast, DPOAE amplitudes in response to low-level stimuli (< 75 dB SPL) decreased significantly. On average, low-level emissions from the amphibian papilla disappeared within 6 min for cardioectomy, and after 13 min for CNS destruction. In the basilar papilla, low-level DPOAEs disappeared more slowly: on average after 34 min following cardioectomy, and after 58 min for CNS destruction. The difference in physiological vulnerability between low- and high-level emissions is similar to that in mammals and a lizard. The difference between the DPOAE decay rate of the frog's amphibian and basilar papillae suggests important differences between the hearing mechanisms of the papillae.

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.

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)].

Recently, Boege and Janssen [J. Acoust. Soc. Am. 111, 1810-1818 (2002)] fit linear equations to distortion product otoacoustic emission (DPOAE) input/output (UO) functions after the DPOAE level (in dB SPL) was converted into pressure (in microPa). Significant correlations were observed between these DPOAE thresholds and audiometric thresholds. The present study extends their work by (1) evaluating the effect of frequency, (2) determining the behavioral thresholds in those conditions that did not meet inclusion criteria, and (3) including a wider range of stimulus levels. DPOAE I/O functions were measured in as many as 278 ears of subjects with normal and impaired hearing. Nine f2 frequencies (500 to 8000 Hz in 1/2-octave steps) were used, L2 ranged from 10 to 85 dB SPL (5-dB steps), and L1 was set according to the equation L1 = 0.4L2 + 39 dB [Kummer et al., J. Acoust. Soc. Am. 103, 3431-3444 (1998)] for L2 levels up to 65 dB SPL, beyond which L1 = L2. For the same conditions as those used by Boege and Janssen, we observed a frequency effect such that correlations were higher for mid-frequency threshold comparisons. In addition, a larger proportion of conditions not meeting inclusion criteria at mid and high frequencies had hearing losses exceeding 30 dB HL, compared to lower frequencies. These results suggest that DPOAE I/O functions can be used to predict audiometric thresholds with greater accuracy at mid and high frequencies, but only when certain inclusion criteria are met. When the SNR inclusion criterion is not met, the expected amount of hearing loss increases. Increasing the range of input levels from 20-65 dB SPL to 10-85 dB SPL increased the number of functions meeting inclusion criteria and increased the overall correlation between DPOAE and behavioral thresholds.

Background: Low-frequency modulated DPOAEs were registrated to investigate whether the subjective symptom of aural fullness can indicate an endolymphatic hydrops., Method: The cochlear partition is periodically moved towards scala vestibuli and scala tympani by a low-frequency suppressor tone. The level of simultaneously registrated DPOAEs is modulated depending on the phase of the suppressor. This modulation may be reduced when the displacement of the organ of Corti is inhibited by mechanical stiffening of the basilar membrane (e. g. in endolymphatic hydrops)., Subjects: Low-frequency modulated DPOAEs were registrated in 15 patients with Menière's disease, in 8 patients with aural fullness and tinnitus, but without vertigo, and in 21 normal hearing adults., Results: In both patient groups the modulation depth is high significantly lower than in the control group. The results do not differ significantly in the patients with and without vertigo., Conclusion: The reduction of the modulation depth can be interpreted as a sign of an endolymphatic hydrops. In the group of patients with aural fullness a cochlear hydrops can be assumed. The measurement of low-frequency modulated DPOAEs is a new tool to diagnose and monitor the course of endolymphatic hydrops and to evaluate the effectiveness of therapeutic methods.

The "temporal processing hypothesis" suggests that individuals with specific language impairments (SLIs) and dyslexia have severe deficits in processing rapidly presented or brief sensory information, both within the auditory and visual domains. This hypothesis has been supported through evidence that language-impaired individuals have excess auditory backward masking. This paper presents an analysis of masking results from several studies in terms of a model of temporal resolution. Results from this modeling suggest that the masking results can be better explained by an "auditory efficiency" hypothesis. If impaired or immature listeners have a normal temporal window, but require a higher signal-to-noise level (poor processing efficiency), this hypothesis predicts the observed small deficits in the simultaneous masking task, and the much larger deficits in backward and forward masking tasks amongst those listeners. The difference in performance on these masking tasks is predictable from the compressive nonlinearity of the basilar membrane. The model also correctly predicts that backward masking (i) is more prone to training effects, (ii) has greater inter- and intrasubject variability, and (iii) increases less with masker level than do other masking tasks. These findings provide a new perspective on the mechanisms underlying communication disorders and auditory masking.

To investigate the physiology of noise-induced hearing loss, the sound-induced vibrations of the basilar membrane (BM) of the inner ear were measured in living anesthetized guinea pigs before and after intense sound exposure. The vibrations were measured using a laser Doppler velocimeter after placing reflective glass beads on the BM. Pseudo-random noise waveforms containing frequencies between 4 and 24 kHz were used to generate velocity tuning curves. Before overstimulation, sharp response peaks were seen at stimulus frequencies between 15 and 17 kHz, consistent with the expected best frequency of the recording location. The response to low level stimuli lagged the high level ones by up to 90 degrees at the characteristic frequency. Following exposure to loud sound, the BM vibrations showed a pronounced reduction in amplitude, primarily at low stimulus levels, and the best frequency moved to approximately 12 kHz. At higher levels, the reduction was either absent or much smaller. In addition to the amplitude changes, increased phase lags were seen at frequencies near the characteristic frequency. In animals with more severe exposures, response phases were altered also at frequencies showing no change of the amplitude. The phase was independent of stimulus level after severe exposures.

DPOAE sources are modeled by intermodulation distortion generated near the f2 place and a reflection of this distortion near the DP place. In a previous paper, inverse fast Fourier transforms (IFFTs) of DPOAE filter functions in normal ears were consistent with this model [Konrad-Martin et al., J. Acoust. Soc. Am. 109, 2862-2879 (2001)]. In the present article, similar measurements were made in ears with specific hearing-loss configurations. It was hypothesized that hearing loss at f2 or DP frequencies would influence the relative contributions to the DPOAE from the corresponding basilar membrane places, and would affect the relative magnitudes of SFOAEs at frequencies equal to f2 and fDP. DPOAEs were measured with f2 = 4 kHz, f1 varied, and a suppressor near fDP. L2 was 25-55 dB SPL (L1 = L2 + 10 dB). SFOAEs were measured at f2 and at 2.7 kHz (the average fDP produced by the f1 sweep) for stimulus levels of 20-60 dB SPL. SFOAE results supported predictions of the pattern of amplitude differences between SFOAEs at 4 and 2.7 kHz for sloping losses, but did not support predictions for the rising- and flat-loss categories. Unsuppressed IFFTs for rising losses typically had one peak. IFFTs for flat or sloping losses typically have two or more peaks; later peaks were more prominent in ears with sloping losses compared to normal ears. Specific predictions were unambiguously supported by the results for only four of ten cases, and were generally supported in two additional cases. Therefore, the relative contributions of the two DPOAE sources often were abnormal in impaired ears, but not always in the predicted manner.

Sensorineural hearing loss has frequently been shown to result in a loss of frequency selectivity. Less is known about its effects on the level dependence of selectivity that is so prominent a feature of normal hearing. The aim of the present study is to characterize such changes in nonlinearity as manifested in the auditory filter shapes of listeners with mild/moderate hearing impairment. Notched-noise masked thresholds at 2 kHz were measured over a range of stimulus levels in hearing-impaired listeners with losses of 20-50 dB. Growth-of-masking functions for different notch widths are more parallel for hearing-impaired than for normal-hearing listeners, indicating a more linear filter. Level-dependent filter shapes estimated from the data show relatively little change in shape across level. The loss of nonlinearity is also evident in the input/output functions derived from the fitted filter shapes. Reductions in nonlinearity are clearly evident even in a listener with only 20-dB hearing loss.

DPOAE input/output (I/O) functions were measured at 7f2 frequencies (1 to 8 kHz; f2/f1 = 1.22) over a range of levels (-5 to 95 dB SPL) in normal-hearing and hearing-impaired human ears. L1-L2 was level dependent in order to produce the largest 2f1-f2 responses in normal ears. System distortion was determined by collecting DP data in six different acoustic cavities. These data were used to derive a multiple linear regression model to predict system distortion levels. The model was tested on cochlear-implant users and used to estimate system distortion in all other ears. At most but not all f2's, measurements in cochlear implant ears were consistent with model predictions. At all f2 frequencies, the ears with normal auditory thresholds produced I/O functions characterized by compressive nonlinear regions at moderate levels, with more rapid growth at low and high stimulus levels. As auditory threshold increased, DPOAE threshold increased, accompanied by DPOAE amplitude reductions, notably over the range of levels where normal ears showed compression. The slope of the I/O function was steeper in impaired ears. The data from normal-hearing ears resembled direct measurements of basilar membrane displacement in lower animals. Data from ears with hearing loss showed that the compressive region was affected by cochlear damage; however, responses at high levels of stimulation resembled those observed in normal ears.

Cell death has been documented in bird auditory inner ear epithelia after induced damage. This cell death is quickly followed by an increase in supporting cell division and regeneration of the epithelium, thereby suggesting a possible relationship between these two processes. However, aspects of this relationship still need to be better understood. The Belgian Waterslager (BWS) canary is an ideal system in which to study cell death and subsequent cell division. In contrast to mixed breed (MB) canaries, cell division normally occurs in the auditory end organ of the BWS without any external manipulation. In addition, some of the cells in the auditory epithelium may be dying through an apoptotic-like process. In the present study two methods were used to quantify dying cells in the BWS and MB canary auditory epithelia: morphological criteria and TUNEL. Results confirm that some of the abnormal hair cells in the BWS auditory epithelium are apoptotic-like. The presence of both cell death and cell division indicates that these processes act concurrently in the adult end organ. Future studies are needed to determine if cell death is a stimulus for the observed cell division.

Differential gene expression forms the basis for development, differentiation, regeneration, and plasticity of tissues and organs. We describe two methods to identify differentially expressed genes. Differential display, a PCR-based approach, compares the expression of subsets of genes under two or more conditions. Gene arrays, or DNA microarrays, contain cDNAs from both known genes and novel genes spotted on a solid support (nylon membranes or glass slides). Hybridization of the arrays with RNA isolated from two different experimental conditions allows the simultaneous analysis of large numbers of genes, from hundreds to thousands to whole genomes. Using differential display to examine differential gene expression after noise trauma in the chick basilar papilla, we identified the UBE3B gene that encodes a new member of the E3 ubiquitin ligase family (UBE3B). UBE3B is highly expressed immediately after noise in the lesion, but not in the undamaged ends, of the chick basilar papilla. UBE3B is most similar to a ubiquitin ligase gene from Caenorhabditis elegans, suggesting that this gene has been conserved throughout evolution. We also describe preliminary experiments to profile gene expression in the cochlea and brain with commercially available low density gene arrays on nylon membranes and discuss potential applications of this and DNA microarray technology to the auditory system.

The subjective recording of the masked threshold of short acoustical stimuli with a loud tone of 30 Hz (phase audiogram) has been used for the clinical diagnosis of endolymphatic hydrops (EH). In normally-hearing subjects, a marked modulation of the threshold was found, depending on the phase of the low-frequency tone. A very small dependence was found in patients with Menière's disease, due to the micromechanical changes in the basilar membrane (BM). The same phase relationship becomes apparent in low-frequency suppression of otoacoustic emissions. The amplitudes of TEOAEs are controlled by the phase-dependent displacement of the BM. The suppressed TEOAEs have to be measured separately in each phase relationship. During recording of suppressed DPOAEs, the low-frequency suppressor is permanently superimposed on the pair of primary tones. After time averaging and a moving short-time FFT, the spectral values of the DPOAEs are obtained depending on the phase of the low-frequency tone. Modulation depends also on the masker level, the levels of the primary tones, and on their frequency range. The method of low-frequency suppressed DPOAEs is an objective method to diagnose EH and could be a useful tool in human inner ear research.

An immunohistochemical study was performed on surgically obtained human fresh cochlear tissue, using synaptophysin antibodies. After immediate aldehyde fixation and decalcification in Na-EDTA serial cryosections were made of the cochlea including the round window membrane (RWM). Apart from highly specific immunostaining of spiral ganglion cells and unmyelinated nerve fibers an immunoreactive neuroreceptor could be demonstrated at the postero-medial insertion of the RWM. The perikaryon showed intense synaptophysin immunoreativity with a distal process projecting into the fibrous stroma of the RWM displaying structural specializations suggestive of a mechanoreceptor function. It is speculated whether the neuroreceptor may be involved in the proprioception and/or mechanoreception of tensile forces generated within the lamina propria during displacement of the yielding RWM in the bony labyrinth. Such a function could be important for the regulation of perilymph pressure.