Lateralization of virtual sound sources with a binaural cochlear-implant sound coding strategy inspired by the medial olivocochlear reflex.

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.

Mechanical Effects of Cochlear Implant on Acoustic Hearing.

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.

Investigating time-efficiency of forward masking paradigms for estimating basilar membrane input-output characteristics.

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.

Comparing auditory filter bandwidths, spectral ripple modulation detection, spectral ripple discrimination, and speech recognition: Normal and impaired hearing.

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.

Further tests of the local nonlinear interaction-based mechanism for simultaneous suppression of tone burst-evoked otoacoustic emissions.

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.

A mouse model for human deafness DFNB22 reveals that hearing impairment is due to a loss of inner hair cell stimulation.

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.

Post-processing analysis of transient-evoked otoacoustic emissions to detect 4 kHz-notch hearing impairment--a pilot study.

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.

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

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

The clinical value of extratympanic electrocochleography in the diagnosis of Ménière's disease.

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.

A superior semicircular canal dehiscence-induced air-bone gap in chinchilla.

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.

Eyes as fenestrations to the ears: a novel mechanism for high-frequency and ultrasonic hearing.

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.

Temporal masking curves for hearing-impaired listeners.

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.

[Diagnosis of endolymphatic hydrops using low frequency modulated distortion product otoacoustic emissions]. / Diagnostik des endolymphatischen Hydrops mit tieftonmodulierten DPOAE.

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.

Masker phase effects in normal-hearing and hearing-impaired listeners: evidence for peripheral compression at low signal frequencies.

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.

Alterations of basilar membrane response phase and velocity after acoustic overstimulation.

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.

Sources of DPOAEs revealed by suppression experiments, inverse fast Fourier transforms, and SFOAEs in impaired ears.

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.

Auditory filter nonlinearity in mild/moderate hearing impairment.

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.

Phase-dependent suppression of transient evoked and distortion product otoacoustic emissions by a low-frequency tone.

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.

Incomplete recovery of chicken distortion product otoacoustic emissions following acoustic overstimulation.

Distortion product otoacoustic emissions (DPOAEs) were measured in chickens before and after exposure to a 525-Hz pure tone (120 dB SPL, 48 h). The exposure caused extensive hair cell loss and destroyed the tectorial membrane along the abneural edge of the basilar papilla in the low-to-mid-frequency region of the cochlea. Although the lesion was restricted, DPOAEs were greatly depressed at all frequencies immediately after the exposure. The high-frequency DPOAEs gradually recovered to preexposure values after the exposure; however, there was little or no improvement in DPOAEs at test frequencies equal to or slightly above the exposure frequency even after 16 weeks of recovery. By 28 days of recovery, the previously damaged region of the basilar papilla had been repopulated by hair cells and the lower honeycomb layer of the tectorial membrane had regenerated, but not the upper fibrous layer. The upper fibrous layer of the tectorial membrane was still missing after 16 weeks of recovery and the region of damage corresponded closely to the frequency regions where the DPOAEs were depressed.

[Diagnosis of endolymphatic hydrops with low tone masked otoacoustic emissions]. / Diagnostik des endolymphatischen Hydrops mit tieftonmaskierten otoakustischen Emissionen.

BACKGROUND: A new method of diagnosis of endolymphatic hydrops by recording low-tone masked evoked otoacoustic emissions (TEOAE) is presented. METHODS: A short acoustic stimulus and a masker tone of 30 Hz are applied in an adjustable phase relation simultaneously to the same ear. In the normal hearing ear the masker shows little influence on the TEOAE at 0 degrees, whereas the suppression at phase 270 degrees (maximal rarefaction at the eardrum) is nearly complete. However, in cases of endolymphatic hydrops this masking effect is reduced or absent, indicating impaired mobility of the basilar membrane. RESULTS: The masked TEOAE were recorded of patients with normal hearing, Menière's disease, and sudden hearing loss without vertigo. In Menière cases with supposed endolymphatic hydrops, the amplitude modulation of the emissions was found to be much less than in the other groups. CONCLUSIONS: Where TEOAE can be recorded, low-tone masking is a quick, objective, and noninvasive method for the diagnosis of endolymphatic hydrops.