Deciphering compromised speech-in-noise intelligibility in older listeners: the role of cochlear synaptopathy.

Speech intelligibility declines with age and sensorineural hearing damage (SNHL). However, it remains unclear whether cochlear synaptopathy (CS), a recently discovered form of SNHL, significantly contributes to this issue. CS refers to damaged auditory-nerve synapses that innervate the inner hair cells and there is currently no go-to diagnostic test available.

Toward an Individual Binaural Loudness Model for Hearing Aid Fitting and Development.

The individual loudness perception of a patient plays an important role in hearing aid satisfaction and use in daily life. Hearing aid fitting and development might benefit from individualized loudness models (ILMs), enabling better adaptation of the processing to individual needs. The central question is whether additional parameters are required for ILMs beyond non-linear cochlear gain loss and linear attenuation common to existing loudness models for the hearing impaired (HI).

Enhancing the sensitivity of the envelope-following response for cochlear synaptopathy screening in humans: The role of stimulus envelope.

Auditory de-afferentation, a permanent reduction in the number of inner-hair-cells and auditory-nerve synapses due to cochlear damage or synaptopathy, can reliably be quantified using temporal bone histology and immunostaining. However, there is an urgent need for non-invasive markers of synaptopathy to study its perceptual consequences in live humans and to develop effective therapeutic interventions. While animal studies have identified candidate auditory-evoked-potential (AEP) markers for synaptopathy, their interpretation in humans has suffered from translational issues related to neural generator differences, unknown hearing-damage histopathologies or lack of measurement sensitivity.

Neural Representation of Loudness: Cortical Evoked Potentials in an Induced Loudness Reduction Experiment.

Loudness context effects comprise differences in judgments of the loudness of a target stimulus depending on the presence of a preceding inducer tone. Interstimulus intervals (ISIs) between inducer tone and target tone of about 200 ms and above cause an induced loudness reduction (ILR) of the target tone. As the ILR increases, respectively, the perceived loudness of the target stimuli decreases with increasing ISI.

Physiologically motivated individual loudness model for normal hearing and hearing impaired listeners.

A loudness model with a central gain is suggested to improve individualized predictions of loudness scaling data from normal hearing and hearing impaired listeners. The current approach is based on the loudness model of Pieper [(2016). J.

Individual Differences in Auditory Brainstem Response Wave Characteristics: Relations to Different Aspects of Peripheral Hearing Loss.

Little is known about how outer hair cell loss interacts with noise-induced and age-related auditory nerve degradation (i.e., cochlear synaptopathy) to affect auditory brainstem response (ABR) wave characteristics.

Physiological motivated transmission-lines as front end for loudness models.

The perception of loudness is strongly influenced by peripheral auditory processing, which calls for a physiologically correct peripheral auditory processing stage when constructing advanced loudness models. Most loudness models, however, rather follow a functional approach: a parallel auditory filter bank combined with a compression stage, followed by spectral and temporal integration. Such classical loudness models do not allow to directly link physiological measurements like otoacoustic emissions to properties of their auditory filterbank.

On the Interplay Between Cochlear Gain Loss and Temporal Envelope Coding Deficits.

Hearing impairment is characterized by two potentially coexisting sensorineural components: (i) cochlear gain loss that yields wider auditory filters, elevated hearing thresholds and compression loss, and (ii) cochlear neuropathy, a noise-induced component of hearing loss that may impact temporal coding fidelity of supra-threshold sound. This study uses a psychoacoustic amplitude modulation (AM) detection task in quiet and multiple noise backgrounds to test whether these aspects of hearing loss can be isolated in listeners with normal to mildly impaired hearing ability. Psychoacoustic results were compared to distortion-product otoacoustic emission (DPOAE) thresholds and envelope-following response (EFR) measures.

Suprathreshold auditory processing deficits in noise: Effects of hearing loss and age.

People with sensorineural hearing loss generally suffer from a reduced ability to understand speech in complex acoustic listening situations, particularly when background noise is present. In addition to the loss of audibility, a mixture of suprathreshold processing deficits is possibly involved, like altered basilar membrane compression and related changes, as well as a reduced ability of temporal coding. A series of 6 monaural psychoacoustic experiments at 0.

Modeling cochlear dynamics: interrelation between cochlea mechanics and psychoacoustics.

A model of the cochlea was used to bridge the gap between model approaches commonly used to investigate phenomena related to otoacoustic emissions and more filter-based model approaches often used in psychoacoustics. In the present study, a nonlinear and active one-dimensional transmission line model was developed that accounts for several aspects of physiological data with a single fixed parameter set. The model shows plausible excitation patterns and an input-output function similar to the linear-compressive-linear function as hypothesized in psychoacoustics.

Investigating possible mechanisms behind the effect of threshold fine structure on amplitude modulation perception.

Detection thresholds for sinusoidal amplitude modulation at low levels are higher (worse) when the carrier of the signal falls in a region of high pure-tone sensitivity (a minimum of the fine structure of the threshold in quiet) than when it falls at a fine-structure maximum. This study explores possible mechanisms behind this phenomenon by measuring modulation detection thresholds as a function of modulation frequency (experiment 1) and of carrier level for tonal carriers (experiment 2) and for 32-Hz wide noise carriers (experiment 3). The carriers could either fall at a fine-structure minimum, a fine-structure maximum, or in a region without fine structure.

Threshold fine structure affects amplitude modulation perception.

Modulation detection thresholds of a sinusoidally amplitude-modulated tone were measured for two different positions of the low-level carrier relative to the fine structure of the threshold in quiet. Modulation detection thresholds were higher for a carrier at a fine-structure minimum than for a carrier at a fine-structure maximum, regardless of whether the carriers had the same sound pressure level or the same sensation level. This indicates that even for small variations of the carrier frequency, the sensitivity to amplitude modulation can vary substantially due to the frequency characteristics of the threshold in quiet.

Automatic screening and detection of threshold fine structure.

Audiograms measured with a high frequency resolution often show quasi-periodic ripples of up to 15 dB in normal-hearing listeners. This fine structure of the threshold in quiet is commonly associated with the active processes in the cochlea. Therefore its absence is discussed in the literature as an indicator of cochlear vulnerability.

Differences in loudness of positive and negative Schroeder-phase tone complexes as a function of the fundamental frequency.

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.

The effects of neural synchronization and peripheral compression on the acoustic-reflex threshold.

This study investigates the acoustic reflex threshold (ART) dependency on stimulus phase utilizing low-level reflex audiometry [Neumann et al., Audiol. Neuro-Otol.

Distortion product otoacoustic emission (DPOAE) input/output functions and the influence of the second DPOAE source.

Distortion product otoacoustic emissions (DPOAEs) at 2f1-f2 (f2/f1 = 1.2) have two components from different cochlear sources, i.e.

Fine structure of hearing threshold and loudness perception.

Hearing thresholds measured with high-frequency resolution show a quasiperiodic change in level called threshold fine structure (or microstructure). The effect of this fine structure on loudness perception over a range of stimulus levels was investigated in 12 subjects. Three different approaches were used.