Age-Related Central Gain Compensation for Reduced Auditory Nerve Output in Non-Tinnitus Patients with Normal Hearing

2021 ◽  
Author(s):  
Peter T. Johannesen ◽  
Enrique Lopez-Poveda
Keyword(s):  
Auditory Nerve ◽  
Normal Hearing ◽  
Age Related ◽  
Gain Compensation

scholarly journals Age-related differences in binaural masking level differences: behavioral and electrophysiological evidence

2018 ◽  
Vol 120 (6) ◽  
pp. 2939-2952 ◽  
Author(s):  
Samira Anderson ◽  
Robert Ellis ◽  
Julie Mehta ◽  
Matthew J. Goupell
Keyword(s):  
Aging Effect ◽  
Normal Hearing ◽  
Behavioral Experiment ◽  
Spatial Cues ◽  
Sound Sources ◽  
Frequency Following Response ◽  
Binaural Processing ◽  
Threshold Difference ◽  
Age Related ◽  
Effects Of Aging

The effects of aging and stimulus configuration on binaural masking level differences (BMLDs) were measured behaviorally and electrophysiologically, using the frequency-following response (FFR) to target brainstem/midbrain encoding. The tests were performed in 15 younger normal-hearing (<30 yr) and 15 older normal-hearing (>60 yr) participants. The stimuli consisted of a 500-Hz target tone embedded in a narrowband (50-Hz bandwidth) or wideband (1,500-Hz bandwidth) noise masker. The interaural phase conditions included NoSo (tone and noise presented interaurally in-phase), NoSπ (noise presented interaurally in-phase and tone presented out-of-phase), and NπSo (noise presented interaurally out-of-phase and tone presented in-phase) configurations. In the behavioral experiment, aging reduced the magnitude of the BMLD. The magnitude of the BMLD was smaller for the NoSo–NπSo threshold difference compared with the NoSo–NoSπ threshold difference, and it was also smaller in narrowband compared with wideband conditions, consistent with previous measurements. In the electrophysiology experiment, older participants had reduced FFR magnitudes and smaller differences between configurations. There were significant changes in FFR magnitude between the NoSo to NoSπ configurations but not between the NoSo to NπSo configurations. The age-related reduction in FFR magnitudes suggests a temporal processing deficit, but no correlation was found between FFR magnitudes and behavioral BMLDs. Therefore, independent mechanisms may be contributing to the behavioral and neural deficits. Specifically, older participants had higher behavioral thresholds than younger participants for the NoSπ and NπSo configurations but had equivalent thresholds for the NoSo configuration. However, FFR magnitudes were reduced in older participants across all configurations. NEW & NOTEWORTHY Behavioral and electrophysiological testing reveal an aging effect for stimuli presented in wideband and narrowband noise conditions, such that behavioral binaural masking level differences and subcortical spectral magnitudes are reduced in older compared with younger participants. These deficits in binaural processing may limit the older participant's ability to use spatial cues to understand speech in environments containing competing sound sources.

scholarly journals Noise-induced and age-related hearing loss:  new perspectives and potential therapies

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 927 ◽  
Author(s):  
M Charles Liberman
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Sensorineural Hearing Loss ◽  
Hair Cells ◽  
Auditory Nerve ◽  
Cell Loss ◽  
Sensorineural Hearing ◽  
Hair Cell Loss ◽  
Age Related ◽  
Age Related Hearing Loss

The classic view of sensorineural hearing loss has been that the primary damage targets are hair cells and that auditory nerve loss is typically secondary to hair cell degeneration. Recent work has challenged that view. In noise-induced hearing loss, exposures causing only reversible threshold shifts (and no hair cell loss) nevertheless cause permanent loss of >50% of the synaptic connections between hair cells and the auditory nerve. Similarly, in age-related hearing loss, degeneration of cochlear synapses precedes both hair cell loss and threshold elevation. This primary neural degeneration has remained a “hidden hearing loss” for two reasons: 1) the neuronal cell bodies survive for years despite loss of synaptic connection with hair cells, and 2) the degeneration is selective for auditory nerve fibers with high thresholds. Although not required for threshold detection when quiet, these high-threshold fibers are critical for hearing in noisy environments. Research suggests that primary neural degeneration is an important contributor to the perceptual handicap in sensorineural hearing loss, and it may be key to the generation of tinnitus and other associated perceptual anomalies. In cases where the hair cells survive, neurotrophin therapies can elicit neurite outgrowth from surviving auditory neurons and re-establishment of their peripheral synapses; thus, treatments may be on the horizon.

Neural Presbyacusis in Humans Inferred from Age-Related Differences in Auditory Nerve Function and Structure

2021 ◽  
pp. JN-RM-1747-21
Author(s):  
Kelly C. Harris ◽  
Jayne B. Ahlstrom ◽  
James W. Dias ◽  
Lilyana B. Kerouac ◽  
Carolyn M. McClaskey ◽  
...  
Keyword(s):  
Auditory Nerve ◽  
Nerve Function ◽  
Age Related

Identifying Subclinical Hearing Loss: Extended Audiometry and Word Recognition in Noise

2021 ◽  
pp. 1-10
Author(s):  
Ward R. Drennan
Keyword(s):  
Word Recognition ◽  
Significant Relationship ◽  
High Frequency ◽  
Recognition Task ◽  
Normal Hearing ◽  
Normal Range ◽  
Closed Set ◽  
Age Related ◽  
High Frequency Audiometry ◽  
Hearing Problems

<b><i>Introduction:</i></b> Normal-hearing people often have complaints about the ability to recognize speech in noise. Such disabilities are not typically assessed with conventional audiometry. Suprathreshold temporal deficits might contribute to reduced word recognition in noise as well as reduced temporally based binaural release of masking for speech. Extended high-frequency audibility (&#x3e;8 kHz) has also been shown to contribute to speech perception in noise. The primary aim of this study was to compare conventional audiometric measures with measures that could reveal subclinical deficits. <b><i>Methods:</i></b> Conventional and extended high-frequency audiometry was done with 119 normal-hearing people ranging in age from 18 to 72. The ability to recognize words in noise was evaluated with and without differences in temporally based spatial cues. A low-uncertainty, closed-set word recognition task was used to limit cognitive influences. <b><i>Results:</i></b> In normal-hearing listeners, word recognition in noise ability decreases significantly with increasing pure-tone average (PTA). On average, signal-to-noise ratios worsened by 5.7 and 6.0 dB over the normal range, for the diotic and dichotic conditions, respectively. When controlling for age, a significant relationship remained in the diotic condition. Measurement error was estimated at 1.4 and 1.6 dB for the diotic and dichotic conditions, respectively. Controlling for both PTA and age, EHF-PTAs showed significant partial correlations with SNR50 in both conditions (<i>ρ</i> = 0.30 and 0.23). Temporally based binaural release of masking worsened with age by 1.94 dB from 18 to 72 years old but showed no significant relationship with either PTA. <b><i>Conclusions:</i></b> All three assessments in this study demonstrated hearing problems independently of those observed in conventional audiometry. Considerable degradations in word recognition in noise abilities were observed as PTAs increased within the normal range. The use of an efficient words-in-noise measure might help identify functional hearing problems for individuals that are traditionally normal hearing. Extended audiometry provided additional predictive power for word recognition in noise independent of both the PTA and age. Temporally based binaural release of masking for word recognition decreased with age independent of PTAs within the normal range, indicating multiple mechanisms of age-related decline with potential clinical impact.

scholarly journals SUBCLINICAL AGE-RELATED HEARING LOSS IS INVERSELY ASSOCIATED WITH DEPRESSIVE SYMPTOMS

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S552-S552
Author(s):  
Justin S Golub ◽  
Katharine K Brewster ◽  
Adam Brickman ◽  
Adam Ciarleglio ◽  
José Luchsinger ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Depressive Symptoms ◽  
Pure Tone ◽  
Depression Scale ◽  
Pure Tone Audiometry ◽  
Normal Hearing ◽  
Health Study ◽  
Late Life Depression ◽  
Age Related ◽  
Age Related Hearing Loss

Abstract Age-related hearing loss (HL), defined by a pure-tone average (PTA) &gt;25 decibels (dB) has been associated with depressive symptoms. We aimed to assess whether this association is present when hearing is better than the arbitrary, but widely-used, 25 dB threshold. The sampled population was the multicentered Hispanic Community Health Study (n=5,165). Cross-sectional data from 2008-2011 were available. Hearing was measured with pure tone audiometry. Clinically-significant depressive symptoms (CSDS) were defined by a score ≥10 on the 10-item Center for Epidemiologic Studies Depression Scale (CESD-10). Participants’ mean age was 58.3 years (SD=6.2, range=50-76). Among those with classically-defined normal hearing (PTA ≤25 dB), a 10 dB increase in HL was associated with 1.26 times the odds (95% CI=1.11, 1.42) of CSDS, adjusting for age, gender, education, vascular disease, and hearing aid use (p25 dB; p&lt;0.001). Results held even for a stricter HL cutpoint of 15 dB. Among subjects with strictly normal hearing (PTA ≤15 dB), a 10 dB increase in HL was associated with 1.47 (1.14, 1.90) times the odds of CSDS, adjusting for confounders (p&lt;0.01). Results also held when defining CSDS by an alternative CESD-10 score ≥16. In conclusion, increasing hearing thresholds were independently associated with CSDS among adults with subclinical HL (PTA ≤25 dB). Studies investigating whether treating HL can prevent late life depression should consider a lower threshold for defining HL.

scholarly journals Synaptic Transmission at the Cochlear Nucleus Endbulb Synapse During Age-Related Hearing Loss in Mice

2005 ◽  
Vol 94 (3) ◽  
pp. 1814-1824 ◽  
Author(s):  
Yong Wang ◽  
Paul B. Manis
Keyword(s):  
Hearing Loss ◽  
Synaptic Transmission ◽  
Cochlear Nucleus ◽  
Auditory Nerve ◽  
High Frequency ◽  
Nerve Activity ◽  
Synaptic Release ◽  
Endbulb Of Held ◽  
Age Related ◽  
Age Related Hearing Loss

Age-related hearing loss (AHL) typically starts from high-frequency regions of the cochlea and over time invades lower-frequency regions. During this progressive hearing loss, sound-evoked activity in spiral ganglion cells is reduced. DBA mice have an early onset of AHL. In this study, we examined synaptic transmission at the endbulb of Held synapse between auditory nerve fibers and bushy cells in the anterior ventral cochlear nucleus (AVCN). Synaptic transmission in hearing-impaired high-frequency areas of the AVCN was altered in old DBA mice. The spontaneous miniature excitatory postsynaptic current (mEPSC) frequency was substantially reduced (about 60%), and mEPSCs were significantly slower (about 115%) and smaller (about 70%) in high-frequency regions of old (average age 45 days) DBA mice compared with tonotopically matched regions of young (average age 22 days) DBA mice. Moreover, synaptic release probability was about 30% higher in high-frequency regions of young DBA than that in old DBA mice. Auditory nerve–evoked EPSCs showed less rectification in old DBA mice, suggesting recruitment of GluR2 subunits into the AMPA receptor complex. No similar age-related changes in synaptic release or EPSCs were found in age-matched, normal hearing young and old CBA mice. Taken together, our results suggest that auditory nerve activity plays a critical role in maintaining normal synaptic function at the endbulb of Held synapse after the onset of hearing. Auditory nerve activity regulates both presynaptic (release probability) and postsynaptic (receptor composition and kinetics) function at the endbulb synapse after the onset of hearing.

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

2020 ◽  
Author(s):  
Viacheslav Vasilkov ◽  
Markus Garrett ◽  
Manfred Mauermann ◽  
Sarah Verhulst
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Sensorineural Hearing Loss ◽  
Auditory Nerve ◽  
Outer Hair Cell ◽  
Cell Damage ◽  
Modulation Depth ◽  
Auditory Evoked Potential ◽  
Sensorineural Hearing ◽  
Age Related

AbstractAuditory de-afferentation, a permanent reduction in the number of innerhair-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. To render AEP-based markers of synaptopathy more sensitive and differential to the synaptopathy aspect of sensorineural hearing loss, we followed a combined computational and experimental approach. Starting from the known characteristics of auditory-nerve physiology, we optimized the stimulus envelope to stimulate the available auditory-nerve population optimally and synchronously to generate strong envelope-following-responses (EFRs). We further used model simulations to explore which stimuli evoked a response that was sensitive to synaptopathy, while being maximally insensitive to possible co-existing outer-hair-cell pathologies. We compared the model-predicted trends to AEPs recorded in younger and older listeners (N=44, 24f) who had normal or impaired audiograms with suspected age-related synaptopathy in the older cohort. We conclude that optimal stimulation paradigms for EFR-based quantification of synaptopathy should have sharply rising envelope shapes, a minimal plateau duration of 1.7-2.1 ms for a 120-Hz modulation rate, and inter-peak intervals which contain near-zero amplitudes. From our recordings, the optimal EFR-evoking stimulus had a rectangular envelope shape with a 25% duty cycle and a 95% modulation depth. Older listeners with normal or impaired audiometric thresholds showed significantly reduced EFRs, which were consistent with how (age-induced) synaptopathy affected these responses in the model.Significance StatementCochlear synaptopathy was in 2009 identified as a new form of sensorineural hearing loss (SNHL) that also affects primates and humans. However, clinical practice does not routinely screen for synaptopathy, and hence its consequences for degraded sound and speech perception remain unclear. Cochlear synaptopathy may thus remain undiagnosed and untreated in the aging population who often report self-reported hearing difficulties. To enable an EEG-based differential diagnosis of synaptopathy in humans, it is crucial to develop a recording method that evokes a robust response and emphasizes inter-individual differences. These differences should reflect the synaptopathy aspect of SNHL, while being insensitive to other aspects of SNHL (e.g. outer-hair-cell damage). This study uniquely combines computational modeling with experiments in normal and hearing-impaired listeners to design an EFR stimulation and recording paradigm that can be used for the diagnosis of synaptopathy in humans.

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