Clinician, student and faculty perspectives on the audiology-industry interface: implications for ethics education.

Objective: Supporting audiologists to work ethically with industry requires theory-building research. This study sought to answer: How do audiologists view their relationship with industry in terms of ethical implications? What do audiologists do when faced with ethical tensions? How do social and systemic structures influence these views and actions? Design: A constructivist grounded theory study was conducted using semi-structured interviews of clinicians, students and faculty. Study sample: A purposive sample of 19 Canadian and American audiologists was recruited with representation across clinical, academic, educational and industry work settings. Theoretical sampling of grey literature occurred alongside audiologist sampling. Interpretations were informed by the concepts of ethical tensions as ethical uncertainty, dilemmas and distress. Results: Findings identified the audiology-industry relationship as symbiotic but not wholly positive. A range of responses included denying ethical tensions to avoiding any industry interactions altogether. Several of our participants who had experienced ethical distress quit their jobs to resolve the distress. Systemic influences included the economy, professional autonomy and the hidden curriculum. Conclusions: In direct response to our findings, the authors suggest a move to include virtues-based practice, an explicit curriculum for learning ethical industry relations, theoretically-aligned ethics education approaches and systemic and structural change.

Cochlear Synaptopathy and Noise-Induced Hidden Hearing Loss.

Recent studies on animal models have shown that noise exposure that does not lead to permanent threshold shift (PTS) can cause considerable damage around the synapses between inner hair cells (IHCs) and type-I afferent auditory nerve fibers (ANFs). Disruption of these synapses not only disables the innervated ANFs but also results in the slow degeneration of spiral ganglion neurons if the synapses are not reestablished. Such a loss of ANFs should result in signal coding deficits, which are exacerbated by the bias of the damage toward synapses connecting low-spontaneous-rate (SR) ANFs, which are known to be vital for signal coding in noisy background. As there is no PTS, these functional deficits cannot be detected using routine audiological evaluations and may be unknown to subjects who have them. Such functional deficits in hearing without changes in sensitivity are generally called "noise-induced hidden hearing loss (NIHHL)." Here, we provide a brief review to address several critical issues related to NIHHL: (1) the mechanism of noise induced synaptic damage, (2) reversibility of the synaptic damage, (3) the functional deficits as the nature of NIHHL in animal studies, (4) evidence of NIHHL in human subjects, and (5) peripheral and central contribution of NIHHL.

Animal-to-Human Translation Difficulties and Problems With Proposed Coding-in-Noise Deficits in Noise-Induced Synaptopathy and Hidden Hearing Loss.

Noise induced synaptopathy (NIS) and hidden hearing loss (NIHHL) have been hot topic in hearing research since a massive synaptic loss was identified in CBA mice after a brief noise exposure that did not cause permanent threshold shift (PTS) in 2009. Based upon the amount of synaptic loss and the bias of it to synapses with a group of auditory nerve fibers (ANFs) with low spontaneous rate (LSR), coding-in-noise deficit (CIND) has been speculated as the major difficult of hearing in subjects with NIS and NIHHL. This speculation is based upon the idea that the coding of sound at high level against background noise relies mainly on the LSR ANFs. However, the translation from animal data to humans for NIS remains to be justified due to the difference in noise exposure between laboratory animals and human subjects in real life, the lack of morphological data and reliable functional methods to quantify or estimate the loss of the afferent synapses by noise. Moreover, there is no clear, robust data revealing the CIND even in animals with the synaptic loss but no PTS. In humans, both positive and negative reports are available. The difficulty in verifying CINDs has led a re-examination of the hypothesis that CIND is the major deficit associated with NIS and NIHHL, and the theoretical basis of this idea on the role of LSR ANFs. This review summarized the current status of research in NIS and NIHHL, with focus on the translational difficulty from animal data to human clinicals, the technical difficulties in quantifying NIS in humans, and the problems with the SR theory on signal coding. Temporal fluctuation profile model was discussed as a potential alternative for signal coding at high sound level against background noise, in association with the mechanisms of efferent control on the cochlea gain.

Synaptopathy in Guinea Pigs Induced by Noise Mimicking Human Experience and Associated Changes in Auditory Signal Processing.

Noise induced synaptopathy (NIS) has been researched extensively since a large amount of synaptic loss without permanent threshold shift (PTS) was found in CBA mice after a brief noise exposure. However, efforts to translate these results to humans have met with little success-and might not be possible since noise exposure used in laboratory animals is generally different from what is experienced by human subjects in real life. An additional problem is a lack of morphological data and reliable functional methods to quantify loss of afferent synapses in humans. Based on evidence for disproportionate synaptic loss for auditory nerve fibers (ANFs) with low spontaneous rates (LSR), coding-in-noise deficits (CIND) have been speculated to be the major difficulty associated with NIS without PTS. However, no robust evidence for this is available in humans or animals. This has led to a re-examination of the role of LSR ANFs in signal coding in high-level noise. The fluctuation profile model has been proposed to support a role for high-SR ANFs in the coding of high-level noise in combination with efferent control of cochlear gain. This study aimed to induce NIS by a low-level, intermittent noise exposure mimicking what is experienced in human life and examined the impact of the NIS on temporal processing under masking. It also evaluated the role of temporal fluctuation in evoking efferent feedback and the effects of NIS on this feedback.

Sensitivity of the human binaural cortical steady state response to interaural level differences.

OBJECTIVES: Periodic alternations of the interaural correlation of a noise stimulus evoke an auditory steady state response that can be measured at the scalp, providing an objective measure of binaural integration. The purpose of this study was to examine the effect of interaural level differences on this steady state response. DESIGN: Auditory steady state responses at 4 and 8 Hz were recorded to 4 Hz cycles of interaural correlation change of a Gaussian noise in normal-hearing listeners. Responses were recorded with symmetric presentation levels of 80, 60, and 40 dB SPL and with interaural asymmetries ranging from 10 to 40 dB, varying in 10-dB steps. RESULTS: The 8 Hz response was sensitive to interaural level asymmetry and fell to 50% strength at an asymmetry of 18 dB, although the response was detectable to an asymmetry of 30 dB. A simultaneously present 4 Hz response showed no sensitivity to interaural level difference. Significant responses were recorded in all participants. CONCLUSIONS: The 8 Hz auditory steady state response to a 4 Hz change in noise interaural correlation might be useful as an objective measure of binaural integration in asymmetric hearing loss. Response amplitude is more negatively affected by small amounts of interaural asymmetry than by large reductions in overall presentation level.

Temporary Versus Permanent Synaptic Loss from Repeated Noise Exposure in Guinea Pigs and C57 Mice.

A single brief noise exposure can cause a significant loss of cochlear afferent synapses without causing permanent threshold shift. Previously we reported that the initial synaptic loss is partially reversible in Guinea pigs, indicating that synaptic loss can be categorized as either temporary or permanent. Since synaptic loss is biased to innervating auditory nerve fibers (ANFs) with low spontaneous spike rates (SSR), which are critical to the coding of in-background noise, coding-in-noise deficits (CIND) have been predicted to result from noise-induced synaptic damage. However, recent study of the noise masking of amplitude-modulation (AM) evoked compound action potentials (CAP) tailed to find evidence for such deficits in either mice or Guinea pigs. The present study sought to determine the effects of repeated noise exposure on temporary and permanent synaptic loss in Guinea pigs and C57 mice, whether such effects were additive, and whether repeated noise exposure induced CIND in Guinea pigs. The results show that the second noise exposure caused much less temporary synaptic loss and no additional permanent loss in Guinea pigs; however, an additional permanent loss was seen after the second noise was in the mice, although it was not significant. In Guinea pigs, the observed increased masking of the AM CAP provides evidence for CIND after repeated noise exposure.

Coding-in-Noise Deficits are Not Seen in Responses to Amplitude Modulation in Subjects with cochlear Synaptopathy Induced by a Single Noise Exposure.

Since the first report of noise-induced synaptic damage in animals without permanent threshold shifts (PTSs), the concept of noise-induced hidden hearing loss (NIHHL) has been proposed to cover the functional deficits in hearing associated with noise-induced synaptopathy. Moreover, the potential functional deficit associated with the noise-induced synaptopathy has been largely attributed to the loss of auditory nerve fibers (ANFs) with a low spontaneous spike rate (SSR). As this group of ANFs is critical for coding at suprathreshold levels and in noisy background, coding-in-noise deficit (CIND) has been considered to be main consequence of the synaptopathy. However, such deficits have not been verified after a single, brief exposure to noise without PTS. In the present study, synaptopathy was generated by such noise exposure in both mice and guinea pigs. Responses to amplitude modulation (AM) were recorded at a high sound level in combination with masking to evaluate the existence of CINDs that might be associated with loss of low-SSR ANFs. An overall reduction in response amplitude was seen in AM-evoked compound action potential (CAP). However, no such reduction was seen in the scalp-recorded envelope following response (EFR), suggesting a compensation due to increased central gain. Moreover, there was no significant difference in masking effect between the control and noise groups. The results suggest that either there is no significant CIND after the synaptopathy we created, or the AM response tested with our protocol was not sufficiently sensitive to detect such a deficit; far-field EFR is not sensitive to cochlear pathology.

Preliminary Investigation of the Passively Evoked N400 as a Tool for Estimating Speech-in-Noise Thresholds.

PURPOSE: Speech-in-noise testing relies on a number of factors beyond the auditory system, such as cognitive function, compliance, and motor function. It may be possible to avoid these limitations by using electroencephalography. The present study explored this possibility using the N400. METHOD: Eleven adults with typical hearing heard high-constraint sentences with congruent and incongruent terminal words in the presence of speech-shaped noise. Participants ignored all auditory stimulation and watched a video. The signal-to-noise ratio (SNR) was varied around each participant's behavioral threshold during electroencephalography recording. Speech was also heard in quiet. RESULTS: The amplitude of the N400 effect exhibited a nonlinear relationship with SNR. In the presence of background noise, amplitude decreased from high (+4 dB) to low (+1 dB) SNR but increased dramatically at threshold before decreasing again at subthreshold SNR (-2 dB). CONCLUSIONS: The SNR of speech in noise modulates the amplitude of the N400 effect to semantic anomalies in a nonlinear fashion. These results are the first to demonstrate modulation of the passively evoked N400 by SNR in speech-shaped noise and represent a first step toward the end goal of developing an N400-based physiological metric for speech-in-noise testing.

Coding deficits in hidden hearing loss induced by noise: the nature and impacts.

Hidden hearing refers to the functional deficits in hearing without deterioration in hearing sensitivity. This concept is proposed based upon recent finding of massive noise-induced damage on ribbon synapse between inner hair cells (IHCs) and spiral ganglion neurons (SGNs) in the cochlea without significant permanent threshold shifts (PTS). Presumably, such damage may cause coding deficits in auditory nerve fibers (ANFs). However, such deficits had not been detailed except that a selective loss of ANFs with low spontaneous rate (SR) was reported. In the present study, we investigated the dynamic changes of ribbon synapses and the coding function of ANF single units in one month after a brief noise exposure that caused a massive damage of ribbon synapses but no PTS. The synapse count and functional response measures indicates a large portion of the disrupted synapses were re-connected. This is consistent with the fact that the change of SR distribution due to the initial loss of low SR units is recovered quickly. However, ANF coding deficits were developed later with the re-establishment of the synapses. The deficits were found in both intensity and temporal processing, revealing the nature of synaptopathy in hidden hearing loss.

A Comparison Between Wireless CROS and Bone-anchored Hearing Devices for Single-sided Deafness: A Pilot Study.

INTRODUCTION: This study compared wireless Contralateral Routing of Signals (CROS) hearing aid and bone-anchored hearing device (BAHD) in patients with single-sided deafness. METHODS: Eight adults with single-sided deafness previously implanted with a BAHD were given a 2-week trial with a CROS hearing aid and tested in unaided and aided conditions. Both devices were compared on head shadow effect reduction, speech perception measures in quiet and in noise, self-assessment questionnaires, and daily diaries. RESULTS: Both the CROS and BAHD significantly reduced the head shadow effect. QuickSIN scores were significantly better with noise presented to the poorer ear, as compared to the better ear, for the unaided condition, the BAHD, and the CROS. Scores showed no significant differences between the CROS and BAHD with noise presented to the better ear, but scores with the CROS were significantly poorer than in the unaided condition with noise presented to the poorer ear. There were no significant differences between BAHD and CROS for the ratings on the Bern Benefit in Single-Sided Deafness and Speech Spatial Qualities questionnaires. Both devices were worn an average of 10 hours per day. Four participants preferred the CROS for sound quality; three preferred the BAHD for comfort. CONCLUSION: Comparisons of CROS and BAHD need to be re-evaluated as both technologies have evolved. In our pilot study, both devices seem comparable, with the CROS avoiding the risks of surgery, and we recommend a trial of CROS in our center for first line treatment of single-sided deafness.

Can otoplasty impact hearing? A prospective randomized controlled study examining the effects of pinna position on speech reception and intelligibility.

OBJECTIVES: Otoplasty is a commonly performed surgical procedure that restores the ideal position of the pinna. Although the pinna is a well-recognized component of the auditory apparatus, no studies have assessed the audiological effects of this procedure. We sought to quantify the impact of pinna repositioning on speech intelligibility and reception. METHODS: Eighteen adults with normal hearing and pinnae were recruited and the pinna positions were randomized in each participant. Intracanal acoustical analysis was performed to calculate the Speech Intelligibility Index (SII). Hearing In Noise Test (HINT) with two azimuth speaker arrangement was also performed. The outcome measures were compared using paired t-tests for both pinna positions. RESULTS: The SII significantly improved with the pinna in forward position (49.3 vs. 45.8, p<0.001). HINT thresholds also improved with the pinna forward (-6.43 dB vs. -5.08 dB, p=0.0003). CONCLUSIONS: Pinna position affects audiological performance, in both speech intelligibility and speech reception in noise. These are novel findings that may impact the informed consent process and decision to treat for patients undergoing otoplasty.

Silent damage of noise on cochlear afferent innervation in guinea pigs and the impact on temporal processing.

Noise-exposure at levels low enough to avoid a permanent threshold shift has been found to cause a massive, delayed degeneration of spiral ganglion neurons (SGNs) in mouse cochleae. Damage to the afferent innervation was initiated by a loss of synaptic ribbons, which is largely irreversible in mice. A similar delayed loss of SGNs has been found in guinea pig cochleae, but at a reduced level, suggesting a cross-species difference in SGN sensitivity to noise. Ribbon synapse damage occurs "silently" in that it does not affect hearing thresholds as conventionally measured, and the functional consequence of this damage is not clear. In the present study, we further explored the effect of noise on cochlear afferent innervation in guinea pigs by focusing on the dynamic changes in ribbon counts over time, and resultant changes in temporal processing. It was found that (1) contrary to reports in mice, the initial loss of ribbons largely recovered within a month after the noise exposure, although a significant amount of residual damage existed; (2) while the response threshold fully recovered in a month, the temporal processing continued to be deteriorated during this period.