Acoustic reflexes: should we be paying more attention?

OBJECTIVE: The clinical audiology test battery often involves playing physically simple sounds with questionable ecological value to the listener. In this technical report, we revisit how valid this approach is using an automated, involuntary auditory response; the acoustic reflex threshold (ART). DESIGN: The ART was estimated four times in each individual in a quasi-random ordering of task conditions. The baseline condition (referred to as Neutral) measured the ART following a standard clinical practice. Three experimental conditions were then used in which a secondary task was performed whilst the reflex was measured: auditory attention, auditory distraction and visual distraction tasks. STUDY SAMPLE: Thirty-eight participants (27 males) with a mean age of 23 years were tested. All participants were audiometrically healthy. RESULTS: The ART was elevated when a visual task was performed at the same time as the measurements were taken. Performing an auditory task did not affect the ART. CONCLUSIONS: These data indicate that simple audiometric measures widely used in the clinic, can be affected by central, non-auditory processes even in healthy, normal-hearing volunteers. The role of cognition and attention on auditory responses will become ever more important in the coming years.

The Role of the Clinically Obtained Acoustic Reflex as a Research Tool for Subclinical Hearing Pathologies.

The acoustic reflex (AR) shows promise as an objective test for the presence of cochlear synaptopathy in rodents. The AR has also been shown to be reduced in humans with tinnitus compared to those without. The aim of the present study was twofold: (a) to determine if AR strength (quantified as both threshold and growth) varied with lifetime noise exposure, and thus provided an estimate of the degree of synaptopathy and (b) to identify which factors should be considered when using the AR as a quantitative measure rather than just present/absent responses. AR thresholds and growth functions were measured using ipsilateral and contralateral, broadband and tonal elicitors in adults with normal hearing and varying levels of lifetime noise exposure. Only the clinical standard 226 Hz probe tone was used. AR threshold and growth were not related to lifetime noise exposure, suggesting that routine clinical AR measures are not a sensitive measure when investigating the effects of noise exposure in audiometrically normal listeners. Our secondary, exploratory analyses revealed that AR threshold and growth were significantly related to middle-ear compliance. Listeners with higher middle-ear compliance (though still in the clinically normal range) showed lower AR thresholds and steeper AR growth functions. Furthermore, there was a difference in middle-ear compliance between the sexes, with males showing higher middle-ear compliance values than females. Therefore, it may be necessary to factor middle-ear compliance values into any analysis that uses the AR as an estimate of auditory function.

Relationship Between Diet, Tinnitus, and Hearing Difficulties.

OBJECTIVES: Diet may affect susceptibility of the inner ear to noise and age-related effects that lead to tinnitus and hearing loss. This study used complementary single nutrient and dietary pattern analysis based on statistical grouping of usual dietary intake in a cross-sectional analysis of tinnitus and hearing difficulties in a large population study sample. DESIGN: The research was conducted using the UK Biobank resource. Tinnitus was based on report of ringing or buzzing in one or both ears that lasts more than five minutes at a time and is currently experienced at least some of the time. Identification of a hearing problem was based on self-reported difficulties with hearing. Usual dietary intake and dietary patterns (involving statistical grouping of intake to account for how foods are combined in real-life diets) were estimated based on between two and five administrations of the Oxford Web-Q 24-hour dietary recall questionnaire over the course of a year for 34,576 UK adult participants aged 40 to 69. RESULTS: In a multivariate model, higher intake of vitamin B12 was associated with reduced odds of tinnitus, while higher intakes of calcium, iron, and fat were associated with increased odds (B12, odds ratio [OR] 0.85, 95% confidence interval [CI] 0.75 to 0.97; Calcium, OR 1.20, 95% CI 1.08 to 1.34; Iron, OR 1.20, 95% CI 1.05 to 1.37; Fat, OR 1.33, 95% CI 1.09 to 1.62, respectively, for quintile 5 versus quintile 1). A dietary pattern characterised by high protein intake was associated with reduced odds of tinnitus (OR 0.90, 95% CI 0.82 to 0.99 for quintile 5 versus quintile 1). Higher vitamin D intake was associated with reduced odds of hearing difficulties (OR 0.90, 95% CI 0.81 to 1.00 for quintile 5 versus quintile 1), as were dietary patterns high in fruit and vegetables and meat and low in fat (Prudent diet: OR 0.89, 95% CI 0.83 to 0.96; High protein: OR 0.88, 95% CI 0.82 to 0.95; High fat: OR 1.16, 95% CI 1.08 to 1.24, respectively, for quintile 5 versus quintile 1). CONCLUSIONS: There were associations between both single nutrients and dietary patterns with tinnitus and hearing difficulties. Although the size of the associations was small, universal exposure for dietary factors indicates that there may be a substantial impact of diet on levels of tinnitus and hearing difficulties in the population. This study showed that dietary factors might be important for hearing health.

No Effect of Interstimulus Interval on Acoustic Reflex Thresholds.

The acoustic reflex (AR), a longstanding component of the audiological test battery, has received renewed attention in the context of noise-induced cochlear synaptopathy-the destruction of synapses between inner hair cells and auditory nerve fibers. Noninvasive proxy measures of synaptopathy are widely sought, and AR thresholds (ARTs) correlate closely with synaptic survival in rodents. However, measurement in humans at high stimulus frequencies-likely important when testing for noise-induced pathology-can be challenging; reflexes at 4 kHz are frequently absent or occur only at high stimulus levels, even in young people with clinically normal audiograms. This phenomenon may partly reflect differences across stimulus frequency in the temporal characteristics of the response; later onset of the response, earlier onset of adaptation, and higher rate of adaptation have been observed at 4 kHz than at 1 kHz. One temporal aspect of the response that has received little attention is the interstimulus interval (ISI); inadequate duration of ISI might lead to incomplete recovery of the response between successive presentations and consequent response fatigue. This research aimed to test for effects of ISI on ARTs in normally hearing young humans, measured at 1 and 4 kHz. Contrary to our hypotheses, increasing ISIs from 2.5 to 8.5 s did not reduce ART level, nor raise ART reliability. Results confirm that clinically measured ARTs-including those at 4 kHz-can exhibit excellent reliability and that relatively short (2.5 s) ISIs are adequate for the measurement of sensitive and reliable ARTs.

Effects of Age and Noise Exposure on Proxy Measures of Cochlear Synaptopathy.

Although there is strong histological evidence for age-related synaptopathy in humans, evidence for the existence of noise-induced cochlear synaptopathy in humans is inconclusive. Here, we sought to evaluate the relative contributions of age and noise exposure to cochlear synaptopathy using a series of electrophysiological and behavioral measures. We extended an existing cohort by including 33 adults in the age range 37 to 60, resulting in a total of 156 participants, with the additional older participants resulting in a weakening of the correlation between lifetime noise exposure and age. We used six independent regression models (corrected for multiple comparisons), in which age, lifetime noise exposure, and high-frequency audiometric thresholds were used to predict measures of synaptopathy, with a focus on differential measures. The models for auditory brainstem responses, envelope-following responses, interaural phase discrimination, and the co-ordinate response measure of speech perception were not statistically significant. However, both age and noise exposure were significant predictors of performance on the digit triplet test of speech perception in noise, with greater noise exposure (unexpectedly) predicting better performance in the 80 dB sound pressure level (SPL) condition and greater age predicting better performance in the 40 dB SPL condition. Amplitude modulation detection thresholds were also significantly predicted by age, with older listeners performing better than younger listeners at 80 dB SPL. Overall, the results are inconsistent with the predicted effects of synaptopathy.

Earplug-induced changes in acoustic reflex thresholds suggest that increased subcortical neural gain may be necessary but not sufficient for the occurrence of tinnitus.

The occurrence of tinnitus is associated with hearing loss and neuroplastic changes in the brain, but disentangling correlation and causation has remained difficult in both human and animal studies. Here we use earplugs to cause a period of monaural deprivation to induce a temporary, fully reversible tinnitus sensation, to test whether differences in subcortical changes in neural response gain, as reflected through changes in acoustic reflex thresholds (ARTs), could explain the occurrence of tinnitus. Forty-four subjects with normal hearing wore an earplug in one ear for either 4 (n = 27) or 7 days (n = 17). Thirty subjects reported tinnitus at the end of the deprivation period. ARTs were measured before the earplug period and immediately after taking the earplug out. At the end of the earplug period, ARTs in the plugged ear were decreased by 5.9 ±â€¯1.1 dB in the tinnitus-positive group, and by 6.3 ±â€¯1.1 dB in the tinnitus-negative group. In the control ear, ARTs were increased by 1.3 ±â€¯0.8 dB in the tinnitus-positive group, and by 1.6 ±â€¯2.0 dB in the tinnitus-negative group. There were no significant differences between the groups with 4 and 7 days of auditory deprivation. Our results suggest that either the subcortical neurophysiological changes underlying the ART reductions might not be related to the occurrence of tinnitus, or that they might be a necessary component of the generation of tinnitus, but with additional changes at a higher level of auditory processing required to give rise to tinnitus. This article is part of a Special Issue entitled: Hearing Loss, Tinnitus, Hyperacusis, Central Gain.

Acoustic Middle-Ear-Muscle-Reflex Thresholds in Humans with Normal Audiograms: No Relations to Tinnitus, Speech Perception in Noise, or Noise Exposure.

The acoustic middle-ear-muscle reflex (MEMR) has been suggested as a sensitive non-invasive measure of cochlear synaptopathy, the loss of synapses between inner hair cells and auditory nerve fibers. In the present study, clinical MEMR thresholds were measured for 1-, 2-, and 4-kHz tonal elicitors, using a procedure shown to produce thresholds with excellent reliability. MEMR thresholds of 19 participants with tinnitus and normal audiograms were compared to those of 19 age- and sex-matched controls. MEMR thresholds did not differ significantly between the two groups at any frequency. These 38 participants were included in a larger sample of 70 participants with normal audiograms. For this larger group, MEMR thresholds were compared to a measure of spatial speech perception in noise (SPiN) and a detailed self-report estimate of lifetime noise exposure. MEMR thresholds were unrelated to either SPiN or noise exposure, despite a wide range in both measures. It is possible that thresholds measured using a clinical paradigm are less sensitive to synaptopathy than those obtained using more sophisticated measurement techniques; however, we had good sensitivity at the group level, and even trends in the hypothesized direction were not observed. To the extent that MEMR thresholds are sensitive to cochlear synaptopathy, the present results provide no evidence that tinnitus, SPiN, or noise exposure are related to synaptopathy in the population studied.

No evidence for enhanced processing of speech that is low-pass filtered near the edge frequency of cochlear dead regions in children.

OBJECTIVES: Cochlear dead regions (DRs) are regions in the cochlea where the inner hair cells and/or neurons are not functioning. Adults with extensive high-frequency DRs have enhanced abilities in processing sounds with frequencies just below the edge frequency, fedge, of the DR. It was assessed whether the same is true for children. DESIGN: Performance was compared for children aged 8 to 13 years with: DRs (group DR), hearing impairment but without DRs (group NODR), and normal hearing (group NH). Seven ears in each group were tested. Each ear in the DR group was matched in age and low-frequency hearing with an ear in the NODR group, and in age with an ear in the NH group, giving seven "triplets". Within each triplet, the percent correct identification of vowel-consonant-vowel stimuli was measured using stimuli that were low-pass filtered at fedge and 0.67fedge, based on the ear with a DR. For the hearing-impaired ears, stimuli were given frequency-selective amplification as prescribed by DSL 4.1. RESULTS: No significant differences in performance were found between groups for either low-pass cut-off frequency. CONCLUSION: Unlike adults, the children with DRs did not show enhanced discrimination of speech stimuli with frequencies below fedge.

Supra-threshold auditory brainstem response amplitudes in humans: Test-retest reliability, electrode montage and noise exposure.

The auditory brainstem response (ABR) is a sub-cortical evoked potential in which a series of well-defined waves occur in the first 10 ms after the onset of an auditory stimulus. Wave V of the ABR, particularly wave V latency, has been shown to be remarkably stable over time in individual listeners. However, little attention has been paid to the reliability of wave I, which reflects auditory nerve activity. This ABR component has attracted interest recently, as wave I amplitude has been identified as a possible non-invasive measure of noise-induced cochlear synaptopathy. The current study aimed to determine whether ABR wave I amplitude has sufficient test-retest reliability to detect impaired auditory nerve function in an otherwise normal-hearing listener. Thirty normal-hearing females were tested, divided equally into low- and high-noise exposure groups. The stimulus was an 80 dB nHL click. ABR recordings were made from the ipsilateral mastoid and from the ear canal (using a tiptrode). Although there was some variability between listeners, wave I amplitude had high test-retest reliability, with an intraclass correlation coefficient (ICC) comparable to that for wave V amplitude. There were slight gains in reliability for wave I amplitude when recording from the ear canal (ICC of 0.88) compared to the mastoid (ICC of 0.85). The summating potential (SP) and ratio of SP to wave I were also quantified and found to be much less reliable than measures of wave I and V amplitude. Finally, we found no significant differences in the amplitude of any wave components between low- and high-noise exposure groups. We conclude that, if the other sources of between-subject variability can be controlled, wave I amplitude is sufficiently reliable to accurately characterize individual differences in auditory nerve function.

Impaired speech perception in noise with a normal audiogram: No evidence for cochlear synaptopathy and no relation to lifetime noise exposure.

In rodents, noise exposure can destroy synapses between inner hair cells and auditory nerve fibers ("cochlear synaptopathy") without causing hair cell loss. Noise-induced cochlear synaptopathy usually leaves cochlear thresholds unaltered, but is associated with long-term reductions in auditory brainstem response (ABR) amplitudes at medium-to-high sound levels. This pathophysiology has been suggested to degrade speech perception in noise (SPiN), perhaps explaining why SPiN ability varies so widely among audiometrically normal humans. The present study is the first to test for evidence of cochlear synaptopathy in humans with significant SPiN impairment. Individuals were recruited on the basis of self-reported SPiN difficulties and normal pure tone audiometric thresholds. Performance on a listening task identified a subset with "verified" SPiN impairment. This group was matched with controls on the basis of age, sex, and audiometric thresholds up to 14 kHz. ABRs and envelope-following responses (EFRs) were recorded at high stimulus levels, yielding both raw amplitude measures and within-subject difference measures. Past exposure to high sound levels was assessed by detailed structured interview. Impaired SPiN was not associated with greater lifetime noise exposure, nor with any electrophysiological measure. It is conceivable that retrospective self-report cannot reliably capture noise exposure, and that ABRs and EFRs offer limited sensitivity to synaptopathy in humans. Nevertheless, the results do not support the notion that noise-induced synaptopathy is a significant etiology of SPiN impairment with normal audiometric thresholds. It may be that synaptopathy alone does not have significant perceptual consequences, or is not widespread in humans with normal audiograms.

Effects of noise exposure on young adults with normal audiograms II: Behavioral measures.

An estimate of lifetime noise exposure was used as the primary predictor of performance on a range of behavioral tasks: frequency and intensity difference limens, amplitude modulation detection, interaural phase discrimination, the digit triplet speech test, the co-ordinate response speech measure, an auditory localization task, a musical consonance task and a subjective report of hearing ability. One hundred and thirty-eight participants (81 females) aged 18-36 years were tested, with a wide range of self-reported noise exposure. All had normal pure-tone audiograms up to 8 kHz. It was predicted that increased lifetime noise exposure, which we assume to be concordant with noise-induced cochlear synaptopathy, would elevate behavioral thresholds, in particular for stimuli with high levels in a high spectral region. However, the results showed little effect of noise exposure on performance. There were a number of weak relations with noise exposure across the test battery, although many of these were in the opposite direction to the predictions, and none were statistically significant after correction for multiple comparisons. There were also no strong correlations between electrophysiological measures of synaptopathy published previously and the behavioral measures reported here. Consistent with our previous electrophysiological results, the present results provide no evidence that noise exposure is related to significant perceptual deficits in young listeners with normal audiometric hearing. It is possible that the effects of noise-induced cochlear synaptopathy are only measurable in humans with extreme noise exposures, and that these effects always co-occur with a loss of audiometric sensitivity.

Using acoustic reflex threshold, auditory brainstem response and loudness judgments to investigate changes in neural gain following acute unilateral deprivation in normal hearing adults.

Unilateral auditory deprivation induces a reduction in the acoustic reflex threshold (ART) and an increase in loudness. These findings have been interpreted as a compensatory change in neural gain, governed by changes in excitatory and inhibitory neural inputs. There is also evidence to suggest that changes in neural gain can be measured using the auditory brainstem response (ABR). The present study extended Munro et al. (2014) [J. Acoust. Soc. Am. 135, 315-322] by investigating changes after 4 days of unilateral earplug use to: (i) ART, (ii) ABR and (iii) loudness. Because changes may occur during the post-deprivation test session (day 4), ART measurements were taken 1 h and 2 h post-earplug removal. There was a significant reduction in ART in the treatment ear immediately after the removal of the earplug, which is consistent with a compensatory increase in neural gain. A novel finding was the significant return of ARTs to baseline within 2 h of earplug removal. A second novel finding was a significant decrease in the mean amplitude of ABR wave V in the treatment ear, but a significant increase in the control ear, both after 4 days of deprivation. These changes in the ABR are in the opposite direction to those predicted. We were unable to replicate the change in loudness reported in previous deprivation studies; however, the short period of earplug use may have contributed to this null finding.

Effects of noise exposure on young adults with normal audiograms I: Electrophysiology.

Noise-induced cochlear synaptopathy has been demonstrated in numerous rodent studies. In these animal models, the disorder is characterized by a reduction in amplitude of wave I of the auditory brainstem response (ABR) to high-level stimuli, whereas the response at threshold is unaffected. The aim of the present study was to determine if this disorder is prevalent in young adult humans with normal audiometric hearing. One hundred and twenty six participants (75 females) aged 18-36 were tested. Participants had a wide range of lifetime noise exposures as estimated by a structured interview. Audiometric thresholds did not differ across noise exposures up to 8 kHz, although 16-kHz audiometric thresholds were elevated with increasing noise exposure for females but not for males. ABRs were measured in response to high-pass (1.5 kHz) filtered clicks of 80 and 100 dB peSPL. Frequency-following responses (FFRs) were measured to 80 dB SPL pure tones from 240 to 285 Hz, and to 80 dB SPL 4 kHz pure tones amplitude modulated at frequencies from 240 to 285 Hz (transposed tones). The bandwidth of the ABR stimuli and the carrier frequency of the transposed tones were chosen to target the 3-6 kHz characteristic frequency region which is usually associated with noise damage in humans. The results indicate no relation between noise exposure and the amplitude of the ABR. In particular, wave I of the ABR did not decrease with increasing noise exposure as predicted. ABR wave V latency increased with increasing noise exposure for the 80 dB peSPL click. High carrier-frequency (envelope) FFR signal-to-noise ratios decreased as a function of noise exposure in males but not females. However, these correlations were not significant after the effects of age were controlled. The results suggest either that noise-induced cochlear synaptopathy is not a significant problem in young, audiometrically normal adults, or that the ABR and FFR are relatively insensitive to this disorder in young humans, although it is possible that the effects become more pronounced with age.

Tinnitus with a normal audiogram: Relation to noise exposure but no evidence for cochlear synaptopathy.

In rodents, exposure to high-level noise can destroy synapses between inner hair cells and auditory nerve fibers, without causing hair cell loss or permanent threshold elevation. Such "cochlear synaptopathy" is associated with amplitude reductions in wave I of the auditory brainstem response (ABR) at moderate-to-high sound levels. Similar ABR results have been reported in humans with tinnitus and normal audiometric thresholds, leading to the suggestion that tinnitus in these cases might be a consequence of synaptopathy. However, the ABR is an indirect measure of synaptopathy and it is unclear whether the results in humans reflect the same mechanisms demonstrated in rodents. Measures of noise exposure were not obtained in the human studies, and high frequency audiometric loss may have impacted ABR amplitudes. To clarify the role of cochlear synaptopathy in tinnitus with a normal audiogram, we recorded ABRs, envelope following responses (EFRs), and noise exposure histories in young adults with tinnitus and matched controls. Tinnitus was associated with significantly greater lifetime noise exposure, despite close matching for age, sex, and audiometric thresholds up to 14 kHz. However, tinnitus was not associated with reduced ABR wave I amplitude, nor with significant effects on EFR measures of synaptopathy. These electrophysiological measures were also uncorrelated with lifetime noise exposure, providing no evidence of noise-induced synaptopathy in this cohort, despite a wide range of exposures. In young adults with normal audiograms, tinnitus may be related not to cochlear synaptopathy but to other effects of noise exposure.

No change in the acoustic reflex threshold and auditory brainstem response following short-term acoustic stimulation in normal hearing adults.

Unilateral auditory deprivation or stimulation can induce changes in loudness and modify the sound level required to elicit the acoustic reflex. This has been explained in terms of a change in neural response, or gain, for a given sound level. However, it is unclear if these changes are driven by the asymmetry in auditory input or if they will also occur following bilateral changes in auditory input. The present study used a cross-over trial of unilateral and bilateral amplification to investigate changes in the acoustic reflex thresholds (ARTs) and the auditory brainstem response (ABR) in normal hearing listeners. Each treatment lasted 7 days and there was a 7-day washout period between the treatments. There was no significant change in the ART or ABR with either treatment. This null finding may have occurred because the amplification was insufficient to induce experience-related changes to the ABR and ART. Based on the null findings from the present study, and evidence of a change in ART in previous unilateral hearing aid use in normal hearing listeners, the threshold to trigger adaptive changes appears to be around 5 days of amplification with real ear insertion gain greater than 13-17 dB.

Time course and frequency specificity of sub-cortical plasticity in adults following acute unilateral deprivation.

Auditory deprivation and stimulation can change the threshold of the acoustic reflex, but the mechanisms underlying these changes remain largely unknown. In order to elucidate the mechanism, we sought to characterize the time-course as well as the frequency specificity of changes in acoustic reflex thresholds (ARTs). In addition, we compared ipsilateral and contralateral measurements because the pattern of findings may shed light on the anatomical location of the change in neural gain. Twenty-four normal-hearing adults wore an earplug continuously in one ear for six days. We measured ipsilateral and contralateral ARTs in both ears on six occasions (baseline, after 2, 4 and 6 days of earplug use, and 4 and 24 h after earplug removal), using pure tones at 0.5, 1, 2 and 4 kHz and a broadband noise stimulus, and an experimenter-blinded design. We found that ipsi- as well as contralateral ARTs were obtained at a lower sound pressure level after earplug use, but only when the reflex was elicited by stimulating the treatment ear. Changes in contralateral ARTs were not the same as changes in ipsilateral ARTs when the stimulus was presented to the control ear. Changes in ARTs were present after 2 days of earplug use, and reached statistical significance after 4 days, when the ipsilateral and contralateral ARTs were measured in the treatment ear. The greatest changes in ARTs occurred at 2 and 4 kHz, the frequencies most attenuated by the earplug. After removal of the earplug, ARTs started to return to baseline relatively quickly, and were not significantly different from baseline by 4-24 h. There was a trend for the recovery to occur quicker than the onset. The changes in ARTs are consistent with a frequency-specific gain control mechanism operating around the level of the ventral cochlear nucleus in the treatment ear, on a time scale of hours to days. These findings, specifically the time course of change, could be applicable to other sensory systems, which have also shown evidence of a neural gain control mechanism.

Using probe-microphone measurements to improve the match to target gain and frequency response slope, as a function of earmould style, frequency, and input level.

OBJECTIVE: Matching a prescription gain target at 60-65 dB SPL does not ensure audibility of lower input levels, nor does it mean the fitted frequency response slope is conducive to good sound quality. The aim of the present study was to evaluate the use of probe-microphone measurements to match target gain and slope, as a function of earmould style, frequency, and input level. DESIGN: The real-ear insertion gain was calculated for an input of 50, 65, and 80 dB SPL for the manufacturer's 'initial fit' (IF) settings and after adjustment to target in 49 and 51 open slim-tube and custom earmould fittings, respectively. STUDY SAMPLE: One hundred adults with median age 74 years (range 32-93). RESULTS: Some 18%-67% of the IF settings were within 10 dB of the target gain but this increased to >85% after adjustment. Some 47%-71% of the IF settings were within 10 dB of the target slope but, with the exception of 2-4 kHz, this increased to >88% after adjustment. CONCLUSIONS: The results indicate that IF settings are inadequate, at least for the model of hearing aid used in the present study; however, significant discrepancies remained, even after adjustment.

Enhanced intensity discrimination in the intact ear of adults with unilateral deafness.

Physiological measures of neural activity in the auditory cortex have revealed plasticity following unilateral deafness. Central projections from the remaining ear reorganize to produce a stronger cortical response than normal. However, little is known about the perceptual consequences of this increase. One possibility is improved sound intensity discrimination. Intensity difference limens were measured in 11 individuals with unilateral deafness that were previously shown to exhibit increased cortical activity to sounds heard by the intact ear. Significantly smaller mean difference limens were observed compared with controls. These results provide evidence of the perceptual consequences of plasticity in humans following unilateral deafness.

Auditory acclimatization and hearing aids: late auditory evoked potentials and speech recognition following unilateral and bilateral amplification.

The aim of this study was to investigate changes in central auditory processing following unilateral and bilateral hearing aid fitting using a combination of physiological and behavioral measures: late auditory event-related potentials (ERPs) and speech recognition in noise, respectively. The hypothesis was that for fitted ears, the ERP amplitude would increase over time following hearing aid fitting in parallel with improvement in aided speech recognition. The N1 and P2 ERPs were recorded to 500 and 3000 Hz tones presented at 65, 75, and 85 dB sound pressure level to either the left or right ear. New unilateral and new bilateral hearing aid users were tested at the time of first fitting and after 12 weeks hearing aid use. A control group of long-term hearing aid users was tested over the same time frame. No significant changes in the ERP were observed for any group. There was a statistically significant 2% improvement in aided speech recognition over time for all groups, although this was consistent with a general test-retest effect. This study does not support the existence of an acclimatization effect observable in late ERPs following 12 weeks' hearing aid use.

Plasticity and modified loudness following short-term unilateral deprivation: evidence of multiple gain mechanisms within the auditory system.

Auditory deprivation and stimulation can change the threshold of the acoustic middle ear reflex as well as loudness in adult listeners. However, it has remained unclear whether changes in these measures are due to the same mechanism. In this study, deprivation was achieved using a monaural earplug that was worn by listeners for 7 days. Acoustic reflex thresholds (ARTs) and categorical loudness ratings were measured using a blinded design in which the experimenter was unaware of which ear had been plugged. Immediately after terminating unilateral deprivation, ARTs were obtained at a lower sound pressure level in the ear that had been fitted with an earplug and at a higher sound pressure level in the control ear. In contrast, categorical judgments of loudness changed in the same direction in both ears with a given stimulus level reported as louder after unilateral deprivation. The relationship between changes to the ART and loudness judgments was not statistically significant. For both the ARTs and the categorical loudness judgments, most of the changes had disappeared within 24 h after earplug removal. The changes in ARTs, as a consequence of unilateral sound deprivation, are consistent with a gain control mechanism; however, the lack of relationship with the categorical loudness judgments, and the different pattern of findings for each measure, suggests the possibility of multiple gain mechanisms.