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.
People with high-frequency sensorineural hearing loss differ in the benefit they gain from amplification of high frequencies when listening to speech. Using vowel-consonant-vowel (VCV) stimuli in quiet that were amplified and then low pass filtered with various cutoff frequencies, Vickers et aL [J. Acoust. Soc. Am. 110, 1164-1175 (2001)] found that the benefit from amplification of high-frequency components was related to the presence or absence of a cochlear dead region at high frequencies. For hearing-impaired subjects without dead regions, performance improved with increasing cutoff frequency up to 7.5 kHz (the highest value tested). Subjects with high-frequency dead regions showed no improvement when the cutoff frequency was increased above about 1.7 times the edge frequency of the dead region. The present study was similar to that of Vickers et al. but used VCV stimuli presented in background noise. Ten subjects with high-frequency hearing loss, including eight from the study of Vickers et al., were tested. Five had dead regions starting below 2 kHz, and five had no dead regions. Speech stimuli at a nominal level of 65 dB were mixed with spectrally matched noise, amplified according to the "Cambridge" prescriptive formula for each subject and then low pass filtered. The noise level was chosen separately for each subject to give a moderate reduction in intelligibility relative to listening in quiet. For subjects without dead regions, performance generally improved with increasing cutoff frequency up to 7.5 kHz, on average more so in noise than in quiet. For most subjects with dead regions, performance improved with cutoff frequency up to 1.5-2 times the edge frequency of the dead region, but hardly changed with further increases. Calculations of speech audibility using a modified version of the articulation index showed that application of the Cambridge formula was at least partially successful in making high-frequency components of the speech audible for subjects with dead regions, and that such subjects often failed to benefit from increased audibility of the speech at high frequencies.
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.
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