Jessica de Boer

Auditory brainstem responses (ABRs) to broadband clicks are strongly affected by dyssynchrony, or “latency dispersion”, of their frequency-specific cochlear contributions. Optimized chirp stimuli, designed to compensate for cochlear dispersion, can afford substantial increase in broadband ABR amplitudes, particularly for the prominent wave-V deflection. Reports on the smaller wave I, however, which may be useful for measuring cochlear synaptopathy, have been mixed. This study aimed to test previous claims that ABR latency dispersion differs between waves I and V, and between males and females, and thus that using wave- and/or sex-tailored chirps may provide more reliable wave-I benefit. Using the derived-band technique, we measured responses from frequency-restricted (one-octave-wide) cochlear regions to energy-matched click and chirp stimuli. The derived-band responses’ latencies were used to assess any wave- and/or sex-related dispersion differences across bands, and their amplitudes, to evaluate any within-band dispersion differences. Our results suggest that sex-related dispersion difference within the lowest-frequency cochlear regions (< 1 kHz), where dispersion is generally greatest, may be a predominant driver of the often-reported sex difference in broadband ABR amplitude. At the same time, they showed no systematic dispersion difference between waves I and V. Instead, they suggest that reduced chirp benefit on wave I may arise as a result of chirp-induced desynchronization of on- and off-frequency responses generated at the same cochlear places, and resultant reduction in response contributions from higher-frequency cochlear regions, to which wave I is thought to be particularly sensitive.

It is commonly assumed that difficulty in listening to speech in noise is at least partly due to deficits in neural temporal processing. Given that noise reduces the temporal fidelity of the auditory brainstem response (ABR) to speech, it has been suggested that the speech ABR may serve as an index of such neural deficits. However, the temporal fidelity of ABRs, to both speech and non-speech sounds, is also known to be influenced by the cochlear origin of the response, as responses from higher-frequency cochlear regions are faster and more synchronous than responses from lower-frequency regions. Thus, if noise caused a reweighting of response contributions from higher- to lower-frequency cochlear regions, the temporal fidelity of the aggregate response should be reduced even in the absence of any changes in neural processing. This ‘place mechanism’ has been demonstrated for non-speech ABRs. The aim of this study was to test whether it also applies to speech ABRs. We used the so-called ‘derived-band’ method to isolate response contributions from frequency-limited cochlear regions. Broadband and derived-band speech ABRs were measured both in quiet and in noise. Whilst the noise caused significant changes to the temporal properties of the broadband response, its effects on the derived-band responses were mostly restricted to the response amplitudes. Importantly, the amplitudes of the higher-frequency derived-band responses were much more strongly affected than those of the lower-frequency responses, suggesting that the noise indeed caused a reweighting effect. Our results indicate that, as for non-speech ABRs, the cochlear place mechanism can represent a potentially substantial confound to speech-ABR-in-noise measurements.

Previous findings have suggested that auditory attention causes not only enhancement in neural processing gain, but also sharpening in neural frequency tuning in human auditory cortex. The current study was aimed to reexamine these findings. Specifically, we aimed to investigate whether attentional gain enhancement and frequency sharpening emerge at the same or different processing levels and whether they represent independent or cooperative effects. For that, we examined the pattern of attentional modulation effects on early, sensory-driven cortical auditory-evoked potentials occurring at different latencies. Attention was manipulated using a dichotic listening task and was thus not selectively directed to specific frequency values. Possible attention-related changes in frequency tuning selectivity were measured with an adaptation paradigm. Our results show marked disparities in attention effects between the earlier N1 deflection and the subsequent P2 deflection, with the N1 showing a strong gain enhancement effect, but no sharpening, and the P2 showing clear evidence of sharpening, but no independent gain effect. They suggest that gain enhancement and frequency sharpening represent successive stages of a cooperative attentional modulation mechanism that increases the representational bandwidth of attended versus unattended sounds.

In background noise, the timing precision of the auditory brainstem response to speech (speech-ABR) is disrupted and the response latency increases. The severity of the disruption has been correlated with listeners' ability to understand speech-in-noise. To date, although a central mechanism is assumed, the locus of the speech-ABR timing disruption is not clear. The present study aimed to investigate the contribution of different cochlear mechanisms to noise-induced latency increases. A first experiment examined the 'cochlear place' mechanism, by which the latency of the response increases as cochlear origin moves towards lower frequency regions. The results showed that the speech-ABR reflects an average over responses from a broad range of cochlear regions, which respond with substantial relative delays. This implies that cochlear place can potentially have large effects on masked speech-ABR latency. Another mechanism that is known to be involved in noise-induced ABR latency increases is neural adaptation. This is presumed to occur at the inner hair cell-nerve junction and is thought to reflect cochlear masking. Thus, if this mechanism contributes to speech-ABR latency increases in noise, we would expect this contribution to depend on cochlear frequency selectivity and amplification gain. This hypothesis is tested in the second experiment.