Abstract

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.

Highlights

  • The ability to understand speech in noise (SiN) is often degraded as a result of hearing loss (Festen and Plomp 1990; Smoorenburg 1992) or in consequence of ageing (Dubno et al 1984; Helfer and Wilber 1990), but can be impaired in younger people and when hearing is clinically normal (Guest et al 2018; Hind et al 2011; Hope et al 2013; Pienkowski 2017)

  • 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

  • Several studies have reported an association between SiN performance and the latencies of some of the speech ABR peaks, with poorer SiN performance generally associated with longer peak latencies (Cunningham et al 2001; Parbery-Clark et al 2009; Anderson et al 2010; Hornickel et al 2011; Parbery-Clark et al 2011; see, de Boer et al 2012)

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Summary

Introduction

The ability to understand speech in noise (SiN) is often degraded as a result of hearing loss (Festen and Plomp 1990; Smoorenburg 1992) or in consequence of ageing (Dubno et al 1984; Helfer and Wilber 1990), but can be impaired in younger people and when hearing is clinically normal (Guest et al 2018; Hind et al 2011; Hope et al 2013; Pienkowski 2017). The speech ABR is typically evoked by a synthetic consonant-vowel syllable, /da/ (Anderson and Kraus 2010; Johnson et al 2005), and consists of a series of peaks, which broadly follow the stimulus waveform and are thought to reflect synchronised neural responses from the DE BOER ET AL.: Noise-Induced Changes of the Speech ABR rostral brainstem. The stimulus-to-response correlation, which measures the degree of time locking between the response and stimulus waveform, is reduced, and the composition of the response frequency spectrum, which relates to the response shape, is altered. Some of these measures were sometimes found to be associated with SiN performance. Some studies have reported an association of SiN performance with the stimulus-to-response correlation of the speech ABR (Cunningham et al 2001; Parbery-Clark et al 2009, 2011, 2012), and some studies have found an association with the fundamental frequency and/or higher harmonics of the response frequency spectrum (Cunningham et al 2001; Anderson et al 2011; Song et al 2011; Strait et al 2012)

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