Abstract
Objective: This study evaluated cortical encoding of voice onset time (VOT) in quiet and noise, and their potential associations with the behavioral categorical perception of VOT in children with auditory neuropathy spectrum disorder (ANSD).Design: Subjects were 11 children with ANSD ranging in age between 6.4 and 16.2 years. The stimulus was an /aba/-/apa/ vowel-consonant-vowel continuum comprising eight tokens with VOTs ranging from 0 ms (voiced endpoint) to 88 ms (voiceless endpoint). For speech in noise, speech tokens were mixed with the speech-shaped noise from the Hearing In Noise Test at a signal-to-noise ratio (SNR) of +5 dB. Speech-evoked auditory event-related potentials (ERPs) and behavioral categorization perception of VOT were measured in quiet in all subjects, and at an SNR of +5 dB in seven subjects. The stimuli were presented at 35 dB SL (re: pure tone average) or 115 dB SPL if this limit was less than 35 dB SL. In addition to the onset response, the auditory change complex (ACC) elicited by VOT was recorded in eight subjects.Results: Speech evoked ERPs recorded in all subjects consisted of a vertex positive peak (i.e., P1), followed by a trough occurring approximately 100 ms later (i.e., N2). For results measured in quiet, there was no significant difference in categorical boundaries estimated using ERP measures and behavioral procedures. Categorical boundaries estimated in quiet using both ERP and behavioral measures closely correlated with the most-recently measured Phonetically Balanced Kindergarten (PBK) scores. Adding a competing background noise did not affect categorical boundaries estimated using either behavioral or ERP procedures in three subjects. For the other four subjects, categorical boundaries estimated in noise using behavioral measures were prolonged. However, adding background noise only increased categorical boundaries measured using ERPs in three out of these four subjects.Conclusions: VCV continuum can be used to evaluate behavioral identification and the neural encoding of VOT in children with ANSD. In quiet, categorical boundaries of VOT estimated using behavioral measures and ERP recordings are closely associated with speech recognition performance in children with ANSD. Underlying mechanisms for excessive speech perception deficits in noise may vary for individual patients with ANSD.
Highlights
Auditory neuropathy spectrum disorder (ANSD) is a form of hearing impairment characterized by normal outer hair cell function, as indicated by the presence of cochlear microphonics (CMs) and/or otoacoustic emissions (OAE), in conjunction with an aberrant auditory neural system, as revealed by an absent or abnormal auditory brainstem response (ABR)
This study investigated the behavioral categorical perception of voice onset time (VOT) and event-related potentials (ERPs) evoked by VOT in children with ANSD in quiet and speech-shaped background noise
Behavioral categorical perception of VOT and speech evoked ERPs were measured from subjects in both quiet and noise conditions
Summary
Auditory neuropathy spectrum disorder (ANSD) is a form of hearing impairment characterized by normal outer hair cell function, as indicated by the presence of cochlear microphonics (CMs) and/or otoacoustic emissions (OAE), in conjunction with an aberrant auditory neural system, as revealed by an absent or abnormal auditory brainstem response (ABR). ANSD is estimated to be present in 5–10% of newly identified hearing loss cases each year (Rance, 2005; Vlastarakos et al, 2008; Berlin et al, 2010; Bielecki et al, 2012). The presence of ANSD has been linked to several risk factors including premature birth, neonatal distress (e.g., hyperbilirubinemia, anoxia, artificial ventilation), infection (e.g., mumps, meningitis), neuropathic disorders (e.g., Charcot-Marie-Tooth syndrome, Friedreich’s Ataxia), genetic factors (e.g., mutations in the otoferlin gene), and ototoxic drugs (e.g., carboplatin; Rance et al, 1999; Madden et al, 2002). Cases of ANSD with no apparent risk factors or medical comorbidities have been reported (Berlin et al, 2010; Teagle et al, 2010; Roush et al, 2011; Bielecki et al, 2012; Pelosi et al, 2012). Proposed sites of lesions include, but are not limited to, cochlear inner hair cells, synapses between inner hair cells and Type I auditory nerve fibers, and synapses between neurons in the auditory pathway
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