Fei Chen1,2,3, Hao Zhang4, Hongwei Ding4, Suiping Wang5, Gang Peng2, Yang Zhang3. 1. School of Foreign Languages, Hunan University, Changsha, China. 2. Research Centre for Language, Cognition, and Neuroscience & Department of Chinese and Bilingual Studies, The Hong Kong Polytechnic University, Hong Kong SAR, China. 3. Department of Speech-Language-Hearing Sciences & Center for Neurobehavioral Development, University of Minnesota, Twin Cities, Minnesota, USA. 4. Speech-Language-Hearing Center, School of Foreign Languages, Shanghai Jiao Tong University, Shanghai, China. 5. School of Psychology, South China Normal University, Guangzhou, China.
Abstract
The presence of vowel exaggeration in infant-directed speech (IDS) may adapt to the age-appropriate demands in speech and language acquisition. Previous studies have provided behavioral evidence of atypical auditory processing towards IDS in children with autism spectrum disorders (ASD), while the underlying neurophysiological mechanisms remain unknown. This event-related potential (ERP) study investigated the neural coding of formant-exaggerated speech and nonspeech in 24 4- to 11-year-old children with ASD and 24 typically-developing (TD) peers. The EEG data were recorded using an alternating block design, in which each stimulus type (exaggerated/non-exaggerated sound) was presented with equal probability. ERP waveform analysis revealed an enhanced P1 for vowel formant exaggeration in the TD group but not in the ASD group. This speech-specific atypical processing in ASD was not found for the nonspeech stimuli which showed similar P1 enhancement in both ASD and TD groups. Moreover, the time-frequency analysis indicated that children with ASD showed differences in neural synchronization in the delta-theta bands for processing acoustic formant changes embedded in nonspeech. Collectively, the results add substantiating neurophysiological evidence (i.e., a lack of neural enhancement effect of vowel exaggeration) for atypical auditory processing of IDS in children with ASD, which may exert a negative effect on phonetic encoding and language learning. LAY SUMMARY: Atypical responses to motherese might act as a potential early marker of risk for children with ASD. This study investigated the neural responses to such socially relevant stimuli in the ASD brain, and the results suggested a lack of neural enhancement responding to the motherese even in individuals without intellectual disability.
The presence of vowel exaggeration in infant-directed speech (IDS) may adapt to the age-appropriate demands in speech and language acquisition. Previous studies have provided behavioral evidence of atypical auditory processing towards IDS in children with autism spectrum disorders (ASD), while the underlying neurophysiological mechanisms remain unknown. This event-related potential (ERP) study investigated the neural coding of formant-exaggerated speech and nonspeech in 24 4- to 11-year-old children with ASD and 24 typically-developing (TD) peers. The EEG data were recorded using an alternating block design, in which each stimulus type (exaggerated/non-exaggerated sound) was presented with equal probability. ERP waveform analysis revealed an enhanced P1 for vowel formant exaggeration in the TD group but not in the ASD group. This speech-specific atypical processing in ASD was not found for the nonspeech stimuli which showed similar P1 enhancement in both ASD and TD groups. Moreover, the time-frequency analysis indicated that children with ASD showed differences in neural synchronization in the delta-theta bands for processing acoustic formant changes embedded in nonspeech. Collectively, the results add substantiating neurophysiological evidence (i.e., a lack of neural enhancement effect of vowel exaggeration) for atypical auditory processing of IDS in children with ASD, which may exert a negative effect on phonetic encoding and language learning. LAY SUMMARY: Atypical responses to motherese might act as a potential early marker of risk for children with ASD. This study investigated the neural responses to such socially relevant stimuli in the ASD brain, and the results suggested a lack of neural enhancement responding to the motherese even in individuals without intellectual disability.