Testing the auditory steady-state response (ASSR) to 40-Hz and 27-Hz click trains in children with autism spectrum disorder and their first-degree biological relatives: A high-density electroencephalographic (EEG) study

对自闭症谱系障碍儿童及其一级亲属进行40 Hz和27 Hz点击序列听觉稳态反应(ASSR)测试:一项高密度脑电图(EEG)研究

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Abstract

MOTIVATION: Altered auditory processing likely contributes to core social and attentional impairments in autism spectrum disorder (ASD). The auditory steady-state response (ASSR)- a neural measure of auditory processing and cortical excitatory-inhibitory balance-has yielded mixed results in ASD. This study uses high density electroencephalography (EEG) to evaluate ASSR in ASD and unaffected siblings to clarify neural mechanisms underlying auditory deficits in autism. METHODS: High-density 70-channel EEG was recorded in children (8-12 years, IQ >80) with ASD (n=53), typically developing (TD) peers (n=35), and unaffected biological siblings (n=26) during 500-ms binaural click trains (27- and 40-Hz) in an active oddball task. RESULTS: No group differences were observed in frequency-following responses (FFR) to 27- or 40-Hz stimuli, although higher 40-Hz power was associated with older age and better behavioral performance in ASD. The broad-band response from 180-250 ms was reduced in ASD for both stimulation frequencies-particularly in the low-frequency (<8 Hz) range-and significantly correlated with IQ and age. Siblings showed intermediate broad-band responses. DISCUSSION: While FFRs appeared intact in ASD, we observed reduced broad-band response in the transition period to the steady state FFR, which was specific to low (<8-Hz) frequencies-potentially reflecting reduced synchronization at timescales that correspond with slower, syllabic rhythms (~4-8 Hz) occurring in natural speech. Intermediate responses in first-degree relatives suggest that this is related to genetic vulnerability for ASD and highlights its clinical relevance. These findings suggest intact sensory processing in ASD alongside possible top-down auditory feedback deficits, which may serve as heritable neurophysiological markers.

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