Zachary J Williams1, Peter G Abdelmessih2, Alexandra P Key3, Tiffany G Woynaroski4. 1. Medical Scientist Training Program, Vanderbilt University School of Medicine, Nashville, Tennessee; Vanderbilt Brain Institute, Vanderbilt University, Nashville, Tennessee; Frist Center for Autism and Innovation, Vanderbilt University, Nashville, Tennessee; Department of Hearing and Speech Sciences, Vanderbilt University Medical Center, Nashville, Tennessee. Electronic address: zachary.j.williams@vanderbilt.edu. 2. Neuroscience Undergraduate Program, Vanderbilt University, Nashville, Tennessee. 3. Department of Hearing and Speech Sciences, Vanderbilt University Medical Center, Nashville, Tennessee; Vanderbilt Kennedy Center, Vanderbilt University Medical Center, Nashville, Tennessee; Department of Psychiatry and Behavioral Sciences, Vanderbilt University Medical Center, Nashville, Tennessee. 4. Vanderbilt Brain Institute, Vanderbilt University, Nashville, Tennessee; Frist Center for Autism and Innovation, Vanderbilt University, Nashville, Tennessee; Department of Hearing and Speech Sciences, Vanderbilt University Medical Center, Nashville, Tennessee; Vanderbilt Kennedy Center, Vanderbilt University Medical Center, Nashville, Tennessee.
Abstract
BACKGROUND: Auditory perceptual abnormalities are common in persons on the autism spectrum. The neurophysiologic underpinnings of these differences have frequently been studied using auditory event-related potentials (ERPs) and event-related magnetic fields (ERFs). However, no study to date has quantitatively synthesized this literature to determine whether early auditory ERP/ERF latencies or amplitudes in autistic persons differ from those of typically developing control subjects. METHODS: We searched PubMed and ProQuest for studies comparing 1) latencies/amplitudes of P1/M50, N1b, N1c, M100, P2/M200, and/or N2 ERP/ERF components evoked by pure tones and 2) paired-click sensory gating (P1/N1b amplitude suppression) in autistic individuals and typically developing control subjects. Effects were synthesized using Bayesian 3-level meta-analysis. RESULTS: In response to pure tones, autistic individuals exhibited prolonged P1/M50 latencies (g = 0.341 [95% credible interval = 0.166, 0.546]), prolonged M100 latencies (g = 0.319 [0.093, 0.550]), reduced N1c amplitudes (g = -0.812 [-1.278, -0.187]), and reduced N2 amplitudes (g = -0.374 [-0.633, -0.179]). There were no practically significant group differences in P2/M200 latencies, N2 latencies, P1/M50 amplitudes, N1b amplitudes, M100 amplitudes, or P2/M200 amplitudes. Paired-click sensory gating was also reduced in autistic individuals (g = -0.389 [-0.619, -0.112]), although this effect was primarily driven by smaller responses to the first click stimulus. CONCLUSIONS: Relative to typically developing control subjects, autistic individuals demonstrate multiple alterations in early cortical auditory processing of simple stimuli. However, most group differences were modest in size and based on small numbers of heterogeneous studies with variable quality. Future work is necessary to understand whether these neurophysiologic measures can predict clinically meaningful outcomes or serve as stratification biomarkers for the autistic population.
BACKGROUND: Auditory perceptual abnormalities are common in persons on the autism spectrum. The neurophysiologic underpinnings of these differences have frequently been studied using auditory event-related potentials (ERPs) and event-related magnetic fields (ERFs). However, no study to date has quantitatively synthesized this literature to determine whether early auditory ERP/ERF latencies or amplitudes in autistic persons differ from those of typically developing control subjects. METHODS: We searched PubMed and ProQuest for studies comparing 1) latencies/amplitudes of P1/M50, N1b, N1c, M100, P2/M200, and/or N2 ERP/ERF components evoked by pure tones and 2) paired-click sensory gating (P1/N1b amplitude suppression) in autistic individuals and typically developing control subjects. Effects were synthesized using Bayesian 3-level meta-analysis. RESULTS: In response to pure tones, autistic individuals exhibited prolonged P1/M50 latencies (g = 0.341 [95% credible interval = 0.166, 0.546]), prolonged M100 latencies (g = 0.319 [0.093, 0.550]), reduced N1c amplitudes (g = -0.812 [-1.278, -0.187]), and reduced N2 amplitudes (g = -0.374 [-0.633, -0.179]). There were no practically significant group differences in P2/M200 latencies, N2 latencies, P1/M50 amplitudes, N1b amplitudes, M100 amplitudes, or P2/M200 amplitudes. Paired-click sensory gating was also reduced in autistic individuals (g = -0.389 [-0.619, -0.112]), although this effect was primarily driven by smaller responses to the first click stimulus. CONCLUSIONS: Relative to typically developing control subjects, autistic individuals demonstrate multiple alterations in early cortical auditory processing of simple stimuli. However, most group differences were modest in size and based on small numbers of heterogeneous studies with variable quality. Future work is necessary to understand whether these neurophysiologic measures can predict clinically meaningful outcomes or serve as stratification biomarkers for the autistic population.
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