EEG microstates suggest atypical resting‐state network activity in high‐functioning children and adolescents with autism spectrum development

地方政府 心理学 脑电图 显著性(神经科学) 自闭症 自闭症谱系障碍 静息状态功能磁共振成像 听力学 默认模式网络 发展心理学 神经科学 认知 医学
作者
Yukari Takarae,Anthony P. Zanesco,Brandon Keehn,Leanne Chukoskie,Ralph‐Axel Müller,Jeanne Townsend
出处
期刊:Developmental Science [Wiley]
卷期号:25 (4) 被引量:23
标识
DOI:10.1111/desc.13231
摘要

EEG microstates represent transient electrocortical events that reflect synchronized activities of large-scale networks, which allows investigations of brain dynamics with sub-second resolution. We recorded resting EEG from 38 children and adolescents with Autism Spectrum Development (ASD) and 48 age, IQ, sex, and handedness-matched typically developing (TD) participants. The EEG was segmented into a time series of microstates using modified k-means clustering of scalp voltage topographies. The frequency and global explained variance (GEV) of a specific microstate (type C) were significantly lower in the ASD group compared to the TD group while the duration of the same microstate was correlated with the presence of ASD-related behaviors. The duration of this microstate was also positively correlated with participant age in the TD group, but not in the ASD group. Further, the frequency and duration of the microstate were significantly correlated with the overall alpha power only in the TD group. The signal strength and GEV for another microstate (type G) was greater in the ASD group than the TD group, and the associated topographical pattern differed between groups with greater variations in the ASD group. While more work is needed to clarify the underlying neural sources, the existing literature supports associations between the two microstates and the default mode and salience networks. The current study suggests specific alterations of temporal dynamics of the resting cortical network activities as well as their developmental trajectories and relationships to alpha power, which has been proposed to reflect reduced neural inhibition in ASD.
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