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自闭症谱系障碍(ASD)和发育正常(TD)儿童空间导航的神经机制:来自脑电图微状态和功能连接分析的见解

Neural mechanisms of spatial navigation in ASD and TD children: insights from EEG microstate and functional connectivity analysis.

作者信息

Wang Yao, Wang Jianing, Lu Chong

机构信息

Cognitive Science and Allied Health School, Beijing Language and Culture University, Beijing, China.

Institute of Life and Health Sciences, Beijing Language and Culture University, Beijing, China.

出版信息

Front Psychiatry. 2025 Apr 4;16:1552233. doi: 10.3389/fpsyt.2025.1552233. eCollection 2025.

DOI:10.3389/fpsyt.2025.1552233
PMID:40256159
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12006063/
Abstract

INTRODUCTION

Autism Spectrum Disorder (ASD) is associated with atypical neural dynamics, affecting spatial navigation and information integration. EEG microstates and functional connectivity (FC) are useful tools for investigating these differences. This study examines alterations in EEG microstates and theta-band FC during map-reading tasks in children with ASD (n = 12) compared to typically developing (TD) peers (n = 12), aiming to uncover neural mechanisms underlying spatial processing deficits in ASD.

METHODS

EEG data were collected from children with ASD (n = 12) and TD controls (n = 12) aged 6-10 years during a map-reading task. Microstate analysis quantified the temporal dynamics of four canonical microstates (A, B, C, and D). Theta-band (4-8 Hz) FC was analyzed to assess interregional neural communication during the task. Statistical tests identified group differences in microstate metrics and FC patterns.

RESULTS

Children with ASD showed significant differences in EEG microstate dynamics compared to TD controls. The ASD group showed reduced occurrence, but longer duration and greater coverage in microstate A, indicating abnormal temporal and spatial brain activity. For microstate B, the ASD group displayed shorter durations and lower coverage, suggesting impairments in cognitive control. In microstate C, the ASD group exhibited reduced duration, coverage, and steady-state distribution, pointing to disruptions in spatial attention. Conversely, microstate D showed increased occurrence and greater coverage in the ASD group, reflecting atypical spatial attention allocation. Theta-band FC analysis revealed significantly reduced connectivity in key brain networks involved in spatial navigation, particularly between fronto-parietal and occipito-temporal regions. This suggests disrupted integration of spatial and cognitive processes in children with ASD.

DISCUSSION

The alterations in EEG microstate patterns and theta-band FC highlight differences in the neural mechanisms underlying spatial navigation and cognitive integration in ASD. These findings suggest that microstate and FC analyses could serve as biomarkers for understanding visual spatial navigation in ASD, related to perceptual abnormalities. This research provides a basis for individualized rehabilitation plans for children with ASD, using qEEG biomarkers to guide neuromodulation techniques, such as transcranial direct current stimulation (tDCS). Future studies should investigate longitudinal changes and intervention effects on these neural dynamics.

摘要

引言

自闭症谱系障碍(ASD)与非典型神经动力学有关,会影响空间导航和信息整合。脑电图微状态和功能连接(FC)是研究这些差异的有用工具。本研究调查了自闭症儿童(n = 12)与发育正常(TD)的同龄人(n = 12)在地图阅读任务期间脑电图微状态和θ波段FC的变化,旨在揭示自闭症中空间处理缺陷背后的神经机制。

方法

在地图阅读任务期间,收集了12名6至10岁的自闭症儿童(n = 12)和TD对照组(n = 12)的脑电图数据。微状态分析量化了四种典型微状态(A、B、C和D)的时间动态。分析θ波段(4 - 8 Hz)FC以评估任务期间的区域间神经通信。统计测试确定了微状态指标和FC模式的组间差异。

结果

与TD对照组相比,自闭症儿童在脑电图微状态动态方面存在显著差异。自闭症组微状态A的出现次数减少,但持续时间更长且覆盖范围更大,表明大脑活动的时间和空间异常。对于微状态B,自闭症组的持续时间较短且覆盖范围较低,表明认知控制受损。在微状态C中,自闭症组的持续时间、覆盖范围和稳态分布均减少,表明空间注意力受到干扰。相反,微状态D在自闭症组中出现次数增加且覆盖范围更大,反映了非典型的空间注意力分配。θ波段FC分析显示,参与空间导航的关键脑网络中的连接显著减少,特别是在额顶叶和枕颞叶区域之间。这表明自闭症儿童的空间和认知过程整合受到干扰。

讨论

脑电图微状态模式和θ波段FC的变化突出了自闭症中空间导航和认知整合背后神经机制的差异。这些发现表明,微状态和FC分析可作为理解自闭症中视觉空间导航的生物标志物,与感知异常有关。本研究为自闭症儿童的个性化康复计划提供了基础,使用定量脑电图生物标志物来指导神经调节技术,如经颅直流电刺激(tDCS)。未来的研究应调查这些神经动力学的纵向变化和干预效果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ec/12006063/8653504cb3f7/fpsyt-16-1552233-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ec/12006063/013ea7584941/fpsyt-16-1552233-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ec/12006063/08c9a105002c/fpsyt-16-1552233-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ec/12006063/8653504cb3f7/fpsyt-16-1552233-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ec/12006063/013ea7584941/fpsyt-16-1552233-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ec/12006063/08c9a105002c/fpsyt-16-1552233-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ec/12006063/f520f22ecbea/fpsyt-16-1552233-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ec/12006063/8653504cb3f7/fpsyt-16-1552233-g004.jpg

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