Research Center for Child Mental Development, Kanazawa University, Kanazawa, Japan; Division of Socio-Cognitive-Neuroscience, Department of Child Development United Graduate School of Child Development, Osaka University, Kanazawa University, Hamamatsu University School of Medicine, Chiba University and University of Fukui, Kanazawa, Japan.
Research Center for Child Mental Development, Kanazawa University, Kanazawa, Japan; Division of Socio-Cognitive-Neuroscience, Department of Child Development United Graduate School of Child Development, Osaka University, Kanazawa University, Hamamatsu University School of Medicine, Chiba University and University of Fukui, Kanazawa, Japan.
Neuroimage Clin. 2021;29:102560. doi: 10.1016/j.nicl.2021.102560. Epub 2021 Jan 14.
Autism spectrum disorder (ASD) often involves dysfunction in general motor control and motor coordination, in addition to core symptoms. However, the neural mechanisms underlying motor dysfunction in ASD are poorly understood. To elucidate this issue, we focused on brain oscillations and their coupling in the primary motor cortex (M1). We recorded magnetoencephalography in 18 children with ASD, aged 5 to 7 years, and 19 age- and IQ-matched typically-developing children while they pressed a button during a video-game-like motor task. The motor-related gamma (70 to 90 Hz) and pre-movement beta oscillations (15 to 25 Hz) were analyzed in the primary motor cortex using an inverse method. To determine the coupling between beta and gamma oscillations, we applied phase-amplitude coupling to calculate the statistical dependence between the amplitude of fast oscillations and the phase of slow oscillations. We observed a motor-related gamma increase and a pre-movement beta decrease in both groups. The ASD group exhibited a reduced motor-related gamma increase and enhanced pre-movement beta decrease in the ipsilateral primary motor cortex. We found phase-amplitude coupling, in which high-gamma activity was modulated by the beta rhythm in the primary motor cortex. Phase-amplitude coupling in the ipsilateral primary motor cortex was reduced in the ASD group compared with the control group. Using oscillatory changes and their couplings, linear discriminant analysis classified the ASD and control groups with high accuracy (area under the receiver operating characteristic curve: 97.1%). The current findings revealed alterations in oscillations and oscillatory coupling, reflecting the dysregulation of motor gating mechanisms in ASD. These results may be helpful for elucidating the neural mechanisms underlying motor dysfunction in ASD, suggesting the possibility of developing a biomarker for ASD diagnosis.
自闭症谱系障碍（ASD）除核心症状外，常伴有运动控制和运动协调功能障碍。然而，ASD 运动功能障碍的神经机制仍不清楚。为阐明这一问题，我们主要关注初级运动皮层（M1）中的脑振荡及其耦合。我们对 18 名 5 至 7 岁 ASD 儿童和 19 名年龄和智商匹配的正常发育儿童进行了脑磁图记录，这些儿童在进行类似于视频游戏的运动任务时按下按钮。采用逆方法对初级运动皮层的运动相关伽马（70-90Hz）和运动前β振荡（15-25Hz）进行分析。为了确定β和γ振荡之间的耦合，我们应用相位-振幅耦合来计算快速振荡的振幅和缓慢振荡的相位之间的统计依赖性。我们观察到两组的运动相关γ增加和运动前β减少。ASD 组表现为同侧初级运动皮层运动相关γ增加减少和运动前β减少增加。我们发现相位-振幅耦合，其中高γ活动受初级运动皮层β节律的调制。与对照组相比，ASD 组同侧初级运动皮层的相位-振幅耦合减少。使用振荡变化及其耦合，线性判别分析可以以高准确率（受试者工作特征曲线下面积：97.1%）对 ASD 和对照组进行分类。目前的研究结果揭示了 ASD 中振荡和振荡耦合的改变，反映了运动门控机制的失调。这些结果可能有助于阐明 ASD 运动功能障碍的神经机制，并为开发 ASD 诊断的生物标志物提供可能性。
