Neural oscillatory activity and connectivity in children who stutter during a non-speech motor task.

IF 4.1 2区 医学 Q1 CLINICAL NEUROLOGY Journal of Neurodevelopmental Disorders Pub Date : 2023-11-15 DOI:10.1186/s11689-023-09507-8
Valeria C Caruso, Amanda Hampton Wray, Erica Lescht, Soo-Eun Chang
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Abstract

Background: Neural motor control rests on the dynamic interaction of cortical and subcortical regions, which is reflected in the modulation of oscillatory activity and connectivity in multiple frequency bands. Motor control is thought to be compromised in developmental stuttering, particularly involving circuits in the left hemisphere that support speech, movement initiation, and timing control. However, to date, evidence comes from adult studies, with a limited understanding of motor processes in childhood, closer to the onset of stuttering.

Methods: We investigated the neural control of movement initiation in children who stutter and children who do not stutter by evaluating transient changes in EEG oscillatory activity (power, phase locking to button press) and connectivity (phase synchronization) during a simple button press motor task. We compared temporal changes in these oscillatory dynamics between the left and right hemispheres and between children who stutter and children who do not stutter, using mixed-model analysis of variance.

Results: We found reduced modulation of left hemisphere oscillatory power, phase locking to button press and phase connectivity in children who stutter compared to children who do not stutter, consistent with previous findings of dysfunction within the left sensorimotor circuits. Interhemispheric connectivity was weaker at lower frequencies (delta, theta) and stronger in the beta band in children who stutter than in children who do not stutter.

Conclusions: Taken together, these findings indicate weaker engagement of the contralateral left motor network in children who stutter even during low-demand non-speech tasks, and suggest that the right hemisphere might be recruited to support sensorimotor processing in childhood stuttering. Differences in oscillatory dynamics occurred despite comparable task performance between groups, indicating that an altered balance of cortical activity might be a core aspect of stuttering, observable during normal motor behavior.

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在非言语运动任务中口吃儿童的神经振荡活动和连通性。
背景:神经运动控制依赖于皮层和皮层下区域的动态相互作用,这反映在振荡活动的调节和多频段的连通性上。运动控制被认为在发育性口吃中受到损害,特别是涉及左半球支持语言、运动启动和时间控制的电路。然而,迄今为止,证据来自成人研究,对儿童运动过程的了解有限,更接近口吃的发病。方法:通过评估在简单的按键运动任务中脑电图振荡活动(功率、按键锁相)和连通性(相位同步)的瞬态变化,研究了口吃儿童和非口吃儿童运动启动的神经控制。我们使用混合模型方差分析,比较了左右脑半球之间以及口吃儿童和非口吃儿童之间这些振荡动态的时间变化。结果:我们发现,与非口吃儿童相比,口吃儿童的左半球振荡功率、按下按钮时的相锁定和相连接的调制减少,这与先前发现的左侧感觉运动电路功能障碍一致。与非口吃儿童相比,口吃儿童的大脑半球间连通性在较低频率(δ, θ)较弱,而在β波段较强。结论:综上所述,这些发现表明,即使在低要求的非言语任务中,口吃儿童对侧左运动网络的参与也较弱,并表明右半球可能被招募来支持儿童口吃的感觉运动加工。尽管两组之间的任务表现相当,但振荡动力学却存在差异,这表明皮层活动平衡的改变可能是口吃的一个核心方面,在正常的运动行为中可以观察到。
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来源期刊
CiteScore
7.60
自引率
4.10%
发文量
58
审稿时长
>12 weeks
期刊介绍: Journal of Neurodevelopmental Disorders is an open access journal that integrates current, cutting-edge research across a number of disciplines, including neurobiology, genetics, cognitive neuroscience, psychiatry and psychology. The journal’s primary focus is on the pathogenesis of neurodevelopmental disorders including autism, fragile X syndrome, tuberous sclerosis, Turner Syndrome, 22q Deletion Syndrome, Prader-Willi and Angelman Syndrome, Williams syndrome, lysosomal storage diseases, dyslexia, specific language impairment and fetal alcohol syndrome. With the discovery of specific genes underlying neurodevelopmental syndromes, the emergence of powerful tools for studying neural circuitry, and the development of new approaches for exploring molecular mechanisms, interdisciplinary research on the pathogenesis of neurodevelopmental disorders is now increasingly common. Journal of Neurodevelopmental Disorders provides a unique venue for researchers interested in comparing and contrasting mechanisms and characteristics related to the pathogenesis of the full range of neurodevelopmental disorders, sharpening our understanding of the etiology and relevant phenotypes of each condition.
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