He Jason L, Fuelscher Ian, Enticott Peter G, Teo Wei-Peng, Barhoun Pamela, Hyde Christian
Deakin Child Study Centre, School of Psychology, Deakin University, Geelong, VIC, Australia.
School of Exercise and Nutrition Sciences, Institute for Physical Activity and Nutrition (IPAN), Deakin University, Geelong, VIC, Australia.
Front Neurol. 2018 Mar 23;9:179. doi: 10.3389/fneur.2018.00179. eCollection 2018.
While the etiology of developmental coordination disorder (DCD) is yet to be established, brain-behavior modeling provides a cogent argument that neuropathology may subserve the motor difficulties typical of DCD. We argue that a number of the core behavioral features of the DCD profile (such as poor surround inhibition, compromised motor inhibition, and the presence of mirror movements) are consistent with difficulties regulating inhibition within the primary motor cortex (M1). This study aimed to be the first account of the integrity of cortical inhibition in motor cortices in DCD.
The sample consisted of eight adults with DCD aged (18-30 years) and 10 aged matched neurotypical controls. Participants received a common battery of single and paired-pulse transcranial magnetic stimulation from which a series of neurophysiological measures classically used to measure intra- [e.g., short-interval cortical inhibition (SICI), long-interval cortical inhibition (LICI), and cortical silent period] and inter hemispheric [e.g., ipsilateral silent period (ISP)] cortical inhibition of the M1 at rest were recorded.
While no group differences were observed for any measure of intrahemispheric cortical inhibition, individuals with DCD demonstrated significantly reduced interhemispheric cortical inhibition relative to controls, shown by consistently lower ISP.
Our findings are consistent with the view that regulation of cortical inhibition of M1 activity may be atypical in individuals with DCD, indicating differential GABAergic operation. This effect, however, appears to be select to cortical inhibition. Importantly, our data support the notion that reduced interhemispheric M1 cortical inhibition may at least partly explain commonly reported difficulties with bimanual motor control in DCD. The neurochemical implications and limitations of this evidence will be discussed.
虽然发育性协调障碍（DCD）的病因尚未明确，但脑-行为模型有力地表明，神经病理学可能是DCD典型运动困难的基础。我们认为，DCD特征的一些核心行为特征（如周围抑制差、运动抑制受损和镜像运动的存在）与初级运动皮层（M1）内抑制调节困难相一致。本研究旨在首次描述DCD患者运动皮层中皮质抑制的完整性。
样本包括8名年龄在18至30岁之间的DCD成年患者和10名年龄匹配的神经典型对照者。参与者接受了一系列常见的单脉冲和双脉冲经颅磁刺激，从中记录了一系列经典用于测量静息状态下M1的半球内[例如，短间隔皮质抑制（SICI）、长间隔皮质抑制（LICI）和皮质静息期]和半球间[例如，同侧静息期（ISP）]皮质抑制的神经生理学指标。
虽然在任何半球内皮质抑制测量中均未观察到组间差异，但与对照组相比，DCD患者的半球间皮质抑制明显降低，表现为ISP持续较低。
我们的研究结果与以下观点一致，即DCD患者中M1活动的皮质抑制调节可能是非典型的，表明GABA能操作存在差异。然而，这种效应似乎仅限于皮质抑制。重要的是，我们的数据支持以下观点，即半球间M1皮质抑制降低可能至少部分解释了DCD中常见的双手运动控制困难。将讨论这一证据的神经化学意义和局限性。
