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Updated: Jan 21, 2026

Corticospinal Excitability Modulation During Action Observation
Published on: December 31, 2013
Activation of Mirror Neuron Regions Is Altered in Developmental Coordination Disorder (DCD)-Neurophysiological
Jessica M Lust1, Hein T van Schie1, Peter H Wilson2
1Behavioural Science Institute (BSI), Radboud University, Nijmegen, Netherlands.
Abstract:
Children with Developmental Coordination Disorder (DCD) have difficulty performing and learning motor skills. Automatic activation of the mirror neuron system (MNS) during action observation and its coupling to the motor output system are important neurophysiological processes that underpin observational motor learning. In the present study, we tested the hypothesis that MNS function is disrupted in children with DCD by using sensitive electroencephalography (EEG)-based measures of MNS activation during action observation. Specifically, we predicted reduced mu-suppression and coherence in DCD compared with typically developing children. Neural activation of the motor network was measured by EEG, specifically event-related desynchronization (ERD) of mu rhythms and fronto-parietal coherence. Children (15 DCD/15 controls) were tested under two task conditions: observational learning (imitation of an observed action) and detection (report a deviant movement after observation). EEG-metrics were compared between groups using linear mixed-effects models. As predicted, children with DCD showed lower levels of mu suppression and reduced modulation of coherence during the observational learning task compared with their non-DCD peers. Notably, mu suppression was reduced in DCD over the entire imitation task (repetitions, and both observation and pause intervals). Action observation can be used for the acquisition of new motor skills. This form of learning entails the transposition of the observed action to the existing internal representations of the observer's own motor system. The present neurophysiological results suggest that this process of learning is impaired in children with DCD. The results are discussed in relation to current hypotheses on mechanisms of DCD.
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