The most common neurodevelopmental disorders (e.g., developmental dyslexia (DD), autism, attention-deficit hyperactivity disorder (ADHD)) have been the subject of numerous neuroimaging studies, leading to certain brain regions being identified as neural correlates of these conditions, referring to a neural signature of disorders. Developmental coordination disorder (DCD), however, remains one of the least understood and studied neurodevelopmental disorders. Given the acknowledged link between motor difficulties and brain features, it is surprising that so few research studies have systematically explored the brains of children with DCD. The aim of the present review was to ascertain whether it is currently possible to identify a neural signature for DCD, based on the 14 magnetic resonance imaging neuroimaging studies that have been conducted in DCD to date. Our results indicate that several brain areas are unquestionably linked to DCD: cerebellum, basal ganglia, parietal lobe, and parts of the frontal lobe (medial orbitofrontal cortex and dorsolateral prefrontal cortex). However, research has been too sparse and studies have suffered from several limitations that constitute a serious obstacle to address the question of a well-established neural signature for DCD.
After spinal cord injury (SCI), the reorganization of the neuromuscular system leads to increased antagonist muscles' co-activation-that is, increased antagonist vs. agonist muscles activation ratio-during voluntary contractions. Increased muscle co-activation is supposed to result from reduced cortical influences on spinal mechanisms inhibiting antagonist muscles. The assessment of the residual interactions between cortical and muscles activity with corticomuscular coherence (CMC) in participants with SCI producing different force levels may shed new lights on the regulation of muscle co-activation. To achieve this aim, we compared the net joint torque, the muscle co-activation and the CMC ~ 10 and ~ 20 Hz with both agonist and antagonist muscles in participants with SCI and healthy participants performing actual isometric elbow flexion contractions at three force levels. For all participants, overall CMC and muscle co-activation decreased with the increase in the net joint torque, but only CMC ~ 10 Hz was correlated with muscle co-activation. Participants with SCI had greater muscle co-activation and lower CMC ~ 10 Hz, at the highest force levels. These results emphasize the importance of CMC as a mechanism that could take part in the modulation of muscle co-activation to maintain a specific force level. Lower CMC ~ 10 Hz in SCI participants may reflect the decreased cortical influence on spinal mechanisms, leading to increased muscle co-activation, although plasticity of the corticomuscular coupling seems to be preserved after SCI to modulate the force level. Clinically, the CMC may efficiently evaluate the residual integrity of the neuromuscular system after SCI and the effects of rehabilitation.
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