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.

Developmental coordination disorder (DCD) is a common and well-recognized neurodevelopmental disorder affecting approximately 5 in every 100 individuals worldwide. It has long been included in standard national and international classifications of disorders (especially the Diagnostic and Statistical Manual of Mental Disorders ). Children and adults with DCD may come to medical or paramedical attention because of poor motor skills, poor motor coordination, and/or impaired procedural learning affecting activities of daily living. Studies show DCD persistence of 30–70% in adulthood for individuals who were diagnosed with DCD as children, with direct consequences in the academic realm and even beyond. In particular, individuals with DCD are at increased risk of impaired handwriting skills. Medium-term and long-term prognosis depends on the timing of the diagnosis, (possible) comorbid disorders (and their diagnosis), the variability of signs and symptoms (number and intensity), and the nature and frequency of the interventions individuals receive. We therefore chose to investigate the signs and symptoms, diagnosis, and rehabilitation of both DCD and developmental dysgraphia, which continues to receive far too little attention in its own right from researchers and clinicians.

There is a general consensus that developmental coordination disorder (DCD) is characterized by impaired motor learning skills. However, actual studies of motor learning in DCD are scarce and, above all, inconsistent. The aims of the present study were therefore to explore the presumed presence of a motor learning deficit among individuals with DCD and to provide a synopsis of the current literature on motor learning in DCD. We begin by defining DCD (etiology, neuropsychology, and brain bases), motor learning (measurement of learning, methods for promoting skill acquisition, scheduling, practice, retention, and feedback) and, of course, the link between the two, focusing on the issue of a possible motor learning deficit in DCD. We then discuss dominant hypotheses and suggest directions for future research in this domain, in the light of research conducted thus far. Particular attention is paid throughout to guide the choice of intervention approaches.

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Developmental dyslexia (DD) and developmental coordination disorder (DCD) co-occur frequently, raising the underlying question of shared etiological bases. We investigated the cognitive profile of children with DD, children with DCD, and children with the dual association (DD + DCD) to determine the inherent characteristics of each disorder and explore the possible additional impact of co-morbidity on intellectual, attentional, and psychosocial functioning. The participants were 8- to 12-year-olds (20 DD, 22 DCD, and 23 DD + DCD). Cognitive abilities were assessed by the Wechsler Intelligence Scale for Children - Fourth Edition (WISC-IV) and the Continuous Performance Test - Second Edition (CPT-II) and behavioral impairments were evaluated by the Child Behavior Checklist (CBCL). No differences were found between the three groups on attention testing (CPT-II) or psychosocial characteristics (CBCL), but a higher percentage of DD + DCD children had pathological scores on psychosocial scales. Significant between-group differences were observed on Processing Speed Index scores and the block design and symbol search subtests, where DD children fared better than DCD children. No significant differences were evident between the co-morbid vs. the pure groups. Our results clearly show significant differences between children with DD only and children with DCD only. In particular, visuo-spatial disabilities and heterogeneity of intellectual profile seem to be good markers of DCD. However, it should be noted that despite these distinct and separate characteristics, a common cognitive profile (weaknesses and strengths) is likely shared by both neurodevelopmental disorders. Surprisingly, concerning co-morbidity, DD + DCD association is not associated with a decrease in intellectual or attentional capacities.