Developmental coordination disorder (DCD) and developmental dyspraxia are often regarded as synonymous. These entities have long remained confusing to clinicians, owing to divergent concepts and lack of precise descriptions. The term DCD was coined in 1987 in the DSM-III-R, and is described as impairment of motor coordination that significantly interferes with activities of daily living and/or academic achievement. The International Statistical Classification of Diseases and Related Health Problems (ICD-10) later stated: ‘It’s usual for the motor clumsiness to be associated with some degree of impaired performance on visuo-spatial cognitive tasks’. Since 1994, following the recommendations of an international consensus conference, the term DCD has been consistently used in research and practice to identify children with mild motor coordination deficits of developmental origin.
Developmental coordination disorder should not be confused with acquired apraxia, seen mainly in adult neurology, although the concept of developmental dyspraxia first emerged with reference to adult apraxia. DCD and acquired apraxia share common features, hence the similarities in some subtype classifications that do not imply similar cerebral involvement. DCD should be distinguished from impairment of the execution of voluntary movement, and should also not be confused with visual or visuoperceptual disorders, which need to be carefully excluded from the diagnosis. Recent systematic studies now allow us to define DCD and identify subtypes of DCD that meet specific clinical criteria.[4, 5] In DCD, motor planning and programming are primarily affected in the absence of any obvious neurological structural abnormality or intellectual and perceptual disability. Three clinical subtypes of DCD can be distinguished: pure ideomotor DCD, pure visuospatial or visuoconstructional DCD, and mixed DCD including features of ideomotor and visuospatial/constructional DCD with additional comorbidities.[5, 6] This recent refinement of the clinical descriptions supports new integrative pathophysiological models and suggests a dysfunction in the cerebello-cerebral network or basal ganglia–thalamocortical circuits. Nevertheless, the neural correlates of DCD remain largely unknown.
Eye movement recordings are used increasingly in clinical neuroscience and are now a routine examination for several neurological conditions in adults. They allow for clinical and neuro-anatomical correlations and help better understanding of the pathophysiology of diseases. In the paediatric field, such recordings have been used less commonly, owing to technical difficulties; however, they have been proved to be feasible.[9-11]
Smooth pursuit eye movements are continuous eye movements that ‘keep the line of regard congruent with the line of interest’. They mature throughout childhood and adolescence. Pursuit studies in children, therefore, require normative data in similar age groups, which have been obtained in a recent study. As motor skills are impaired, impaired oculomotor performance would also be expected in children with DCD, especially with pursuit eye movements, which ‘have the character of habitual movements’. While quantification of global motor skills is difficult, oculomotor performance can be quantitatively assessed, offering new insights on this condition.
A previous study on eight children with DCD showed a reduced velocity gain for horizontal pursuit relative to aged-matched comparison participants. To the best of our knowledge, these results on a small cohort have not been replicated, nor have they been extended to vertical pursuit characteristics.
The purpose of this study was to compare the characteristics of both horizontal and vertical smooth pursuits in children with DCD with age-matched comparison participants without DCD.
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This study is the first to show that in children with DCD aged 7 to 12 years, vertical pursuit is significantly impaired relative to children without DCD. It failed, however, to demonstrate a statistically significant difference in horizontal pursuit, as was the case in a previous study in a smaller population.
One of the reasons for this could be the younger age of the children (5–7y) in the study by Langaas et al. In typical development, horizontal smooth pursuit is mature by the age of 7 years, while vertical smooth pursuit is not mature until late adolescence. If one hypothesizes that children with DCD exhibit a delayed maturation of both pursuit systems, this delay could be picked up at different ages according to the type of pursuit studied: before the age of 7 years for horizontal pursuit and between 7 year and 12 years for vertical pursuit. As the diagnosis of DCD is usually not formally confirmed before the age of 7 years, vertical pursuit studies might appear more relevant for practical purposes. Another reason for this difference could be that the children's phenotype may have been more severe in the study by Langaas et al., as suggested by their young age at diagnosis. The main limitation of the present study is its cross-sectional nature. A longitudinal study would clarify whether this alteration of vertical pursuit in DCD is due to a delayed maturation or a definite abnormality of vertical pursuit.
Recent research allows for more refined hypotheses concerning the pathophysiology of DCD, which suggest a specific disruption of the predictive control of action. Motor adaptation studies suggest cerebellar dysfunction in DCD.[8, 19, 20] Other anatomical structures potentially involved in DCD are the parietal lobe, the corpus callosum, and the basal ganglia. Smooth pursuit is a complex, non-reflexive, conscious function under the control of numerous cerebral structures: the cerebellum, pontine nuclei, central thalamus, medial superior temporal cortex, caudal frontal eye field, and the supplementary eye field. A few studies have specifically investigated the development of smooth pursuit tracking in children.[10, 21-25] Smooth pursuit alteration can result from the dysfunction of many anatomical structures and is encountered in a large variety of neurological and psychiatric diseases. Little is known, however, about delayed maturation of the pursuit system, which may result from distinct processes and can also be observed in children born preterm.[13, 26] Clinically, poor pursuit gains often result from cerebellar or cerebello-cerebral network dysfunctions. Low pursuit indices as found in this study are part of the cerebellar syndrome and are definitely consistent with the hypothesis of a cerebellar involvement in DCD. Yet it has also been hypothesized that visual selective attention, which is probably mediated by the dorsolateral prefrontal cortex, is one of the driving factors in adaptive changes for smooth pursuit.[27, 28] Poor pursuit may, therefore, also result from altered inputs, such as poor visual attention. Impaired ocular pursuit results from similar mechanisms such as impaired non-ocular coordinated movements. It also, in turn, has itself a negative impact on many visually guided coordinated movements; as such, it can be considered as part of a vicious motor impairment circle in DCD.
Intervention is often proposed for these children; however, its nature, pathophysiological bases, and effects are controversial. A few studies have evaluated intervention in DCD; the two main approaches are often referred to as process oriented (e.g. sensory integration and kinaesthetic training) and task oriented (or motor skill intervention). Based on a recent combined systematic review and meta-analysis, Smits-Engelsman et al. concluded that there is evidence only to support task-oriented intervention. In the present study, some children had previously received intervention, but its modalities had been heterogeneous. We chose not to exclude these children, as the usual population of children diagnosed with DCD now comprises many children who have already received intervention. It is, therefore, difficult to draw conclusions regarding the underlying mechanisms of the more accurate vertical pursuit demonstrated in the intervention subgroup, as well as regarding the efficiency of intervention on DCD itself, as oculomotor abnormalities are only one of the various clinical indicators of DCD. This improvement may either reflect the direct effect of intervention itself on oculomotor functions or result from a general improvement in DCD. In adults, simple, short visual training sessions induce significant, lasting improvements in smooth pursuit performance. Adult patients with such improved smooth pursuit performance then better adapt to vestibular dysfunction, as improving one of the preserved inputs of a multisensory process, such as orientation in space, helps to compensate for the deficient input. If oculomotor markers, such as the SPG index used in this study, are proved to be correlated with the severity of DCD, they could become, as for many neurological diseases in adulthood, a useful tool in the initial and longitudinal assessment of children with DCD. The effects of intervention on ocular pursuit, and hence in DCD, would also be better appreciated in an ongoing large, prospective, longitudinal study.