Associations of Postural Knowledge and Basic Motor Skill With Dyspraxia In Autism: Implication for Abnormalities in Distributed Connectivity and Motor Learning

Background: Children with autism often have difficulty performing skilled movements. This “dyspraxia” remains significant after accounting for basic motor skill deficits (Dziuk et al., 2007). Performance of skilled movements also requires knowledge of spatial and temporal representations of the movement, mediated by parietal regions, and transcoding of these spatial representations into movement plans, mediated by premotor circuits. Objectives: The goals of this study were: (1) to determine whether autism is associated with impaired representational knowledge of skilled movements (“postural knowledge”) and (2) to examine the combined contributions of postural knowledge and basic motor skill to dyspraxia in autism. Methods: 34 children with HFA and 37 typically-developing (TD) children, ages 8-13, completed: (1) a postural knowledge test (PKT), a praxis discrimination test assessing knowledge of transitive/intransitive postures (2) a childhood examination of basic motor skills (the PANESS), and (3) a praxis examination including gestures to command, imitation, and tool-use. Results: Children with HFA showed worse postural knowledge than TD controls (F=5.350, p=.02). Hierarchical regression further revealed, that after controlling for age and IQ, both basic motor skill (ΔR2=.11 p=.004) and postural knowledge (ΔR2=0.16 p<0.0001) were significant predictors of praxis performance; nevertheless, the HFA group continued to show significantly poorer praxis than controls after accounting for these abilities (ΔR2=0.19, p<0.0001). Conclusions: The findings suggest that dyspraxia in autism is associated with both impaired formation of spatial representation, as well as transcoding and execution, of skilled movements. This would be consistent with a model in which distributed abnormality across parietal, premotor and motor circuitry, and/or connectivity between these regions, contributes to dyspraxia in autism. The findings might also be explained by a developmental model in which impaired acquisition (learning) leads to anomalous formation of both spatial and motor representations of skilled movements, as well as impaired execution.