by Giuseppe Cossu, Sonia Boria, Cristiana Copioli, Roberta Bracceschi, Virginia Giuberti, Erica Santelli, Vittorio Gallese
Children with Autistic Spectrum Disorders (ASD) are frequently hampered by motor impairment, with difficulties ranging from imitation of actions to recognition of motor intentions. Such a widespread inefficiency of the motor system is likely to interfere on the ontogeny of both motor planning and understanding of the goals of actions, thus delivering its ultimate effects on the emergence of social cognition. Methodology/Principal Findings
We investigate the organization of action representation in 15 high functioning ASD (mean age: 8.11) and in two control samples of typically developing (TD) children: the first one, from a primary school, was matched for chronological age (CA), the second one, from a kindergarten, comprised children of much younger age (CY). We used nine newly designed behavioural motor tasks, aiming at exploring three domains of motor cognition: 1) imitation of actions, 2) production of pantomimes, and 3) comprehension of pantomimes. The findings reveal that ASD children fare significantly worse than the two control samples in each of the inspected components of the motor representation of actions, be it the imitation of gestures, the self-planning of pantomimes, or the (verbal) comprehension of observed pantomimes. In the latter task, owing to its cognitive complexity, ASD children come close to the younger TD children’s level of performance; yet they fare significantly worse with respect to their age-mate controls. Overall, ASD children reveal a profound damage to the mechanisms that control both production and pre-cognitive “comprehension” of the motor representation of actions. Conclusions/Significance
Our findings suggest that many of the social cognitive impairments manifested by ASD individuals are likely rooted in their incapacity to assemble and directly grasp the intrinsic goal-related organization of motor behaviour. Such impairment of motor cognition might be partly due to an early damage of the Mirror Neuron Mechanism (MNM).