Aims: Motor dysfunction is common to both autism and Asperger syndrome, but the underlying neurophysiological impairments are unclear. Neurophysiological examinations of motor dysfunction can provide information about likely sites of functional impairment and can contribute to the debate about whether autism and Asperger syndrome are variants of the same disorder or fundamentally distinct neurodevelopmental conditions.We investigated the neurophysiology of internally determined motor activity in autism and Asperger syndrome via examination of movement-related potentials (MRPs). Method: We used electroencephalography to investigateMRPs, via an internally cued movement paradigm, in the following three groups: (1) individuals with high-functioning autism (14 males, one female;mean age 13y 1mo, SD 4y 2mo, range 7y 8mo to 20y 9mo; mean Full-scale IQ 93.40, SD 20.72); (2) individuals with Asperger syndrome (10males, two females; mean age 13y 7mo, SD 3y 9mo, range 8y 11mo to 20y 4mo; mean Full-scale IQ 103.25, SD 19.37), and (3) a healthy control group (13 males, seven females;mean age 14y 0mo, SD 3y 11mo; range 8y 4mo to 21y 0mo; mean Full-scale IQ 114.25, SD 11.29). Results: Abnormal MRPs can reflect disruption of motor-related neural networks involving the basal ganglia, thalamus, and supplementary motor area. There was evidence for abnormal MRPs in autism (e.g. increased post-movement cortical activity, abnormal peak time) but not in Asperger syndrome. Interpretation: The results support basal ganglia, thalamus, and supplementary motor area involvement as a likely source ofmotor dysfunction in autism, and provide further evidence for the neurobiological separateness of autism and Asperger syndrome. © Mac Keith Press 2009.
CITATION STYLE
Enticott, P. G., Bradshaw, J. L., Iansek, R., Tonge, B. J., & Rinehart, N. J. (2009). Electrophysiological signs of supplementary-motor-area deficits in high-functioning autism but not Asperger syndrome: An examination of internally cued movement-related potentials. Developmental Medicine and Child Neurology, 51(10), 787–791. https://doi.org/10.1111/j.1469-8749.2009.03270.x
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