Decreased connectivity and cerebellar activity in autism during motor task performance.
Although motor deficits are common in autism, the neural correlates underlying the disruption of even basic motor execution are unknown. Motor deficits may be some of the earliest identifiable signs of abnormal development and increased understanding of their neural underpinnings may provide insight into autism-associated differences in parallel systems critical for control of more complex behaviour necessary for social and communicative development. Functional magnetic resonance imaging was used to examine neural activation and connectivity during sequential, appositional finger tapping in 13 children, ages 8-12 years, with high-functioning autism (HFA) and 13 typically developing (TD), age- and sex-matched peers. Both groups showed expected primary activations in cortical and subcortical regions associated with motor execution [contralateral primary sensorimotor cortex, contralateral thalamus, ipsilateral cerebellum, supplementary motor area (SMA)]; however, the TD group showed greater activation in the ipsilateral anterior cerebellum, while the HFA group showed greater activation in the SMA. Although activation differences were limited to a subset of regions, children with HFA demonstrated diffusely decreased connectivity across the motor execution network relative to control children. The between-group dissociation of cerebral and cerebellar motor activation represents the first neuroimaging data of motor dysfunction in children with autism, providing insight into potentially abnormal circuits impacting development. Decreased cerebellar activation in the HFA group may reflect difficulty shifting motor execution from cortical regions associated with effortful control to regions associated with habitual execution. Additionally, diffusely decreased connectivity may reflect poor coordination within the circuit necessary for automating patterned motor behaviour. The findings might explain impairments in motor development in autism, as well as abnormal and delayed acquisition of gestures important for socialization and communication.
Mostofsky
Stewart H
SH
Kennedy Krieger Institute, Baltimore, MD 21205, USA. mostofsky@kennedykrieger.org
Powell
Stephanie K
SK
Simmonds
Daniel J
DJ
Goldberg
Melissa C
MC
Caffo
Brian
B
Pekar
James J
JJ
D001321:Autistic Disorder / Q000503:physiopathology* / Q000523:psychology; D001931:Brain Mapping / Q000379:methods; D016022:Case-Control Studies; D002531:Cerebellum / Q000503:physiopathology*; D002648:Child; D005260:Female; D005385:Fingers / Q000503:physiopathology; D006801:Humans; D007858:Learning / Q000502:physiology; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D009044:Motor Cortex / Q000503:physiopathology; D009068:Movement / Q000502:physiology*; D009434:Neural Pathways / Q000503:physiopathology; D011597:Psychomotor Performance / Q000502:physiology*; D013788:Thalamus / Q000503:physiopathology