Precision Sensorimotor Control and Brain Network Activity in ASD
Objectives: We will update behavioral and functional MRI (fMRI) results on neural processes associated with sensorimotor deficits in ASD.
Methods: Individuals with ASD aged 10-35 years and age-matched controls completed three task-based functional MRI (fMRI) studies. For each study, participants completed visuomotor tasks in which they pressed with their thumb and index finger on a force transducer while viewing a white FORCE bar on a screen that moved upwards with increased force toward a fixed green TARGET bar. Participants were instructed to maintain the FORCE bar at the level of the TARGET bar for 26 seconds. For study 1 (force level study), 20 participants with ASD and 15 controls pressed with their right hand at 20 and 60% of their maximum force. For study 2 (visual gain study), a separate 25 individuals with ASD and 22 controls pressed with their right hand at 15% of their maximum force across three different visual feedback gain levels. At higher visual gains, the white FORCE bar moved a greater distance per change in Newtons of force relative to lower gains. For study 3 (laterality study), 10 participants with ASD and 10 controls have completed the fMRI visuomotor tests separately with their right and left hands.
Results: Across studies, individuals with ASD showed greater force variability relative to controls. During the force level fMRI study, individuals with ASD showed greater activation than controls in ipsilateral premotor/motor cortex (M1) and reduced activation of left angular gyrus during force compared to rest. They also showed reduced activation of cerebellar Crus I compared to controls during the higher force condition. During the visual gain study, individuals with ASD showed reduced M1, SPL and anterior cerebellar activation at low gain compared to controls, but increased activation of SPL and cerebellar lobules I-V at high gain. For the laterality study, data collection and analysis are ongoing.
Conclusions: These studies indicate that increased sensorimotor variability in ASD is associated with dysfunction of sensory processing mechanisms supported by posterior parietal cortex and cerebellum. Parietal-cerebellar circuits are involved in the translation of sensory feedback error information into refined motor commands relayed to motor cortex. Increased ipsilateral M1 activation in ASD during sensorimotor control reflected a failure to de-activate ipsilateral motor cortex during manual actions, suggesting a failure to optimally differentiate hemispheric activity for behavioral demands. Together, these results indicate that dysfunction of neural processes involved in translating sensory feedback into precision behavioral output and atypical lateralization of motor cortical control of precision behavior represent significant components of the neurodevelopmental processes associated with ASD.