The Functional Neuroanatomy of Visuomotor Impairments in ASD

Oral Presentation
Saturday, May 12, 2018: 11:45 AM
Willem Burger Hal (de Doelen ICC Rotterdam)
M. W. Mosconi1, K. E. Unruh1, R. J. Lepping2, Y. Wang3, L. M. Schmitt4, Z. Wang5, S. Lui3, D. E. Vaillancourt6 and J. A. Sweeney7, (1)Kansas Center for Autism Research and Training (K-CART), University of Kansas, Lawrence, KS, (2)Hoglund Brain Imaging Center, University of Kansas, Kansas City, KS, (3)Huaxi MR Research Center (HMRRC), Department of Radiology, West China Hospital of Sichuan University, Chengdu, China, (4)Cincinnati Children's Hospital Medical Center, Cincinnati, OH, (5)Department of Occupational Therapy, University of Florida, Gainesville, FL, (6)Applied Physiology and Kinesiology, University of Florida, Gainesville, FL, (7)Division of Developmental Behavioral and Pediatrics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH
Background: Sensorimotor impairments are common in ASD and associated with worse functional outcomes. We previously documented increased force variability during continuous visuomotor behavior in ASD. Patients’ visuomotor deficits were more severe when the force required or the precision of visual feedback were increased implicating both motor and sensory feedback processes. Characterizing the neural processes associated with visuomotor deficits in ASD will help determine mechanisms of sensorimotor issues and related daily living skills.

Objectives: We will describe new results on neural processes associated with sensory feedback and motor control processes during visuomotor behavior in ASD.

Methods: Individuals with ASD aged 11-30 years and age-matched controls completed three functional MRI (fMRI) studies. For studies 1 and 2, 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, 20 participants with ASD and 15 controls pressed at 20 and 60% of their maximum force. For study 2, a separate 25 individuals with ASD and 22 controls pressed 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, the same participants who performed study 1 completed a resting functional scan.

Results: During study 1, individuals with ASD showed reduced activation of contralateral motor cortex (M1), superior parietal lobule (SPL), and ipsilateral cerebellar lobules V-VI compared to controls. These hypoactivations were more severe at higher force levels. Individuals with ASD also showed greater activation than controls in middle frontal gyrus, supplementary motor area (SMA) and striatum at both force levels. During study 2, reduced M1, SPL and ipsilateral cerebellar activation was seen in ASD relative to controls at low visual gain. At high gain, individuals with ASD showed greater activation than controls in SPL. During rest, reduced SMA and cerebellar ALFF and reduced striatal-cortical and cerebellar-cortical connectivity each were associated with visuomotor deficits in ASD (r’s>.6; p’s<.05 corrected).

Conclusions: These studies indicate that elevated motor variability in ASD is associated with intrinsic alterations of frontal, parietal, striatal and cerebellar function and connectivity. We found that parietal-cerebellar-M1 circuits involved in reactively adjusting motor output in response to visual feedback are underactive and less able to support precise motor behavior in ASD. Elevated frontostriatal activation in ASD suggests that brain systems typically involved in higher-level cognitive control may compensate for visuomotor network underactivity. Greater parietal activation in ASD at high visual gain suggests that deficient motor control during conditions of increased sensory load reflects hyper-reactivity of visual processing brain circuits. Together, these results indicate that atypical neural processes involved in translating sensory feedback into precision behavioral output represents a significant component of the neurodevelopmental processes that cause ASD.