Saccadic eye movement abnormalities in autism spectrum disorder indicate dysfunctions in cerebellum and brainstem.
BACKGROUND
Individuals with autism spectrum disorder (ASD) show atypical scan paths during social interaction and when viewing faces, and recent evidence suggests that they also show abnormal saccadic eye movement dynamics and accuracy when viewing less complex and non-social stimuli. Eye movements are a uniquely promising target for studies of ASD as their spatial and temporal characteristics can be measured precisely and the brain circuits supporting them are well-defined. Control of saccade metrics is supported by discrete circuits within the cerebellum and brainstem - two brain regions implicated in magnetic resonance (MR) morphometry and histopathological studies of ASD. The functional integrity of these distinct brain systems can be examined by evaluating different parameters of visually-guided saccades.


METHODS
A total of 65 participants with ASD and 43 healthy controls, matched on age (between 6 and 44-years-old), gender and nonverbal IQ made saccades to peripheral targets. To examine the influence of attentional processes, blocked gap and overlap trials were presented. We examined saccade latency, accuracy and dynamics, as well as the trial-to-trial variability of participants' performance.


RESULTS
Saccades of individuals with ASD were characterized by reduced accuracy, elevated variability in accuracy across trials, and reduced peak velocity and prolonged duration. In addition, their saccades took longer to accelerate to peak velocity, with no alteration in the duration of saccade deceleration. Gap/overlap effects on saccade latencies were similar across groups, suggesting that visual orienting and attention systems are relatively spared in ASD. Age-related changes did not differ across groups.


CONCLUSIONS
Deficits precisely and consistently directing eye movements suggest impairment in the error-reducing function of the cerebellum in ASD. Atypical increases in the duration of movement acceleration combined with lower peak saccade velocities implicate pontine nuclei, specifically suggesting reduced excitatory activity in burst cells that drive saccades relative to inhibitory activity in omnipause cells that maintain stable fixation. Thus, our findings suggest that both cerebellar and brainstem abnormalities contribute to altered sensorimotor control in ASD.
Center for Autism and Developmental Disabilities, University of Texas Southwestern, 5323 Harry Hines Blvd, Dallas, TX 75390-9086 USA.
Lauren M
LM
Schmitt
Department of Psychiatry, University of Illinois at Chicago, 1747 W. Roosevelt Rd (MC 747), Chicago, IL 60608 USA.
Edwin H
EH
Cook
Center for Autism and Developmental Disabilities, University of Texas Southwestern, 5323 Harry Hines Blvd, Dallas, TX 75390-9086 USA ; Centre for Autism Spectrum Disorders, Bond University, Gold Coast, QLD 4229 Australia.
John A
JA
Sweeney
Center for Autism and Developmental Disabilities, University of Texas Southwestern, 5323 Harry Hines Blvd, Dallas, TX 75390-9086 USA ; Departments of Psychiatry and Pediatrics, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9086 USA.
Matthew W
MW
Mosconi
Autism spectrum disorder (ASD); Brainstem; Cerebellum; Eye movement; Saccade; Sensorimotor