Psychophysical Correlates of Excitatory/Inhibitory Imbalance during Visual Motion Perception in Adults with ASD and Schizophrenia

Friday, May 13, 2016: 11:30 AM-1:30 PM
Hall A (Baltimore Convention Center)
B. D. Adkinson1,2, J. H. Foss-Feig3, W. J. Park4, E. J. Levy5, N. Santamauro6, C. Schleifer7, K. B. Schauder8, K. Deckert5, V. Srihari6, J. Krystal9, D. Tadin4, J. McPartland3 and A. Anticevic6, (1)Department of Psychiatry, Yale School of Medicine, New Haven, CT, (2)Marietta College, Marietta, OH, (3)Child Study Center, Yale School of Medicine, New Haven, CT, (4)Brain and Cognitive Sciences, University of Rochester, Rochester, NY, (5)Yale Child Study Center, New Haven, CT, (6)Yale University School of Medicine, New Haven, CT, (7)Yale University, New Haven, CT, (8)Clinical and Social Sciences in Psychology, University of Rochester, Rochester, NY, (9)Yale University - Psychiatry, New Haven, CT
Background: Recent evidence implicates neural excitatory (E) and inhibitory (I) imbalance as a mechanistic underpinning of autism spectrum disorder (ASD). E/I imbalance is also implicated in other disorders, such as schizophrenia (SZ), that are associated with social and cognitive deficits. While phenotypic similarities across diagnoses suggest common mechanistic origins, no studies have tested the existence of shared markers of E/I imbalance across ASD and SZ. Surround suppression and gain control are two well-established neural processes affecting perception of visual motion that rely on precise E/I balance. Previous studies examining visual motion processing in ASD and SZ have identified surround suppression and gain control abnormalities. However, none of these studies directly compared these processes across both populations.

Objectives: Evaluate E/I balance in the context of surround suppression and gain control affecting visual motion perception in young adults with ASD relative to SZ and healthy controls.

Methods: Participants were 10 young adults with ASD, 9 with SZ, and 14 healthy controls, matched for demographic variables. Recruitment is ongoing with expected final sample sizes of 20 per group. Participants completed three visual processing tasks that involved motion discrimination of gratings that varied by size at high (Task 1) and low (Task 2) contrast, as well as gratings with fixed, small size but varied contrast level (Task 3). Task order was counterbalanced across participants. Duration thresholds were computed for eight different sizes and contrasts. Suppression index (Tasks 1 and 2) and response gain control (Task 3) were computed by contrasting thresholds at the highest level of contrast/largest size to those at the lowest contrast level/smallest size for each task. Group differences were assessed using one-way ANOVAs.

Results: Results revealed few differences between groups in duration thresholds across contrast levels or sizes. Contrary to predictions, response gain control did not differ among ASD, SZ, or controls (F=.070, p=.93). Likewise, at high contrast, the suppression index did not differ by group (F=.556, p=.58). However, at low contrast, there were group differences in suppression index (F=4.378, p=.023), wherein, relative to controls, SZ, but not ASD, was characterized by an unexpected increase in spatial suppression.

Conclusions: Contrary to predictions, differences in surround suppression for high contrast stimuli and gain control with increasing contrast during motion discrimination were not observed in ASD or SZ relative to controls. Moreover, an unexpected increase in suppression was observed at low contrast for SZ participants. These data suggest that, at least in the context of low-level visual motion processing, young adults with ASD and SZ may have intact E/I balance. Transdiagnostic correlations with measures of sensory, social, and cognitive functioning are ongoing to quantify if deficits in surround suppression and gain control are associated with symptoms that cross traditional diagnostic categories.