Neural Mechanisms of Social Prediction Errors in Adolescents with ASD
Objectives: To compare blood oxygen level dependent (BOLD) signals among adolescents with and without ASD during a social prediction error task.
Methods: The sample included 41 12-to-17-year-olds: 21 with high-functioning ASD and 20 with typical development (TD). Prior to the scan, participants were taught to press a “check” every time they saw a symbol (i.e., “cue 1”) that predicted a clear image and an “x” every time they saw a different symbol (i.e., “cue 2”) that predicted a blurry image. In the scanner, participants saw images of smiling faces (i.e., social reward) or blurry faces (i.e., non-reward) across two 7-minute runs. In 20% of trials, the images violated expectations (i.e., “cue 1” predicted a blurry face, rather than a clear face as expected; “cue 2” predicted a clear rather than blurry face). Analyses focused on group differences with respect to the contrast between expected and unexpected reward outcomes, which are known to elicit prediction error signals in the midbrain, striatum, and prefrontal cortex (Ramnani, Elliott, Athwal, & Passingham, 2004),
Results: Data collection is complete and analysis is ongoing. Preliminary analyses found that the TD group demonstrated increased activation in the right inferior frontal gyrus compared to the ASD group when expectations were violated, whereas the ASD group demonstrated increased activation in the right frontal pole. When outcomes were as expected, the TD group demonstrated increased activation in the right frontal pole, whereas the ASD group exhibited increased activation in the left inferior frontal gyrus. Ongoing analyses will examine functional connectivity differences between groups, as well as relations between brain imaging metrics, task related behavior, and ASD symptom severity.
Conclusions: Preliminary results indicate differential activation in prefrontal cortical regions that are critical for eliciting prediction error signals in adolescents with ASD. These differences may provide a mechanistic account of disrupted social reward learning in ASD and contribute to the literature addressing reward processing deficits in ASD.
See more of: Brain Function (fMRI, fcMRI, MRS, EEG, ERP, MEG)