Christian Kindt, Alyssa Ashton, Jay Homewood, and Catie Nielson, Brigham Young University
Social and Behavioral Sciences
Background: Improved understanding of the neural mechanisms of anxiety in ASD may provide targets for etiological research as well as for better treatment specificity. To date, however, there have been no fMRI studies of such mechanisms. Objectives: We report findings from behavioral and functional neuroimaging studies of potentially atypical function. We hypothesize that such atypical function during extinction of learned fear may contribute to difficulty adapting to changing contexts in ASD and lead to subsequent symptoms of uncertainty and anxiety. Methods: Twenty-one adults with ASD ages 18-29 were compared to healthy controls on a classical conditioning task used by Phelps and colleagues (Hartley et al., 2011) during two functional runs of fear acquisition and two extinction runs. Resulting regions of interest were identified with a 2×2 repeated measures ANOVA comparing diagnostic group (ASD vs. controls) and task condition (threat vs. non-threat stimulus). Results: Analyses revealed greater activation in right amygdala and left insula in controls than ASD for threat compared with non-threat stimuli. ROI analysis across all 4 runs revealed that activation patterns for these ROIs show a statistically significant descrease for the CON group, in contrast to an increase for the ASD group that persists into the extinction period. Left amygdala and right insula showed significantly greater activity in the ASD group compared to controls in final extinction run. Conclusions: fMRI data support that fear learning networks in amygdala and insula are less activated in ASD during fear acquisition, but show increased activation during contexts that should be safe. Rather, they are afraid when they should be feeling safe. We hypothesize that chronic everyday anxiety in many individuals diagnosed with ASD may arise from uncertainty regarding contextual cues for fear versus safety.