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The Neurobiology of Emotion Regulation Problems and Co-Occurring Anxiety in ASD
There is a growing recognition that emotion regulation difficulties are common in ASD, resulting in increased symptoms of anxiety. However, the neurobiology of emotion regulation problems in ASD has yet to be fully examined. Data from non-ASD samples suggest that this examination will point to brain systems that we already know function differently in ASD, but are seldom interpreted in terms of emotion regulation. This is particularly true of prefrontal cortex (PFC), where decades of affective neuroscience research have implicated cognitive control structures in the regulation of emotion. This presentation examines data from two functional MRI studies that associate anxiety deficits with abnormal PFC function in ASD.
Objectives: To examine the role of cognitive control (PFC) regions in youth diagnosed with co-occurring anxiety and ASD.
Methods: Both fMRI studies used face-processing tasks that are known to elicit activity in emotion and emotion regulation structures. The first study (N = 81 ASD, 67 control, mean age = 12.5 years) follows a dimensional approach, examining the relationship between anxiety symptoms (measured via the Screen for Child Anxiety Related Emotional Disorders) and PFC function in ASD. The second study follows a categorical approach, including ASD samples with formal anxiety disorder diagnoses (established via the Anxiety Disorder Interview Schedule; n = 15), and without (n = 13). ASD diagnoses were made following a developmental interview with parents and administration of the Autism Diagnostic Observation Schedule.
Results: Both dimensional and categorical approaches strongly associated increased anxiety in ASD with increased activation in multiple portions of PFC, including both dorsal and ventral medial PFC, superior frontal gyrus, and the frontal poles (see Fig. 1 for an illustration of the frontal pole activation). Although ASD studies often interpret activation in many of these regions in terms of mentalizing abilities, they also have known relationships with cognitive control. Given the direction of the results (i.e., increased PFC activity in ASD with anxiety), interpretations of findings in terms of anxiety and emotion regulation seem more parsimonious than those related to mentalizing. Post hoc analyses indicated that the findings from these studies cannot be attributed to differences in core ASD symptoms or intellectual level.
Conclusions:
Findings of altered PFC function in ASD may be best accounted for by models of emotion regulation that integrate cognitive control processes. The direction of effects (increased PFC activation) suggests that individuals with ASD and increased anxiety symptoms are over-engaging brain systems involved in cognitive control and emotion regulation. Future research should explore whether this increase is a compensatory response for increased levels of negative affect, or possibly inefficient communication between PFC and other emotion structures (i.e., amygdala).