A Longitudinal Study of Emotion Processing in ASD and the Relation with Other Clinical Symptoms: The Cpea Early Development Study of Autism

Thursday, May 15, 2014: 2:20 PM
Imperial A (Marriott Marquis Atlanta)
K. M. Burner1, L. J. Sterling2, J. Munson3, A. M. Estes4, G. Dawson5 and S. J. Webb6, (1)Seattle Children's Hospital, Seattle, WA, (2)Psychiatry, UCLA Semel Institute for Neuroscience & Human Behavior, Los Angeles, CA, (3)University of Washington, Seattle, WA, (4)Speech and Hearing Sciences, University of Washington, Seattle, WA, (5)Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC, (6)Psychiatry and behavioral sciences, University of Washington, Seattle, WA
Background:  Behavioral and psychophysiological research suggests that emotion processing is impaired in individuals with autism spectrum disorder (ASD). Underlying neural abnormalities in emotion processing may contribute to the variability in social-emotion functioning in children with autism and negatively influence social interactions and the maintenance of social relationships. However, conditions associated with autism such as anxiety and depression are known to influence emotional processing and hyperarousal to emotional stimuli has been proposed as a risk marker for later elevated symptoms in these domains.

Objectives:  N/A.

Methods:  Participant groups included children who met criteria for ASD at 3-4 years of age and controls (children with neurotypical development and children with developmental delay). Participants were followed longitudinally at age 3, 6, 9 and 15 years of age in the CPEA Early Development Study. Electrophysiological data (using a high density EEG array) was collected during processing of fearful faces and a control face stimulus (neutral or happy faces) at 3, 6 and 9 years of age. Diagnostic, Cognitive, and Face Memory data was available for time points 3-9 years and parent report of internalizing symptoms (via CBCL) was available at 9 and 15 years.

Results:  Using event-related potentials, at 3-4 years of age, children with ASD demonstrated delays in fear processing that are related to social ability, including social orienting, and response to distress. Delays in processing speed were also found at 6 years of age. However, by 9 years of age, as a group, the children with ASD did not differ in their responses to fear faces, neither in amplitude nor speed of the ERP components. Responses at 9 were related to internalizing symptoms, with increased amplitude responses correlated with higher scores. By 15 years, the ASD group reported higher levels of internalizing symptoms. Discussion will focus on both group trajectories in fear processing and later ASD and internalizing symptom levels. The role of early hyper- or hypo-processing of fear may be a risk factor for less optimal outcomes.

Conclusions:  The CPEA Early Development longitudinal Study provides an opportunity for examining very early processing of fear stimuli, assessed through event – related potentials, in children with ASD and control groups embedded in a rich background of information about diagnostic, cognitive and psychological functioning.  This work suggests that early emotion processing vulnerabilities in children with ASD play a role in later social communicative outcomes but also may be related to the susceptibility for internalizing disorders.  Understanding how basic processing of fear is related to larger social constructs may inform our understanding of mechanisms that contribute to the heterogeneity in functioning.