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ERPs Reveal Atypical Neural Response During Empathy for Physical and Social Pain in ASD

Friday, 3 May 2013: 14:00-18:00
Banquet Hall (Kursaal Centre)
C. Mukerji1, A. Naples1, R. Bernier2, R. Tillman3, D. Perszyk4 and J. C. McPartland1, (1)Yale Child Study Center, New Haven, CT, (2)University of Washington, Seattle, WA, (3)Child Study Center, Yale University, New Haven, CT, (4)Northwestern University, Evanston, IL
Background: Empathy is a fundamental social ability affected in autism spectrum disorder (ASD). Study of motor-evoked potentials has suggested reduced embodied empathy during physical pain observation in ASD. Neuroimaging studies in typical development (TD) have indicated that empathy for social pain recruits both distinct mentalizing networks and emotion-encoding regions involved in empathy for physical pain. Our work in TD revealed that autistic traits modulated event-related potential (ERP) markers of empathic processing for both physical and social pain: a rapid negative peak (N110) and a later positive deflection (P3) associated with affective sharing and cognitive evaluation, respectively. Despite its relevance to social function, neural empathic response to social pain in ASD remains unexplored. 

Objectives: This study employed ERPs to (a) contrast temporal dynamics of empathy for physical and social pain in adults with ASD and TD and (b) explore relationships among neural responses to observed social pain, empathic traits, and social function in ASD. We predicted ERPs would reveal atypical affective response to both physical and social pain at the N110 and slower cognitive appraisal of social pain at the P3 in ASD. Social function and trait empathy were hypothesized to correlate with enhanced neural response to social pain in ASD.  

Methods: Participants included 20 adult males with ASD and 20 age- and sex-matched TD controls. Empathic traits and social function were measured using the Empathy Quotient (EQ) and Social Responsiveness Scale (Adult Self-Report; SRS-A-SR). EEG was recorded with a 128-electrode Hydrocel Geodesic Sensor net while participants viewed dynamic and static stimuli displaying hands in physically painful, socially painful, or painless contexts. Participants performed an empathic task (rate distress) or a distractor task (count bracelets). ERPs were extracted for each condition at central leads (C3/C4). 

Results: Preliminary results from a subsample (TD: N=14; ASD: N=7) revealed (a) enhanced N110 amplitude to painful actions in ASD (p=.004) but not in TD (p=.766) and (b) delayed P3 peak latency for social actions in the right hemisphere in ASD (p=.018) but not in TD (p=.207). In addition, social impairment in ASD correlated with N110 amplitude differentiation between observed physical and social pain (r=-.801, p=.030) during the rating task, such that higher social function was associated with enhanced response to social relative to non-social pain. Empathic traits in the subsample correlated with P3 amplitude differentiation between observed physical and social pain (r=-.503, p=.020), such that higher trait empathy was associated with greater amplitude to social relative to non-social pain.  

Conclusions: ERPs revealed disruption of neural mechanisms for regulating affective response to observed pain and a specific delay in neural processing of actions during cognitive empathy in ASD. Empathy was associated with greater salience of social pain during cognitive appraisal across diagnostic categories, affirming the specific importance of neural response to observed social pain to empathic function. Lastly, enhanced salience of social relative to physical pain at the affective stage of processing was associated with overall social function in ASD, indicating emotional sharing as a critical target for intervention and research in this population.

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