Empathy in ASD: Using ERPs to Identify Atypical Neural Responses to Physical and Social Pain

Background: Neuroimaging studies have revealed specific brain systems subserving empathic processing. Research in typical development (TD) indicates that observed physical and social pain evoke distinct affective and cognitive empathic responses in neural circuitry. Our prior work in TD revealed event-related potential (ERP) biomarkers for empathic processing: a rapid negative peak (N110) and a later positive deflection (P3) were associated with affective sharing and cognitive evaluation of pain, respectively. In addition, these biomarkers were modulated by autistic traits. The current research applies these findings to autism spectrum disorder (ASD) and investigates, for the first time, mu wave suppression, an index of mirror neuron system function, as a marker of empathic response to social pain.

Objectives: Using EEG and ERPs, the current study aims to: (i) differentiate the temporal dynamics of brain response to physical and social pain in TD and ASD adults; (ii) examine group differences in suppression of mu wave activity in response to observing others’ pain; and (iii) identify relationships among empathic characteristics, social functioning, and neural response to observed social pain. We predicted atypical embodied and cognitive empathic responses to both physical and social pain in ASD, reflected in changes in N110 and P3 responses. In addition, we expected attenuated mu suppression in ASD relative to TD. We hypothesized that trait empathy and social functioning would correlate with neural response to social pain.

Methods: Participants were 20 adult males with ASD and 20 age-matched TD adult males. EEG was recorded with a 128-electrode Hydrocel Geodesic Sensor net. Participants viewed dynamic and static images of social versus physical pain presented in four counter-balanced blocks; attention to pain was manipulated with an empathic versus distractor task. In each block, 50% of stimuli were painful and 50% were analogous but painless. Empathic traits and social functioning were measured using the Empathy Quotient (EQ) and Social Responsiveness Scale Adult Self-Report (SRS-A-SR). ERPs and oscillatory EEG activity were extracted for each condition at central leads (C3/C4). 

Results: ERP results indicated (i) increased N110 amplitude in response to painless stimuli in ASD compared to TD (p=.001), (ii) marginally longer right hemisphere P3 latency in response to social versus physical pain in ASD (p=.059) but not in TD (p>.05), and (iii) shorter right hemisphere P3 latency to physically painful stimuli in ASD versus TD (p=.012). Greater amplitudes to social versus physical pain at N110 and at P3 correlated with increased social responsiveness within the ASD population and trait empathy across groups (ps=.030 and .002, respectively).

Conclusions: Individuals with ASD display distinct brain responses to social versus painful stimuli relative to TD counterparts. These differences were evident in neural markers of both affective and cognitive empathic responses. Notable differences were also observed in neural response to social and physical pain between groups; these changes correlated with empathic traits, which were characteristically diminished in ASD. The present results help to explain variability in social empathic behavior in ASD and inform targeted intervention strategies focused on affective response versus cognitive awareness of social pain.