Objectives: The objectives of the current study were two-fold. First, we sought to study unconscious modulation of affective perception across a range of negative emotional expressions. Second, we investigated whether subcortical pathway dysfunction, as revealed by subliminal processing of emotional faces, is evident in individuals with subclinical levels of autistic traits.
Methods: Healthy adults were pre-screened with the Autism Spectrum Quotient for high (H-AQ) or low (L-AQ) levels of autistic traits. Event-related potentials (ERPs) were recorded with a 128 channel HydroCel Geodesic Sensor Net during viewing of subliminal (16 ms) and supraliminal (200 ms) presentations of fearful, sad, and neutral faces, backward-masked by scrambled faces. Participants also completed self-report measures assessing cognitive (Systemizing Quotient) and empathic (Empathizing Quotient) style. Amplitude and latency were extracted for early components modulated by the subcortical processing route (N170, N2/P3 complex) and a subsequent component reflecting higher level processing (P3/N4 complex).
Results: Analyses in progress contrast amplitude and latency of ERP components using repeated measures analysis of variance with within-subjects factors of presentation speed (subliminal/supraliminal), emotion (fearful/sad/neutral), and hemisphere (left/right), as well as a between-subjects factor of group (H-AQ/L-AQ). We predict that, in contrast to L-AQ individuals, H-AQ individuals will fail to exhibit modulation of early ERP components in response to subliminally presented emotional expressions. Correlational analyses will explore interrelationships between neural response and cognitive and empathic characteristics.
Conclusions: Results will elucidate the temporal dynamics of emotional face processing and their relationship to subclinical autistic features. The experimental paradigm is the first to contrast conscious and unconscious processing for negative emotional expressions other than fear. Clarifying the integrity of subcortical face processing mechanisms in individuals without autistic social dysfunction is critical to defining the specificity of processing anomalies in ASD to differentiate between core features and broader characteristics distributed more widely in the population. Evidence of common patterns of function and dysfunction within and without the autism spectrum informs understanding of social processing mechanisms in both typical and atypical development.
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