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Abstract
Individuals with autism spectrum disorders (ASDs) have marked impairments in social-emotional reciprocity and social cognition. Deficits in theory of mind (ToM) and social motivation, including disruptions to emotion processing and neural networks, have been proposed as potential underlying mechanisms, however inconsistencies remain. The aim of the present thesis was to utilise specific methodologies to examine the veracity of these hypotheses in a sample of high-functioning adults with ASDs. Ecological validity was pertinent to the investigation of higher-order social cognition in Study 1, and confirmed that individuals with ASDs have significantly impaired advanced ToM (comprehension of sarcasm and lies/deception) while their simple ToM abilities remain intact (comprehension of sincere interactions). Subsequently, psychophysiological measures (skin conductance (SCR, SCL), cardiac responses (ECD, ECA) and facial muscle movements (electromyography; EMG)) were employed to investigate emotional engagement and allocation of significance to neutral faces (Study 2), emotional faces (Study 3), and affective scenes (Study 4). Results consistently demonstrated that SCRs to socially-relevant stimuli are atypical in ASDs, reflective of atypical orienting and allocation of attention. Facial EMG responses were impaired to emotional faces but intact to extreme, highly arousing pleasant and unpleasant stimuli. Collectively, these results highlight specific disruptions in social motivational responses whilst primitive motivational drive appears intact. Importantly, these findings cannot be attributed to a failure to register or detect socially-relevant stimuli, as initial ECD responses were also intact. As well as these implications for the social motivation hypothesis, it also emerged that deficits in cognitive and affective empathy may account for deficits in ToM and (physiological) emotional responsivity, respectively. Finally, Study 5 found that differences in resting arousal (SCL) may account for some of the behavioural variation in ASDs. These findings support past literature suggesting deficits in neural networks in ASDs associated with social cognitive processing and psychophysiological processes, particularly the amygdala, orbitofrontal cortex, anterior cingulate cortex and insula. Important clinical implications include increasing emotional engagement and allocation of significance, as well as individually targeting interventions to resting arousal levels.