Individuals with autism spectrum disorder (ASD) and individuals with conduct disorder (CD) are characterized by notable impairments in social-emotional functioning. In this thesis social-emotional... Show moreIndividuals with autism spectrum disorder (ASD) and individuals with conduct disorder (CD) are characterized by notable impairments in social-emotional functioning. In this thesis social-emotional impairments were investigated using a cognitive neuroscience perspective (i.e., studying cognitive mechanisms and associated neural processes and structures). First, we directly compared groups of ASD and CD to test the hypothesized dissociable deficits in understanding other’s emotions in ASD in contrast to deficits in feeling other’s emotions in CD. This was done by comparing brain activity during basic emotion processing to assess cognitive and affective aspects of empathy, and by comparing white matter tracts that may underlie social-emotional processing. Second, we examined the neural processes at the level of social interactions in ASD and in CD, which has been overlooked by prior work, by studying interactive decision-making in response to other’s emotions. The results of the first part of this thesis show that different neural mechanisms underlie social-emotional difficulties in ASD and CD. Results of the second part imply that uncovering the neural correlates of interacting with others might lead to refined models of social-emotional deficits in ASD and CD that are different from previous accounts based on merely observing other’s emotions. Show less
The work presented in this thesis provides important new clues on the neurobiology of juvenile psychopathic traits in clinically antisocial juveniles. The data specifically shows that these... Show moreThe work presented in this thesis provides important new clues on the neurobiology of juvenile psychopathic traits in clinically antisocial juveniles. The data specifically shows that these traits are ostensibly underpinned by highly specific corticolimbic network dysfunctions, in which amygdala subregional networks seem particularly relevant. That data additionally suggests that some of these network dysfunctions and their associated neurocognitive deficits are possibly driven by alterations in the oxytocinergic system. Interestingly, the data also provides preliminary neurobiological support for the scientific utility of using juvenile psychopathic traits to subtype the highly heterogeneous group of clinically antisocial teens. While these data may represent important new steps towards a deeper understanding of clinical youth antisociality, their significance has to be evaluated by replication studies that further explore and validate the findings presented here. Show less
