This project has established a series of core neuro-biological findings regarding the basis of Conduct Disorder (CD). Over the past year, we have particularly concentrated on forms of function that are compromised in youth with CD and then examined what specific symptom sets are consequent on these forms of dysfunction. In our previous work, we have shown that youth show reduced amygdala responses to the distress of others. This year we have continued this work revealing that patients with CD show reduced amygdala (and connected structure) responses to not only other forms of negative stimuli but also animate stimuli. The amygdala is importantly involved in responding to animacy information as well as emotional information. Children with CD are compromised in both functions and thus show more widespread amygdala dysfunction that previously identified. Notably, both forms of impairment relates to the level of Callous Unemotional symptomatology (i.e., levels of reduced guilt and empathy). Youth with CD show elevated levels of retaliation to social provocation. We examined the neural substrates mediating retaliatory behavior in both healthy youth and youth with CD. We particularly noted that ventromedial prefrontal cortex plays an important modulatory role in the selection of retaliatory responses to social provocation. Youth with CD show impairment in this modulatory role. Moreover, level of impairment in this modulatory role relates to the level of reactive aggression shown by youth with this disorder in their communities. Reactive aggression is anger-based aggression conducted in response to threat, frustration and provocation. Youth with CD show high comorbidity with attention deficit hyperactivity disorder (ADHD). We examined the neural substrates mediating impulsiveness in youth with CD and youth with ADHD. We noted that the recruitment of regions implicated in response control (dorsomedial frontal and anterior insula cortices) was disrupted in youth with CD relative to healthy youth. Notably, the extent of this impairment related to the level of impulsive and ADHD symptoms shown by the youth with CD. However, it did not relate to level of CU traits, reactive aggression or CD symptoms more generally. Critically, this work has allowed us to identify objective biomarkers of specific symptom sets that can be used in on-going work to assess treatment efficacy in this population. Indeed, our group, in other protocols, is about to start examining treatment efficacy using the paradigms developed under this protocol. This project has established a series of core neuro-biological findings regarding the basis of Conduct Disorder (CD). Over the past year, we have particularly concentrated on forms of function that are compromised in youth with CD and then examined what specific symptom sets are consequent on these forms of dysfunction. In our previous work, we have shown that youth show reduced amygdala responses to the distress of others. This year we have continued this work revealing that patients with CD show reduced amygdala (and connected structure) responses to not only other forms of negative stimuli but also animate stimuli. The amygdala is importantly involved in responding to animacy information as well as emotional information. Children with CD are compromised in both functions and thus show more widespread amygdala dysfunction that previously identified. Notably, both forms of impairment relates to the level of Callous Unemotional symptomatology (i.e., levels of reduced guilt and empathy). Youth with CD show elevated levels of retaliation to social provocation. We examined the neural substrates mediating retaliatory behavior in both healthy youth and youth with CD. We particularly noted that ventromedial prefrontal cortex plays an important modulatory role in the selection of retaliatory responses to social provocation. Youth with CD show impairment in this modulatory role. Moreover, level of impairment in this modulatory role relates to the level of reactive aggression shown by youth with this disorder in their communities. Reactive aggression is anger-based aggression conducted in response to threat, frustration and provocation. Youth with CD show high comorbidity with attention deficit hyperactivity disorder (ADHD). We examined the neural substrates mediating impulsiveness in youth with CD and youth with ADHD. We noted that the recruitment of regions implicated in response control (dorsomedial frontal and anterior insula cortices) was disrupted in youth with CD relative to healthy youth. Notably, the extent of this impairment related to the level of impulsive and ADHD symptoms shown by the youth with CD. However, it did not relate to level of CU traits, reactive aggression or CD symptoms more generally. Critically, this work has allowed us to identify objective biomarkers of specific symptom sets that can be used in on-going work to assess treatment efficacy in this population. Indeed, our group, in other protocols, is about to start examining treatment efficacy using the paradigms developed under this protocol.
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