This project has established a series of core neuro-biological findings regarding the basis of Conduct Disorder (CD), particularly CD with Callous-Unemotional (CU) traits (reduced guilt and empathy). Over the past year, our main achievements have been the following: First, in a series of studies we have used structural imaging studies to identify whether it is possible to identify structural anatomical markers of CD with and without CU traits. In the past year we have extended our previous findings by demonstrating that youths with CD showed reduced cortical thickness in the superior temporal cortex and had indications of reduced gyrification in the ventromedial frontal cortex. This was particularly pronounced for youths with CD without comorbid attention-deficit/hyperactivity disorder. There were no group differences in cortical surface area. However, youths with CD also showed reduced amygdala and striatum (putamen and pallidum) volumes. Right temporal cortical thickness was significantly inversely related to severity of CU traits. Second, in earlier work on this protocol, we demonstrated that CD+CU is associated with impaired reward/punishment based decision making and this impairment is related to dysfunction within orbital frontal cortex and caudate. This relates to computational impairments in prediction error signaling (signaling that an outcome is better or worse than the individual expected it to be), a critical signal for learning and expected value (representing the likely reward or punishment that will be received following performance of the action). This view has been confirmed and extended in additional studies of decision making this year with the caudate, dorsomedial prefrontal cortex and anterior insula cortex dysfunction being replicated in a paradigm utilizing environmental reinforcement. In this paradigm failure in the use of expected value information to guide the individual away from poor choices was again observed in youth with CD. Interestingly, this failure does not seem to be specifically related to youth with CD+CU. Further identifying specific deficits common to DBD and specific to CD+CU and CD-CU will be a focus of the group moving forward. Critically, this work has allowed us to identify objective biomarkers 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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