Objective Though there is growing evidence of brain abnormalities among individuals with Conduct Disorder (CD), the structural neuroimaging literature is mixed and frequently aggregates cortical volume rather than differentiating cortical thickness from surface area. The current study assesses CD-related differences in cortical thickness, surface area, and gyrification as well as volume differences in subcortical structures critical to neurodevelopmental models of CD (amygdala; striatum) in a carefully characterized sample. We also examined whether group structural differences were related to severity of callous-unemotional (CU) traits in the CD sample. Method Participants were 49 community adolescents (aged 10-18 years); 22 with CD and 27 healthy comparison youth. Structural MRI was collected and the FreeSurfer image analysis suite was used to provide measures of cortical thickness, surface area and local gyrification as well as subcortical (amygdala and striatum) volumes. Results Youths with CD showed reduced cortical thickness in superior temporal cortex. There were also indications of reduced gyrification in ventromedial frontal cortex particularly for youth with CD without comorbid Attention Deficit Hyperactivity Disorder. There were no group differences in cortical surface area. However, the youth 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. Conclusions Youths with CD show reduced cortical thickness within superior temporal regions, some indication of reduced gyrification within ventromedial frontal cortex and reduced amygdala and striatum (putamen and pallidum) volumes. These results are discussed with reference to neurobiological models of CD.

Background To determine the functional integrity of the neural systems involved in emotional responding, regulation and response control/inhibition in youths (age 10–18) with Disruptive Behavioral Disorder (DBD: Conduct Disorder and/or Oppositional Defiant Disorder) as a function of callous-unemotional (CU) traits. Method 28 healthy youths and 35 youths with DBD (N=18 High CU, N=17 Low CU) performed the fMRI Affective Stroop task. Participants viewed positive, neutral, and negative images under varying levels of cognitive load. A 3-way ANOVA (group by emotion by task) was conducted on the BOLD response data. Results Youths with DBD-HCU showed significantly less activation of ventromedial prefrontal cortex (vmPFC) and amygdala in response to negative stimuli, compared to healthy youths and youths with DBD-LCU. VMPFC responsiveness was inversely related to CU symptoms in DBD. Youths with DBD-LCU showed decreased functional connectivity between amygdala and regions including inferior frontal gyrus in response to emotional stimuli. Youths with DBD (LCU and HCU) additionally showed decreased insula responsiveness to high load (incongruent trials) compared to healthy youths. Insula responsiveness was inversely related to ADHD symptoms in DBD. Conclusion These data reveal two forms of pathophysiology in DBD. One associated with reduced amygdala and vmPFC responses to negative stimuli and related to increased CU traits. Another associated with reduced insula responses during high load task trails and related to ADHD symptoms. Appropriate treatment will need to be individualized according to the patient’s specific pathophysiology.

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Objective Youth with Disruptive Behavior Disorders (DBD: Conduct Disorder/Oppositional Defiant Disorder) are at increased risk for maladaptive reactive aggression. Theory suggests this is due to increased sensitivity of basic threat circuitry implicated in retaliation (amygdala/periaqueductal gray) in youth with DBD and low levels of Callous-Unemotional Traits and dysfunctional regulatory activity within ventromedial prefrontal cortex (vmPFC) in youth with DBD irrespective of callous-unemotional traits. Methods Fifty-six youths participated (23 female) aged 10–18 (26 healthy and 30 with DBD [15 with high and 15 with low callous-unemotional traits]) who completed an Ultimatum Game during functional MRI. Results Youth with DBD and low callous-unemotional traits showed greater increases in activation of basic threat circuitry when punishing others relative to comparison groups and dysfunctional down regulation of vmPFC during retaliation. All youth with DBD showed reduced amygdala-vmPFC connectivity during high provocation relative to healthy youth. VmPFC responsiveness and vmPFC-amygdala connectivity were related to patients’ retaliatory propensity (behavioral responses during task) and parent reported reactive aggression. Conclusions These data suggest differences in the underlying neurobiology of maladaptive reactive aggression in youth with DBD and low relative to high levels of callous-unemotional traits. Youth with DBD and low callous-unemotional traits alone show significantly greater threat responses during retaliation relative to comparison individuals. Moreover, these data suggest that vmPFC-amygdala connectivity is critical for regulating retaliation/reactive aggression and when dysfunctional, contributes to reactive aggression, independent of level of callous-unemotional traits.

The current study examined temporal discounting (the decrease in subjective reward value as a function of increasing delay) in youths with conduct disorder (CD) and the extent to which this was modulated by level of psychopathic traits. In the temporal discounting task, participants were asked to choose between immediate rewards of varying values and a larger reward, held at a constant value ($10), whose receipt was delayed by different time intervals across trials (e.g., 7 days, 360 days). The level of immediate reward necessary for selection over the larger, delayed reward is the measure of temporal discounting. Forty-six youths (21 with CD and 25 healthy youths) participated in this study. Compared with healthy youths, youths with CD chose significantly smaller amounts of immediate reward rather than the larger future rewards. This was the case even in youths with CD without comorbid attention-deficit/hyperactivity disorder. However, level of psychopathic traits did not modulate temporal discounting in this sample. These results are discussed in terms of neurobiological models of CD and psychopathic traits.