Results : In ADHD , deviant prefrontal and cingulate functional activity was associated with increased IA .
Structural alterations were most pronounced in the cingulate cortex .
Subjects with DBDs showed marked cortico‐subcortical dysfunctions .
ADHD and DBDs share similar cortico‐limbic structural and functional alterations .
RI deficits in ADHD highlighted hypoactivity in the dorso/ventro‐lateral PFC , insula , and striatum , while the paralimbic system was primarily dysfunctional in DBDs .
Across disorders , extensively altered cortico‐limbic dysfunctions underlie IA , while RI was mostly associated with aberrant prefrontal activity .
Conclusion : Control network deficits were evidence d across clinical phenotypes in IA and RI .
Dysfunctions at any level within these cortico‐subcortical projections lead to deficient cognitive‐affective control by ascribing emotional salience to otherwise irrelevant stimuli .
HighlightsImpulsive aggression and dysfunctional response inhibition are present in ADHD and DBDs .
Broad fronto‐striatal‐cerebellar dysfunctions have been implicated in ADHD and DBDs .
Prefrontal and cingulate cortical deficits are associated with IA in ADHD.Severe widespread cortico‐subcortical breakdowns are associated with IA in DBDs .
RI deficits have been attributed to hypoactivity in the lateral PFC , insula , and amygdala .
Whether reduced gray matter volumes relate to ADHD and DBDs or if present as an IA epiphenomenon remains debatable .
Background : Although impulsive aggression ( IA ) and dysfunctional response inhibition ( RI ) are hallmarks of attention‐deficit/hyperactivity disorder ( ADHD ) and disrupted behavioral disorders ( DBDs ) , little is known about their shared and distinct deviant neural mechanisms .
Neural Correlates of the Propensity for Retaliatory Behavior in Youths With Disruptive Behavior Disorders.
OBJECTIVE Youths with disruptive behavior disorders ( DBD ) ( conduct disorder and oppositional defiant disorder ) have an elevated risk for maladaptive reactive aggression . Theory suggests that this is due to an elevated sensitivity of basic threat circuitry implicated in retaliation ( amygdala/periaqueductal gray ) in youths with DBD and low levels of callous-unemotional traits and dysfunctional regulatory activity in the ventromedial prefrontal cortex in youths with DBD irrespective of callous-unemotional traits . METHOD A total of 56 youths 10 - 18 years of age ( 23 of them female ) participated in the study : 30 youths with DBD , divided by median split into groups with high and low levels of callous-unemotional traits , and 26 healthy youths . All participants completed an ultimatum game task during functional MRI . RESULTS Relative to the other groups , youths with DBD and low levels of callous-unemotional traits showed greater increases in activation of basic threat circuitry when punishing others and dysfunctional down-regulation of the ventromedial prefrontal cortex during retaliation . Relative to healthy youths , all youths with DBD showed reduced amygdala-ventromedial prefrontal cortex connectivity during high provocation . Ventromedial prefrontal cortex responsiveness and ventromedial prefrontal cortex-amygdala connectivity were related to patients ' retaliatory propensity ( behavioral responses during the task ) and parent-reported reactive aggression . CONCLUSIONS These data suggest differences in the underlying neurobiology of maladaptive reactive aggression in youths with DBD who have relatively low levels of callous-unemotional traits . Youths with DBD and low callous-unemotional traits alone showed significantly greater threat responses during retaliation relative to comparison subjects . These data also suggest that ventromedial prefrontal cortex-amygdala connectivity is critical for regulating retaliation/reactive aggression and , when dysfunctional , contributes to reactive aggression , independent of level of callous-unemotional traits
Results : In ADHD , deviant prefrontal and cingulate functional activity was associated with increased IA .
Structural alterations were most pronounced in the cingulate cortex .
Subjects with DBDs showed marked cortico‐subcortical dysfunctions .
ADHD and DBDs share similar cortico‐limbic structural and functional alterations .
RI deficits in ADHD highlighted hypoactivity in the dorso/ventro‐lateral PFC , insula , and striatum , while the paralimbic system was primarily dysfunctional in DBDs .
Across disorders , extensively altered cortico‐limbic dysfunctions underlie IA , while RI was mostly associated with aberrant prefrontal activity .
Conclusion : Control network deficits were evidence d across clinical phenotypes in IA and RI .
Dysfunctions at any level within these cortico‐subcortical projections lead to deficient cognitive‐affective control by ascribing emotional salience to otherwise irrelevant stimuli .
HighlightsImpulsive aggression and dysfunctional response inhibition are present in ADHD and DBDs .
Broad fronto‐striatal‐cerebellar dysfunctions have been implicated in ADHD and DBDs .
Prefrontal and cingulate cortical deficits are associated with IA in ADHD.Severe widespread cortico‐subcortical breakdowns are associated with IA in DBDs .
RI deficits have been attributed to hypoactivity in the lateral PFC , insula , and amygdala .
Whether reduced gray matter volumes relate to ADHD and DBDs or if present as an IA epiphenomenon remains debatable .
Background : Although impulsive aggression ( IA ) and dysfunctional response inhibition ( RI ) are hallmarks of attention‐deficit/hyperactivity disorder ( ADHD ) and disrupted behavioral disorders ( DBDs ) , little is known about their shared and distinct deviant neural mechanisms .