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 .
Progressive increase of frontostriatal brain activation from childhood to adulthood during event-related tasks of cognitive control.
Higher cognitive inhibitory and attention functions have been shown to develop throughout adolescence , presumably concurrent with anatomical brain maturational changes . The relatively scarce developmental functional imaging literature on cognitive control , however , has been inconsistent with respect to the neurofunctional substrates of this cognitive development , finding either increased or decreased executive prefrontal function in the progression from childhood to adulthood . Such inconsistencies may be due to small subject numbers or confounds from age-related performance differences in block design functional MRI ( fMRI ) . In this study , rapid , r and omized , mixed-trial event-related fMRI was used to investigate developmental differences of the neural networks mediating a range of motor and cognitive inhibition functions in a sizeable number of adolescents and adults .  Functional brain activation was compared between adolescents and adults during three different executive tasks measuring selective motor response inhibition ( Go/no-go task ) , cognitive interference inhibition ( Simon task ) , and attentional set shifting ( Switch task ) .  Adults compared with children showed increased brain activation in task-specific frontostriatal networks , including right orbital and mesial prefrontal cortex and cau date during the Go/no-go task , right mesial and inferior prefrontal cortex , parietal lobe , and putamen during the Switch task and left dorsolateral and inferior frontotemporoparietal regions and putamen during the Simon task . Whole-brain regression analyses with age across all subjects showed progressive age-related changes in similar and extended clusters of task-specific frontostriatal , frontotemporal , and frontoparietal networks . The findings suggest progressive maturation of task-specific frontostriatal and frontocortical networks for cognitive control functions in the transition from childhood to mid-adulthood
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 .