Dissociated functional brain abnormalities of inhibition in boys with pure conduct disorder and in boys with pure attention deficit hyperactivity disorder.
OBJECTIVE
Inhibitory dysfunction may be a transdiagnostic etiopathophysiology of disruptive behavior disorders. Functional magnetic resonance imaging (fMRI) of inhibitory control has only been investigated in patients with attention deficit hyperactivity disorder (ADHD), including comorbidity with conduct disorder, showing frontal-striatal dysfunction. This study investigates differences and commonalities in functional neural networks mediating inhibitory control between medication-naive adolescents with pure conduct disorder and those with pure ADHD to identify biological markers that distinguish these clinically overlapping disorders.


METHODS
Event-related fMRI was used to compare brain activation of 13 boys with noncomorbid conduct disorder, 20 with noncomorbid ADHD, and 20 normal boys during an individually adjusted tracking stop task that measures the neural substrates of inhibition and stopping failure.


RESULTS
During successful inhibition, only patients with ADHD showed reduced activation in the left dorsolateral prefrontal cortex in relation to comparison subjects and patients with conduct disorder. During inhibition failures compared to go responses, both patient groups shared underactivation in the posterior cingulate gyrus in relation to comparison subjects. Patients with conduct disorder showed reduced activation in bilateral temporal-parietal regions compared to the other groups, which did not differ in this measure.


CONCLUSIONS
Patients with pure ADHD or pure conduct disorder show qualitative differences in their brain abnormality patterns during inhibitory control. Inhibition-mediating prefrontal regions appear to be specifically reduced in ADHD, whereas posterior temporal-parietal, performance monitoring networks are specifically dysfunctional in conduct disorder. The findings provide pioneering evidence that distinct neurobiological abnormalities may be underlying the overlapping behavioral phenotype of the two disruptive disorders.
Rubia
Katya
K
Department of Child Psychiatry/MRC Center for Social, Genetic, and Developmental Psychiatry, Institute of Psychiatry, King's College, London SE5 8AF, UK. k.rubia@iop.kcl.ac.uk
Halari
Rozmin
R
Smith
Anna B
AB
Mohammed
Majeed
M
Scott
Steven
S
Giampietro
Vincent
V
Taylor
Eric
E
Brammer
Michael J
MJ
D000293:Adolescent; D001289:Attention Deficit Disorder with Hyperactivity / Q000175:diagnosis / Q000453:epidemiology* / Q000503:physiopathology*; D019958:Attention Deficit and Disruptive Behavior Disorders / Q000175:diagnosis / Q000453:epidemiology / Q000503:physiopathology; D001921:Brain / Q000503:physiopathology*; D002648:Child; D019955:Conduct Disorder / Q000175:diagnosis / Q000453:epidemiology* / Q000503:physiopathology*; D004213:Dissociative Disorders / Q000175:diagnosis / Q000453:epidemiology* / Q000503:physiopathology*; D007839:Functional Laterality / Q000502:physiology; D006801:Humans; D007266:Inhibition, Psychological; D008279:Magnetic Resonance Imaging; D008297:Male; D010296:Parietal Lobe / Q000503:physiopathology; D010641:Phenotype; D017397:Prefrontal Cortex / Q000503:physiopathology; D013702:Temporal Lobe / Q000503:physiopathology