title: Neural correlates of response inhibition in pediatric bipolar disorder.
abstract: OBJECTIVE
  Pediatric bipolar disorder is characterized by core deficits in mood and executive function and commonly co-occurs with attention-deficit/hyperactivity disorder (ADHD). We aimed to examine response inhibition in this population, as an element of executive function, which, if aberrant, may interfere with learning and information processing.
  
  
  METHODS
  Children (9-18 years) with bipolar I or II disorder (BD, n = 26) and age, gender, and intelligence quotient (IQ) comparable healthy children (HC, n = 22) without any psychopathology were given a standardized Go/NoGo computerized task measuring response inhibition. A whole-brain functional magnetic resonance imaging (MRI) group analysis was performed using statistical parametric mapping software (SPM2) for comparing NoGo to Go epochs.
  
  
  RESULTS
  There were no statistically significant group differences between groups in age, gender, or ethnicity. The BD group had high rates of co-morbid disorders, including 81% with ADHD, 62% with oppositional defiant disorder (ODD), and 46% with anxiety disorders. This BD group had fewer correct responses on Go (84% vs. 96%, T[46] = 3.35, p = 0.002) and overall (85% vs. 94%, T[46] = 4.12, p = 0.0002) trials as compared to the HC group. However, there were no statistically significant group differences in response inhibition on NoGo trials (p = 0.11). In the NoGo-Go contrast, the BD group showed increased neural activation in the right dorsolateral prefrontal cortex (DLPFC) compared to HC (T[46] = 4.21, p < 0.001).
  
  
  CONCLUSIONS
  During accurate NoGo but impaired Go trial performance, children with BD showed increased right DLPFC activation versus controls, suggesting increased recruitment of executive control regions for accurate response inhibition. Studies relating these results to mood regulation in pediatric BD are warranted.
authors.affiliation: Pediatric Bipolar Disorders Program, Stanford University School of Medicine, Stanford, California 94305-5719, USA.
authors.forename: Manpreet K
authors.initials: MK
authors.lastname: Singh
authors.forename: Kiki D
authors.initials: KD
authors.lastname: Chang
authors.forename: Paul
authors.initials: P
authors.lastname: Mazaika
authors.forename: Amy
authors.initials: A
authors.lastname: Garrett
authors.forename: Nancy
authors.initials: N
authors.lastname: Adleman
authors.forename: Ryan
authors.initials: R
authors.lastname: Kelley
authors.forename: Meghan
authors.initials: M
authors.lastname: Howe
authors.forename: Allan
authors.initials: A
authors.lastname: Reiss
mesh_terms: D000293:Adolescent; D001008:Anxiety Disorders / Q000453:epidemiology* / Q000473:pathology / Q000523:psychology; D001289:Attention Deficit Disorder with Hyperactivity / Q000453:epidemiology* / Q000473:pathology / Q000523:psychology; D019958:Attention Deficit and Disruptive Behavior Disorders / Q000453:epidemiology* / Q000473:pathology / Q000523:psychology; D001714:Bipolar Disorder / Q000453:epidemiology / Q000503:physiopathology* / Q000523:psychology*; D001921:Brain / Q000503:physiopathology*; D016022:Case-Control Studies; D002648:Child; D003071:Cognition; D015897:Comorbidity; D005260:Female; D006801:Humans; D007091:Image Processing, Computer-Assisted; D007266:Inhibition, Psychological; D008279:Magnetic Resonance Imaging; D008297:Male; D009483:Neuropsychological Tests; D017397:Prefrontal Cortex / Q000503:physiopathology; D011597:Psychomotor Performance