title: Neural circuitry engaged during unsuccessful motor inhibition in pediatric bipolar disorder.
abstract: OBJECTIVE
  Deficits in motor inhibition may contribute to impulsivity and irritability in children with bipolar disorder. Studies of the neural circuitry engaged during failed motor inhibition in pediatric bipolar disorder may increase our understanding of the pathophysiology of the illness. The authors tested the hypothesis that children with bipolar disorder and comparison subjects would differ in ventral prefrontal cortex, striatal, and anterior cingulate activation during unsuccessful motor inhibition. They also compared activation in medicated versus unmedicated children with bipolar disorder and in children with bipolar disorder and attention deficit hyperactivity disorder (ADHD) versus those with bipolar disorder without ADHD.
  
  
  METHODS
  The authors conducted an event-related functional magnetic resonance imaging study comparing neural activation in children with bipolar disorder and healthy comparison subjects while they performed a motor inhibition task. The study group included 26 children with bipolar disorder (13 unmedicated and 15 with ADHD) and 17 comparison subjects matched by age, gender, and IQ.
  
  
  RESULTS
  On failed inhibitory trials, comparison subjects showed greater bilateral striatal and right ventral prefrontal cortex activation than did patients. These deficits were present in unmedicated patients, but the role of ADHD in mediating them was unclear.
  
  
  CONCLUSIONS
  In relation to comparison subjects, children with bipolar disorder may have deficits in their ability to engage striatal structures and the right ventral prefrontal cortex during unsuccessful inhibition. Further research should ascertain the contribution of ADHD to these deficits and the role that such deficits may play in the emotional and behavioral dysregulation characteristic of bipolar disorder.
authors.affiliation: Emotion and Development Branch, mood and Anxiety Disorders Program, NIMH, NIH, Health and Human Services, Bldg. 15K, MSC-2670, Bethesda, MD 20892-2670, USA. leibs@mail.nih.gov
authors.forename: Ellen
authors.initials: E
authors.lastname: Leibenluft
authors.forename: Brendan A
authors.initials: BA
authors.lastname: Rich
authors.forename: Deborah T
authors.initials: DT
authors.lastname: Vinton
authors.forename: Eric E
authors.initials: EE
authors.lastname: Nelson
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Fromm
authors.forename: Lisa H
authors.initials: LH
authors.lastname: Berghorst
authors.forename: Paramjit
authors.initials: P
authors.lastname: Joshi
authors.forename: Adelaide
authors.initials: A
authors.lastname: Robb
authors.forename: Russell J
authors.initials: RJ
authors.lastname: Schachar
authors.forename: Daniel P
authors.initials: DP
authors.lastname: Dickstein
authors.forename: Erin B
authors.initials: EB
authors.lastname: McClure
authors.forename: Daniel S
authors.initials: DS
authors.lastname: Pine
mesh_terms: D000293:Adolescent; D001289:Attention Deficit Disorder with Hyperactivity / Q000175:diagnosis / Q000453:epidemiology / Q000503:physiopathology; D001714:Bipolar Disorder / Q000175:diagnosis* / Q000453:epidemiology / Q000503:physiopathology*; D001931:Brain Mapping; D015897:Comorbidity; D004365:Drugs, Chinese Herbal; D028001:Eleutherococcus; D005071:Evoked Potentials / Q000502:physiology; D005260:Female; D007839:Functional Laterality / Q000502:physiology; D006179:Gyrus Cinguli / Q000503:physiopathology; D006801:Humans; D007266:Inhibition, Psychological; D008279:Magnetic Resonance Imaging / Q000706:statistics & numerical data*; D008297:Male; D009434:Neural Pathways / Q000503:physiopathology*; D009483:Neuropsychological Tests / Q000706:statistics & numerical data; D017397:Prefrontal Cortex / Q000503:physiopathology*; D011597:Psychomotor Performance / Q000502:physiology*; D011930:Reaction Time / Q000502:physiology; D014793:Visual Cortex / Q000503:physiopathology
chemical_list: D004365:Drugs, Chinese Herbal; C400150:Acanthopanax gracilistylus, extract