title: Action monitoring in boys with attention-deficit/hyperactivity disorder, their nonaffected siblings, and normal control subjects: evidence for an endophenotype.
abstract: BACKGROUND
  Attention-deficit/hyperactivity disorder (ADHD) is a very common and highly heritable child psychiatric disorder associated with dysfunctions in fronto-striatal networks that control attention and response organization. The aim of this study was to investigate whether features of action monitoring related to dopaminergic functions represent endophenotypes that are brain functions on the pathway from genes and environmental risk factors to behavior.
  
  
  METHODS
  Action monitoring and error processing as indicated by behavioral and electrophysiological parameters during a flanker task were examined in boys with ADHD combined type according to DSM-IV (n = 68), their nonaffected siblings (n = 18), and healthy control subjects with no known family history of ADHD (n = 22).
  
  
  RESULTS
  Boys with ADHD displayed slower and more variable reaction-times. Error negativity (Ne) was smaller in boys with ADHD compared with healthy control subjects, whereas nonaffected siblings displayed intermediate amplitudes following a linear model predicted by genetic concordance. The three groups did not differ on error positivity (Pe). The N2 amplitude enhancement due to conflict (incongruent flankers) was reduced in the ADHD group. Nonaffected siblings also displayed intermediate N2 enhancement.
  
  
  CONCLUSIONS
  Converging evidence from behavioral and event-related potential findings suggests that action monitoring and initial error processing, both related to dopaminergically modulated functions of anterior cingulate cortex, might be an endophenotype related to ADHD.
authors.affiliation: Child and Adolescent Psychiatry, University of Göttingen, Germany. balbrec@gwdg.de
authors.forename: Bjoern
authors.initials: B
authors.lastname: Albrecht
authors.forename: Daniel
authors.initials: D
authors.lastname: Brandeis
authors.forename: Henrik
authors.initials: H
authors.lastname: Uebel
authors.forename: Hartmut
authors.initials: H
authors.lastname: Heinrich
authors.forename: Ueli C
authors.initials: UC
authors.lastname: Mueller
authors.forename: Marcus
authors.initials: M
authors.lastname: Hasselhorn
authors.forename: Hans-Christoph
authors.initials: HC
authors.lastname: Steinhausen
authors.forename: Aribert
authors.initials: A
authors.lastname: Rothenberger
authors.forename: Tobias
authors.initials: T
authors.lastname: Banaschewski
mesh_terms: D001289:Attention Deficit Disorder with Hyperactivity / Q000175:diagnosis / Q000235:genetics / Q000503:physiopathology; D002648:Child; D003342:Corpus Striatum / Q000503:physiopathology*; D004298:Dopamine / Q000378:metabolism; D004569:Electroencephalography; D004777:Environment; D005071:Evoked Potentials / Q000502:physiology*; D005625:Frontal Lobe / Q000503:physiopathology*; D006179:Gyrus Cinguli / Q000378:metabolism; D006801:Humans; D008297:Male; D009415:Nerve Net / Q000503:physiopathology*; D010641:Phenotype; D011597:Psychomotor Performance / Q000502:physiology*; D011930:Reaction Time; D012307:Risk Factors; D035781:Siblings
chemical_list: D004298:Dopamine