title: Electrophysiological correlates of automatic spreading of activation in patients with psychotic disorder and first-degree relatives.
abstract: BACKGROUND
  Semantic network abnormalities in patients with psychotic disorder were examined using associative prime-target relations with two stimulus asynchronies (SOAs; -250ms and -500ms) to assess the time course of automatic and more controlled processes of semantic priming. To investigate whether an aberrant semantic network system is part of the familial liability for psychosis, healthy siblings of patients with psychotic disorder were additionally examined. The N400 event-related brain potential (ERP) was used as a probe of semantic processing.
  
  
  METHODS
  Twenty-two patients with psychotic disorder, twenty siblings of patients with psychotic disorder and twenty controls participated in a lexical decision task and ERPs were recorded to target words that were associatively, indirectly or not related to their preceding prime word.
  
  
  RESULTS
  Associative priming of the N400 amplitude was found across all participants and both SOAs, but no between-group differences were found for the N400 amplitude (both SOAs). The Group×Condition interaction of the indirect priming N400 latency of the three groups was just short of statistical significance (F2,59=2.7, p=.077). Patients showed an increased indirect priming effect of the N400 latency only at short SOA, with decreased latency of the indirectly related compared to the unrelated condition, while controls did not show an indirect priming N400 latency effect. No between-group differences in N400 latency of indirect priming were found at the long SOA. Only a trend towards a Group×Condition interaction of the indirect priming N400 latency between the sibling and the controls was found, but without a main effect of indirect priming in the sibling group.
  
  
  CONCLUSIONS
  These preliminary results support the assumption of a hyperactive semantic network in patients with psychotic disorder, which develops under automatic processes and decreases with more controlled processes, but does not represent clear trait familial liability.
authors.affiliation: Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research and Teaching Network, EURON, Maastricht University Medical Centre, Maastricht, The Netherlands. s.pfeifer@maastrichtuniversity.nl
authors.forename: Stefanie
authors.initials: S
authors.lastname: Pfeifer
authors.forename: Niels O
authors.initials: NO
authors.lastname: Schiller
authors.forename: Jim
authors.initials: J
authors.lastname: van Os
authors.forename: Wim J
authors.initials: WJ
authors.lastname: Riedel
authors.forename: Petra
authors.initials: P
authors.lastname: Vlamings
authors.forename: Claudia
authors.initials: C
authors.lastname: Simons
authors.forename: Lydia
authors.initials: L
authors.lastname: Krabbendam
mesh_terms: D000293:Adolescent; D000328:Adult; D013181:Cortical Spreading Depression / Q000502:physiology*; D003657:Decision Making / Q000502:physiology*; D004569:Electroencephalography / Q000379:methods; D005071:Evoked Potentials / Q000502:physiology*; D005190:Family / Q000523:psychology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010775:Photic Stimulation / Q000379:methods; D011597:Psychomotor Performance / Q000502:physiology*; D011618:Psychotic Disorders / Q000235:genetics / Q000503:physiopathology* / Q000523:psychology; D011930:Reaction Time / Q000502:physiology; D055815:Young Adult