title: Auditory P300 in patients with bipolar disorder and their unaffected relatives.
abstract: OBJECTIVE
  There is evidence that genetic susceptibility may be shared between bipolar disorder (BD) and schizophrenia, but electrophysiological phenotypes which have been extensively used in studies of genetic susceptibility for schizophrenia remain far less explored in bipolar illness. This study assesses whether auditory P300 latency delays and amplitude reductions, which have been demonstrated in patients with schizophrenia and their unaffected first-degree relatives, are associated with familial liability to psychotic bipolar illness.
  
  
  METHODS
  The P300 auditory evoked potential was obtained using an oddball task from 37 participants with BD who had a history of psychotic symptoms, 38 of their unaffected first-degree relatives and 42 healthy unrelated comparison subjects. Patients and relatives came from families multiply affected with BD or another functional psychotic disorder. P300 amplitude and latency at midline sites were compared between the groups, using linear regression analyses and robust variance estimators for clustered data, including age and gender as covariates.
  
  
  RESULTS
  Bipolar disorder patients with a history of psychosis and their unaffected relatives showed significantly delayed P300 latency at Pz compared to controls. The groups did not differ in P300 amplitude.
  
  
  CONCLUSIONS
  P300 latency delays are associated with both psychotic BD and familial liability for this illness. Sample size limited our ability to test for multimodal distribution of P300 measures among relatives, which might be expected if only a subgroup inherits any deficits. In future it will be of interest to directly compare groups of families with psychotic and non-psychotic forms of BD to explore further the role of psychotic symptoms with regard to P300 measures in the disorder. Our results indicate that delayed P300 latency is a promising candidate endophenotype for psychotic BD, as well as schizophrenia, and may reflect the impact of shared susceptibility genes for both types of psychosis.
authors.affiliation: Division of Psychological Medicine, Institute of Psychiatry, King's College, London, UK. k.schulze@iop.kcl.ac.uk
authors.forename: Katja K
authors.initials: KK
authors.lastname: Schulze
authors.forename: Mei-Hua
authors.initials: MH
authors.lastname: Hall
authors.forename: Colm
authors.initials: C
authors.lastname: McDonald
authors.forename: Nicolette
authors.initials: N
authors.lastname: Marshall
authors.forename: Muriel
authors.initials: M
authors.lastname: Walshe
authors.forename: Robin M
authors.initials: RM
authors.lastname: Murray
authors.forename: Elvira
authors.initials: E
authors.lastname: Bramon
mesh_terms: D000161:Acoustic Stimulation / Q000379:methods; D000293:Adolescent; D000328:Adult; D001714:Bipolar Disorder / Q000503:physiopathology*; D016022:Case-Control Studies; D016001:Confidence Intervals; D018913:Event-Related Potentials, P300 / Q000502:physiology*; D005190:Family; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011601:Psychophysics; D011930:Reaction Time / Q000502:physiology