title: Saccadic disinhibition in patients with acute and remitted schizophrenia and their first-degree biological relatives.
abstract: OBJECTIVE
  Performance on measures of saccadic inhibition and control was investigated in a large family study of schizophrenia to evaluate the utility of using antisaccade task performance as an endophenotypic marker of genetic liability for schizophrenia.
  
  
  METHODS
  Ninety-five patients with acute schizophrenia and 116 of their first-degree biological relatives, 13 schizophrenia patients whose illness was in full remission, 35 patients with acute psychotic affective disorder, and 109 nonpsychiatric comparison subjects were administered antisaccade and prosaccade tasks.
  
  
  RESULTS
  Both schizophrenia patient groups had a greater number of errors on the antisaccade task than did the first-degree relatives and the affective disorder group, which both had more errors than the comparison subjects. Among the first-degree relatives of the probands with acute schizophrenia, relatives of poor-performing patients performed worse on the antisaccade task than relatives of patients with good performance. Reflexive errors were not likely the result of interfering psychotic symptoms, medication, or medication side effects. Although the schizophrenia patients demonstrated other signs of saccadic abnormalities, these problems, which were not observed in their relatives even though they had high antisaccade error rates, seem unlikely to account for the higher antisaccade error rate of the schizophrenia patients.
  
  
  CONCLUSIONS
  These findings suggest that saccadic disinhibition is strongly associated with the genetic liability for schizophrenia.
authors.affiliation: Department of Psychology, University of Minnesota, Minneapolis, MN 55455-0344, USA.
authors.forename: C E
authors.initials: CE
authors.lastname: Curtis
authors.forename: M E
authors.initials: ME
authors.lastname: Calkins
authors.forename: W M
authors.initials: WM
authors.lastname: Grove
authors.forename: K J
authors.initials: KJ
authors.lastname: Feil
authors.forename: W G
authors.initials: WG
authors.lastname: Iacono
mesh_terms: D000208:Acute Disease; D000328:Adult; D000367:Age Factors; D005190:Family; D005260:Female; D005403:Fixation, Ocular / Q000502:physiology; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D017397:Prefrontal Cortex / Q000503:physiopathology; D011597:Psychomotor Performance / Q000502:physiology*; D011618:Psychotic Disorders / Q000175:diagnosis / Q000235:genetics / Q000503:physiopathology; D011930:Reaction Time / Q000502:physiology; D012438:Saccades / Q000235:genetics* / Q000502:physiology; D012559:Schizophrenia / Q000175:diagnosis* / Q000235:genetics* / Q000503:physiopathology; D012565:Schizophrenic Psychology; D014796:Visual Perception / Q000502:physiology