Smooth pursuit ocular motor dysfunction in schizophrenia: evidence for a major gene

Am J Psychiatry. 1992 Oct;149(10):1362-8. doi: 10.1176/ajp.149.10.1362.

Abstract

Objective: Evidence suggests that poor eye tracking relates to genetically transmitted vulnerability for schizophrenia. The authors tested competing models for the genetic transmission of poor eye tracking in a search for major gene effects.

Method: Samples from three studies (conducted in Minneapolis, New York, and Vancouver, B.C.) were pooled. Probands (N = 92) were diagnosed as schizophrenic by DSM-III criteria. Of the comparison subjects (N = 171), Vancouver patients were an epidemiologic first-episode group; at other sites unselected admitted patients were studied. First-degree relatives (N = 146) of 65 probands were also studied. Eye tracking was measured while subjects followed a horizontally moving, sinusoidally driven (0.4 Hz) spot of light on a screen. Performance was quantified by root mean square error. Data analysis was by complex segregation analysis (Bonney's class D regressive models).

Results: A single major gene is needed to account for poor eye tracking in schizophrenic patients and their relatives. This gene alone can explain about two-thirds of the variance in eye tracking performance. A single gene alone (regardless of dominance) will, however, not account for the data; polygenic factors are also required.

Conclusions: Results support postulation of a single gene for ocular motor dysfunction, which may be a risk factor for schizophrenia. Eye tracking may be useful as a gene carrier test in genetic studies of schizophrenia.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adolescent
  • Adult
  • Age Factors
  • Family
  • Female
  • Genetic Markers
  • Humans
  • Male
  • Models, Genetic*
  • Pursuit, Smooth / genetics*
  • Schizophrenia / genetics*
  • Schizophrenia / physiopathology
  • Sex Factors

Substances

  • Genetic Markers