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

William M. Grove, Brett A. Clementz, William G Iacono, Joanna Katsanis

Research output: Contribution to journalArticlepeer-review

66 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1362-1368
Number of pages7
JournalAmerican Journal of Psychiatry
Volume149
Issue number10
DOIs
StatePublished - 1992

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