Am J Psychiatry 1992; 149:1362-1368
Copyright © 1992 by American Psychiatric Association
Smooth pursuit ocular motor dysfunction in schizophrenia: evidence for a major gene
WM Grove, BA Clementz, WG Iacono and J Katsanis
Department of Psychology, University of Minnesota, MN 55455.
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.
