TY - JOUR
T1 - Smooth pursuit ocular motor dysfunction in schizophrenia
T2 - Evidence for a major gene
AU - Grove, William M.
AU - Clementz, Brett A.
AU - Iacono, William G
AU - Katsanis, Joanna
N1 - Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 1992
Y1 - 1992
N2 - 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.
AB - 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.
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U2 - 10.1176/ajp.149.10.1362
DO - 10.1176/ajp.149.10.1362
M3 - Article
C2 - 1530073
AN - SCOPUS:0026657529
SN - 0002-953X
VL - 149
SP - 1362
EP - 1368
JO - American Journal of Psychiatry
JF - American Journal of Psychiatry
IS - 10
ER -