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  Vol. 54 No. 5, May 1997 TABLE OF CONTENTS
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A Quantitative Analysis of Smooth Pursuit Eye Tracking in Monozygotic Twins Discordant for Schizophrenia

Robert E. Litman, MD; E. Fuller Torrey, MD; Daniel W. Hommer, MD; Allan R. Radant, MD; David Pickar; Daniel R. Weinberger, MD

Arch Gen Psychiatry. 1997;54(5):417-426.


Abstract

Background
Previous studies of discordant monozygotic (MZ) twins have suggested that abnormal smooth pursuit eye tracking is an indicator of genetic liability for schizophrenia. We attempted to replicate this in a different sample of twins.

Methods
Probands from 12 sets of MZ twins discordant for schizophrenia who met DSM-III-R criteria for schizophrenia or schizoaffective disorder and their cotwins without psychiatric diagnosis (except 2 with a history of substance abuse) and 12 sets of normal control MZ twins. Psychiatric diagnosis was based on Structured Clinical Interview; monozygosity was based on analysis of 19 red blood cell antigens. Smooth pursuit eye movement gain (equal to the ratio of eye-target velocity) and numbers, amplitudes, and subtypes of saccadic eye movements were compared. Measures were derived from computer analysis of digitized infrared oculographic recordings of constant velocity (16.67%o per second) smooth pursuit eye tracking.

Results
Quantitative measures of eye tracking for the affected twin were inferior to those of the unaffected co-twin, with affected twins showing significant decreases in gain and significant increases in numbers and amplitudes of total and intrusive saccades. Moreover, whereas means for the group of affected twins differed significantly from those of normal controls on measures of gain and total saccades, means for the group of unaffected co-twins were well within the normal range.

Conclusions
These data are consistent with the hypothesis that abnormal eye tracking is associated with the expression of illness, or phenotype, in schizophrenia, at least in this twin sample. The data raise questions regarding the use of eye tracking measurement for identifying putative gene carriers among at-risk relatives in genetic linkage studies of schizophrenia.



Author Affiliations

From the Experimental Therapeutics Branch (Drs Litman and Pickar) and the Clinical Brain Disorders Branch (Drs Torrey and Weinberger), National Institute of Mental Health, and the Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Md (Dr Hommer); and the Veterans Affairs Medical Center, Seattle, Wash (Dr Radant).



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