A Quantitative Analysis of Smooth Pursuit Eye Tracking in Monozygotic Twins Discordant for Schizophrenia

Abstract

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.

Visual Attention Decits in Schizophrenia Can Arise From Inhibitory Dysfunction in Thalamus or Cortex

“…Temporal locations of the high-velocity (saccade-like) eye movements are depicted with vertical black ticks in Figure 7. Compared to healthy controls, schizophrenia patients tend to show greater rms error in smooth pursuit tasks (Allen et al, 1990; Benson et al, 2012; O’Driscoll & Callahan, 2008; Ross et al, 1997) and a larger number of catch-up and intrusive saccades in fixation tasks (Benson et al, 2012; Litman et al, 1997; Rybakowski & Borkowska, 2002). We computed performance measures for the normal epoch (4–6 s period) and the perturbed epoch (6–8 s period).…”

Are eye movement abnormalities indicators of genetic vulnerability to schizophrenia?

“…These observations were consistent with those of Keefe et al [32] who did not find any difference on quantitative parameters (gain and number of large saccades) between relatives of schizophrenic patients and healthy subjects. Litman et al [42], likewise, compared the performances between schizophrenic patients and non-schizophrenic twins and observed that the non-affected twins had better results than the probands but did not differ from healthy subjects. Ross et al [49] did not observe any difference between the less likely carrier relatives and healthy subjects.…”

Eye movement dysfunction in first-degree relatives of patients with schizophrenia: A meta-analytic evaluation of candidate endophenotypes

“…Two studies of healthy twins obtained heritability estimates for closed-loop gain ranging from h 2 =.46 (Katsanis, Taylor, Iacono, & Hammer, 2000) to h 2 =.70 (Blekher, Miller, Yee, Christian, & Abel, 1997). Two additional studies reported significant healthy monozygotic twin intraclass correlations for closed loop gain of h 2 =.60 (Litman et al, 1997), and from h 2 =.91 to .98 depending on target waveform and velocity (Bell, Abel, Wei, Christian, & Yee, 1994). Though the results of these healthy twin investigations is consistent with a genetic influence on closed loop gain, three investigations of schizophrenia families reporting non-twin, discordant sibling intraclass correlations for closed loop gain are conflicting (Ettinger et al, 2004; Hong et al, 2006; Litman et al, 1997), reported as ranging from small and non-significant to significant (r=.44, Ettinger et al, 2004).…”