Article

Abnormal pursuit eye movements in schizophrenia: Evidence for a genetic marker

Archives of General Psychiatry (Impact Factor: 13.75). 08/1977; 34(7):802-5.
Source: PubMed

ABSTRACT Disordered smooth-pursuit eye movements occur in a high percentage of schizophrenic patients and their first-degree relatives. A Test of the hypothesis that these disorders represent a genetic indicator of schizophrenia was undertaken by testing pursuit eye movements in a sample of monozygotic and dizygotic twins discordant for clinical schizophrenia. Deviant eye tracking is significantly concordant within monozygotic twin pairs, and less so with dizygotic twin pairs discordant for schizophrenia. A genetic interpretation is consistent with these results.

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    • "Multiple replications of the familial aggregation of ETD in relatives of schizophrenia patients also followed, suggesting that it might be heritable. Studies of twins discordant for schizophrenia as well as healthy twins supported the idea that eye tracking performance was under genetic control (Holzman et al. 1977, 1988; Iacono and Lykken 1979; Bell et al. 1994; Katsanis et al. 2000). The elevated rate of ETD in clinically adopted in psychopathology laboratories is that they can be mapped to specific neural structures [for overviews see (Thier and Ilg 2005; Leigh and Zee 2006)]. "
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    ABSTRACT: Eye tracking dysfunction (ETD) is one of the most widely replicated behavioral deficits in schizophrenia and is over-represented in clinically unaffected first-degree relatives of schizophrenia patients. Here, we provide an overview of research relevant to the characterization and pathophysiology of this impairment. Deficits are most robust in the maintenance phase of pursuit, particularly during the tracking of predictable target movement. Impairments are also found in pursuit initiation and correlate with performance on tests of motion processing, implicating early sensory processing of motion signals. Taken together, the evidence suggests that ETD involves higher-order structures, including the frontal eye fields, which adjust the gain of the pursuit response to visual and anticipated target movement, as well as early parts of the pursuit pathway, including motion areas (the middle temporal area and the adjacent medial superior temporal area). Broader application of localizing behavioral paradigms in patient and family studies would be advantageous for refining the eye tracking phenotype for genetic studies.
    Current Topics in Behavioral Neurosciences 01/2010; 4(4):311-47. DOI:10.1007/7854_2010_60
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    • "Patients with schizophrenia show cognitive and behavioral problems such as deficits in performance on the Wisconsin Card Sorting Test (Weinberger et al., 1986), smooth pursuit eye movement (Holzman et al., 1977) and performance on spatial working memor y tasks (Park and Holzman, 1992) that are frequently associated with frontal lobe lesions in humans — see recent review of effects of prefrontal lesions (Knight et al., 1999). Additionally, both lesion and recording data in nonhuman primates implicate the prefrontal cortex in performance on analogs of these tasks, as well as more complex 'executive' behavior [reviewed by Miller (Miller, 1999)]. "
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    ABSTRACT: Functional measures have consistently shown prefrontal abnormalities in schizophrenia. However, structural magnetic resonance imaging (MRI) findings of prefrontal volume reduction have been less consistent. In this study, we evaluated prefrontal gray matter volume in first episode (first hospitalized) patients diagnosed with schizophrenia, compared with first episode patients diagnosed with affective psychosis and normal comparison subjects, to determine the presence in and specificity of prefrontal abnormalities to schizophrenia. Prefrontal gray and white matter volumes were measured from first episode patients with schizophrenia (n = 17), and from gender and parental socio-economic status-matched subjects with affective (mainly manic) psychosis (n = 17) and normal comparison subjects (n = 17), age-matched within a narrow age range (18--29 years). Total (left and right) prefrontal gray matter volume was significantly reduced in first episode schizophrenia compared with first episode affective psychosis and comparison subjects. Follow-up analyses indicated significant left prefrontal gray matter volume reduction and trend level reduction on the right. Schizophrenia patients showed 9.2% reduction on the left and 7.7% reduction on the right compared with comparison subjects. White matter volumes did not differ among groups. These data suggest that prefrontal cortical gray matter volume reduction is selectively present at first hospitalization in schizophrenia but not affective psychosis.
    Cerebral Cortex 05/2001; 11(4):374-81. DOI:10.1093/cercor/11.4.374 · 8.67 Impact Factor
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    • "E ye tracking dysfunction is one of the best established familial markers of risk for schizophrenia (Clementz and Sweeney 1990; Levy et al 1994). The dysfunction is common in schizophrenic patients (Holzman et al 1974; Katsanis and Iacono 1991; Sweeney et al 1994a; Friedman et al 1995; Abel et al 1991) and their biological relatives (Iacono et al 1992; Clementz et al 1990; Holzman et al 1977; Whicker et al 1985), and has been replicated in several laboratories. Despite over 20 years of active investigation of this abnormality, a clear understanding of its pathophysiological basis has not been developed. "
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    ABSTRACT: Eye tracking deficits are robust abnormalities in schizophrenia, but the neurobiological disturbance underlying these deficits is not known. To clarify the pathophysiology of eye tracking disturbances in schizophrenia, we tested 12 first-episode treatment-naive schizophrenic patients and 10 matched healthy individuals on foveofugal and foveopetal step-ramp pursuit tasks. On foveopetal tasks, the initiation of pursuit eye movements was delayed in schizophrenic patients, and their steady-state pursuit gain was reduced particularly at slower target speeds (8 and 16 deg/sec). In foveofugal step-ramp tasks, their primary catch-up saccades were normal in latency and accuracy, but their postsaccadic pursuit in the first 100 msec after the primary catch-up saccade was significantly reduced even relative to their slow steady-state pursuit, especially during and immediately after an acute episode of illness. These observations indicate that motion-sensitive areas in posterior temporal cortex provide sufficiently intact information about moving targets to guide accurate catch-up saccades, but that the sensory processing of motion information is not being used effectively for pursuit eye movements. Low-gain pursuit after the early stage of pursuit initiation suggests that the use of extraretinal signals about target motion (e.g., anticipatory prediction) only partially compensates for this deficit. The pattern of low-gain pursuit, impaired pursuit initiation, and intact processing of motion information for catch-up saccades but not pursuit eye movements, was consistent in the schizophrenic patients tested at five time points over a 2-year follow-up period, and implicates the frontal eye fields or their efferent or afferent pathways in the pathophysiology of eye tracking abnormalities in schizophrenia.
    Biological Psychiatry 11/1998; 44(8):698-708. DOI:10.1016/S0006-3223(98)00035-3 · 10.25 Impact Factor
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