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

Archives of General Psychiatry (Impact Factor: 14.48). 08/1977; 34(7):802-5.
Source: PubMed


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.

6 Reads
    • "SPEM are controlled by both retinal and extraretinal signals (including internal representations of target and eye velocity). SPEM dysfunction is present in 60 – 80% of patients with schizophrenia (Holzman et al. 1977; Hutton et al. 1998), even in drug-na ï ve patients (Campion et al. 1992), in about 50% of their non-schizophrenic relatives (Holzman et al. 1974; Karoumi et al. 2001; Louchart-de la Chapelle et al. 2005), in monozygotic twins discordant for schizophrenia (Holzman et al. 1980) as well as in childhood onset schizophrenia (Kumra et al. 2001) as compared to 10 – 20% of normal controls. SPEM impairments occur with a higher frequency in subjects with high schizotypal scores or schizotypal disorders (Siever et al. 1984, 1990). "
    [Show abstract] [Hide abstract]
    ABSTRACT: The neurophysiological components that have been proposed as biomarkers or as endophenotypes for schizophrenia can be measured through electroencephalography (EEG) and magnetoencephalography (MEG), transcranial magnetic stimulation (TMS), polysomnography (PSG), registration of event-related potentials (ERPs), assessment of smooth pursuit eye movements (SPEM) and antisaccade paradigms. Most of them demonstrate deficits in schizophrenia, show at least moderate stability over time and do not depend on clinical status, which means that they fulfil the criteria as valid endophenotypes for genetic studies. Deficits in cortical inhibition and plasticity measured using non-invasive brain stimulation techniques seem promising markers of outcome and prognosis. However the utility of these markers as biomarkers for predicting conversion to psychosis, response to treatments, or for tracking disease progression needs to be further studied.
    The World Journal of Biological Psychiatry 08/2015; 16(5):280-90. DOI:10.3109/15622975.2015.1050061 · 4.18 Impact Factor
  • Source
    • "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)]. "
    [Show abstract] [Hide abstract]
    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
  • Source
    • "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)]. "
    [Show abstract] [Hide abstract]
    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
Show more

Similar Publications