Poor performance in smooth pursuit and antisaccadic eye-movement tasks in healthy siblings of patients with schizophrenia

Karoumi, Bouchaı̈b; Saoud, Mohamed; d’Amato, Thierry; Rosenfeld, Frederic; Denise, Pierre; Gutknecht, Christian; Gaveau, Valérie; Beaulieu, Flore-Estelle; Daléry, J; Rochet, Thierry

doi:10.1016/s0165-1781(01)00227-x

Cited by 56 publications

(52 citation statements)

References 53 publications

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“…Consistent with the involvement of genetic factors in schizophrenia, cognitive (3,4), neurologic (5,6) and neurobiological (7,8) abnormalities have been found in the unaffected relatives of schizophrenia subjects, generally in attenuated form.…”

supporting

confidence: 53%

“…Evidence from family, twin and adoption studies suggest that genetic factors play an important role in the pathogenesis of schizophrenia (1,2). Consistent with the involvement of genetic factors in schizophrenia, cognitive (3,4), neurologic (5,6) and neurobiological (7,8) abnormalities have been found in the unaffected relatives of schizophrenia subjects, generally in attenuated form. …”

mentioning

confidence: 64%

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Basal Ganglia Shape Abnormalities in the Unaffected Siblings of Schizophrenia Patients

Mamah¹,

Harms²,

Wang³

et al. 2008

Biological Psychiatry

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Objective-Abnormalities of basal ganglia structure in schizophrenia have been attributed to the effects of antipsychotic drugs. Our aim was to test the hypothesis that abnormalities of basal ganglia structure are intrinsic features of schizophrenia, by assessing basal ganglia volume and shape in the unaffected siblings of schizophrenia subjects.Method-The study involved 25 pairs of schizophrenia subjects and their unaffected siblings and 40 pairs of healthy controls and their siblings. Large deformation, high-dimensional brain mapping was used to obtain surface representations of the caudate, putamen, and globus pallidus. Surfaces were derived from transformations of anatomical templates and shapes were analyzed using reduceddimensional measures of surface variability (i.e. principal components and canonical analysis). Canonical functions were derived using schizophrenia and control groups, and were then used to compare shapes in the sibling groups. To visualize shape differences, maps of the estimated surface displacement between groups were created.Results-In the caudate, putamen and globus pallidus, the degree of shape abnormality observed in the siblings of the schizophrenia subjects was intermediate between the schizophrenia subjects and the controls. In the schizophrenia subjects, significant correlations were observed between measures of caudate, putamen and globus pallidus structure and the selected measures of lifetime psychopathology.Conclusions-Attenuated abnormalities of basal ganglia structure are present in the unaffected siblings of schizophrenia subjects. This finding implies that basal ganglia structural abnormalities observed in subjects with schizophrenia are at least in part an intrinsic feature of the illness. KeywordsSchizophrenia; Siblings; Basal Ganglia; Caudate; Putamen; Globus Pallidus Corresponding Author: Daniel Mamah, M.D., M.P.E. Department of Psychiatry (Box 8134), Washington University School of Medicine, 660 S. Euclid, St. Louis, MO 63110, (314) 747-2160, Fax: (314) 747-2182, E-mail: mamahd@psychiatry.wustl.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Evidence from family, twin and adoption studies suggest that genetic factors play an important role in the pathogenesis of schizophrenia (1,2). Consistent with the involvement of genetic factors in schizophrenia, cognitive (3,4), neurologic (5,6) and neurobiological (7,8) abnormalities have been found in the unaffected relatives of schizophrenia subjects, generally in attenuated form. NIH Public AccessA number of lines of research suggest that basal ganglia abnormalities mi...

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confidence: 53%

mentioning

confidence: 64%

Basal Ganglia Shape Abnormalities in the Unaffected Siblings of Schizophrenia Patients

Mamah¹,

Harms²,

Wang³

et al. 2008

Biological Psychiatry

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“…Furthermore, deficits such as a higher error rate in memory-guided saccades and lower acuity in predictive saccades have been reported (Krebs et al, 2001; Hutton et al, 2004; Keedy et al, 2006). In chronic patients, all these deficits have been observed (e.g., Karoumi et al, 2001; Brownstein et al, 2003; Reuter et al, 2006; Radant et al, 2007; Amado et al, 2008; Landgraf et al, 2008). In addition, chronic patients have shown lower acuity in memory-guided saccades (Crawford et al, 1995a; Park et al, 1995; McDowell and Clementz, 1996; Radant et al, 1997; Karoumi et al, 1998; McDowell et al, 2001).…”

Section: The Vision Perspective On Schizophreniamentioning

confidence: 96%

“To see or not to see: that is the question.” The “Protection-Against-Schizophrenia” (PaSZ) model: evidence from congenital blindness and visuo-cognitive aberrations

Landgraf¹,

Osterheider²

2013

Front. Psychol.

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The causes of schizophrenia are still unknown. For the last 100 years, though, both “absent” and “perfect” vision have been associated with a lower risk for schizophrenia. Hence, vision itself and aberrations in visual functioning may be fundamental to the development and etiological explanations of the disorder. In this paper, we present the “Protection-Against-Schizophrenia” (PaSZ) model, which grades the risk for developing schizophrenia as a function of an individual's visual capacity. We review two vision perspectives: (1) “Absent” vision or how congenital blindness contributes to PaSZ and (2) “perfect” vision or how aberrations in visual functioning are associated with psychosis. First, we illustrate that, although congenitally blind and sighted individuals acquire similar world representations, blind individuals compensate for behavioral shortcomings through neurofunctional and multisensory reorganization. These reorganizations may indicate etiological explanations for their PaSZ. Second, we demonstrate that visuo-cognitive impairments are fundamental for the development of schizophrenia. Deteriorated visual information acquisition and processing contribute to higher-order cognitive dysfunctions and subsequently to schizophrenic symptoms. Finally, we provide different specific therapeutic recommendations for individuals who suffer from visual impairments (who never developed “normal” vision) and individuals who suffer from visual deterioration (who previously had “normal” visual skills). Rather than categorizing individuals as “normal” and “mentally disordered,” the PaSZ model uses a continuous scale to represent psychiatrically relevant human behavior. This not only provides a scientific basis for more fine-grained diagnostic assessments, earlier detection, and more appropriate therapeutic assignments, but it also outlines a trajectory for unraveling the causes of abnormal psychotic human self- and world-perception.

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“…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(Siever et al , 1990.…”

Section: Smooth Pursuit Eye Movements (Spem) Antisaccade Paradigmsmentioning

confidence: 99%

Consensus paper of the WFSBP Task Force on Biological Markers: Criteria for biomarkers and endophenotypes of schizophrenia part I: Neurophysiology

Thibaut

Boutros

Jarema

et al. 2015

The World Journal of Biological Psychiatry

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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.

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Poor performance in smooth pursuit and antisaccadic eye-movement tasks in healthy siblings of patients with schizophrenia

Cited by 56 publications

References 53 publications

Basal Ganglia Shape Abnormalities in the Unaffected Siblings of Schizophrenia Patients

Basal Ganglia Shape Abnormalities in the Unaffected Siblings of Schizophrenia Patients

“To see or not to see: that is the question.” The “Protection-Against-Schizophrenia” (PaSZ) model: evidence from congenital blindness and visuo-cognitive aberrations

Consensus paper of the WFSBP Task Force on Biological Markers: Criteria for biomarkers and endophenotypes of schizophrenia part I: Neurophysiology

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