Saccadic eye movement abnormalities in relatives of patients with schizophrenia

Thaker, Gunvant K.; Ross, David E.; Cassady, Shawn L.; Adami, Helene; Medoff, Deborah R.; Sherr, Jay D.

doi:10.1016/s0920-9964(99)00193-0

Cited by 59 publications

(43 citation statements)

References 29 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: 54%

“…Volumes were compared across the four subject groups using a mixed linear model that specified group, hemisphere (for basal ganglia only), the interaction of group with hemisphere, and gender as fixed effects. Using this model, there was a significant effect of group status on cerebral volume (F [3,46] …”

Section: Volume Analysesmentioning

confidence: 99%

“…When either (1) lifetime history of alcohol and cannabis dependence or (2) total grams of alcohol consumed over the previous two years were included as covariates in the mixed-model analysis (but not cerebral volume), the main effect of group on caudate volume remained significant (F [3,50]=3.2,p=0.03 and F [3,50]=3.9, p=0.01 respectively) None of the substance use variables themselves had a significant effect on the volume of any basal ganglia structure. However, there was a trend towards significance of the effect of cannabis dependence on globus pallidus volume (F[1,94]=3.7,p=0.06).…”

Section: Substance and Alcohol Effects On Volumesmentioning

confidence: 99%

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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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supporting

confidence: 54%

Section: Volume Analysesmentioning

confidence: 99%

Section: Substance and Alcohol Effects On Volumesmentioning

confidence: 99%

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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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“…43,44 The ability of some probands (60-70%) with schizophrenia to follow a smooth pendulum movement with their eyes is deficient. 45 Instead of describing smooth movements following a pendulum stimulus, some show jerky and irregular (delayed and catch-up movements) tracking patterns. Also, antisacade eye movements (those directed away from a stimulus) are also abnormal in persons with the illness.…”

Section: Cognitionmentioning

confidence: 99%

“…Also, antisacade eye movements (those directed away from a stimulus) are also abnormal in persons with the illness. 45,46 Prepulse inhibition (PPI) is a normal phenomena evident across all sensory modalities, where a small initial ('pre') stimulus decreases the electrophysiological response to a second higher intensity stimulus. In schizophrenia, many probands show abnormal PPI, as do unaffected family members.…”

Section: Cognitionmentioning

confidence: 99%

Phenotype of schizophrenia: a review and formulation

2004

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The discovery of the pathophysiology(ies) for schizophrenia is necessary to direct rational treatment directions for this brain disorder. Firm knowledge about this illness is limited to areas of phenomenology, clinical electrophysiology, and genetic risk; some aspects of dopamine pharmacology, cognitive symptoms, and risk genes are known. Basic questions remain about diagnostic heterogeneity, tissue neurochemistry, and in vivo brain function. It is an illness ripe for molecular characterization using a rational approach with a confirmatory strategy; drug discovery based on knowledge is the only way to advance fully effective treatments. This paper reviews the status of general knowledge in this area and proposes an approach to discovery, including identifying brain regions of dysfunction and subsequent localized, hypothesis-driven molecular screening.

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