Literature DB >> 15652873

Abnormalities in visually guided saccades suggest corticofugal dysregulation in never-treated schizophrenia.

James L Reilly1, Margret S H Harris, Matcheri S Keshavan, John A Sweeney.   

Abstract

BACKGROUND: Previous studies have reported intact visually guided saccades in schizophrenia, but these are limited by potential acute and long-term pharmacological treatment effects, small sample sizes, and a failure to follow patients over time.
METHODS: Visually guided saccades were examined in 44 antipsychotic-naive patients experiencing their first episode of schizophrenia prior to treatment and again after 6, 26, and 52 weeks of antipsychotic treatment. Thirty-nine matched healthy individuals were followed over the same period.
RESULTS: Before treatment, patients showed faster saccade latencies to unpredictable visual targets, suggesting reduced inhibitory regulation of brainstem saccade generators by neocortical attentional systems. Risperidone treatment reduced this deficit, suggesting a facilitation of attentional function, but haloperidol treatment did not. However, there was also a modest decline in saccade accuracy after risperidone treatment. The ability to sustain fixation of static central and peripheral targets was unimpaired before and after treatment.
CONCLUSIONS: These findings provide evidence for impairments in neocortical attentional systems that cause reduced corticofugal regulation of brainstem systems in schizophrenia. This dysfunction appears to be minimized by the atypical antipsychotic risperidone but at the cost of a subtle reduction in saccade accuracy, possibly mediated via adverse effects on cerebellar vermis function.

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Year:  2005        PMID: 15652873     DOI: 10.1016/j.biopsych.2004.10.024

Source DB:  PubMed          Journal:  Biol Psychiatry        ISSN: 0006-3223            Impact factor:   13.382


  26 in total

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5.  Impact of antipsychotic treatment on attention and motor learning systems in first-episode schizophrenia.

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8.  Pharmacogenetic associations of the type-3 metabotropic glutamate receptor (GRM3) gene with working memory and clinical symptom response to antipsychotics in first-episode schizophrenia.

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