ArticleJournal of abnormal psychology2013
Testing sensory and cognitive explanations of the antisaccade deficit in schizophrenia.
Article in Journal of abnormal psychology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Individual differences in first saccade latency predict overt behavior during search for a contour integration target.Visual cognition · 2024Article
- Attention in Schizophrenia.Current topics in behavioral neurosciences · 2023Article
- The Hyperfocusing Hypothesis: A New Account of Cognitive Dysfunction in Schizophrenia.Schizophrenia bulletin · 2019Review
- Effects of ketamine on brain function during response inhibition.Psychopharmacology · 2018Article
- Electrophysiological Evidence for Hyperfocusing of Spatial Attention in Schizophrenia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Psychophysiological endophenotypes to characterize mechanisms of known schizophrenia genetic loci.Psychological medicine · 2017Article
- Hyperfocusing of attention on goal-related information in schizophrenia: Evidence from electrophysiology.Journal of abnormal psychology · 2017Article
- Hyperfocusing in schizophrenia: Evidence from interactions between working memory and eye movements.Journal of abnormal psychology · 2014Article
- Relationships between divided attention and working memory impairment in people with schizophrenia.Schizophrenia bulletin · 2014Article
- Enhanced distraction by magnocellular salience signals in schizophrenia.Neuropsychologia · 2014Article
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Authors and funding
8 authors.
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Abstract
Recent research has suggested that people with schizophrenia (PSZ) have sensory deficits, especially in the magnocellular pathway, and this has led to the proposal that dysfunctional sensory processing may underlie higher-order cognitive deficits. Here we test the hypothesis that the antisaccade deficit in PSZ reflects dysfunctional magnocellular processing rather than impaired cognitive processing, as indexed by working memory capacity. This is a plausible hypothesis because oculomotor regions have direct magnocellular inputs, and the stimuli used in most antisaccade tasks strongly activate the magnocellular visual pathway. In the current study, we examined both prosaccade and antisaccade performance in PSZ (N = 22) and matched healthy control subjects (HCS; N = 22) with Gabor stimuli designed to preferentially activate the magnocellular pathway, the parvocellular pathway, or both pathways. We also measured working memory capacity. PSZ exhibited impaired antisaccade performance relative to HCS across stimulus types, with impairment even for stimuli that minimized magnocellular activation. Although both sensory thresholds and working memory capacity were impaired in PSZ, only working memory capacity was correlated with antisaccade accuracy, consistent with a cognitive rather than sensory origin for the antisaccade deficit.
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