Testing sensory and cognitive explanations of the antisaccade deficit in schizophrenia.

Bibliographic Data

ID23136335
AuthorsMordechai Z Cohen (0000-0002-8584-6982, corresponding author), Carly J Leonard (0000-0003-1302-7491), Benjamin M Robinson, Samuel T Kaiser, Britta Hahn (0000-0002-1968-8453), Clara McClenon, Alex N Harvey, Steven J Luck (0000-0002-3725-1474), James M Gold (0000-0002-0109-9554)
Year2013
Volume122
Issue4
Pages1111-1120
Publication date2013-11-01
Peer ReviewedYes
Open AccessNo
TypeARTICLE
VenueJournal of Abnormal Psychology (JOURNAL)
Journal identifiersISSN: 0021-843X • E-ISSN: 1939-1846
PublisherAmerican Psychological Association (APA) (PUBLISHER)
DOI10.1037/a0034956
PMID24364614
PMCIDPMC3929125
OpenAlexW24364614
LanguageEN
Citations received17

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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