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

Leonard, Carly J.; Robinson, Benjamin M.; Kaiser, Samuel T.; Hahn, Britta; McClenon, Clara; Harvey, Alex; Luck, Steven J.; Gold, James M.

doi:10.1037/a0034956

Cited by 12 publications

(15 citation statements)

References 66 publications

(97 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast to the current results, Leonard, et al (in press) found that the antisaccade deficit in PSZ was equivalent for stimuli designed to preferentially activate the magnocellular, parvocellular, or both pathways. Unlike the antisaccade task, in which only a single object is presented on the screen, the current task involves simultaneous competition between the target and multiple distractors.…”

Section: Discussioncontrasting

confidence: 99%

“…When the target is presented in isolation in the antisaccade task, it captures attention so strongly that the weighting of the magnocellular and parvocellular signals will have little or no effect on the initial capture. The exaggerated antisaccade effect in PSZ appears to reflect impairments in higher-level executive processes rather than dysregulation of the magnocellular pathway (Leonard, et al, in press). …”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Enhanced distraction by magnocellular salience signals in schizophrenia

et al. 2014

Self Cite

View full text Add to dashboard Cite

Research on schizophrenia has provided evidence of both impaired attentional control and dysfunctional magnocellular sensory processing. The present study tested the hypothesis that these impairments may be related, such that people with schizophrenia would be differentially distracted by stimuli that strongly activate the magnocellular pathway. To accomplish this, we used a visual attention paradigm from the basic cognitive neuroscience literature designed to assess the capture of attention by salient but irrelevant stimuli. Participants searched for a target shape in an array of non-target shapes. On some trials, a salient distractor was presented that either selectively activated the parvocellular system (parvo-biased distractors) or activated both the magnocellular and parvocellular systems (magno+parvo distractors). For both manual reaction times and eye movement measures, the magno+parvo distractors captured attention more strongly than the parvo-biased distractors in people with schizophrenia, but the opposite pattern was observed in matched healthy control participants. These results indicate that attentional control deficits in schizophrenia may arise, at least in part, by means of an interaction with magnocellular sensory dysfunction.

show abstract

Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Enhanced distraction by magnocellular salience signals in schizophrenia

et al. 2014

Self Cite

View full text Add to dashboard Cite

show abstract

“…Antisaccade here is measured as the proportion of trials in which the participant initially looked toward the spot of light, rather than away from it. Antisaccade eye movement has long been a strong candidate endophenotype for schizophrenia, replicated in dozens of studies over recent decades (Radant et al 2010; Leonard et al 2013). Antisaccade eye tracking error is highly heritable (Vaidyanathan et al 2014 b ), present in first-degree relatives of individuals with schizophrenia, and co-segregates within families (Calkins et al 2004; Radant et al 2010).…”

Section: Methodsmentioning

confidence: 99%

Psychophysiological endophenotypes to characterize mechanisms of known schizophrenia genetic loci

et al. 2016

View full text Add to dashboard Cite

Background Endophenotypes are laboratory-based measures hypothesized to lie in the causal chain between genes and clinical disorder, and to serve as a more powerful way to identify genes associated with the disorder. One promise of endophenotypes is that they may assist in elucidating the neurobehavioral mechanisms by which an associated genetic polymorphism affects disorder risk in complex traits. We evaluated this promise by testing the extent to which variants discovered to be associated with schizophrenia through large-scale meta-analysis show associations with psychophysiological endophenotypes. Method We genome-wide genotyped and imputed 4905 individuals. Of these, 1837 were whole-genome-sequenced at 11× depth. In a community-based sample, we conducted targeted tests of variants within schizophrenia-associated loci, as well as genome-wide polygenic tests of association, with 17 psychophysiological endophenotypes including acoustic startle response and affective startle modulation, antisaccade, multiple frequencies of resting electroencephalogram, electrodermal activity and P300 event-related potential. Results Using single variant tests and gene-based tests we found suggestive evidence for an association between contactin 4 (CNTN4) and antisaccade and P300. We were unable to find any other variant or gene within the 108 schizophrenia loci significantly associated with any of our 17 endophenotypes. Polygenic risk scores indexing genetic vulnerability to schizophrenia were not related to any of the psychophysiological endophenotypes after correction for multiple testing. Conclusions The results indicate significant difficulty in using psychophysiological endophenotypes to characterize the genetically influenced neurobehavioral mechanisms by which genome-wide association study-identified risk loci affect disorder risk.

show abstract

“…With regard to schizophrenia, the role of early visual dysfunction (Butler et al, 2005) and their relation to higher cognitive deficits (Haenschel et al, 2007) has previously been shown, raising the question to what extent the frequent observation of increased antisaccade direction errors in schizophrenia (Hutton & Ettinger, 2006) is a consequence of visual system dysfunction. Importantly, however, it was recently demonstrated in an elegant experiment that the increase in antisaccade direction errors in schizophrenia is not due to dysfunctional visual processing in the magnocellular pathway but instead reflects deficient top-down control over automatic oculomotor responses (Leonard et al, 2013).…”

Section: Patients With Schizophreniamentioning

confidence: 99%

Response inhibition and interference control: Effects of schizophrenia, genetic risk, and schizotypy

Ettinger

Aichert²,

Wöstmann³

et al. 2017

Journal of Neuropsychology

View full text Add to dashboard Cite

The ability to inhibit inappropriate responses and suppress irrelevant information is a core feature of executive control. In this study, we provide a detailed analysis of prepotent response inhibition and interference in patients with schizophrenia. To further test the role of genetic factors and subclinical schizophrenia-like traits, we additionally studied clinically unaffected, first-degree relatives of schizophrenia patients and assessed dimensions of schizotypy in both relatives and healthy controls. Inhibition and interference control were assessed using a battery comprising the antisaccade, Stroop, stop signal, go/no-go, flanker, and Simon tasks. Schizophrenia patients differed from both relatives and controls in making more errors on the antisaccade task and having longer response times on the Stroop task, especially the incongruent condition. Patients also had general, that is, condition independent, increases in reaction times on the go/no-go and flanker tasks and made more errors on the flanker and Simon tasks, suggesting general performance impairments independent of inhibitory demand. Relatives were characterized by hypometric antisaccade amplitude gain despite normal prosaccades, suggesting a selective deficit in non-standard sensorimotor transformations. Schizotypy was correlated with inhibitory performance across a number of tasks in both relatives and controls. Generally, these effects were independent of verbal intelligence levels. Overall, the findings point to rather selective impairments of inhibitory control in the schizophrenia spectrum and confirm a previously observed deficit in antisaccade spatial accuracy as an endophenotype of schizophrenia.

show abstract

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

Cited by 12 publications

References 66 publications

Enhanced distraction by magnocellular salience signals in schizophrenia

Enhanced distraction by magnocellular salience signals in schizophrenia

Psychophysiological endophenotypes to characterize mechanisms of known schizophrenia genetic loci

Response inhibition and interference control: Effects of schizophrenia, genetic risk, and schizotypy

Contact Info

Product

Resources

About