Error detection in the stop signal task

Chevrier, Andre; Schachar, Russell

doi:10.1016/j.neuroimage.2010.06.056

Cited by 46 publications

(59 citation statements)

References 92 publications

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“…Our finding that d-amphetamine selectively reduced post-error slowing is consistent with evidence that structures modulating dopamine output play a key role in processing errors (Chevrier and Schachar 2010) and can be viewed in the context of several of these theories.…”

Section: Discussionsupporting

confidence: 88%

Effect of d-amphetamine on post-error slowing in healthy volunteers

2011

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Rationale Post-error slowing has long been considered a sign of healthy error detection and an important component of cognitive function. However, the neuropharmacological processes underlying post-error slowing are poorly understood. Objectives This study investigated the effect of the dopamine agonist d-amphetamine on post-error slowing and secondarily, the potential mediator of drug-induced euphoria and potential moderators of personality and baseline task performance. Methods Healthy male and female participants (N=110) completed four study sessions, at which d-amphetamine (placebo 5, 10, 20 mg) was administered under double-blind, counter-balanced conditions. At each session, participants completed subjective drug effect assessments and a working memory task (N-back) to measure post-error slowing. They completed the Multidimensional Personality Questionnaire (MPQ) during screening. Results Amphetamine (20 mg) reduced post-error slowing, consistent with a dampened behavioral reactivity to errors. This was not related to drug-induced euphoria. Although higher scores on MPQ constraint were related to less post-error slowing under placebo conditions, neither personality nor baseline cognitive performance moderated the effects of amphetamine on post-error slowing. Conclusions The finding that amphetamine reduced post-error slowing supports the idea that dopamine plays a role in error stimulus processing. The finding is discussed in relation to an existing literature on the mechanisms and function of behavioral and electrophysiological indices of error sensitivity.

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Section: Discussionsupporting

confidence: 88%

Effect of d-amphetamine on post-error slowing in healthy volunteers

2011

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“…Supporting this explanation, differential activation patterns of pFC during error detection and subsequent processing have indeed been shown when these phases were analyzed as separate within-trial processes. For instance, Chevrier and Schachar (2010) showed deactivation of medial pFC during error detection but increased activity in the same regions during subsequent PES. Activity within these structures was also found to decrease during cognitive tasks requiring mental effort or goaldirected behaviors (Tomasi, Ernst, Caparelli, & Chang, 2006;Greicius & Menon, 2004;Raichle et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Spatio-temporal Brain Dynamics Mediating Post-error Behavioral Adjustments

Manuel

Bernasconi

Murray

et al. 2012

Journal of Cognitive Neuroscience

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Abstract■ Optimal behavior relies on flexible adaptation to environmental requirements, notably based on the detection of errors. The impact of error detection on subsequent behavior typically manifests as a slowing down of RTs following errors. Precisely how errors impact the processing of subsequent stimuli and in turn shape behavior remains unresolved. To address these questions, we used an auditory spatial go/no-go task where continual feedback informed participants of whether they were too slow. We contrasted auditory-evoked potentials to left-lateralized go and right no-go stimuli as a function of performance on the preceding go stimuli, generating a 2 × 2 design with "preceding performance" (fast hit [FH], slow hit [SH]) and stimulus type (go, no-go) as within-subject factors. SH trials yielded SH trials on the following trials more often than did FHs, supporting our assumption that SHs engaged effects similar to errors. Electrophysiologically, auditory-evoked potentials modulated topographically as a function of preceding performance 80-110 msec poststimulus onset and then as a function of stimulus type at 110-140 msec, indicative of changes in the underlying brain networks. Source estimations revealed a stronger activity of prefrontal regions to stimuli after successful than error trials, followed by a stronger response of parietal areas to the no-go than go stimuli. We interpret these results in terms of a shift from a fast automatic to a slow controlled form of inhibitory control induced by the detection of errors, manifesting during low-level integration of task-relevant features of subsequent stimuli, which in turn influences response speed. ■

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“…Extensive research has shown that performance monitoring engages a widespread network of cortical and subcortical brain regions (for a recent review see Ullsperger et al, 2014). The prefrontal cortex (PFC) has been identified as a key node for executive control (Alvarez and Emory, 2006;Garavan et al, 2002), while the basal ganglia (BG) and mediofrontal structures, here particularly the anterior cingulate cortex (ACC), are critically involved in error and feedback processing (Ullsperger et al, 2014;Nee et al, 2011;Hollerman et al, 2000;Chevrier and Schachar, 2010). The cerebellum has been shown to also contribute to performance monitoring.…”

Section: Introductionmentioning

confidence: 99%