On the basis of a review of the extant literature describing emotion-cognition interactions, the authors propose 4 methodological desiderata for studying how task-irrelevant affect modulates cognition and present data from an experiment satisfying them. Consistent with accounts of the hemispheric asymmetries characterizing withdrawal-related negative affect and visuospatial working memory (WM) in prefrontal and parietal cortices, threat-induced anxiety selectively disrupted accuracy of spatial but not verbal WM performance. Furthermore, individual differences in physiological measures of anxiety statistically mediated the degree of disruption. A second experiment revealed that individuals characterized by high levels of behavioral inhibition exhibited more intense anxiety and relatively worse spatial WM performance in the absence of threat, solidifying the authors' inference that anxiety causally mediates disruption. These observations suggest a revision of extant models of how anxiety sculpts cognition and underscore the utility of the desiderata.
Changing between cognitive tasks requires a reorganization of cognitive processes. Behavioural evidence suggests this can occur in advance of the stimulus. However, the existence or detectability of an anticipatory task-set reconfiguration process remains controversial, in part because several neuroimaging studies have not detected extra brain activity during preparation for a task switch relative to a task repeat. In contrast, electrophysiological studies have identified potential correlates of preparation for a task switch, but their interpretation is hindered by the scarcity of evidence on their relationship to performance. We aimed to: (i) identify the brain potential(s) reflecting effective preparation for a task-switch in a task-cuing paradigm that shows clear behavioural evidence for advance preparation, and (ii) characterize this activity by means of temporal segmentation and source analysis. Our results show that when advance preparation was effective (as indicated by fast responses), a protracted switchrelated component, manifesting itself as widespread posterior positivity and concurrent right anterior negativity, preceded stimulus onset for 300 ms, with sources primarily in the left lateral frontal, right inferior frontal and temporal cortices. When advance preparation was ineffective (as implied by slow responses), or made impossible by a short cue-stimulus interval (CSI), a similar component, with lateral prefrontal generators, peaked 300 ms poststimulus. The protracted prestimulus component (which we show to be distinct from P3 or contingent negative variation, CNV) also correlated over subjects with a behavioural measure of preparation. Furthermore, its differential lateralization for word and picture cues was consistent with a role for verbal self-instruction in preparatory task-set reconfiguration.
In human electrophysiology, a considerable corpus of studies using event-related potentials have investigated inhibitory processes by employing the 'go-nogo' paradigm, which requires responding to one type of event while withholding the response to another type of event. Two event-related potential waveform features (N2 and P3) have been associated with larger amplitude in nogo trials than in go trials. Traditionally, these differences were thought to reflect response inhibition. Recently, the source localization of N2 to the anterior cingulate cortex, as well as the colocalization of N2 with error-related negativity, has been interpreted in terms of conflict monitoring. In order to isolate the contribution of inhibitory processes, we matched the frequency of the go and nogo events, thus minimizing differences in response conflict between event types. A data-driven analytical procedure contrasted go with nogo events across the entire event-related potential segment and found that N2 reliably differentiated between the two conditions while P3 did not. Tomographical analyses of the N2 difference observed in conditions of equal go and nogo trial frequency localized N2 to the right ventral and dorsolateral prefrontal cortex. Because a growing body of evidence implicates these brain regions in inhibitory processes, we conclude that N2 does, at least in part, reflect inhibition.
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