15 research outputs found

    fMRI and EEG error markers.

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    <p>A. Error-related dACC activation. Statistical maps of activation at 6 s in the contrast of error vs. correct are displayed on the inflated medial cortical surfaces. The dACC ROI is outlined in black. Warm colors indicate stronger activation on errors. The gray masks cover subcortical regions in which activity is displaced in a surface rendering. Line graphs show hemodynamic response functions for correct and error trials in the vertices with maximal error-related activation in the dACC. B. The ERN. The left panel shows grand average waveforms for correct (black) and error (red) trials, time locked to the onset of the saccade. The right panel shows the difference waveform, obtained by subtracting the correct waveform from the error waveform. The thin lines on either side of the waveforms represent the standard error of the mean at each time point.</p

    Genetic dissociation between error-related dACC activation and the ERN.

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    <p>Both error markers are shown in standardized units as a function of risk allele load (677T for <i>MTHFR C677T</i>, -521C for <i>DRD4 C-521T</i>). Error bars represent within subject confidence intervals <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101784#pone.0101784-Loftus1" target="_blank">[75]</a> for each allele combination.</p

    Genetic modulation of error-related dACC activation.

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    <p>A: <i>MTHFR C677T</i>. B: <i>DRD4 C-521T</i>. Statistical maps show regressions of activation in the error vs. correct contrast on allele load. Blue colors represent a negative correlation, i.e., stronger activation associated with more 677T (A) or -521C (B) alleles. The gray masks cover subcortical regions in which activity is displaced in a surface rendering.</p

    Antisaccade paradigm.

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    <p>Schematic and timeline of the three conditions: easy, hard, and fake-hard. Each trial lasted 4 s and began with an instructional cue (300 ms), either a blue or yellow “X” that indicated whether the trial was hard or easy. The mapping of cue color to trial type was counterbalanced across participants. The cue was horizontally flanked by two white squares of 0.4° width that marked the potential locations of stimulus appearance, 10° left and right of center. The squares remained visible for the duration of each run. At 300 ms, the instructional cue was replaced by a white fixation ring of 1.3° diameter at the center of the screen. At 1800 ms, the fixation ring disappeared (200 ms gap). At 2000 ms, the fixation ring reappeared at one of the two stimulus locations, right or left with equal probability. This was the imperative stimulus to which the participant responded by making a saccade in the opposite direction. The ring remained in the peripheral location for 1000 ms and then returned to the center, where participants were instructed to return their gaze for 1000 ms before the start of the next trial. Fixation epochs were simply a continuation of this fixation display. Hard trials were distinguished by a 3 db increase in luminance of the peripheral squares starting during the gap. Except for the hard cue, fake-hard trials were identical to easy trials.</p

    Genetic modulation of the ERN.

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    <p>A: <i>MTHFR</i> C677T. B: <i>DRD4 C-</i>521T. Correct and error trial waveforms are shown for every allele combination of each polymorphism. The error-correct difference waveforms for each allele combination is shown on the right column. The thin lines on either side of the waveforms represent the standard error of the mean at each time point.</p
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