Electrophysiological and behavioral evidence reveals the effects of trait anxiety on contingent attentional capture.

Few studies have investigated the effects of anxiety on contingent attentional capture. The present study examined contingent attentional capture in trait anxiety by applying a rapid serial visual presentation (RSVP) paradigm during electroencephalographic recording. Overall, the behavioral and electrophysiological results showed a larger capture effect when a distractor was the same color as the target compared to when the distractor was not of the target color. Moreover, high-anxiety individuals showed a larger N2pc in the target colored distractor condition and nontarget colored distractor condition compared to the distractor-absent condition. In addition, the reaction time was slower when distractors were presented in the left visual field compared to when they were in the right visual field. This pattern was not seen in low-anxiety individuals. The findings may indicate that high-anxiety individuals allocate attention to the target less efficiently and have reduced suppression of distractors compared to low-anxiety individuals who could suppress attention to the distractors more efficiently. Future work could valuably investigate the consequences of such differences in terms of benefits and disruption associated with attentional capture differences in a range of anxious populations in different risk monitoring situations.

Cancellation but not restraint ability is modulated by trait anxiety: An event-related potential and oscillation study using Go-Nogo and stop-signal tasks.

BACKGROUND: Trait anxiety has a detrimental effect on attention, which further leads to dysfunction of inhibitory control. However, there is no study examining how trait anxiety modulates inhibitory abilities on restraint and cancellation in the same subjects. Therefore, we aimed to use electrophysiological recordings to interrogate whether and to what extent trait anxiety modulated these two kinds of inhibitory functions. The Cognitive Failures Questionnaire (CFQ), a self-reported assessment of daily absentmindedness, was also used to examine its association with inhibition-related electrophysiological indicators. METHODS: Forty subjects were recruited from the top 10% (Higher Trait Anxiety [HTA], n= 20) and last 10% (Lower Trait Anxiety [LTA], n= 20) of the trait anxiety score distribution from 400 college students. During electrophysiological recordings, the Go-Nogo and stop-signal tasks were performed, which evaluated the abilities of restraint and cancellation, respectively. RESULTS: The HTA and LTA groups showed a comparable behavioral performance of restraint and cancellation abilities. However, the results of time-frequency analysis revealed that those with HTA demonstrated a stronger power of alpha oscillations (600‒1000 ms) in response to Stop trials in the stop-signal task, compared with individuals with LTA. Such oscillatory activity was positively correlated with the CFQ score. There was no significant between-group difference of the brain activation in the Go-Nogo task. LIMITATIONS: Future studies can recruit both individuals with trait anxiety and anxiety disorders to clarify the boundaries between healthy and pathological worries in terms of cancellation ability. CONCLUSIONS: cancellation, but not restraint, is modulated by trait anxiety.

Effects of Trait Anxiety on Error Processing and Post-error Adjustments: An Event-Related Potential Study With Stop-Signal Task.

The present study aimed to use event-related potentials with the stop-signal task to investigate the effects of trait anxiety on inhibitory control, error monitoring, and post-error adjustments. The stop-signal reaction time (SSRT) was used to evaluate the behavioral competence of inhibitory control. Electrophysiological signals of error-related negativity (ERN) and error positivity (Pe) were used to study error perception and error awareness, respectively. Post-error slowing (PES) was applied to examine the behavioral adjustments after making errors. The results showed that SSRT and PES did not differ significantly between individuals with high trait anxiety (HTA) and those with low trait anxiety (LTA). However, individuals with HTA demonstrated reduced ERN amplitudes and prolonged Pe latencies than those with LTA. Prolonged Pe latencies were also significantly associated with poorer post-error adjustments. In conclusion, HTA led to reduced cortical responses to error monitoring. Furthermore, inefficient conscious awareness of errors might lead to maladaptive post-error adjustments.

Altered mismatch response precedes gray matter atrophy in subjective cognitive decline.

The cross-sectional identification of subjective cognitive decline (SCD) in cognitively normal adults is particularly important for the early effective prevention or intervention of the future development of mild cognitive impairments (MCI) or Alzheimer's disease (AD). A pre-attentive neurophysiological signal that reflects the brain's ability to detect the changes of the environment is called mismatch negativity (MMN) or its magnetic counterpart (MMNm). It has been shown that patients with MCI or AD demonstrate reduced MMN/MMNm responses, while the exact profile of MMN/MMNm in SCD is substantially unknown. We applied magnetoencephalographic recordings to interrogate MMNm activities in healthy controls (HC, n = 29) and individuals with SCD (n = 26). Furthermore, we analyzed gray matter (GM) volumes in the MMNm-related regions through voxel-based morphometry and performed apolipoprotein E4 (APOE4) genotyping for all the participants. Our results showed that there were no significant differences in GM volume and proportions of APOE4 carriers between HC and SCD groups. However, individuals with SCD exhibited weakened z-corrected MMNm responses in the left inferior parietal lobule and right inferior frontal gyrus (IFG) as compared to HC. Based on the regions showing significant between-group differences, z-corrected MMNm amplitudes of the right IFG significantly correlated with the memory performance among the SCD participants. Our data suggest that neurophysiological changes of the brain, as indexed by MMNm, precede structural atrophy in the individuals with SCD compared to those without SCD.