Total sleep deprivation (TSD) leads to cognitive decline; however, the neurophysiological mechanisms underlying resting-state electroencephalogram (EEG) changes after TSD remain unclear. In this study, 42 healthy adult participants were subjected to 36 h of sleep deprivation (36 h TSD), and resting-state EEG data were recorded at baseline, after 24 h of sleep deprivation (24 h TSD), and after 36 h TSD. The analysis of resting-state EEG at baseline, after 24 h TSD, and after 36 h TSD using source localization analysis, power spectrum analysis, and functional connectivity analysis revealed a decrease in alpha-band power and a significant increase in delta-band power after TSD and impaired functional connectivity in the default mode network, precuneus, and inferior parietal lobule. The cortical activities of the precuneus, inferior parietal lobule, and superior parietal lobule were significantly reduced, but no difference was found between the 24 h and 36 h TSD groups. This may indicate that TSD caused some damage to the participants, but this damage temporarily slowed during the 24 h to 36 h TSD period.

Background: Previous studies revealed that sleep deprivation (SD) impairs risk perception and leads to poor decision-making efficiency. However, how risk perception is related to brain regions’ communication after SD has not been elucidated. In this study, we investigated the neuropsychological mechanisms of SD-impaired risk perception. Methods: Nineteen healthy male adults were recruited and underwent resting-state functional magnetic resonance imaging during a state of rested wakefulness and after nearly 36 h of total SD. They then completed the balloon analog risk task, which was used to measure the risk perception ability of risky decision-making. Regional homogeneity (ReHo) and voxel-wise functional connectivity were used to investigate neurobiological changes caused by SD. Correlation analysis was used to investigate the relationship between changes in ReHo, function, and risk perception. Results: At the behavioral level, risk perception decreased after 36 h of SD. At the neural level, SD induced a significant increase in ReHo in the right postcentral gyrus and was positively correlated with risk perception changes. The functional connectivity between the right postcentral gyrus, left medial temporal gyrus, and right inferior temporal gyrus was enhanced. Critically, increased right postcentral gyrus and right inferior temporal gyrus connectivity positively correlated with changes in risk perception. Conclusions: SD impairs the risk perception associated with altered postcentral connectivity. The brain requires more energy to process and integrate sensory and perceptual information after SD, which may be one possible reason for decreased risk perception ability after SD.

Sleep deprivation leads to reduced inhibitory control in individuals. However, the underlying neural mechanisms are poorly understood. Accordingly, this study aimed to investigate the effects of total sleep deprivation (TSD) on inhibitory control and their neuroelectrophysiological mechanisms from the perspective of the time course of cognitive processing and brain network connectivity, using event-related potential (ERP) and resting-state functional connectivity techniques. Twenty-five healthy male participants underwent 36 h of TSD (36-h TSD), completing Go/NoGo tasks and resting-state data acquisition before and after TSD; their behavioral and electroencephalogram data were recorded. Compared to baseline, participants’ false alarms for NoGo stimuli increased significantly (t = −4.187, p < 0.001) after 36-h TSD. ERP results indicated that NoGo-N2 negative amplitude increased and latency was prolonged (t = 4.850, p < 0.001; t = −3.178, p < 0.01), and NoGo-P3 amplitude significantly decreased and latency was prolonged (t = 5.104, p < 0.001; t = −2.382, p < 0.05) after 36-h TSD. Functional connectivity analysis showed that the connectivity of the default mode and visual networks in the high alpha band was significantly reduced after TSD (t = 2.500, p = 0.030). Overall, the results suggest that the negative amplitude increase in N2 after 36-h TSD may reveal that more attention and cognitive resources are invested after TSD; the significant decrease in P3 amplitude may indicate the impairment of advanced cognitive processing. Further functional connectivity analysis indicated impairment of the brain’s default mode network and visual information processing after TSD.

Purpose: This study explores the status of pandemic fatigue, predictors, and their mechanisms of action based on a stress-response framework and a parallel model of future-oriented response. Patients and methods: Study 1 investigated 8426 Chinese adult residents’ understanding of and willingness to cooperate with the pandemic prevention and control policies and Study 2 surveyed 1635 Chinese residents on their activeness of pandemic prevention and control (APPC), pandemic risk perception, perceived stress, and future-oriented coping. Results: Study 1 found that public understanding of and willingness to cooperate with prevention policies were significantly lower in 2022 than in 2020 and 2021. Study 2 found that risk perception negatively predicted the APPC; perceived stress and preventive coping significantly mediated the relationship between risk perception and APPC; but perceived stress and proactive coping did not significantly mediate the relationship between risk perception and APPC. Conclusion: This revealed an increase in public fatigue in the third year of the pandemic. Pandemic fatigue can be predicted by pandemic risk perception, but the direct pathway of action is not significant and requires the mediation of perceived stress and preventive coping.

Previous studies have shown that males with substance use disorder (SUD) in their first mandatory detoxification experience high rates of depression. It is unknown whether this high depression incidence contributes to impaired inhibition. In this work, two studies were undertaken to examine the role of depression in cognitive inhibition in heroin and methamphetamine withdrawal. We used the Beck Depression Inventory (BDI) and the self-control scale (SCS) to explore the relationship between depression and impulse inhibition in patients participating in mandatory drug treatment for the first time (Study 1). The results showed that depression negatively predicted impulse inhibition. The Stroop color–word interference task was used to explore the role of patients’ depression in their inhibitory abilities (Study 2). The results showed that the high-depression group had weaker inhibition performances in the Stroop color–word interference task compared to the low-depression group. This study shows that cognitive inhibition is weaker in people with high-depression addiction than in those with low depression. This result suggests that attention should be paid to the role of depressive comorbidity when conducting working memory training treatment for substance addiction.

Patients with heroin use disorder (HUD) often exhibit trait impulsivity, which may be an important factor in and a good predictor of addiction. However, the factor structure of HUD trait impulsivity (motor, attentional, and nonplanning) and its neural correlates are not yet known. A total of 24 male volunteers with HUD and 16 healthy control volunteers were recruited for this cross-sectional study. The Barratt Impulsiveness Scale (BIS-11) and resting-state functional magnetic resonance imaging (rs-fMRI) were employed using the insula as a seed point in an effort to understand the association between trait impulsivity and its intrinsic factors and functional connectivity (FC) between the insula and the whole brain. The HUD group in this study exhibited higher total trait impulsivity scores, motor impulsivity, and nonplanning impulsivity than the control group. Changes in FC between the right insula and the lateral occipital cortex and the right angular gyrus were significantly positively correlated with total trait impulsivity scores, motor impulsivity, and nonplanning impulsivity, whereas changes in the FC between the left insula and the left superior frontal gyrus and left frontopolar brain region were significantly negatively correlated with trait impulsivity. Thus, the insula may serve as an important biomarker for identifying trait impulsivity and its intrinsic factor structure in patients with HUDs.