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.
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.
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.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.