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.

Background: Spatial working memory is crucial for processing visual and spatial information, serving as a foundation for complex cognitive tasks. However, the effects of prolonged sleep deprivation on its dynamics and underlying neural mechanisms remain unclear. This study aims to investigate the specific trends and neural mechanisms underlying spatial working memory alterations during 36 h of acute sleep deprivation. Methods: Twenty participants underwent a 36 h protocol of acute sleep deprivation. Utilizing the spatial 2-back task for assessing spatial working memory, combined with event-related potential (ERP) technology, we compared behavioral and neural responses at four critical time points—before deprivation, and after 12, 24, and 36 h of sleep deprivation—to uncover dynamic cognitive changes. Results: The findings indicate that the impact of sleep deprivation on spatial working memory exhibits significant temporal dependence. After 24 h of deprivation, both behavioral performance and ERP component amplitudes showed significant declines. During the period from 24 to 36 h, the amplitudes of the P2, N2, and P3 components exhibited a recovery trend, potentially reflecting neural compensatory mechanisms. Conclusions: The impact of 36 h acute sleep deprivation on spatial working memory is characterized by time-dependent and phase-specific effects. Initially, sleep deprivation leads to severe cognitive depletion, followed by an adaptive compensatory phase where neural mechanisms may partially restore function. These findings highlight the non-linear nature of cognitive impairment due to sleep deprivation, involving complex self-regulatory and compensatory mechanisms, with implications for understanding cognitive resilience and adaptive processes.

The impact of sleep deprivation on working memory can only be reversed by recovery sleep (RS). However, there are limited electrophysiological studies on the effect of RS on the improvement in working memory after sleep deprivation, and the changes in the early components of event-related potentials (ERPs) before and after RS are still unclear. Therefore, this study aims to explore the effects of RS on the earlier ERP components related to object working memory following 36 h of total sleep deprivation (TSD). Twenty healthy male participants performed an object working memory task after 36 h of TSD and after 8 h of RS. Electroencephalogram data were recorded accordingly while the task was performed. Repeated ANOVA showed that P2 amplitudes related to object working memory decreased significantly after 8 h of RS compared to after a 36 h period of TSD, but there was no significant difference from baseline (BS), which indicates a trend of recovery to the baseline state. An 8 h RS can partially improve impaired object working memory caused by TSD. However, a longer period of RS is needed for the complete recovery of cognitive function after a long period of TSD.

Sleep is crucial for optimal sensorimotor integration, a fundamental process enabling coordinated motor responses to sensory inputs. However, the neurophysiological mechanisms through which acute sleep deprivation impairs this integration remain incompletely understood. This study investigates the impact of acute sleep deprivation on postural balance and elucidates the underlying multilayered mechanisms using a combination of behavioral, psychophysiological, and neuroimaging indicators. Twenty-five healthy young participants underwent 36 hours of total sleep deprivation. Before and after the deprivation period, data were collected on postural stability metrics, psychomotor vigilance (PVT), critical flicker fusion frequency (CFF), resting-state electroencephalography (EEG), and resting-state functional magnetic resonance imaging (fMRI). Correlation analyses were performed to examine the associations between changes in behavioral performance (postural balance, PVT, and CFF) and alterations in psychophysiological measures (EEG spectral power and fMRI resting-state activity). Sleep deprivation significantly impaired balance, particularly with eyes closed, and was associated with reduced alertness and increased visual fatigue. EEG revealed elevated low-frequency power in occipital and frontal regions. fMRI showed altered activity in sensorimotor-related areas, especially the caudate nucleus, cerebellum, and thalamus. Acute sleep deprivation impairs postural stability by disrupting key nodes and networks involved in sensorimotor integration. This disruption manifests as reduced visual cortical excitability (affecting sensory input), weakened cognitive regulation within the frontoparietal network (impairing sensory processing and motor planning), and altered functional status of subcortical sensorimotor hubs (compromising motor coordination and feedback). These findings demonstrate that sleep deprivation compromises the neural circuitry governing the transformation of sensory information into appropriate motor outputs for balance control. This study provides comprehensive multimodal neuroimaging evidence for the neurobiological mechanisms linking insufficient sleep to impaired sensorimotor function.