Working memory is very sensitive to acute sleep deprivation, and many studies focus on the brain areas or network activities of working memory after sleep deprivation. However, little is known about event-related potential (ERP)-related changes in working memory after sleep loss. The purpose of this research was to explore the effects of 36 h of total sleep deprivation (TSD) on working memory through ERPs. Sixteen healthy college students performed working memory tasks while rested and after 36 h of TSD, and electroencephalography (EEG) data were simultaneously recorded while the subjects completed working memory tasks that included different types of stimulus materials. ERP data were statistically analyzed using repeated measurements analysis of variance to observe the changes in the working memory-related N2-P3 components. Compared with baseline before TSD, the amplitude of N2-P3 components related to working memory decreased, and the latency was prolonged after TSD. However, the increased amplitude of the P2 wave and the prolonged latency were found after 36 h of TSD. Thus, TSD can impair working memory capacity, which is characterized by lower amplitude and prolonged latency.

Sleep deprivation (SD) is very common in modern society and has a profound effect on cognitive function, in particular on working memory (WM). This type of memory is required for completion of many tasks and is adversely affected by SD. However, the cognitive neural mechanism by which SD affects WM, remains unclear. In this study, we investigated the changes in the brain network involved in WM after SD. Twentytwo healthy subjects underwent functional magnetic resonance imaging scan while in a state of resting wakefulness and again after 36 h of total SD and performed a WM task before each scanning session. Nineteen main nodes of the default mode network (DMN), dorsal attention network (DAN), fronto-parietal network (FPN), salience network (SN), and other networks were selected for functional analysis of brain network connections. Functional connectivity measures were computed between seed areas for region of interest (ROI)-to-ROI analysis and to identify patterns of ROI-to-ROI connectivity. The relationship between the significant changes in functional connectivity in the brain network and WM performance were then examined by Pearson's correlation analysis. WM performance declined significantly after SD. Compared with the awake state, the functional connectivity between DAN and DMN significantly increased after SD while that between FPN and DMN significantly decreased. Correlation analysis showed that the enhanced functional connectivity between DAN and DMN was negatively correlated with the decline in WM performance and that the decline in functional connectivity between FPN and DMN was positively correlated with decreased WM performance. These findings suggested that SD may affect WM by altering the functional connectivity among DMN, DAN, and FPN.

Total sleep deprivation (TSD) negatively affects cognitive function. Previous research has focused on individual variation in cognitive function following TSD, but we know less about how TSD influences the lateralization of spatial working memory. This study used event-related-potential techniques to explore asymmetry in spatial-working-memory impairment. Fourteen healthy male participants performed a two-back task with electroencephalogram (EEG) recordings conducted at baseline and after 36 h of TSD. We selected 12 EEG points corresponding to left and right sides of the brain and then observed changes in N2 and P3 components related to spatial working memory. Before TSD, P3 amplitude differed significantly between the left and right sides of the brain. This difference disappeared after TSD. Compared with baseline, P3 amplitude decreased for a duration as extended as the prolonged latency of N2 components. After 36 h of TSD, P3 amplitude decreased more in the right hemisphere than the left. We therefore conclude that TSD negatively affected spatial working memory, possibly through removing the right hemisphere advantage.

Sleep deprivation (SD) induces a negative emotional experience due to a prolonged time spent awake. However, few studies have focused on the mechanism underlying communication within brain networks or alterations during this emotional deterioration. We propose that negative reward judgment is important in poor emotional processing after SD, which will be reflected in functional connectivity in the reward network. We sought to analyze alterations in functional connectivity within the reward network and cerebral cortex. Furthermore, we analyzed changes in functional connectivity correlation with negative emotional experience after SD. Twenty-six healthy volunteers participated in this study. Two resting-state fMRI scans were obtained from the participants, once during resting wakefulness, and once after 36 h of total SD. The bilateral nucleus accumbens (NAc) was selected as a seed region for region of interest (ROI)-to-ROI functional connectivity analysis. Correlation analyses between functional connectivity alterations within the reward network and negative emotional experience were also performed. We found that SD decreased functional connectivity between the left NAc and anterior cingulate cortex (ACC) compared with resting wakefulness. There was a decreased functional connectivity with the ACC and right inferior frontal gyrus (IFG) after SD in the right NAc. Furthermore, decreased functional connectivity between the right NAc and right IFG, and NAc and ACC was negatively correlated with emotional experience scores. Sleep deprivation decreased functional connectivity within the reward network. This may be associated with the enhanced negative emotional experience that was found after total sleep deprivation.

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