Abstract:Working memory (WM) components are altered after total sleep deprivation (TSD), both with respect to information replacement and result judgment. However, the electrophysiological mechanisms of WM alterations following sleep restriction remain largely unknown. To identify such mechanisms, event-related potentials were recorded during the n-back WM task, before and after 36 h sleep deprivation. Thirty-one young volunteers participated in this study and performed a two-back WM task with simultaneous electroencep… Show more
“…For working memory tasks, the effects of repetitive partial sleep deprivation (PSD) and TSD are not related to the level of execution load, and the effects of PSD are observed to be small ( Lo et al, 2012 ). Although in this study we only selected spatial working memory tasks, sleep deprivation also reduces the quality of information storage in pronunciation working memory ( Zhang et al, 2019 ) and damages the performance of the entire working memory system ( Peng et al, 2020 ).…”
Section: Discussionmentioning
confidence: 99%
“…Reduced amplitude and sustained latency of the P3 and N2 component are associated with prolonged sobriety ( Koslowsky and Babkoff, 1992 ; Morris et al, 1993 ; Jones and Harrison, 2001 ). A decrease in P3 volatility may reflect a reduction in individual attention and discernment of target stimuli ( Zhang et al, 2019 ). Research in the field of sleep using these techniques has linked TSD with response inhibition and working memory, and shown that working memory would be impaired after TSD.…”
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.
“…For working memory tasks, the effects of repetitive partial sleep deprivation (PSD) and TSD are not related to the level of execution load, and the effects of PSD are observed to be small ( Lo et al, 2012 ). Although in this study we only selected spatial working memory tasks, sleep deprivation also reduces the quality of information storage in pronunciation working memory ( Zhang et al, 2019 ) and damages the performance of the entire working memory system ( Peng et al, 2020 ).…”
Section: Discussionmentioning
confidence: 99%
“…Reduced amplitude and sustained latency of the P3 and N2 component are associated with prolonged sobriety ( Koslowsky and Babkoff, 1992 ; Morris et al, 1993 ; Jones and Harrison, 2001 ). A decrease in P3 volatility may reflect a reduction in individual attention and discernment of target stimuli ( Zhang et al, 2019 ). Research in the field of sleep using these techniques has linked TSD with response inhibition and working memory, and shown that working memory would be impaired after TSD.…”
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.
“…Growing evidence has demonstrated the critical impairments of SD on various cognitive abilities, especially on working memory both in younger and older healthy adults, after total SD or partial SD [14,15,[39][40][41][42][43]. Behavioral results of almost all these past studies found that subjects showed a significantly lower response accuracy rate, longer reaction time, and higher lapse rate on the working memory test after SD 4…”
Section: Working Memory and Alff Changes After Sdmentioning
Objective. To investigate whether and how the working memory impairment induced by sleep deprivation (SD) could be recovered by using repetitive transcranial magnetic stimulation (rTMS), as well as to clarify the corresponding brain activity changes. Methods. Seventeen healthy adults received one session of 5.0 Hz rTMS over the left dorsolateral prefrontal cortex (DLPFC) following 24 hours of SD. Resting state functional magnetic resonance imaging (fMRI) and working memory test were performed during a rested waking period, after SD and rTMS. The amplitude of low-frequency fluctuations (ALFF) was used to detect the spontaneous neural activity changes after both SD and rTMS. The relationship between ALFF and the performance of working memory was also assessed by using correlation analysis. Results. After SD, the participants exhibited lower response accuracies and longer reaction times on the working memory tests of letters and numbers. The decreased response accuracy of numbers was significantly improved after rTMS similarly to the state of the rested waking period after a normal night of sleep. ALFF values decreased from the rested waking period state to the state of SD in the brain regions involving the frontal gyrus, precuneus, angular gyrus, and parietal lobe which showed significantly increased ALFF after rTMS. Furthermore, significantly positive correlations were observed between changes of response accuracy and the changes of ALFF value of the inferior frontal gyrus and supramarginal gyrus. Conclusion. These results indicate that high-frequency rTMS applied over left DLPFC may contribute to the recovery of the impaired working memory after SD by modulating the neural activity of related brain regions.
“…The change to the P2 wave in working memory requirements is also very sensitive ( Smith et al, 2002 ). A study has shown that sleep pressure can significantly reduce the P2 peak amplitude in working memory and increase the latency ( Zhang L. et al, 2019 ). There are two potential reasons for the decrease in P2 peak amplitude: information processing changes and damage to information in early recognition.…”
Section: Discussionmentioning
confidence: 99%
“…Moreover, most studies have focused on long-term SD; therefore, whether low homeostatic sleep pressure has an adverse effect on individual cognitive processing and changes in the early ERP components has not yet been systematically concluded. Furthermore, there have been inconsistencies among some research findings ( Evans and Federmeier, 2007 ; Wiggins et al, 2018 ; Zhang L. et al, 2019 ).…”
Homeostatic sleep pressure can cause cognitive impairment, in which executive function is the most affected. Previous studies have mainly focused on high homeostatic sleep pressure (long-term sleep deprivation); thus, there is still little related neuro-psycho-physiological evidence based on low homeostatic sleep pressure (12 h of continuous wakefulness) that affects executive function. This study aimed to investigate the impact of lower homeostatic sleep pressure on executive function. Our study included 14 healthy young male participants tested using the Go/NoGo task in normal resting wakefulness (10:00 am) and after low homeostatic sleep pressure (10:00 pm). Behavioral data (response time and accuracy) were collected, and electroencephalogram (EEG) data were recorded simultaneously, using repeated measures analysis of variance for data analysis. Compared with resting wakefulness, the participants’ response time to the Go stimulus was shortened after low homeostatic sleep pressure, and the correct response rate was reduced. Furthermore, the peak amplitude of Go–P2 decreased significantly, and the peak latency did not change significantly. For NoGo stimulation, the peak amplitude of NoGo–P2 decreased significantly (p < 0.05), and the peak latency was significantly extended (p < 0.05). Thus, the P2 wave is likely related to the attention and visual processing and reflects the early judgment of the perceptual process. Therefore, the peak amplitude of Go–P2 and NoGo–P2 decreased, whereas the peak latency of NoGo–P2 increased, indicating that executive function is impaired after low homeostatic sleep pressure. This study has shown that the P2 wave is a sensitive indicator that reflects the effects of low homeostatic sleep pressure on executive function, and that it is also an important window to observe the effect of homeostatic sleep pressure and circadian rhythm on cognitive function.
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