scholarly journals Total sleep deprivation reduces top-down regulation of emotion without altering bottom-up affective processing

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0256983
Author(s):  
Anthony R. Stenson ◽  
Courtney A. Kurinec ◽  
John. M. Hinson ◽  
Paul Whitney ◽  
Hans P. A. Van Dongen

Sleep loss is reported to influence affective processing, causing changes in overall mood and altering emotion regulation. These aspects of affective processing are seldom investigated together, making it difficult to determine whether total sleep deprivation has a global effect on how affective stimuli and emotions are processed, or whether specific components of affective processing are affected selectively. Sixty healthy adults were recruited for an in-laboratory study and, after a monitored night of sleep and laboratory acclimation, randomly assigned to either a total sleep deprivation condition (n = 40) or a rested control condition (n = 20). Measurements of mood, vigilant attention to affective stimuli, affective working memory, affective categorization, and emotion regulation were taken for both groups. With one exception, measures of interest were administered twice: once at baseline and again 24 hours later, after the sleep deprived group had spent a night awake (working memory was assessed only after total sleep deprivation). Sleep deprived individuals experienced an overall reduction in positive affect with no significant change in negative affect. Despite the substantial decline in positive affect, there was no evidence that processing affectively valenced information was biased under total sleep deprivation. Sleep deprived subjects did not rate affective stimuli differently from rested subjects, nor did they show sleep deprivation-specific effects of affect type on vigilant attention, working memory, and categorization tasks. However, sleep deprived subjects showed less effective regulation of negative emotion. Overall, we found no evidence that total sleep deprivation biased the processing of affective stimuli in general. By contrast, total sleep deprivation appeared to reduce controlled processing required for emotion regulation.

2020 ◽  
Vol 30 (10) ◽  
pp. 2050051
Author(s):  
Feng Fang ◽  
Thomas Potter ◽  
Thinh Nguyen ◽  
Yingchun Zhang

Emotion and affect play crucial roles in human life that can be disrupted by diseases. Functional brain networks need to dynamically reorganize within short time periods in order to efficiently process and respond to affective stimuli. Documenting these large-scale spatiotemporal dynamics on the same timescale they arise, however, presents a large technical challenge. In this study, the dynamic reorganization of the cortical functional brain network during an affective processing and emotion regulation task is documented using an advanced multi-model electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) technique. Sliding time window correlation and [Formula: see text]-means clustering are employed to explore the functional brain connectivity (FC) dynamics during the unaltered perception of neutral (moderate valence, low arousal) and negative (low valence, high arousal) stimuli and cognitive reappraisal of negative stimuli. Betweenness centralities are computed to identify central hubs within each complex network. Results from 20 healthy subjects indicate that the cortical mechanism for cognitive reappraisal follows a ‘top-down’ pattern that occurs across four brain network states that arise at different time instants (0–170[Formula: see text]ms, 170–370[Formula: see text]ms, 380–620[Formula: see text]ms, and 620–1000[Formula: see text]ms). Specifically, the dorsolateral prefrontal cortex (DLPFC) is identified as a central hub to promote the connectivity structures of various affective states and consequent regulatory efforts. This finding advances our current understanding of the cortical response networks of reappraisal-based emotion regulation by documenting the recruitment process of four functional brain sub-networks, each seemingly associated with different cognitive processes, and reveals the dynamic reorganization of functional brain networks during emotion regulation.


2007 ◽  
Vol 21 (6) ◽  
pp. 787-795 ◽  
Author(s):  
Travis H. Turner ◽  
Sean P. A. Drummond ◽  
Jennifer S. Salamat ◽  
Gregory G. Brown

2020 ◽  
Vol 14 ◽  
Author(s):  
Ziyi Peng ◽  
Cimin Dai ◽  
Xiaoping Cai ◽  
Lingjing Zeng ◽  
Jialu Li ◽  
...  

2017 ◽  
Vol 40 ◽  
pp. e110
Author(s):  
A. Gerhardsson ◽  
H. Fischer ◽  
M. Lekander ◽  
G. Kecklund ◽  
J. Axelsson ◽  
...  

SLEEP ◽  
2017 ◽  
Vol 40 (suppl_1) ◽  
pp. A56-A57
Author(s):  
E Hennecke ◽  
D Lange ◽  
J Fronczek ◽  
A Bauer ◽  
D Aeschbach ◽  
...  

2020 ◽  
Author(s):  
Zi-Yi Peng ◽  
Yi Wang ◽  
Ci-Min Dai ◽  
Le-Tong Wang ◽  
Song-Yue Xie ◽  
...  

Abstract Background: Considering the well-known detrimental effects of sleep deprivation (SD) on cognitive function and quality of life, sleep disturbances represent a major physical and mental health issue. Because working memory plays an important role in many complex cognitive processes, it is necessary to identify strategies that can effectively counteract the negative effects of SD on working memory. Methods: In the present study, we utilized event-related potentials (ERPs) to investigate the restorative effect of 8 h of recovery sleep (RS) on working memory impairments induced by 36 h of total sleep deprivation (TSD). We analyzed data from 16 healthy male participants. All participants completed a 2-back working memory task before and after 36 h of TSD and after 8 h of RS. Electroencephalography (EEG) data were recorded during the task. Results: N2 and P3 components related to working memory exhibited low-amplitude slow-wave characteristics following 36 h of TSD. Significant decreases in the latency of the N2 component were observed after 8 h of RS. RS also induced significant increases in the amplitude of the P3 component, along with significant decreases in P3 latency. Conclusions: Eight hours of RS also attenuated decreases in working memory performance caused by 36 h of TSD. However, the effects of RS appear to be limited.


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