Examining the Causal Effects of Sleep Deprivation on Emotion Regulation and Its Neural Mechanisms

2020 ◽  
Vol 32 (7) ◽  
pp. 1289-1300
Author(s):  
Maheen Shermohammed ◽  
Laurel E. Kordyban ◽  
Leah H. Somerville
Keyword(s):  
Negative Affect ◽  
Sleep Deprivation ◽  
Control Systems ◽  
Emotional Reactivity ◽  
Neural Mechanisms ◽  
Causal Effects ◽  
Neural Responses ◽  
Active Regulation ◽  
Rate Deceleration ◽  
The Way

Cognitive reappraisal (CR) is a strategy used to regulate emotions that is thought to be effective but effortful, relying on higher-order cognitive control systems to engage in active regulation. Sleep deprivation is believed to impair the functioning of these control systems, suggesting that it may impede the ability to implement CR effectively. This study tested the causal effects of sleep deprivation on emotional reactivity and the neurobiological systems underlying CR. We employed a within-subject crossover design in which participants underwent fMRI scanning twice, once when fully rested and once after a night of total sleep deprivation. During scans, participants passively viewed or used CR to down-regulate their emotional response to negative and neutral images. Contrary to hypotheses, both self-reported negative affect ratings and neural responses to the images indicated no difference in the way participants implemented CR when sleep deprived and when fully rested. Meanwhile, neural regions that showed distinct reactivity responses to negative relative to neutral images lost this specificity under deprived conditions. Negative affect ratings and heart rate deceleration, a physiological response typically evoked by aversive pictures, exhibited a similar blunting. Together, these results suggest that, although sleep deprivation may reduce the discrimination between emotional reactivity responses to negative and neutral stimuli, it does not impact CR the way it is presently studied.

scholarly journals 0262 An Exploratory Examination of the Relationship Between Negative Affect, Stress and Emotional Reactivity, Mindfulness, and Sleep Incompatible Behaviors

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A100-A100
Author(s):  
S Nagy ◽  
S M Pickett ◽  
J Sosa ◽  
A Garcell
Keyword(s):  
Negative Affect ◽  
Stress Management ◽  
Emotional Reactivity ◽  
Rating Scale ◽  
Negative Emotion ◽  
Sleep Hygiene ◽  
Poor Sleep ◽  
Dispositional Mindfulness ◽  
Sleep Behaviors ◽  
The Relationship

Abstract Introduction Stress has been identified as a barrier to engaging in positive health behaviors. Sleep interventions, including sleep hygiene recommendations, highlight stress management as an important treatment component. However, the relationship between negative emotion, stress management or emotion regulation, and positive sleep behaviors has largely been unexamined. Therefore, the current study, through secondary analyses, examined the relationships between negative affect, stress and emotional reactivity and sleep incompatible behaviors. Lastly, the indirect effect that dispositional mindfulness, as a possible self-regulatory mechanism, may have on the relationship was also examined. It was hypothesized that greater levels of stress, emotional reactivity, and negative arousal along with lower levels of dispositional mindfulness would predict higher engagement in sleep incompatible behaviors. Methods Participants (n=308) identified mostly as female (55.8%) and White/Caucasian (83.2%) and with an average age of 36.76 (SD = 12.20). Participants completed the Perceived Stress and Reactivity Scale (PSRS), the Positive and Negative Affect Scale (PANAS), the Sleep Behaviors Self-Rating Scale, and the Five Facet Mindfulness Questionnaire (FFMQ). A multiple regression analysis was conducted using the relevant subscales from the PSRS, PANAS, and FFMQ to predict the occurrence of behaviors incompatible with healthy sleep. Results The hypothesis was partially supported. Results indicated that the model significantly predicted sleep incompatible behavior (R2= .108, F(9, 299) = 4.042, p < .001), with only negative affect (β= .163, t(299) = 2.555, p = .011) and nonreactivity (β= -.219, t(299) = -2.484, p = .014) remaining significant when all variables were entered in the model. Conclusion The findings demonstrate that negative affect and reactivity are significant predictors of engagement in poor sleep hygiene practices. They also suggest that certain facets of dispositional mindfulness has an indirect relationship with sleep incompatible behaviors. The results may contribute to the development of sleep health interventions and highlight the need for future research. Support N/A

Acetaminophen Reduces Social Pain

2010 ◽  
Vol 21 (7) ◽  
pp. 931-937 ◽  
Author(s):  
C. Nathan DeWall ◽  
Geoff MacDonald ◽  
Gregory D. Webster ◽  
Carrie L. Masten ◽  
Roy F. Baumeister ◽  
...  
Keyword(s):  
Brain Activity ◽  
Brain Regions ◽  
Daily Basis ◽  
Social Rejection ◽  
Neural Mechanisms ◽  
Anterior Cingulate ◽  
Neural Responses ◽  
Physical Pain ◽  
Social Pain ◽  
Dorsal Anterior Cingulate Cortex

Pain, whether caused by physical injury or social rejection, is an inevitable part of life. These two types of pain—physical and social—may rely on some of the same behavioral and neural mechanisms that register pain-related affect. To the extent that these pain processes overlap, acetaminophen, a physical pain suppressant that acts through central (rather than peripheral) neural mechanisms, may also reduce behavioral and neural responses to social rejection. In two experiments, participants took acetaminophen or placebo daily for 3 weeks. Doses of acetaminophen reduced reports of social pain on a daily basis (Experiment 1). We used functional magnetic resonance imaging to measure participants’ brain activity (Experiment 2), and found that acetaminophen reduced neural responses to social rejection in brain regions previously associated with distress caused by social pain and the affective component of physical pain (dorsal anterior cingulate cortex, anterior insula). Thus, acetaminophen reduces behavioral and neural responses associated with the pain of social rejection, demonstrating substantial overlap between social and physical pain.

Dream-Sharing and Human Self-Domestication

2021 ◽  
Author(s):  
Mark Blagrove ◽  
Julia Lockheart
Keyword(s):  
Emotional Reactivity ◽  
Social Evolution ◽  
Cultural Practices ◽  
Neural Mechanisms ◽  
The Social ◽  
Primary Driver ◽  
Group Members ◽  
Human Social Evolution ◽  
Dream Sharing ◽  
Experimental Findings

There are many theories of the function of dreams, such as memory consolidation, emotion processing, threat simulation and social simulation. In general, such theories hold that the function of dreams occurs within sleep; occurs for unrecalled dreams as well as for dream that are recalled on awakening; and that conscious recall of dreams is not necessary for their function to occur. In contrast, we propose that dreams have an effect of enhancing empathy and group bonding when dreams are shared and discussed with others. We propose also that this effect would have occurred in history and pre-history and, as it would have enhanced the cohesiveness and mutual understanding of group members, the fictional and engaging characteristics of dream content would have been selected for during human social evolution, interacting with cultural practices of dream-sharing. Such dream-sharing may have taken advantage of the long REM periods that occur for biological reasons near the end of the night. Dream-production and dream-sharing may have developed alongside story-telling, utilising common neural mechanisms. Dream-sharing hence would have contributed to Human Self-Domestication, held by many researchers to be the primary driver of the evolution of human prosociality, tolerance and reduced intragroup emotional reactivity. We note that within-sleep theories of dream function rely on correlational rather than experimental findings, and have as yet untested and speculative mechanisms, whereas post-sleep effects of dream-sharing are easily testable and have mechanisms congruent with the social processes proposed by the theory of Human Self-Domestication.

scholarly journals 0183 Both Positive and Negative Affect Are Impacted by Sleep Deprivation

SLEEP ◽  
2018 ◽  
Vol 41 (suppl_1) ◽  
pp. A72-A72
Author(s):  
H K Ritchie ◽  
O A Knauer ◽  
M K Guerin ◽  
E R Stothard ◽  
K P Wright
Keyword(s):  
Negative Affect ◽  
Sleep Deprivation ◽  
Positive And Negative Affect

scholarly journals Neural mechanisms underlying regulation of empathy and altruism by beliefs of others' pain

2021 ◽  
Author(s):  
Tao Yu ◽  
Shihui Han
Keyword(s):  
Real Life ◽  
Stimulus Onset ◽  
Neural Mechanisms ◽  
Altruistic Behavior ◽  
Emotional States ◽  
Neural Responses ◽  
Temporoparietal Junction ◽  
Subjective Estimation ◽  
Show Evidence

Perceived cues signaling others' pain induce empathy that in turn motivates altruistic behavior toward those who appear suffering. This perception-emotion-behavior reactivity is the core of human altruism but does not always occur in real life situations. Here, by integrating behavioral and multimodal neuroimaging measures, we investigate neural mechanisms underlying the functional role of beliefs of others' pain in modulating empathy and altruism. We show evidence that decreasing (or enhancing) beliefs of others' pain reduces (or increases) subjective estimation of others' painful emotional states and monetary donations to those who show pain expressions. Moreover, decreasing beliefs of others' pain attenuates neural responses to perceived cues signaling others' pain within 200 ms after stimulus onset and modulate neural responses to others' pain in the frontal cortices and temporoparietal junction. Our findings highlight beliefs of others' pain as a fundamental cognitive basis of human empathy and altruism and unravel the intermediate neural architecture.

scholarly journals 0081 Habitual Sleep Duration is Negatively Correlated with Emotional Reactivity within the Rostral Anterior Cingulate Cortex in Individuals with PTSD

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A32-A33
Author(s):  
R King ◽  
D Jecmen ◽  
J Mitchell ◽  
K Ralston ◽  
J Gould ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Anterior Cingulate Cortex ◽  
Sleep Duration ◽  
Emotional Reactivity ◽  
Brain Activation ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Functional Brain ◽  
Rostral Anterior Cingulate Cortex ◽  
Reward Network

Abstract Introduction Sleep difficulties, such as insomnia, are highly prevalent in individuals with Post-Traumatic Stress Disorder (PTSD). However, sleep deprivation can also increase emotional reactivity to positive (as well as negative) stimuli. While the effects of sleep loss on emotional perception healthy individuals has been documented, it remains unclear how lack of sleep in individuals with PTSD may affect their emotional reactivity to positive stimuli. We hypothesized that lower habitual sleep duration would be associated with greater functional brain activation changes in response to subliminally presented happy faces in brain areas of the reward network, such as the rostral anterior cingulate cortex (rACC). Methods Thirty-nine individuals with DSM-5 confirmed PTSD were administered the Pittsburgh Sleep Quality Index (PSQI) as a measure of their average nightly sleep duration over the past month. Participants then underwent fMRI imagining while viewing subliminal presentations of faces displaying happiness, using a backward masked facial affect paradigm to minimize conscious awareness of the expressed emotion. Brain activation to masked happy expressions was regressed against sleep duration in SPM12. Results There was a negative correlation between habitual sleep duration and activation within the rACC in response to the masked happy faces (x=14,y=40,z=0; k=102, pFWE-corr= 0.008). Conclusion Individuals with PTSD who average less sleep at night showed greater emotional reactivity, as indexed by greater functional brain activation changes within an area of the reward network, than individuals who obtained more sleep per night. Future research involving actual sleep duration manipulation will be necessary to determine whether this finding reflects the well-known antidepressant effect of sleep deprivation or a form of greater emotional expression error monitoring among traumatized patients when lacking sleep. Regardless, these findings suggest that insufficient sleep could affect unconsciously perceived emotion in faces and potentially affect social and emotional responses among individuals with PTSD. Support US Army Medical Research and Materiel Command: W81XWH-14-1-0570

Emotional reactivity in chronic schizophrenia: structural and functional brain correlates and the influence of adverse childhood experiences

2010 ◽  
Vol 41 (3) ◽  
pp. 509-519 ◽  
Author(s):  
F. Benedetti ◽  
D. Radaelli ◽  
S. Poletti ◽  
A. Falini ◽  
R. Cavallaro ◽  
...  
Keyword(s):  
Adverse Childhood Experiences ◽  
Emotional Reactivity ◽  
Chronic Schizophrenia ◽  
Neural Responses ◽  
Emotional Stimuli ◽  
Childhood Experiences ◽  
Functional Brain ◽  
Healthy Humans ◽  
Adverse Childhood ◽  
Brain Correlates

BackgroundDespite behavioural signs of flattened affect, patients affected by schizophrenia show enhanced sensitivity to negative stimuli. The current literature concerning neural circuitry for emotions supports dysregulations of cortico-limbic networks, but gives contrasting results. Adverse childhood experiences (ACEs) could persistently influence emotional regulation and neural correlates of response to emotional stimuli in healthy humans. This study evaluated the effect of ACEs and chronic undifferentiated schizophrenia on neural responses to emotional stimuli (negative facial expression).MethodBrain blood-oxygen-level-dependent functional magnetic resonance imaging neural responses to a face-matching paradigm, and regional grey matter (GM) volumes were studied at 3.0 T in the amygdala, hippocampus, anterior cingulated cortex (ACC) and prefrontal cortex (PFC). The severity of ACEs was assessed. Participants included 20 consecutively admitted in-patients affected by chronic undifferentiated schizophrenia, and 20 unrelated healthy volunteers from the general population.ResultsPatients reported higher ACEs than controls. Worse ACEs proportionally led to decreasing responses in the amygdala and hippocampus, and to increasing responses in the PFC and ACC in all participants. Patients showed higher activations in the amygdala and hippocampus, and lower activations in the PFC and ACC. Higher ACEs were associated with higher GM volumes in the PFC and ACC, and schizophrenia was associated with GM reduction in all studied regions.ConclusionsStructural and functional brain correlates of emotional reactivity are influenced by both current chronic undifferentiated schizophrenia and the severity of past ACEs.

scholarly journals Sympathetic neural responses to 24-hour sleep deprivation in humans: sex differences

2012 ◽  
Vol 302 (10) ◽  
pp. H1991-H1997 ◽  
Author(s):  
Jason R. Carter ◽  
John J. Durocher ◽  
Robert A. Larson ◽  
Joseph P. DellaValla ◽  
Huan Yang
Keyword(s):  
Sex Differences ◽  
Sleep Deprivation ◽  
Muscle Sympathetic Nerve Activity ◽  
Operating Point ◽  
Neural Responses ◽  
Short Sleep Duration ◽  
Short Sleep ◽  
Baroreflex Function ◽  
Normal Sleep ◽  
Spontaneous Fluctuations

Sleep deprivation has been linked to hypertension, and recent evidence suggests that associations between short sleep duration and hypertension are stronger in women. In the present study we hypothesized that 24 h of total sleep deprivation (TSD) would elicit an augmented pressor and sympathetic neural response in women compared with men. Resting heart rate (HR), blood pressure (BP), and muscle sympathetic nerve activity (MSNA) were measured in 30 healthy subjects (age, 22 ± 1; 15 men and 15 women). Relations between spontaneous fluctuations of diastolic arterial pressure and MSNA were used to assess sympathetic baroreflex function. Subjects were studied twice, once after normal sleep and once after TSD (randomized, crossover design). TSD elicited similar increases in systolic, diastolic, and mean BP in men and women (time, P < 0.05; time × sex, P > 0.05). TSD reduced MSNA in men (25 ± 2 to 16 ± 3 bursts/100 heart beats; P = 0.02), but not women. TSD did not alter spontaneous sympathetic or cardiovagal baroreflex sensitivities in either sex. However, TSD shifted the spontaneous sympathetic baroreflex operating point downward and rightward in men only. TSD reduced testosterone in men, and these changes were correlated to changes in resting MSNA ( r = 0.59; P = 0.04). Resting HR, respiratory rate, and estradiol were not altered by TSD in either sex. In conclusion, TSD-induced hypertension occurs in both sexes, but only men demonstrate altered resting MSNA. The sex differences in MSNA are associated with sex differences in sympathetic baroreflex function (i.e., operating point) and testosterone. These findings may help explain why associations between sleep deprivation and hypertension appear to be sex dependent.

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