scholarly journals Reconfigurations in brain networks upon awakening from slow wave sleep: Interventions and implications in neural communication

2021 ◽  
Author(s):  
Cassie J Hilditch ◽  
Kanika Bansal ◽  
Ravi Chachad ◽  
Lily R Wong ◽  
Nicholas G Bathurst ◽  
...  

Sleep inertia is the brief period of impaired alertness and performance experienced immediately after waking. While the neurobehavioral symptoms of sleep inertia are well-described, less is known about the neural mechanisms underlying this phenomenon. A better understanding of the neural processes during sleep inertia may offer insight into the cognitive impairments observed and the awakening process generally. We observed brain activity following abrupt awakening from slow wave sleep during the biological night. Using electroencephalography (EEG) and a network science approach, we evaluated power, clustering coefficient, and path length across frequency bands under both a control condition and a blue-enriched light intervention condition in a within-subject design. We found that under control conditions, the awakening brain is typified by an immediate reduction in global theta, alpha, and beta power. Simultaneously, we observed a decrease in the clustering coefficient and an increase in path length within the delta band. Exposure to blue-enriched light immediately after awakening ameliorated these changes, but only for clustering. Our results suggest that long-range network communication within the brain is crucial to the waking process and that the brain may prioritize these long-range connections during this transitional state. Our study highlights a novel neurophysiological signature of the awakening brain and provides a potential mechanistic explanation for the effect of light in improving performance after waking.

2012 ◽  
Vol 24 (1) ◽  
pp. 119-132 ◽  
Author(s):  
Juliana Yordanova ◽  
Vasil Kolev ◽  
Ullrich Wagner ◽  
Jan Born ◽  
Rolf Verleger

The number reduction task (NRT) allows us to study the transition from implicit knowledge of hidden task regularities to explicit insight into these regularities. To identify sleep-associated neurophysiological indicators of this restructuring of knowledge representations, we measured frequency-specific power of EEG while participants slept during the night between two sessions of the NRT. Alpha (8–12 Hz) EEG power during slow wave sleep (SWS) emerged as a specific marker of the transformation of presleep implicit knowledge to postsleep explicit knowledge (ExK). Beta power during SWS was increased whenever ExK was attained after sleep, irrespective of presleep knowledge. No such EEG predictors of insight were found during Sleep Stage 2 and rapid eye movement sleep. These results support the view that it is neuronal memory reprocessing during sleep, in particular during SWS, that lays the foundations for restructuring those task-related representations in the brain that are necessary for promoting the gain of ExK.


1964 ◽  
Vol 207 (6) ◽  
pp. 1379-1386 ◽  
Author(s):  
H. Kawamura ◽  
C. H. Sawyer

A study has been made of d-c potential changes in the brain during various states of sleep and wakefulness in the unrestrained unanesthetized rabbit with chronically implanted electroencephalogram and d-c electrodes. In preliminary acute experiments with an occipital bone reference electrode, the direction of the d-c potential change induced by stimulation of the midbrain reticular formation was the same in cortical and subcortical sites. With frontal and occipital bones as reference points the cortical d-c potential changes were similar to one another, but arousal stimuli readily elicited positive d-c shifts with the frontal reference electrode. In the chronic rabbit with an occipital reference electrode, cortical and hypothalamic d-c potentials shifted strongly to the positive side during slow-wave sleep and after injection of pentobarbital; from these conditions stimulation of the reticular formation induced a marked negative shift. During paradoxical sleep both cortical and subcortical d-c electrodes showed negative shifts similar to those seen during an arousal reaction. Grooming and eating elicited strong positive shifts in both cortical and hypothalamic d-c electrodes.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A31-A32 ◽  
Author(s):  
E E Flynn-Evans ◽  
C J Hilditch ◽  
R Chachad ◽  
K Bansal ◽  
L R Wong ◽  
...  

Abstract Introduction Waking from sleep is associated with reduced alertness due to sleep inertia. Light acutely improves alertness during sleep deprivation. In this study we assessed the influence of light on brain activity and connectivity after waking from slow wave sleep (SWS). Methods Twelve participants kept an actigraphy-confirmed stable sleep schedule with 8.5 hours for five nights and five hours for one night prior to an overnight laboratory visit. Participants completed two three-minute Karolinska Drowsiness Tests (KDT) before going to bed at their habitual bedtime. They were monitored continuously using high-density EEG (32-channel; Brain Products GmbH). Participants were woken twice and exposed to red light (0.01 melanopic-lux; control) or blue-enriched light (63.62 melanopic-lux) for one hour, in a randomized order, following at least five minutes of SWS. EEG artifact were removed algorithmically and the spectral composition of each electrode (i.e., fast fourier transform, FFT) and effective connectivity (i.e., partial directed coherence, PDC) between each electrode were estimated. A graphical analysis was conducted to extract features relevant to the facilitation of efficient communication between electrodes. All data were averaged within frequency bins of interest that correspond to delta (1-3Hz), theta (4-7Hz), alpha (8-12Hz), and beta (13-25Hz) bands and expressed relative to the pre-sleep baseline. Results Compared to the pre-sleep baseline, participants exposed to blue-enriched light experienced reduced theta and alpha activity; however, these results were not significantly different from the control. In contrast, the communication of frontal electrodes significantly increased across all frequency bands compared to the control, and this effect was most prominent in the alpha (t(11)=3.80, p=.005) and beta bands (t(11)=3.92, p=.004). Conclusion Exposure to blue-enriched light immediately after waking from SWS may accelerate the process of waking and help to improve alertness by facilitating communication between brain regions. Future analyses will explore the temporal persistence and granularity of the communicative properties associated with this response. Support Naval Postgraduate School Grant. NASA Airspace Operations and Safety Program, System-Wide Safety Project.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A69-A70 ◽  
Author(s):  
C J Hilditch ◽  
N H Feick ◽  
L R Wong ◽  
N G Bathurst ◽  
E E Flynn-Evans

Abstract Introduction Waking from sleep, especially slow wave sleep (SWS), is associated with reduced alertness known as sleep inertia. Light improves alertness during sleep deprivation and circadian misalignment. In this study, we assessed the efficacy of light to improve alertness and mood immediately after waking from SWS. Methods Twelve participants kept a sleep schedule of 8.5 h for 5 nights and 5 h for one night prior to the overnight laboratory visit (confirmed by actigraphy). Participants went to bed at their scheduled habitual bedtime in the laboratory and were monitored by standard polysomnography. After at least 5 min of SWS, participants were awoken and exposed to either red ambient light (control) or blue-enriched bright light (light) for 1 h. During this time, participants completed a subjective scale of alertness (Karolinska Sleepiness Scale, KSS) and visual analogue scales (VAS) of mood at 2 min, 17 min, 32 min, and 47 min after waking. Following this sleep inertia measurement period, all lights were turned off and participants were allowed to return to sleep. They were then awoken again from their subsequent SWS period and exposed to the opposite condition (control or light). A linear mixed-effects model with fixed effects of condition, time, and condition*time and a random effect of participant was used to determine the impact of light across the testing period. An average of baseline responses (pre-sleep) was included as a covariate. Results Compared to the control condition, participants exposed to blue-enriched bright light reported feeling more alert (KSS: F1,77=4.955, p=.029; VASalert: F1,77=8.226, p=.005), more cheerful (VAScheerful: F1,77=8.615, p=.004), less depressed (VASdepressed: F1,77=4.649, p=.034), and less lethargic (VASlethargic: F1,77=5.652, p=.020). Conclusion Exposure to blue-enriched bright light immediately after waking from SWS may help to improve subjective alertness and mood. Future analyses will explore whether these findings extend to effects on cognitive performance. Support Naval Postgraduate School Grant. NASA Airspace Operations and Safety Program, System-Wide Safety Project.


Electronics ◽  
2021 ◽  
Vol 10 (23) ◽  
pp. 2978
Author(s):  
Giovanni Chiarion ◽  
Luca Mesin

The electroencephalogram (EEG) of patients suffering from inflammatory diseases of the brain may show specific waveforms called slow biphasic complexes (SBC). Recent studies indicated a correlation between the severity of encephalitis and some features of SBCs, such as location, amplitude and frequency of appearance. Moreover, EEG rhythms were found to vary before the onset of an SBC, as if the brain was preparing to the discharge (actually with a slowing down of the EEG oscillation). Here, we investigate possible variations of EEG functional connectivity (FC) in EEGs from pediatric patients with different levels of severity of encephalitis. FC was measured by the maximal crosscorrelation of EEG rhythms in different bipolar channels. Then, the indexes of network patterns (namely strength, clustering coefficient, efficiency and characteristic path length) were estimated to characterize the global behavior when they are measured during SBCs or far from them. EEG traces showed statistical differences in the two conditions: clustering coefficient, efficiency and strength are higher close to an SBC, whereas the characteristic path length is lower. Moreover, for more severe conditions, an increase in clustering coefficient, efficiency and strength and a decrease in characteristic path length were observed in the delta–theta band. These outcomes support the hypothesis that SBCs result from the anomalous coordination of neurons in different brain areas affected by the inflammation process and indicate FC as an additional key for interpreting the EEG in encephalitis patients.


2021 ◽  
Vol 16 (3) ◽  
pp. 34-45
Author(s):  
I. A. Sadekov ◽  
A. V. Polyakov ◽  
I. V. Sadekova ◽  
E. A. Tupikina ◽  
V. Yu. Kochmar ◽  
...  

In this work, we have analyzed the results of observation of 200 children aged from 3 to 15 years old, who had various neuropsychiatric disorders in combination with benign childhood epileptiform patterns on the electroencephalogram. A hypothesis has been put forward about functional disorders of the developing nervous system with prolonged persistence of benign focal epileptiform discharge of childhood on electroencephalogram, mainly in slow-wave sleep. The possibilities of therapeutic correction of these disorders are discussed.


2022 ◽  
Vol 15 ◽  
Author(s):  
Caglar Cakan ◽  
Cristiana Dimulescu ◽  
Liliia Khakimova ◽  
Daniela Obst ◽  
Agnes Flöel ◽  
...  

During slow-wave sleep, the brain is in a self-organized regime in which slow oscillations (SOs) between up- and down-states travel across the cortex. While an isolated piece of cortex can produce SOs, the brain-wide propagation of these oscillations are thought to be mediated by the long-range axonal connections. We address the mechanism of how SOs emerge and recruit large parts of the brain using a whole-brain model constructed from empirical connectivity data in which SOs are induced independently in each brain area by a local adaptation mechanism. Using an evolutionary optimization approach, good fits to human resting-state fMRI data and sleep EEG data are found at values of the adaptation strength close to a bifurcation where the model produces a balance between local and global SOs with realistic spatiotemporal statistics. Local oscillations are more frequent, last shorter, and have a lower amplitude. Global oscillations spread as waves of silence across the undirected brain graph, traveling from anterior to posterior regions. These traveling waves are caused by heterogeneities in the brain network in which the connection strengths between brain areas determine which areas transition to a down-state first, and thus initiate traveling waves across the cortex. Our results demonstrate the utility of whole-brain models for explaining the origin of large-scale cortical oscillations and how they are shaped by the connectome.


1991 ◽  
Vol 3 (2) ◽  
pp. 88-92
Author(s):  
Toshinori Kobayashi ◽  
◽  
Yoichi Tsuji ◽  
Yoshinobu Iguchi

In order to study the psychophysiological function of ""slow wave sleep (SWS), we are trying to identify the control mechanism of SWS. It is well known that the amount of SWS found in a sleep episode depends upon the length of wakefulness prior to the sleep episode. But Karakan et al. (1970) and Miyashita et al (1978) reported that SWS of a sleep episode was also influenced by SWS of the preceding sleep episode. So, we examined the hypothesis that SWS of a sleep episode depended not only on prior wakefulness to the sleep episode but also on SWS of the preceding sleep episode by the use of mathematical models and the experiment. Two models were prepared to examine the hypothesis: one is MODEL (CO), in which SWS of a sleep episode depends upon both prior wakefulness and SWS carried over from the preceding sleep episode, the other is MODEL (nCO), in which SWS of a sleep episode depends on only prior wakefulness to the sleep episode. Four pairs of night sleep and dayti,me naps were recorded in the experiment for eight healthy university students (aged 18 to 25) as follows: (1) Morning nap (0900-1300) was recorded after the mid night sleep (23000300) or early morning sleep (0300-0700), and (2) evening nap (1700-2100) after mid night sleep or early morning sleep. We compared SWS of night sleep and daytime naps estimated by two models with those obtained by the experiment. There was close agreement between SWS estimated by MODEL (CO) and that obtained by the experiment. This result indicates that there is carry over of SWS from night sleep to daytime nap. So, SWS of a sleep episode depends on both prior wakefulness to the sleep episode and SWS carried over from the preceding sleep episode. SWS is accumulated in proportion to the length of wakefulness prior to a sleep episode during waking and is released according to sleep progression during sleep. When SWS is relatively large compared with the length of sleep episode, all SWS is not completely released in the sleep episode. A part of SWS remains in the brain. The remainder of SWS is carried over to the following sleep episode. When SWS is considered as an index of a kind of fatigue in the brain, it is accumulated during waking and is restored during sleep. When the fatigue is not fully restored in a sleep episode, it carries over into the following sleep episode.


2000 ◽  
Vol 279 (3) ◽  
pp. R793-R802 ◽  
Author(s):  
Fang-Chia Chang ◽  
Mark R. Opp

We hypothesize that corticotropin-releasing hormone (CRH), a regulator of the hypothalamic-pituitary-adrenal (HPA) axis, is involved in sleep-wake regulation on the basis of observations that the CRH receptor antagonist astressin, after a delay of several hours, reduces waking and increases slow-wave sleep (SWS) in rats. This delay suggests a cascade of events that begins with the HPA axis and culminates with actions on sleep regulatory systems in the central nervous system. One candidate mediator in the brain for these actions is interleukin (IL)-1. IL-1 promotes sleep, and glucocorticoids inhibit IL-1 synthesis. In this study, central administration of 12.5 μg astressin into rats before dark onset reduced corticosterone 4 h after injection and increased mRNA expression for IL-1α and IL-1β but not for IL-6 or tumor necrosis factor-α in the brain 6 h after injection. To determine directly whether IL-1 is involved in astressin-induced alterations in sleep-wake behavior, we then pretreated rats with 20 μg anti-IL-1β antibodies before injecting astressin. The increase in SWS and the reduction in waking that occur after astressin are abolished when animals are pretreated with anti-IL-1β. These data indicate that IL-1 is a mediator of astressin-induced alterations in sleep-wake behavior.


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