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Consciousness, EEG, Sleep and Emotions
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
In non-REM (slow-wave) sleep, a person passes through four stages: In stage 1, the α waves are interspersed with lower-frequency (4–6 Hz) theta (θ) waves.This progresses to stage 2, which is marked by the appearance of high-frequency bursts called sleep spindles (12–14 Hz) and occasional large, slow biphasic potentials called K complexes.In stage 3, there are slow (1–2 Hz) high-voltage δ waves with occasional sleep spindles.In stage 4, large-amplitude, rhythmic, slow δ waves become synchronized.Approximately every 90 minutes, the slow-wave sleep waves change to REM sleep. The EEG becomes desynchronized, with low-voltage (amplitude), high-frequency and asynchronous waves.
What Actually Is Sleep?
Published in Zippi Dolev, Mordechai Zalesch, Judy Kupferman, Sleep and Women's Health, 2019
Zippi Dolev, Mordechai Zalesch, Judy Kupferman
Slow-wave sleep is characterized by a decrease in the frequency of the electrical activity waves of the brain, along with increase in wave intensity, and by the relaxation of the body while maintaining muscle tension and closed and quiet eyelids. This state is divided into three phases, corresponding to the frequency of the waves. The slowest waves are the stage of the deepest sleep.
EEG changes between sleeping and wakefulness
Published in Philip N. Murphy, The Routledge International Handbook of Psychobiology, 2018
Julia K. M. Chan, Christian L. Nicholas
A number of factors can affect the distribution of sleep stages (sleep architecture) across the night (Carskadon & Dement, 2017). One of these is the use and withdrawal of drugs such as sedatives (e.g. benzodiazapines), which while they are being used cause the suppression of slow-wave sleep.
Physical Activity and Cognition: A Mediating Role of Efficient Sleep
Published in Behavioral Sleep Medicine, 2018
Kristine A. Wilckens, Kirk I. Erickson, Mark E. Wheeler
Awakenings during sleep are less likely to occur during the deepest stage of sleep, slow-wave sleep (Neckelmann & Ursin, 1993). Slow-wave sleep involves neural synchrony predominantly over the prefrontal cortex, reflecting synchronized depolarizing of neurons (Steriade et al., 1993). Such neural synchrony over the prefrontal cortex may potentiate synapses within networks important for executive control. Slow-wave sleep has been shown to increase with exercise (Kline et al., 2013), and is linked to executive control and memory consolidation (Anderson & Horne, 2003; Mander et al., 2013; Wilckens et al., 2016). One proposed mechanism supporting a link between physical activity and sleep is the restoration hypothesis, which proposes that energy expenditure stimulates a restoration process whereby sleep allows the body and brain to recuperate (Buman & King, 2010; Driver & Taylor, 2000; Lopez, 2008). Accordingly, slow-wave sleep has been proposed to preferentially “restore” prefrontal cortex function (Anderson & Horne, 2003; Maquet et al., 1997; Muzur, Pace-Schott, & Hobson, 2002; Picchioni, Duyn, & Horovitz, 2013; Wilckens et al., 2016). Additionally, low sleep efficiency may reflect the disruption of multiple sleep features involved in cognition, including stage N2 spindles and rapid eye movement sleep. Future research will determine whether the sleep mechanism linking physical activity with executive control is synchronized neural firing, a restoration processes, or a combination of sleep features working together to enhance executive control.
Does breaking up prolonged sitting when sleep restricted affect postprandial glucose responses and subsequent sleep architecture? – a pilot study
Published in Chronobiology International, 2018
Grace E. Vincent, Sarah M. Jay, Charli Sargent, Katya Kovac, Michele Lastella, Corneel Vandelanotte, Nicola D. Ridgers, Sally A. Ferguson
In this study, regularly breaking up prolonged sitting with light-intensity walking was associated with small increases in stage N3 sleep (slow-wave sleep) and a decrease in stage N2 sleep and WASO. These findings partially support one previous study which investigated sleep of hypertensive adults using sit–stand desks compared to continuous sitting across two simulated 8-h workdays (Kline et al. 2017). Some subjective (WASO, sleep-onset latency and awakenings) but not objective (measured by wrist-actigraphy) improvements in sleep quality were reported (Kline et al. 2017). A recent review of the previous literature showed that acute exercise results in small increases in slow-wave sleep (Chennaoui et al. 2015). Slow-wave sleep plays a crucial role in recovery and sleep consolidation (Roth 2009), but the mechanisms linking physical activity and increases in slow-wave sleep are unclear. Further, it is unknown what characteristics of the physical activity (e.g. intermittent, amount) in the current study contributed to the increase in slow-wave sleep. The observed increase in the amount of slow-wave sleep with subsequent days of sleep restriction is supported by previous literature (Wu et al. 2010). Further research is needed to explore what aspects of breaking up sitting have benefits for subsequent sleep.
Association between sleep disorders and morning blood pressure in hypertensive patients
Published in Clinical and Experimental Hypertension, 2018
Xinran Li, Jiangbo Li, Kai Liu, Shenzhen Gong, Rufeng Shi, Pei Pan, Yujie Yang, Xiaoping Chen
The general characteristics of the subjects are shown in Table 1. Overall, our sample had a mean age of 57.4 ± 15.4 years (n = 144), 63.9% of the subjects were males, and 48.6% of the subjects had diabetes. Higher night-time systolic BP (SBP) (P < 0.001), night-time diastolic BP (DBP) (P < 0.001) and FBG (P = 0.033) existed in the morning hypertension group. The sleep characteristics of subjects are shown in Table 2. Compared with normal sleep characteristics, which are over 95% sleep efficiency, 47%-60% proportion of light sleep and 13%-23% proportion of slow wave sleep (28), our subjects showed decreases in sleep efficiency and the proportion of slow wave sleep, increases in the proportion of light sleep and MI. There were no significant differences between subjects with and without morning hypertension in the parameters of sleep architecture and sleep respiratory and severity of OSA (all P > 0.05) (Table 2).