Slow-wave sleep

About: Slow-wave sleep is a research topic. Over the lifetime, 6543 publications have been published within this topic receiving 320663 citations. The topic is also known as: deep sleep.

Sleep and quantitative EEG in patients with progressive supranuclear palsy

Abstract: Sleep architecture and quantitative EEG from wakefulness and REM sleep were studied in six patients (mean age, 70.5 years) with progressive supranuclear palsy (PSP) and compared with that of six control subjects (mean age, 69.8 years). Particular attention was given to quantifying REM sleep variables because of the known PSP-associated degeneration of the pedunculopontine tegmentum (PPT)--a critical structure in REM sleep generation. Patients with PSP had a shorter total sleep time, a lower sleep efficiency, a drastic reduction in sleep spindles, an atonic slow-wave sleep, and a lower percentage of REM sleep. The lower percentage of REM sleep was the result of both a reduction in the number of REM periods and a reduction in mean period of duration. REM density was also reduced while REM efficiency, atonia, and phasic EMG were similar to control values. REM sleep findings are consistent with the known role of the PPT in REM sleep induction. A slowing of the awake EEG was found for the six frontal leads and for C4, P4, and T4 in PSP patients. The frontal EEG slowing found in wakefulness is in accord with imaging and neuropsychological studies showing impairment of the frontal lobes in these patients. REM sleep EEG was not significantly slower in any regions. Because all previous studies on PSP have relied on visual inspection of the EEG tracings, the present finding of EEG slowing in the frontal lobes (rather than in the temporal regions or diffusely) suggests that our quantitative EEG approach may be more useful in determining specific regions of impaired cortical activity.

Circadian Variation of Sleep During the Follicular and Luteal Phases of the Menstrual Cycle

Abstract: SLEEP COMPLAINTS ARE PREVALENT IN WOMEN, WHO, DESPITE FINDINGS OF UNAFFECTED POLYSOMNOGRAPHIC (PSG) SLEEP MACROSTRUCTURE,1 ARE 1.5-2 times as likely to report insomnia symptoms as men.2 The variation of reproductive hormones across the menstrual cycle, including progesterone, which is low throughout the follicular phase (FP) and rises during the luteal phase (LP), can affect sleep.3 Overall, previous studies documenting nocturnal PSG sleep indicate sleep onset latency (SOL), sleep efficiency (SE), and slow wave sleep (SWS) are stable across the menstrual cycle, whereas decreases in REM sleep are observed during LP compared to FP.3 Nevertheless, PSG findings are not unequivocal, and inconsistencies persist regarding the variation of SWS4–6 and REM sleep across the menstrual cycle.6–9 Changes in reproductive hormones are also thought to affect the expression of circadian rhythms, though findings are equivocal.3 During LP, high progesterone levels are associated with significant alterations in core body temperature (CBT) rhythms, including increased daily values of 0.3°-0.4°C, blunted nocturnal decline, and reduced circadian amplitude.10–13 Inconsistencies appear when considering the timing of the temperature rhythm across the menstrual cycle, as studies have reported phase delays7,12 or unchanged phase4,10,11 during LP compared to FP. As for melatonin, a pineal hormone whose high nocturnal secretion pattern makes it a reliable circadian marker, it remains unclear whether its rhythm is affected by menstrual phase. There are prior reports of decreases,13 increases,14 phase-delays,12 or no change15 in melatonin secretion during LP compared to FP. Finally, though limited in number, studies investigating the circadian variation of cortisol across the menstrual cycle have been similarly inconsistent, with rhythms either phase-advanced, phase-delayed, or decreased in amplitude during LP.16 Modifications in circadian rhythms across the menstrual cycle are pertinent since sleep is regulated by a complex interaction between circadian and homeostatic processes.17 Experiments manipulating the timing of the sleep-wake cycle (e.g., by forced desynchrony or ultra-rapid sleep-wake cycle [URSW] procedures17–19) have illustrated the circadian variation of sleep propensity and architecture, and how these are related to CBT and melatonin rhythms. Specifically, increased sleep and REM sleep propensity as well as decreased SOL and REM sleep onset latency (ROL) are observed near the CBT nadir when endogenous melatonin levels are high.17,19 In the present study, we utilized the URSW at the mid-follicular (MF) and mid-luteal (ML) phases of the menstrual cycle to quantify the circadian variation of sleep propensity and organization in healthy women. This design allowed us to observe nocturnal sleep at different menstrual phases, to study variation in circadian rhythms of CBT and melatonin across the menstrual cycle under highly controlled conditions, and to document how the circadian variation of sleep is modified by different phases of the menstrual cycle. This investigation will therefore explore the interaction between circadian and menstrual processes as it affects sleep and alertness in healthy women. As such, this line of investigation has the potential to shed light on factors contributing to the increased susceptibility for sleep disruptions and reports of poor sleep in women.2

The BDNF Val66Met polymorphism modulates sleep intensity: EEG frequency- and state-specificity.

Abstract: Study objectives EEG slow waves are the hallmark of deep NREM sleep and may reflect the restorative functions of sleep. Evidence suggests that increased sleep slow waves after sleep deprivation reflect plastic synaptic processes, and that brain-derived neurotrophic factor (BDNF) is causally involved in their homeostatic regulation. The functional Val66Met polymorphism of the gene encoding pro-BDNF causes impaired activity-dependent secretion of mature BDNF protein. We investigated whether this polymorphism contributes to the pronounced inter-individual variation in sleep slow wave activity (SWA) in humans. Setting Sleep laboratory in temporal isolation unit. Participants Eleven heterozygous Met allele carriers and 11 individually sex- and age-matched Val/Val homozygotes. Interventions Forty hours prolonged wakefulness. Measurements and results Cognitive performance, subjective state, and waking and sleep EEG in baseline and after sleep deprivation were studied. Val/Val homozygotes showed better response accuracy than Met allele carriers on a verbal 2-back working memory task. This difference did not reflect genotype-dependent differences in sleepiness, well-being, or sustained attention. In baseline and recovery nights, deep stage 4 sleep and NREM sleep intensity as quantified by EEG SWA (0.75-4.5 Hz) were higher in Val/Val compared to Val/Met genotype. Similar to sleep deprivation, the difference was most pronounced in the first NREM sleep episode. By contrast, increased activity in higher EEG frequencies (> 6 Hz) in wakefulness and REM sleep was distinct from the effects of prolonged wakefulness. Conclusion BDNF contributes to the regulation of sleep slow wave oscillations, suggesting that genetically determined variation in neuronal plasticity modulates NREM sleep intensity in humans.