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 activity rhythms are related to circadian phase in the blind.

Abstract: Study objectives: Sleep is controlled by both circadian and homeostatic mechanisms. As the light-dark cycle is the most important time cue in humans, blind individuals may have circadian rhythm disorders including sleep. The aim of the study was to assess sleep with simultaneous measurement of an endogenous marker of the circadian clock, namely 6-sulphatoxymelatonin (aMT6s). Setting and participants: 59 registered blind subjects were studied in their own homes. Design: Subjects completed daily sleep and nap diaries for at least four weeks, wore activity monitors continuously, and collected urine samples over 48 hours each week for 3-5 weeks for assessment of aMT6s rhythms. Results: The most sensitive indicator of a circadian rhythm disorder was day-time napping. Subjects with normally entrained (NE) aMT6s rhythms had fewer naps of a shorter duration than abnormally entrained (AE) or free- running (FR) subjects. The timing of these naps was not random; significantly more naps occurred within a five-hour range before and after the aMT6s acrophase (phi (I�)) than outside this range. Disorders in the timing and duration of night sleep in AE subjects manifested as either a permanent advance (advanced sleep phase syndrome, ASPS) or delay (delayed sleep phase syndrome, DSPS). In FR subjects there were transient advances and delays in sleep timing that paralleled aMT6s timing with increased night sleep duration and reduced number and duration of day-time naps associated with a normal aMT6s phase. Conclusions: Changes in sleep and activity rhythms reflect changes in circadian phase.

Increased sleep need and daytime sleepiness 6 months after traumatic brain injury: a prospective controlled clinical trial.

Abstract: Post-traumatic sleep-wake disturbances are common after acute traumatic brain injury. Increased sleep need per 24 h and excessive daytime sleepiness are among the most prevalent post-traumatic sleep disorders and impair quality of life of trauma patients. Nevertheless, the relation between traumatic brain injury and sleep outcome, but also the link between post-traumatic sleep problems and clinical measures in the acute phase after traumatic brain injury has so far not been addressed in a controlled and prospective approach. We therefore performed a prospective controlled clinical study to examine (i) sleep-wake outcome after traumatic brain injury; and (ii) to screen for clinical and laboratory predictors of poor sleep-wake outcome after acute traumatic brain injury. Forty-two of 60 included patients with first-ever traumatic brain injury were available for follow-up examinations. Six months after trauma, the average sleep need per 24 h as assessed by actigraphy was markedly increased in patients as compared to controls (8.3 ± 1.1 h versus 7.1 ± 0.8 h, P < 0.0001). Objective daytime sleepiness was found in 57% of trauma patients and 19% of healthy subjects, and the average sleep latency in patients was reduced to 8.7 ± 4.6 min (12.1 ± 4.7 min in controls, P = 0.0009). Patients, but not controls, markedly underestimated both excessive sleep need and excessive daytime sleepiness when assessed only by subjective means, emphasizing the unreliability of self-assessment of increased sleep propensity in traumatic brain injury patients. At polysomnography, slow wave sleep after traumatic brain injury was more consolidated. The most important risk factor for developing increased sleep need after traumatic brain injury was the presence of an intracranial haemorrhage. In conclusion, we provide controlled and objective evidence for a direct relation between sleep-wake disturbances and traumatic brain injury, and for clinically significant underestimation of post-traumatic sleep-wake disturbances by trauma patients.

Lactation is associated with an increase in slow-wave sleep in women

Abstract: Major physiological changes occur following parturition and the onset of lactation, including the withdrawal of oestrogen and progesterone, with a consequent increase in circulating prolactin (PRL). Changes in other circulating hormones are well known to alter sleep architecture in other circumstances. We therefore aimed to assess whether sleep architecture is altered in fully lactating women as a result of hormonal changes associated with lactation. A descriptive comparison study was undertaken on 12 fully breastfeeding women (B/F), 12 age-matched control women (CTRL), and seven postnatal women who had chosen to bottle-feed their infants (BOTTLE). Maternal age, infant age and body mass index (BMI) were similar between all three groups. We performed overnight polysomnography utilizing the Portable Compumedics P-series. The total sleep time (TST) and rapid eye movement (REM) sleep time were similar in the three groups of women. However, B/F women demonstrated a marked increase in slow wave sleep (SWS), 182 +/- 41 min compared with CTRL (86 +/- 22 min, P < 0.001 compared with B/F) and BOTTLE subjects (63 +/- 29 min, P < 0.001 compared with B/F). There was a compensatory reduction in light non-rapid eye movement (NREM) sleep in B/F when compared with CTRL and BOTTLE. The most likely explanation for the altered sleep architecture noted to occur in women who are fully breastfeeding their infants is an increase in circulating PRL, which occurs in lactating women. Enhanced SWS may be another important factor to support breastfeeding in the postnatal period.