Non-rapid eye movement sleep

About: Non-rapid eye movement sleep is a research topic. Over the lifetime, 8661 publications have been published within this topic receiving 389465 citations. The topic is also known as: NREM.

Reported chronic insomnia is independent of poor sleep as measured by electroencephalography.

Abstract: OBJECTIVE Several behavioral, physiological, and subjective variables were examined in subjects reporting chronic insomnia (IN group) and subjects with no complaint of insomnia (NC group) to determine factors predictive of poor sleep as measured by electroencephalography (EEG sleep). METHODS A total of 177 subjects (121 in the IN group and 56 in the NC group) were evaluated on the basis of EEG sleep, subjective sleep, sleepiness, performance, mood, personality, and metabolic parameters during a 36-hour laboratory stay. RESULTS Equal percentages of subjects in each group had 0, 1, or 2 nights of poor EEG sleep, indicating that the IN group was not more likely to have impaired sleep in the laboratory. Results of the Minnesota Multiphasic Personality Inventory showed that subjects in the IN group had more pathological personality profiles, and results of laboratory studies showed that these subjects had worse mood ratings, less subjective sleepiness, poorer memory performance, and longer midafternoon sleep latencies. Subjects in the IN group also rated their laboratory sleep as poorer in quality with more time awake after sleep onset and longer sleep latencies, but no differences in EEG sleep were observed. Poor nights of EEG sleep were associated with being male, increasing age, and a history of more time awake after sleep onset; among the laboratory tests, poor EEG sleep was associated with worse mood ratings, poorer memory performance, longer sleep latencies (as indicated by higher scores on the Multiple Sleep Latency Test), higher sleep/wake ratios for metabolic parameters, lower ratings of sleep quality, and longer perceived sleep latencies. CONCLUSIONS A history of chronic insomnia does not predict poor EEG sleep. Both chronic insomnia and poor EEG sleep are associated independently with dysphoria, hyperarousal, diminished waking function, and negative subjective sleep quality. Separate arousal and sleep systems are posited to account for these results.

Sleep initiation and initial sleep intensity: interactions of homeostatic and circadian mechanisms.

Abstract: Sleep initiation and sleep intensity in humans show a dissimilar time course. The propensity of sleep initiation (PSI), as measured by the multiple sleep latency test, remains at a relatively constant level throughout the habitual period of waking or exhibits a midafternoon peak. When waking is extended into the sleep period, PSI rises rapidly within a few hours. In contrast, sleep intensity, as measured by electroencephalographic slow-wave activity during naps, shows a gradual increase during the period of habitual waking. In the two-process model of sleep regulation, it corresponds to the rising limb of the homeostatic Process S. We propose that PSI is determined by the difference between Process S and the threshold H defining sleep onset, which is modulated by the circadian process C. In contrast to a previous version of the model, the parameters of H (amplitude, phase, skewness) differ from those of threshold L, which defines sleep termination. The present model is able to simulate the time course of PSI under baseline conditions as well as following recovery sleep after extended sleep deprivation. The simulations suggest that during the regular period of waking, a circadian process counteracts the increasing sleep propensity induced by a homeostatic process. Data obtained in the rat indicate that during the circadian period of predominant waking, a circadian process prevents a major intrusion of sleep.

Age-related changes in the cognitive function of sleep.

Abstract: Healthy aging is characterized by a diminished quality of sleep with decreased sleep duration and increased time awake after sleep onset. Older adults awaken more frequently and tend to awaken less from rapid eye movement (REM) sleep and more from non-REM (nREM) sleep than young adults. Sleep architecture also begins changing in middle age leading to a dramatic decrease in the deepest stage of nREM-slow wave sleep (SWS)-as aging progresses. Other less marked nREM changes include reduced numbers of sleep spindles and K-complexes. In contrast, the amount of REM diminishes only slightly. Both circadian and homeostatic sleep-regulatory processes are affected by aging. Circadian rhythms of temperature, melatonin, and cortisol are phase advanced and their amplitude diminished. An increased number of nocturnal awakenings and diminished daytime sleepiness suggest diminished homeostatic sleep pressure. A variety of endocrine and neuromodulatory changes (e.g., reduced growth hormone and dopamine levels) also accompany healthy aging. Healthy aging is characterized by declines in working memory and new episodic memory performance with relative sparing of semantic memory, recognition memory, and priming. Memory systems impacted by aging are associated with volumetric and functional changes in fronto-striatal circuits along with more limited changes in medial temporal structures (in which larger aging-related changes suggest neuropathology). Cross-sectional studies generally associate poorer sleep quality with poorer neuropsychological functioning. However, paradoxically, older adults appear to be more resistant to the cognitive effects of sleep deprivation, restriction, and fragmentation than younger adults. A new and expanding field examines the interaction between aging and sleep-dependent memory consolidation. Among forms of learning displaying prominent sleep-dependent consolidation in young adults, motor-sequence learning displays loss of sleep-dependent consolidation with aging whereas sleep-dependent consolidation of verbal declarative memory appears spared. Findings suggest that improving sleep through behavioral or pharmacological treatments may enhance cognition and performance in older adults.