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.

Age-related changes in the circadian and homeostatic regulation of human sleep.

Abstract: The reduction of electroencephalographic (EEG) slow-wave activity (SWA) (EEG power density between 075-45 Hz) and spindle frequency activity, together with an increase in involuntary awakenings during sleep, represent the hallmarks of human sleep alterations with age It has been assumed that this decrease in non-rapid eye movement (NREM) sleep consolidation reflects an age-related attenuation of the sleep homeostatic drive To test this hypothesis, we measured sleep EEG characteristics (ie, SWA, sleep spindles) in healthy older volunteers in response to high (sleep deprivation protocol) and low sleep pressure (nap protocol) conditions Despite the fact that the older volunteers had impaired sleep consolidation and reduced SWA levels, their relative SWA response to both high and low sleep pressure conditions was similar to that of younger persons Only in frontal brain regions did we find an age-related diminished SWA response to high sleep pressure On the other hand, we have clear evidence that the circadian regulation of sleep during the 40 h nap protocol was changed such that the circadian arousal signal in the evening was weaker in the older study participants More sleep occurred during the wake maintenance zone, and subjective sleepiness ratings in the late afternoon and evening were higher than in younger participants In addition, we found a diminished melatonin secretion and a reduced circadian modulation of REM sleep and spindle frequency-the latter was phase-advanced relative to the circadian melatonin profile Therefore, we favor the hypothesis that age-related changes in sleep are due to weaker circadian regulation of sleep and wakefulness Our data suggest that manipulations of the circadian timing system, rather than the sleep homeostat, may offer a potential strategy to alleviate age-related decrements in sleep and daytime alertness levels

Effects of two nights sleep deprivation and two nights recovery sleep on response inhibition.

Abstract: This study examined the effects of two nights of total sleep deprivation (TSD) and two nights of recovery sleep on response inhibition. Thirty-eight young, healthy adults performed a Go-NoGo task at 14 : 00 after: (1) a normal night of sleep; (2) each of two consecutive nights of TSD; and (3) each of two consecutive nights of recovery sleep; they also performed the task at 05 : 00 during the first night of sleep deprivation. We hypothesized that TSD would lead to an impaired ability to withhold a response that would be reversed with recovery sleep. Subjects did experience a significant increase in false positive responses throughout all of TSD, errors of omission (i.e. missed 'go' targets) were not significant until after the second night of TSD. Both components (withholding a response and automatic responding) of the task returned to baseline levels after one night of recovery sleep. These data suggest that individuals experience difficulty in withholding an inappropriate response during TSD, even when they are able to attend to the incoming stimuli and respond accurately to appropriate stimuli.

Consequences of sleep deprivation

Abstract: This paper presents the history of research and the results of recent studies on the effects of sleep deprivation in animals and humans Humans can bear several days of continuous sleeplessness, experiencing deterioration in wellbeing and effectiveness; however, also a shorter reduction in the sleep time may lead to deteriorated functioning Sleeplessness accounts for impaired perception, difficulties in keeping concentration, vision disturbances, slower reactions, as well as the appearance of microepisodes of sleep during wakefulness which lead to lower capabilities and efficiency of task performance and to increased number of errors Sleep deprivation results in poor memorizing, schematic thinking, which yields wrong decisions, and emotional disturbances such as deteriorated interpersonal responses and increased aggressiveness The symptoms are accompanied by brain tissue hypometabolism, particularly in the thalamus, prefrontal, frontal and occipital cortex and motor speech centres Sleep deficiency intensifies muscle tonus and coexisting tremor, speech performance becomes monotonous and unclear, and sensitivity to pain is higher Sleeplessness also relates to the changes in the immune response and the pattern of hormonal secretion, of the growth hormone in particular The risk of obesity, diabetes and cardiovascular disease increases The impairment of performance which is caused by 20-25 hours of sleeplessness is comparable to that after ethanol intoxication at the level of 010% blood alcohol concentration The consequences of chronic sleep reduction or a shallow sleep repeated for several days tend to accumulate and resemble the effects of acute sleep deprivation lasting several dozen hours At work, such effects hinder proper performance of many essential tasks and in extreme situations (machine operation or vehicle driving), sleep loss may be hazardous to the worker and his/her environment

Variation of electroencephalographic activity during non-rapid eye movement and rapid eye movement sleep with phase of circadian melatonin rhythm in humans

Abstract: 1. The circadian pacemaker regulates the timing, structure and consolidation of human sleep. The extent to which this pacemaker affects electroencephalographic (EEG) activity during sleep remains unclear. 2. To investigate this, a total of 1.22 million power spectra were computed from EEGs recorded in seven men (total, 146 sleep episodes; 9 h 20 min each) who participated in a one-month-long protocol in which the sleep-wake cycle was desynchronized from the rhythm of plasma melatonin, which is driven by the circadian pacemaker. 3. In rapid eye movement (REM) sleep a small circadian variation in EEG activity was observed. The nadir of the circadian rhythm of alpha activity (8.25-10.5 Hz) coincided with the end of the interval during which plasma melatonin values were high, i.e. close to the crest of the REM sleep rhythm. 4. In non-REM sleep, variation in EEG activity between 0.25 and 11.5 Hz was primarily dependent on prior sleep time and only slightly affected by circadian phase, such that the lowest values coincided with the phase of melatonin secretion. 5. In the frequency range of sleep spindles, high-amplitude circadian rhythms with opposite phase positions relative to the melatonin rhythm were observed. Low-frequency sleep spindle activity (12.25-13.0 Hz) reached its crest and high-frequency sleep spindle activity (14.25-15.5 Hz) reached its nadir when sleep coincided with the phase of melatonin secretion. 6. These data indicate that the circadian pacemaker induces changes in EEG activity during REM and non-REM sleep. The changes in non-REM sleep EEG spectra are dissimilar from the spectral changes induced by sleep deprivation and exhibit a close temporal association with the melatonin rhythm and the endogenous circadian phase of sleep consolidation.