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.

Effects of exercise on sleep

Abstract: We tested the hypothesis that EEG sleep stages 3 and 4 (slow-wave sleep, SWS) would be increased as a function of either acute of chronic exercise. Ten distance runners were matched with 10 nonrunners, and their sleep was recorded under both habitual (runners running and nonrunners not running, 3 night) and abruptly changed (runners not running and nonrunners running, 1 night) conditions. Analyses of both visually scored SWS and computer measures of delta activity during non-rapid eye-movement (NREM) sleep failed to support the SWS-exercise hypothesis. The runners showed a significantly higher proportion and a greater absolute amount of NREM sleep than the nonrunners. The runners showed less rapid eye-movement activity during sleep than the nonrunners under both experimental conditions, indicating a strong and unexpected effect of physical fitness on this measure. Modest afternoon exercise in nonrunners was associated with a strong trend toward elevated heart rate during sleep. Mood tests and personality profiles revealed few differences, either between groups or within groups, as a function of exercise.

Serotonergic antidepressants are associated with REM sleep without atonia.

Abstract: STUDY OBJECTIVES Rapid eye movement (REM) sleep behavior disorder (RBD) is generally observed in older men and in individuals with specific neurologic diseases. There are case reports of RBD in individuals taking serotonergic antidepressants. Our objective was to assess electromyogram (EMG) activity during REM sleep in individuals taking serotonergic antidepressants and in a matched control group not on such medication. DESIGN Chart review of clinical and polysomnographic data. SETTING Sleep laboratory affiliated with a general hospital. PARTICIPANTS 15 subjects taking a serotonergic antidepressant and 15 age-matched individuals not on such medication. MEASUREMENTS Submental and anterior tibialis tonic and phasic EMG activity during REM sleep, REM latency, time in REM, apnea-hypopnea index, periodic leg movements of sleep index, and sleep-architecture measures. RESULTS Tonic, but not phasic, submental EMG activity during REM sleep was significantly more common in the antidepressant-treated group than in the control group (P < .02). Tonic REM submental EMG activity correlated with REM latency (r = .42, P = .02) and inversely with REM time (r = -.36, P = .05). Subject age correlated with tonic REM submental EMG activity (r = .58, P = .02) in the antidepressant group There were also trends for more phasic activity in the anterior tibialis (P = .09) and submental (P = .07) EMG in REM sleep in the antidepressant group than in the control group. CONCLUSIONS Subjects taking serotonergic antidepressants had more EMG activity in the submental lead during REM sleep than did controls. This correlated with measures of REM suppression and age. Individuals taking such medications may be at increased risk of developing REM sleep behavior disorder, particularly with increasing age.

Melatonin as a therapy in REM sleep behavior disorder patients: an open-labeled pilot study on the possible influence of melatonin on REM-sleep regulation.

Abstract: REM sleep behavior disorder (RBD) is clinically impressive by virtue of its vigorous sleep behaviors usually accompanying vivid, striking dreams. The main feature of the disorder, REM sleep without muscle atonia, has been shown in a variety of diseases; therefore, the disorder might possibly be underestimated. In an open-labeled trial, we treated six consecutive RBD patients over a 6-week period with 3 mg melatonin given within 30 minutes before bedtime. There was a dramatic clinical improvement in five of the six patients within a week which extended beyond the end of treatment for weeks or months. A second polysomnogram performed 6 weeks after the beginning of treatment showed a significant tendency toward normalization of the percentage of REM sleep, a significant reduction of 30-second epochs, scored as REM sleep without muscle atonia, a significant reduction of stage-shifts in REM, and a significant reduction in epochs considered as movement time in REM. All other sleep parameters were not changed consistently. We hypothesize that internal desynchrony might be a part of the underlying pathophysiology in RBD. Our data might give first evidence to the hypothesis that exogenous melatonin, administered to patients with internal desynchrony at the time of the maximal rise of melatonin secretion, might increase the overall amplitude of the circadian pacemaker by reentraining the suprachiasmatic nucleus and thereby restore circadian driven rhythms, one of them being the circadian modulation of REM sleep.