Topic
Rapid eye movement sleep
About: Rapid eye movement sleep is a research topic. Over the lifetime, 3740 publications have been published within this topic receiving 183415 citations. The topic is also known as: REM sleep & REMS.
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TL;DR: Shortly after initiation of mirtazapine treatment in four patients with parkinsonism, the authors observed the appearance of REM sleep behavior disorder (RBD), which was accompanied by hallucinations and confusion in two patients with severe motor symptoms.
Abstract: Shortly after initiation of mirtazapine (a noradrenergic and serotonergic antidepressant) treatment in four patients with parkinsonism, the authors observed the appearance of REM sleep behavior disorder (RBD). In the two patients with severe motor symptoms, RBD was accompanied by hallucinations and confusion. These disturbances resolved with drug discontinuation, and remained resolved by 12- to 24-month follow-up, suggesting that RBD can be triggered by a drug lacking anticholinergic activity.
115 citations
TL;DR: The concept of a Sleep Onset Period, characterized by lengthening response times and intermittent response failure (thereby reflecting neither true sleep nor wakefulness), may provide a useful resolution to this definitional dilemma.
Abstract: In this report, a sleep deprivation/multiple arousal paradigm was used in which response time (RT) and respiratory and electroencephalographic (EEG) measures were combined with a continuous behavioral index of arousal (a deadman switch) and frequently repeated Stanford Sleepiness Scale ratings to examine the process of falling asleep. Sleep was defined behaviorally as failure to respond to the faint auditory RT cue. Although response rates decreased significantly as EEG stages passed from W through 1 to 2, responding continued in both light "sleep" stages. Respiratory, subjective, and DM changes were more pronounced between Stages W and 1 than between Stages 1 and 2. If the criterion for wakefulness is cognitive response to external stimulation, accurate distinctions between sleep and wakefulness can only be made in EEG Stages 3, 4, and rapid eye movement sleep. If EEG is the criterion, then the data suggest that cognitive response is possible during Stages 1 and 2 "sleep". The concept of a Sleep Onset Period, characterized by lengthening response times and intermittent response failure (thereby reflecting neither true sleep nor wakefulness), may provide a useful resolution to this definitional dilemma.
115 citations
TL;DR: It was showed that patients with schizophrenia have significantly shorter total sleep time, longer sleep onset latency, more wake time after sleep onset, lower sleep efficiency, and decreased stage 4 sleep, slow wave sleep, and duration and latency of rapid eye movement sleep compared to healthy controls.
115 citations
TL;DR: PBL neuronal activity in behaving animals and the anatomical features of these neurons in relation to behavioral state control are reviewed and tentative mechanisms of REM sleep generation, PGO waves generation, and the cortical activation process are outlined.
115 citations
TL;DR: The data suggest that in vivo 5-HT at the LDT nuclei suppresses REM sleep expression and total REM phasic activity was reduced because of less REM sleep after 5- HT.
Abstract: Serotonin [5-hydroxytryptamine (5-HT)] is believed to play an important inhibitory role in the regulation of rapid-eye-movement (REM) sleep. 5-HT may exert this effect on neurons of the laterodorsal tegmental (LDT) nuclei that are implicated as important in the generation of REM sleep and phasic REM events such as ponto-geniculo-occipital (PGO) waves and respiratory variability. In rat brainstem in vitro , 5-HT hyperpolarizes and inhibits the bursting properties of LDT neurons assumed to be involved in generating REM sleep and PGO waves. This study tests the hypothesis that in vivo 5-HT at the LDT nuclei suppresses REM sleep and phasic REM events. Ten rats were implanted with bilateral cannulae aimed at the LDT and with electrodes for recording the electroencephalogram, neck electromyogram, PGO waves, and diaphragm electromyogram. During REM sleep, 5-HT (100 nl; 1–1.5 mm), saline, or sham microinjections were performed; repeated microinjections were separated by ∼1 hr. After the first microinjection, REM sleep as a percent of the total sleep time was reduced with 5-HT (mean percent REM, 19.9 ± 2.5% for 5-HT vs 26.8 ± 2.4% for saline; p = 0.02). REM duration was reduced by 37% with 5-HT ( p = 0.01), but REM episode frequency was changed less consistently ( p = 0.21), suggesting that 5-HT mainly disrupted REM sleep maintenance. Per unit time of REM sleep, 5-HT had no effect on the amount or variability of REM PGO activity ( p > 0.740) or on the mean or coefficient of variation of REM respiratory rate ( p > 0.11). With subsequent microinjections, the effects of 5-HT on REM sleep were similar. A dose-dependent REM sleep suppression with 5-HT was observed in five rats tested. These data suggest that in vivo 5-HT at the LDT nuclei suppresses REM sleep expression. Although 5-HT did not disproportionately reduce the occurrence of phasic events within REM, total REM phasic activity was reduced because of less REM sleep after 5-HT.
115 citations