Topic
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.
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TL;DR: The progressive decrease in the number of SS and slow-wave sleep time with age suggests that SS are part of sleep promoting mechanisms, and the negative correlation found between SS density and sleep efficiency in the present study is congruent with the sleep maintenance role of SS.
200 citations
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TL;DR: It is concluded that while sleep/wake patterns are significantly disturbed in AD, this phenomenon is not diagnostically useful for discrimination of mild stage AD.
Abstract: We examined the ability of sleep/wake measures to discriminate 45 control subjects from 44 mild Alzheimer's disease (AD) patients. Sleep fragmentation was observed as indicated by significant increases in time awake (37-52%) and number of awakenings (31-36%) during the night as compared to controls. Further, slow wave sleep (SWS) was significantly reduced (22%) in AD patients relative to controls. These findings are consistent with our earlier observations of increased wakefulness and decreased SWS in mild-moderate, moderate-severe, and severe stage AD patients. However, when we used these sleep/wake stage measures in discriminant analyses to classify the current AD subjects vs control subjects, the analyses failed to confirm our earlier high classification rate (90%). The present groups were discriminated at overall classification rates of only 63-67%. We conclude that while sleep/wake patterns are significantly disturbed in AD, this phenomenon is not diagnostically useful for discrimination of mild stage AD.
200 citations
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TL;DR: The sleep phenotype of HD includes insomnia, advanced sleep phase, periodic leg movements, REM sleep behavior disorders, and reduced REM sleep but not narcolepsy.
Abstract: Background Sleep disorders including insomnia, movements during sleep, and daytime sleepiness are common but poorly studied in Huntington disease (HD). Objective To evaluate the HD sleep-wake phenotype (including abnormal motor activity during sleep) in patients with various HD stages and the length of CAG repeats. Because a mild hypocretin deficiency has been found in the brains of some patients with HD (hereinafter referred to as HD patients), we also tested the HD patients for narcolepsy. Design and Patients Twenty-five HD patients (including 2 premanifest carriers) underwent clinical interview, nighttime video and sleep monitoring, and daytime multiple sleep latency tests. Their results were compared with those of patients with narcolepsy and control patients. Results The HD patients had frequent insomnia, earlier sleep onset, lower sleep efficiency, increased stage 1 sleep, delayed and shortened rapid eye movement (REM) sleep, and increased periodic leg movements. Three HD patients (12%) had REM sleep behavior disorders. No sleep abnormality correlated with CAG repeat length. Reduced REM sleep duration (but not REM sleep behavior disorders) was present in premanifest carriers and patients with very mild HD and worsened with disease severity. In contrast to narcoleptic patients, HD patients had no cataplexy, hypnagogic hallucinations, or sleep paralysis. Four HD patients had abnormally low ( Conclusions The sleep phenotype of HD includes insomnia, advanced sleep phase, periodic leg movements, REM sleep behavior disorders, and reduced REM sleep but not narcolepsy. Reduced REM sleep may precede chorea. Mutant huntingtin may exert an effect on REM sleep and motor control during sleep.
200 citations
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200 citations
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TL;DR: It is proposed that reactivations during sleep are a general mechanism underlying the abstraction of temporally stable invariants from a flow of input that is solely structured in time, thus representing a basic mechanism of memory formation.
Abstract: Sleep is known to support memory consolidation. Here we review evidence for an active system consolidation occurring during sleep. At the beginning of this process is sleep's ability to preserve episodic experiences preferentially encoded in hippocampal networks. Repeated neuronal reactivation of these representations during slow-wave sleep transforms episodic representations into long-term memories, redistributes them toward extrahippocampal networks, and qualitatively changes them to decontextualized schema-like representations. Electroencephalographic (EEG) oscillations regulate the underlying communication: Hippocampal sharp-wave ripples coalescing with thalamic spindles mediate the bottom-up transfer of reactivated memory information to extrahippocampal regions. Neocortical slow oscillations exert a supraordinate top-down control to synchronize hippocampal reactivations of specific memories to their excitable up-phase, thus allowing plastic changes in extrahippocampal regions. We propose that reactiv...
198 citations