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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.


Papers
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Journal ArticleDOI
TL;DR: All patients receiving efavirenz had longer sleep latencies and shorter duration of deep sleep, although poor sleepers also showed reduced sleep efficiency and shorterduration of rapid eye movement sleep.
Abstract: Ambulatory electroencephalogram monitoring was performed for 18 HIV-infected subjects treated with efavirenz with and without insomnia and for 13 healthy control subjects. All patients receiving efavirenz had longer sleep latencies and shorter duration of deep sleep, although poor sleepers also showed reduced sleep efficiency and shorter duration of rapid eye movement sleep. Efavirenz plasma levels were higher in patients with insomnia and/or reduced sleep efficiency.

130 citations

Journal ArticleDOI
TL;DR: It was suggested that men, but not women, with MDD show impaired SWA regulation that is evident from 20 to 40 years of age, and it is suggested that maturational effects on SWA in depression differ from those observed in healthy individuals.
Abstract: The amplitude and time course of slow-wave activity (SWA) during NREM sleep were compared in 76 outpatients with depression and 55 healthy control subjects. Lower SWA amplitude was evident in the depressed group, especially among depressed men. For the most part, significant differences between patients and control subjects were restricted to the first NREM period and only in those 20-30 years of age. Significant age-related declines in SWA amplitude were evident in control subjects but not in depressed patients. In addition, sex differences in the depressed group were twice as large as those seen in control subjects. The time course of SWA amplitude, presumed to reflect homeostatic sleep regulation of SWA, was only abnormal in depressed men with lower accumulation and slower dissipation over NREM sleep. Depressed women showed no evidence of an abnormal SWA time course. Furthermore, no sex differences in the time course of SWA were evident in control subjects, and age-related changes in this aspect of regulation were not striking in any group. Thus, the amplitude of SWA showed strong age effects in healthy individuals but not in those with MDD whereas the time course showed very subtle age effects. It was suggested that men, but not women, with MDD show impaired SWA regulation that is evident from 20 to 40 years of age. These findings provide further support that the pathophysiology of depression differs for men and women and suggest that maturational effects on SWA in depression differ from those observed in healthy individuals.

130 citations

Journal ArticleDOI
01 Nov 1997-Sleep
TL;DR: Recent work investigating the influence of these various neuropeptides on sleep is reviewed, finding that in elderly subjects, sleep deteriorates after acute administration of somatostatin but improves after chronic treatment with vasopressin.
Abstract: Results from preclinical studies have validated the participation of neuropeptides in sleep regulation. In recent human and clinical studies it has been shown that peripheral administration of various peptides results in specific changes in the sleep electroencephalogram in humans. Furthermore, it has been demonstrated that certain peptides are common regulators of the electrophysiological and neuroendocrine components of sleep. It is now well established that the balance between the neuropeptides growth hormone-releasing hormone (GHRH) and cortico-tropin-releasing hormone (CRH) plays a key role in normal and pathological sleep regulation. In young normal subjects. GHRH stimulates slow-wave sleep and growth hormone secretion but inhibits cortisol release, whereas CRH has the opposite effect. During normal aging and during acute depression, the GHRH:CRH ratio is changed in favor of CRH, resulting in disturbances in sleep endocrine activity. In addition to GHRH, galanin, growth hormone-releasing peptide, and neuropeptide Y also promote sleep, unlike ACTH(4-9), which disturbs sleep. In elderly subjects, sleep deteriorates after acute administration of somatostatin but improves after chronic treatment with vasopressin. Vasoactive intestinal polypeptide decelerates the non-rapid eye movement-rapid eye movement cycle and advances the occurrence of the cortisol nadir. The impact of delta sleep-inducing peptide, cholecystokinin. and thyrotropin-releasing hormone on human sleep regulation is not yet clear. This paper reviews recent work investigating the influence of these various neuropeptides on sleep.

129 citations

Journal ArticleDOI
TL;DR: Human somatic evoked responses (SERs) were recorded from the scalps of eleven subjects to percutaneous shock stimulation of median nerve during waking, slow wave and REM sleep to suggest the release of neural activity inhibited in waking and REM.

129 citations

Journal ArticleDOI
TL;DR: Olanzapine produced substantial and highly significant dose-related increases in SWS in humans probably via blockade of brain 5-HT(2C) receptors, which may account for some of the therapeutic and adverse effects of olanZapine therapy.

129 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202364
2022103
2021171
2020163
2019166
2018152