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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.


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Journal ArticleDOI
TL;DR: The results show the effectiveness of EMA in the treatment of OSA and indicate that polysomnographic severity of O SA and the site of airway closure should not be used to exclude patients from this oral device treatment.
Abstract: Oral mandibular advancement devices are becoming an increasingly important treatment alternative for obstructive sleep apnea (OSA). The first aim of the study was to determine whether a new oral elastic mandibular advancement device (EMA) prevents pharyngeal airway closure during sleep in patients with OSA. The second aim of the study was to determine if the polysomnographic response to the oral mandibular advancement device was dependent on the site of airway closure. Overnight polysomnograms were performed in 28 untreated OSA subjects with and without EMA. A third polysomnogram was performed in 12 of the subjects to determine the site of airway closure without the device. Site of airway closure above or below the oropharynx was determined by measuring the respective presence or absence of respiratory fluctuations in oropharyngeal pressure during induced occlusions in non‐rapid eye movement (NREM) sleep. Mean apnea‐hypopnea index (AHI) was 52.6 6 28.2 (SD) events/h without the device and 21.2 6 19.3 events/h with the device. Nineteen subjects (68%) had at least a 50% reduction in AHI with the device. The change in AHI with the device (AHI without device 2 AHI with device) was directly related to the AHI without the device. All three subjects with airway closure in the lower pharyngeal airway had a greater than 80% reduction in AHI with the device. Two of the nine subjects with airway closure in the velopharynx had a similar therapeutic response. The results show the effectiveness of EMA in the treatment of OSA. The results also indicate that polysomnographic severity of OSA and the site of airway closure should not be used to exclude patients from this oral device treatment. Henke KG, Frantz DE, Kuna ST. An oral elastic mandibular advancement device for obstructive sleep apnea. AM J RESPIR CRIT CARE MED 2000;161:420‐425.

114 citations

Journal ArticleDOI
TL;DR: Schizophrenic patients were found to have a more disturbed sleep compared to controls, although no distinction was apparent between patients with or without stage IV present, and differences in time of onset, duration, and number of sleep stage changes were noted between schizophrenic and control subjects.

114 citations

Journal ArticleDOI
TL;DR: The extent of hypocretin neuronal loss together with an accompanying loss of cells in the lateral hypothalamus may explain the differences in severity of symptoms seen in human narcolepsy.

113 citations

Journal ArticleDOI
TL;DR: A steep increase in vagal tone at 37-38 weeks CA, with stability afterwards, and a more regular increase in sympathetic tone from 31 to 41 weeks CA are suggested, suggesting maturation of the Autonomic Nervous System and sleep states.

113 citations

Journal ArticleDOI
TL;DR: The homeostatic response of the lower-range SWA was markedly and specifically reduced after NA depletion, suggesting that the wake-dependent accumulation of sleep need is causally related to cellular changes dependent on NA release, such as the induction of LTP-related genes, and support the hypothesis that sleep SWA homeostasis may be related to synaptic potentiation during wakefulness.
Abstract: Sleep intensity is regulated by the duration of previous wakefulness, suggesting that waking results in the progressive accumulation of sleep need (Borbely and Achermann, 2000). In mammals, sleep intensity is reflected by slow-wave activity (SWA) in the nonrapid eye movement (NREM) sleep electroencephalogram, which increases in proportion to the time spent awake. However, the mechanisms responsible for the increase of NREM SWA after wakefulness remain unclear. According to a recent hypothesis (Tononi and Cirelli, 2003), the increase in SWA occurs because during wakefulness, many cortical circuits undergo synaptic potentiation, as evidenced by the widespread induction of long-term potentiation (LTP)-related genes in the brain of awake animals. A direct prediction of this hypothesis is that manipulations interfering with the induction of LTP-related genes should result in a blunted SWA response. Here, we examined SWA response in rats in which cortical norepinephrine (NA) was depleted, a manipulation that greatly reduces the induction of LTP-related genes during wakefulness (Cirelli and Tononi, 2004). We found that the homeostatic response of the lower-range SWA was markedly and specifically reduced after NA depletion. These data suggest that the wake-dependent accumulation of sleep need is causally related to cellular changes dependent on NA release, such as the induction of LTP-related genes, and support the hypothesis that sleep SWA homeostasis may be related to synaptic potentiation during wakefulness.

113 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023229
2022453
2021353
2020283
2019315
2018221