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.

Effect of wake-sleep transitions and rapid eye movement sleep on pharyngeal muscle response to negative pressure in humans.

Abstract: 1. Genioglossus (GG) activation in response to upper airway negative pressure may be an important mechanism in the maintenance of airway patency. This reflex occurs during wakefulness but is diminished during stable non-rapid eye movement (NREM) sleep. Since obstructive events occur more commonly at wake-sleep transitions and during rapid eye movement (REM) sleep than during stable NREM sleep, we assessed the GG reflex during these two vulnerable states. 2. Seventeen healthy adults were studied throughout one evening and overnight. Electroencephalograms (EEGs), electro-oculograms (EOGs), submental electromyogram (EMG), GG EMG (intramuscular electrodes), and choanal plus epiglottic pressures were recorded. The GG reflex response to pulses of -8 cmH2O choanal pressure applied via nose mask during early inspiration was quantified repeatedly during relaxed wakefulness, within five breaths of wake-sleep transition (EEG alpha-theta transition) and during REM sleep. Only trials without EEG arousal were analysed, resulting in data from 14 subjects during sleep onset and 10 subjects during REM sleep (overall, 174-491 trials per state). 3. During wakefulness there was brisk GG reflex activation in response to negative pressure (amplitude: +78.5 +/- 28.3 % baseline (mean +/- s.e.m.); latency to maximal response: 177 +/- 16 ms). 4. At sleep onset, although there was marked variability among individuals, there was no significant reduction in the magnitude of the GG reflex for the group as a whole (amplitude: +33.2 +/- 8.2 % baseline; latency: 159 +/- 15 ms). 5. In contrast, during REM sleep there was a reduction of GG reflex (amplitude: -12.6 +/- 8.3 % baseline (P = 0.017 vs. awake); latency: 160 +/- 10 ms (n.s. vs. awake)) and greater airway collapsibility during the applied pressures (P = 0.043 vs. awake). 6. We conclude that there was no systematic reduction in the GG reflex to negative pressure at sleep onset. Nonetheless, it remains possible that sleep-deprived normal subjects and patients with sleep apnoea could react differently. 7. The apparent inhibition of the GG reflex during REM sleep may help explain why the upper airway is vulnerable to collapse during this state.

EEG sigma and slow-wave activity during NREM sleep correlate with overnight declarative and procedural memory consolidation

Abstract: SUMMARY Previous studies suggest that sleep-specific brain activity patterns such as sleep spindles and electroencephalographic slow-wave activity contribute to the consolidation of novel memories. The generation of both sleep spindles and slow-wave activity relies on synchronized oscillations in a thalamo-cortical network that might be implicated in synaptic strengthening (spindles) and downscaling (slow-wave activity) during sleep. This study further examined the association between electroencephalographic power during non-rapid eye movement sleep in the spindle (sigma, 12–16 Hz) and slow-wave frequency range (0.1– 3.5 Hz) and overnight memory consolidation in 20 healthy subjects (10 men, 27.1 ± 4.6 years). We found that both electroencephalographic sigma power and slow-wave activity were positively correlated with the pre–post-sleep consolidation of declarative (word list) and procedural (mirror-tracing) memories. These results, although only correlative in nature, are consistent with the view that processes of synaptic strengthening (sleep spindles) and synaptic downscaling (slow-wave activity) might act in concert to promote synaptic plasticity and the consolidation of both declarative and procedural memories during sleep.

Effect of Inhaled 3% CO2 on Cheyne-Stokes Respiration in Congestive Heart Failure

Abstract: Cheyne-Stokes respiration (CSR) in severe stable congestive heart failure (CHF) may be associated with significant nocturnal arterial oxygen desaturation and sleep disruption. Previous investigations of inhaled CO2 in CSR have been uncontrolled and of short duration, sleep has not been monitored electroencephalographically, and most patients studied have had neurological disease with or without cardiac disease. The purpose of our study was to document the effects of inhaled CO2 on CSR in patients with severe stable CHF (left ventricular ejection fraction < 35% and NYHA class 3 or 4 dyspnea) in controlled all-night polysomnographic studies. Six patients were studied for 3 nights and days: adaptation, control and inhalation of CO2. These patients received a constant F1CO2 = 0.03 in air (with a 4-5 mm Hg increase in PaCO2) on night 3. This caused virtual abolition of CSR as reflected by CSR duration/total sleep time (62-2.2%; p = 0.0012) and CSR duration/nonrapid eye movement (NREM) sleep time (73-2.4%; p = 0.00064), and NREM apnea index was reduced from 33.5 to zero (p = 0.026). The apparatus used to accurately control F1CO2, however, was intrusive and some features of sleep structure such as sleep latency were adversely affected. We conclude that inhalation of CO2 with a constant F1CO2 = 0.03 virtually eradicates CSR in all-night polysomnographically monitored studies in patients with severe stable CHF. The clinical significance of these findings remains to be determined.