"REM rebound"

, including nightmares.[11] The increased physiological arousal that occurs during REM rebound may be dangerous for patients with peptic ulcers or a history of cardiovascular problems. Newer medications for insomnia have reduced adverse effects.[12]The sleep of hospitalized patients is likely to be frequently interrupted by treatment schedules, hospital routines, and roommates, which singularly , and variations from normal periods of rapid eye movement (REM) sleep and non-REM sleep are common. It is important to taper hypnotic medications slowly, or the variations in normal sleep patterns can become even more pronounced, with the majority of time spent in REM sleep in a condition known as REM rebound.[30,31]Table 3 lists the drug categories and specific medications, including doses, commonly used

, and the potential for apnea during rapid eye movement (REM) sleep on the third or fourth postoperative day (i.e., “REM rebound”), as sleep patterns are reestablished. Postoperative interventions to manage OSA patients who may be susceptible to the above risks include the topics of (1) postoperative analgesia, (2) oxygenation, (3) patient positioning, and (4) monitoring.Postoperative Analgesia.The literature

amounts of REM towards the end of usual sleep, where REM's qualitative changes indicate reduced sleep pressure, 4) as in infancy, some of our adult REM remains replaceable by EW (without REM rebounds), mostly in this final REM episode whenever EW need prevails. Accordingly, our adult sleep duration is adaptable to habitual shortening via this REM episode substituted by purposeful EW, which could provide

+/-3.1 min) groups. Relative to the baseline on the recovery night the FM group showed increased sleep efficiency (83.7+/-7.8 to 88.1+/-9.2%) relative to the RA (83.9+/-8.6 to 80.9+/-13.3%) and HC (90.1+/-5.0 to 87.4+/-7.6%) groups due primarily to reduced wake after sleep onset. The groups did not differ in recovery night sleep stages with the exception that the FM group showed REM rebound (21.6+/-6.5 to 25.2+/-6.0%), which was not found in the RA (20.4+/-7.4 to 17.8+/-6.5%) or HC (16.6+/-6.6 to 17.5+/-6.0%) groups. Compared to RA and HC, people with FM responded to reduced bedtime with a comparable increase in sleepiness and greater recovery sleep efficiency, suggesting that homeostatic sleep mechanisms are functional in FM. People with FM uniquely showed REM rebound on recovery from reduced bedtime

not alter social exploratory behavior. The potentiation of anxiety produced by prior repeated fear was temporary; exaggerated fear was present 1 day but not 4 days following acute stress. Interestingly, exposure to acute stress reduced rapid eye movement (REM) and non-REM (NREM) sleep during the hours immediately following acute stress. This initial reduction in sleep was followed by robust REM rebound and diurnal rhythm flattening of sleep/wake behavior. Prior repeated fear extended the acute stress-induced REM and NREM sleep loss, impaired REM rebound, and prolonged the flattening of the diurnal rhythm of NREM sleep following acute stressor exposure. These data suggest that impaired recovery of sleep/wake behavior following acute stress could contribute to the mechanisms by which a history of prior

on the time of day expression profiles of AcPb and IL1. We hypothesized that the magnitude of the responses to sleep loss would be strain- and time of day-dependent. In WT mice, NREMS and REMS rebounds occurred regardless of when they were deprived of sleep. In contrast, when AcPbKO mice were sleep deprived from ZT10 to 20 NREMS and REMS rebounds were absent. The AcPbKO mice expressed sleep rebound if sleep

to changes in sleep cycle length. However, alcohol did not reduce SOL, or result in a REM rebound following reduced REM in the first half of the night. The results suggest that the effects of alcohol on sleep are modified by sleep's prevailing developmental stage.

of the drug on Nights 4-6, and then withdrawal effects were recorded on Nights 7-9. The subjective effects of the drug and EEG sleep variables were determined on these nights. The results showed that the drug might have had dose related effects. REM-sleep was increased by 10 mg doses, which also caused an increase in SW sleep. There was no significant change after the 20 mg dose. Significant REM rebound

, is sufficient to induce marked sleep changes. MAO inhibitor-induced receptor changes are proposed to account for the time course of the REM suppression and the REM rebound observed upon withdrawal.

moclobemide, REM sleep was slightly suppressed. Drug cessation was followed by REM rebound. In contrast to REM sleep, NPT was not affected by the drug. The nocturnal cortisol concentration was elevated under moclobemide and this effect persisted after withdrawal. No influences on growth hormone, prolactin, testosterone, luteinizing hormone or follicle-stimulating hormone were found.

of clomipramine for 10 days, and finally placebo after withdrawal for 8 days. Under clomipramine, rapid eye movement (REM) sleep was suppressed markedly; an REM rebound occurred after withdrawal. Awake and stages 1 and 2 increased while slow wave sleep was diminished under clomipramine. Those non-REM parameters returned to baseline values after drug cessation. NPT was reduced simultaneously with REM sleep under

under 150 mg brofaremine, while stages 1 and 2 increased. In comparison to the effect of irreversible MAOIs the REM suppression was shorter and did not persist after withdrawal. A decrease of the plasma concentration of the drug coincided with a return of sleep variables to baseline values. A REM rebound occurred after withdrawal of brofaremine. REM sleep and NPT showed a dissociation; NPT variables

an increase of stage II and with the highest dose an increase of stage III + IV. An increase of REM-latency together with a decrease of REM-periods was also seen, and while pentobarbital gave a decrease in REM-density, promethazine did not cause any changes in the phasic REM-component. A REM-rebound was seen in the first night of withdrawal with an increase of per cent REM from 19.9%-25.1%. The mean for the whole withdrawal period was 23.1%. Promethazine in the highest dose, 200 mg, gave drowsiness and hangover effects in 14 nights out of 20. The REM-depressing effect of promethazine together with its relatively weak REM-rebound effect may explain its value in the treatment of withdrawal symptoms following abuse of alcohol and barbiturates.

administration. For the rapid-eye-movement (REM) stage, a significant decrease (P less than 0.05) in mean REM percent was noted during the drug period despite an increase in mean absolute REM time. No REM rebound occurred upon drug withdrawal. There were no significant changes in mean percentages for stages 3 and 4 during the drug period and the withdrawal period. Adverse reactions were rare (chiefly some

Rapid Eye Movement Sleep Debt Accrues in Mice Exposed to Volatile Anesthetics. General anesthesia has been likened to a state in which anesthetized subjects are locked out of access to both rapid eye movement (REM) sleep and wakefulness. Were this true for all anesthetics, a significant REM rebound after anesthetic exposure might be expected. However, for the intravenous anesthetic propofol

be a withdrawal syndrome with rapid eye movement (REM) rebound. Two newer benzodiazepine-like agents, zolpidem and zaleplon, have fewer side effects, yet good efficacy. Other agents for insomnia include sedating antidepressants and over-the-counter sleep products (sedating antihistamines). Nonpharmacologic behavioral methods may also have therapeutic benefit. An understanding of the electrophysiologic

in the average length of REMS. Group C exhibited maximum REMS rebound on the first recovery night with an increased number of REMS episodes, as well as significant reductions in the first REMS latency. Our findings suggest that physostigmine alters REMS rebound following REMS deprivation.

a modest REM rebound. Techniques of neurosurgery, chemical injection, electroencephalography, positron emission tomography, and reports of dreamers upon waking, have all been used to study this phase of sleep.[3]Contents * 1 Physiology * 1.1 Electrical activity in the brain * 1.1.1 Brain stem * 1.1.2 Forebrain * 1.2 Chemicals in the brain * 1.2.1 Models of REM regulation than in slow-wave sleep.[17]Deprivation effects[edit]Selective REMS deprivation causes a significant increase in the number of attempts to go into REM stage while asleep. On recovery nights, an individual will usually move to stage 3 and REM sleep more quickly and experience a REM rebound, which refers to an increase in the time spent in REM stage over normal levels. These findings are consistent