Rapid eye movement sleep

About: Rapid eye movement sleep is a research topic. Over the lifetime, 3740 publications have been published within this topic receiving 183415 citations. The topic is also known as: REM sleep & REMS.

Shining evolutionary light on human sleep and sleep disorders.

Abstract: Sleep is essential to cognitive function and health in humans, yet the ultimate reasons for sleep-i.e. 'why' sleep evolved-remain mysterious. We integrate findings from human sleep studies, the ethnographic record, and the ecology and evolution of mammalian sleep to better understand sleep along the human lineage and in the modern world. Compared to other primates, sleep in great apes has undergone substantial evolutionary change, with all great apes building a sleeping platform or 'nest'. Further evolutionary change characterizes human sleep, with humans having the shortest sleep duration, yet the highest proportion of rapid eye movement sleep among primates. These changes likely reflect that our ancestors experienced fitness benefits from being active for a greater portion of the 24-h cycle than other primates, potentially related to advantages arising from learning, socializing and defending against predators and hostile conspecifics. Perspectives from evolutionary medicine have implications for understanding sleep disorders; we consider these perspectives in the context of insomnia, narcolepsy, seasonal affective disorder, circadian rhythm disorders and sleep apnea. We also identify how human sleep today differs from sleep through most of human evolution, and the implications of these changes for global health and health disparities. More generally, our review highlights the importance of phylogenetic comparisons in understanding human health, including well-known links between sleep, cognitive performance and health in humans.

Interleukin-1β has a Role in Cerebral Cortical State-Dependent Electroencephalographic Slow-Wave Activity

Abstract: STUDY OBJECTIVES To investigate the hypothesis that interleukin (IL)-1beta is involved in mediating localized electroencephalogram synchronization. DESIGN We evaluated bilateral cortical electroencephalograms after unilateral local application of IL-1beta onto the somatosensory cortex of rats. Furthermore, we investigated the effects of unilateral application of an IL-1beta inhibitor, the IL-1 soluble receptor, on spontaneous sleep and sleep rebound after sleep deprivation. SETTING University research laboratory. INTERVENTIONS N/A. PARTICIPANTS Rats. MEASUREMENTS AND RESULTS Neither dose of IL-1beta or the IL-1 soluble receptor affected the duration of non-rapid eye movement sleep or rapid eye movement sleep. Unilateral application of IL-1beta induced state- and frequency-dependent electroencephalogram asymmetries. During non-rapid eye movement sleep, but not during other states, electroencephalographic slow-wave activity was greater on the side that received IL-1beta (10- and 50-ng doses). Electroencephalographic power in the higher frequencies was not affected by IL-1beta in any state. Unilateral application of the IL-1 soluble receptor (0.1, 1.0 and 5.0 microg) had no effect on the spontaneous sleep electroencephalogram. In contrast, unilateral application of the IL-1 soluble receptor (5.0 microg) attenuated sleep deprivation-enhanced electroencephalographic slow-wave power ipsilaterally during non-rapid eye movement sleep. CONCLUSIONS Results suggest that IL-1beta can induce state-dependent localized increases of electroencephalographic delta wave power, suggesting an enhancement of sleep intensity within the cortex.

The effect of memantine on sleep behaviour in dementia with Lewy bodies and Parkinson's disease dementia.

Abstract: OBJECTIVE: Two common and characteristic sleep disturbances have been described in dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD); excessive daytime sleepiness and REM sleep behaviour disorder (RBD). This study is an analysis of a secondary outcome measure of a larger study already reported, aimed to determine whether memantine has an effect on the sleep disturbances in DLB and PDD patients. METHODS: Patients with DLB or PDD were included in a placebo-controlled, randomised controlled study of memantine (20 mg per day) for 24 weeks. The Stavanger Sleep Questionnaire and the Epworth Sleepiness Scale were used to evaluate the effect on sleep disturbances. RESULTS: Forty two patients started treatment; 20 with memantine and 22 with placebo. The primary analysis was the comparison of change between the two groups during a 24-week period, using the modified ITT population (last observation carried forward). At 24 weeks, patients treated with memantine were less physically active during sleep while patients in the placebo group worsened. Mean difference between the groups (0.5 [0.05-0.90]) was significant (p = 0.006). No significant change was observed in severity of excessive daytime sleepiness. CONCLUSIONS: Memantine decreases probable REM sleep behaviour disorder in patients with DLB and PDD. Both diagnostic groups contributed equally to the outcome. (Less)

Effects of lesions of the histaminergic tuberomammillary nucleus on spontaneous sleep in rats.

Abstract: Study Objectives— Extensive evidence suggests that histaminergic neurons promote wakefulness. Histaminergic neurons are found exclusively in the tuberomammillary nucleus (TMN), and electrolytic lesions of the posterior hypothalamus, where the TMN resides, produce intense hypersomnolence. However, electrolytic lesions disrupt fibers of passage, and the effects of fibersparing, cell-specific TMN lesions on sleep and wakefulness are unknown. Hence, we placed cellspecific lesions in the TMN to determine its role in spontaneous wakefulness. Design— TMN neurons in rats are relatively resistant to excitotoxins. Hence, we ablated them using saporin conjugated to hypocretin 2, which ablates hypocretin receptor-bearing neurons such as TMN neurons. One to 2 weeks after bilateral injections of Hcrt2-SAP into Sprague-Dawley rats, we correlated loss of TMN neurons with changes in sleep. Setting—N/A Participants—N/A Interventions—N/A Measurements and Results—Four days after injections with hypocretin-2–saporin, the number of TMN neurons was markedly decreased, and most were lost after 12 days, as determined by immunohistochemistry for adenosine deaminase, a marker of TMN neurons. Nearby nonhistaminergic neurons were similarly ablated. Rats with an average 82.5% loss of TMN cells (determined 2 weeks after injection) did not have marked changes in total sleep amounts compared to saline-treated rats 1 or 2 weeks following the injection, except for a slight decrease in rapid eye movement sleep during the lights-on period for the first week only. The percentage of remaining TMN neurons positively correlated with the average duration of wake bouts during the lights-off period. Conclusion—The absence of gross changes in sleep after extensive loss of histaminergic neurons suggests that this system is not critical for spontaneous wakefulness.

Excessive daytime somnolence and increased rapid eye movement pressure in myotonic dystrophy.

Abstract: STUDY OBJECTIVES Sleep studies at Duke University Medical Center were retrospectively reviewed to investigate causes of excessive daytime sleepiness (EDS) in our myotonic dystrophy1 (DM1) patient population, identified by an abnormal CTG expansion on chromosome 19. Excessive daytime sleepiness, an accentuated desire for sleep or the occurrence of sleep episodes that interfere with normal wakefulness, is common in patients with DM1. Sleep abnormalities, such as central and obstructive sleep apnea, have been extensively reported; however, many DM1 patients suffer from EDS in the absence of any identified respiratory dysrhythmia. DESIGN Nineteen DM1 patients, with the clinical diagnosis and genetic confirmation in the proband or a related family member, had a sleep evaluation. Polysomnogram (PSG) and mean sleep latency test (MSLT) results were retrospectively reviewed. SETTING N/A. PARTICIPANTS N/A. INTERVENTIONS N/A. MEASUREMENTS AND RESULTS Most DM1 patients demonstrated grade 3 (distal weakness) or grade 4 (mild to moderate proximal weakness) on the myotonic dystrophy impairment rating scale. All patents had a PSG, with 13 patients having an MSLT the following day. Clinically significant respiratory abnormalities on PSG, defined in this study as a respiratory disturbance index > 15 and/or upper airway resistance syndrome, could not explain the EDS observed in 14 of 19 patients. Decreased mean sleep latency was observed in 12 of 13 patients evaluated by MSLT, while sleep onset REM sleep was seen in 8 of 13 patients. Pathologic REM onset (2 or more SOREMs on MSLT) was seen in 5 of 13 patients, with 3 of those 5 patients having a PSG with RDI < or = 5. CONCLUSIONS Most DM1 patients did not have significant respiratory abnormalities on PSG to explain the manifested EDS. Objective sleepiness is common in DM1, and pathologic REM pressure can be commonly observed. These observations imply an intrinsic hypersomnolence sometimes accompanied by abnormal REM pressure may be an integral part of EDS in DM1 patients.