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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.


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Journal ArticleDOI
TL;DR: The hypothesis that GABA release in the posterior hypothalamus mediates inhibition of posterior hypothalamic neurons, thereby facilitating slow-wave sleep (SWS) is supported.
Abstract: The activity of neurons in the posterior hypothalamus (PH) is thought to contribute to the production of wakefulness and electroencephalograph desynchronization. Inactivation of neuronal activity in this area is known to induce sleep. Most PH neurons decrease unit discharge during slow-wave sleep (SWS) relative to wake and rapid eye movement sleep. In the present study, we sought to examine potential sources of inhibition or disfacilitation underlying the reduction of PH unit activity during SWS in the cat. We employed the microdialysis technique in conjunction with high-performance liquid chromatography methods for the quantification of glutamate, glycine, and gamma-aminobutyric acid (GABA) release. We found a selective increase in GABA release during SWS in the PH. Glutamate and glycine levels were unchanged across the sleep-wake cycle. microinjection of the GABAA-receptor agonist muscimol, into the same areas from which microdialysis samples were collected, increased SWS time. Our studies support the hypothesis that GABA release in the posterior hypothalamus mediates inhibition of posterior hypothalamic neurons, thereby facilitating SWS.

137 citations

Journal ArticleDOI
01 Apr 2016-Brain
TL;DR: Neuromelanin-sensitive imaging provides an early marker of non-dopaminergic alpha-synucleinopathy that can be detected on an individual basis in patients with idiopathic rapid eye movement sleep behaviour.
Abstract: Idiopathic rapid eye movement sleep behaviour disorder is characterized by nocturnal violence, increased muscle tone during rapid eye movement sleep and the lack of any other neurological disease. However, idiopathic rapid eye movement sleep behaviour disorder can precede parkinsonism and dementia by several years. Using 3 T magnetic resonance imaging and neuromelanin-sensitive sequences, we previously found that the signal intensity was reduced in the locus coeruleus/subcoeruleus area of patients with Parkinson’s disease and rapid eye movement sleep behaviour disorder. Here, we studied the integrity of the locus coeruleus/subcoeruleus complex with neuromelanin-sensitive imaging in 21 patients with idiopathic rapid eye movement sleep behaviour disorder and compared the results with those from 21 age- and gender-matched healthy volunteers. All subjects underwent a clinical examination, motor, cognitive, autonomous, psychological, olfactory and colour vision tests, and rapid eye movement sleep characterization using video-polysomnography and 3 T magnetic resonance imaging. The patients more frequently had preclinical markers of alpha-synucleinopathies, including constipation, olfactory deficits, orthostatic hypotension, and subtle motor impairment. Using neuromelanin-sensitive imaging, reduced signal intensity was identified in the locus coeruleus/subcoeruleus complex of the patients with idiopathic rapid eye movement sleep behaviour. The mean sensitivity of the visual analyses of the signal performed by neuroradiologists who were blind to the clinical diagnoses was 82.5%, and the specificity was 81% for the identification of idiopathic rapid eye movement sleep behaviour. The results confirm that this complex is affected in idiopathic rapid eye movement sleep behaviour (to the same degree as it is affected in Parkinson’s disease). Neuromelanin-sensitive imaging provides an early marker of non-dopaminergic alpha-synucleinopathy that can be detected on an individual basis.

137 citations

Journal ArticleDOI
TL;DR: Evidence linking sleep disturbance and dementia is summarized, which highlights the potential importance of identifying and treating sleep problems and disorders in middle‐aged and older adults as a strategy to prevent cognitive decline and dementia.
Abstract: Approximately half of older people report sleep disturbances, which are associated with various health conditions, including neurodegenerative disease and dementia. Indeed, 60 to 70% of people with cognitive impairment or dementia have sleep disturbances, which are linked to poorer disease prognosis. Sleep disturbances in people with dementia have long been recognized and studied; however, in the past 10 years, researchers have begun to study disturbed sleep, including sleep fragmentation, abnormal sleep duration, and sleep disorders, as risk factors for dementia. In this review the authors summarize evidence linking sleep disturbance and dementia. They describe how specific aspects of sleep (e.g., quality, duration) and the prevalence of clinical sleep disorders (e.g., sleep-disordered breathing, rapid eye movement sleep behavior disorder) change with age; how sleep parameters and sleep disorders are associated with the risk of dementia; how sleep can be disturbed in dementia; and how disturbed sleep affects dementia prognosis. These findings highlight the potential importance of identifying and treating sleep problems and disorders in middle-aged and older adults as a strategy to prevent cognitive decline and dementia. The authors also review recent evidence linking sleep disturbances to the pathophysiology underlying dementing conditions, and briefly summarize available treatments for sleep disorders in people with dementia.

137 citations

Journal ArticleDOI
TL;DR: Stable MMP patients have more sleep architecture abnormalities than controls and a higher prevalence of central sleep apnoea and further studies are needed to confirm these findings.
Abstract: Aims. To explore the possibility that stable MMP patients have sleep-disordered breathing (SDB) and abnormal sleep architecture defined by nocturnal sleep stages and sleep efficiency. Design. Observational. Setting. Regional Methadone Service and sleep disorders laboratory in a university affiliated hospital. Participants and measurements. Ten stable MMP patients and nine normal subjects were assessed clinically and with overnight polysomnography. Findings. There were no differences in age, sex and body mass index between the groups. The methadone dose ranged between 50 and 120 mg/day. Six patients had central apnoea index (CAI) greater than 5, four had a CAI greater than 10 and three of these exhibited periodic breathing. No normal subject had central sleep apnoea. The patients had lower sleep efficiency ( p < 0.05), less slow wave sleep ( p < 0.01), less rapid eye movement sleep ( p < 0.05) and more Stage 2 sleep ( p < 0.05) than controls. Conclusions. Stable MMP patients have more sleep architecture abnormalities than controls and a higher prevalence of central sleep apnoea. Further studies are needed to confirm these findings, to delineate the mechanisms for the abnormalities and to assess whether the SDB is related to sudden death in stable MMP patients. We recommend that MMP patients have awake and sleep respiration assessed to identify those potentially at risk.

136 citations

Journal ArticleDOI
TL;DR: The PGO wave-generating network has been postulated to inform the visual system about eye movements, to promote brain development, and to facilitate the response to novel environmental stimuli.
Abstract: 1. Pontogeniculooccipital (PGO) waves are recorded during rapid eye movement (REM) sleep from the pontine reticular formation, lateral geniculate bodies, and occipital cortex of many species. 2. PGO waves are associated with increased visual system excitability but arise spontaneously and not via stimulation of the primary visual afferents. Both auditory and somatosensory stimuli influence PGO wave activity. 3. Studies using a variety of techniques suggest that the pontine brain stem is the site of PGO wave generation. Immediately prior to the appearance of PGO waves, neurons located in the region of the brachium conjunctivum exhibit bursts of increased firing, while neurons in the dorsal raphe nuclei show a cessation of firing. 4. The administration of pharmacological agents antagonizing noradrenergic or serotonergic neurotransmission increases the occurrence of PGO waves independent of REM sleep. Cholinomimetic administration increases the occurrence of both PGO waves and other components of REM sleep. 5. Regarding function, the PGO wave-generating network has been postulated to inform the visual system about eye movements, to promote brain development, and to facilitate the response to novel environmental stimuli.

136 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202353
2022115
2021116
2020107
201995
201883