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International Journal of Environmental... Dec 2021Standard polysomnographic analysis of sleep has not provided evidence of an objective measure of sleep quality; however, factors such as sleep duration and sleep... (Review)
Review
Standard polysomnographic analysis of sleep has not provided evidence of an objective measure of sleep quality; however, factors such as sleep duration and sleep efficiency are those more consistently associated with the subjective perception of sleep quality. Sleep reduction as currently occurs in our 24/7 society has had a profound impact on sleep quality; the habitual sleep period should fit within what is a limited nighttime window and may not be sufficient to satisfy the whole sleep process; moreover, the use of artificial light during the evening and early night hours can delay and disturb the circadian rhythms, especially affecting REM sleep. The correct phase relationship of the sleep period with the circadian pacemaker is an important factor to guarantee adequate restorative sleep duration and sleep continuity, thus providing the necessary background for a good night's sleep. Due to the fact that REM sleep is controlled by the circadian clock, it can provide a window-like mechanism that defines the termination of the sleep period when there is still the necessity to complete the sleep process (not only wake-related homeostasis) and to meet the circadian end of sleep timing. An adequate amount of REM sleep appears necessary to guarantee sleep continuity, while periodically activating the brain and preparing it for the return to consciousness.
Topics: Brain; Circadian Rhythm; Sleep; Sleep Quality; Sleep, REM
PubMed: 34948586
DOI: 10.3390/ijerph182412976 -
Science (New York, N.Y.) Oct 2021Sleep is crucial for healthy cognition, including memory. The two main phases of sleep, REM (rapid eye movement) and non-REM sleep, are associated with characteristic... (Review)
Review
Sleep is crucial for healthy cognition, including memory. The two main phases of sleep, REM (rapid eye movement) and non-REM sleep, are associated with characteristic electrophysiological patterns that are recorded using surface and intracranial electrodes. These patterns include sharp-wave ripples, cortical slow oscillations, delta waves, and spindles during non-REM sleep and theta oscillations during REM sleep. They reflect the precisely timed activity of underlying neural circuits. Here, we review how these electrical signatures have been guiding our understanding of the circuits and processes sustaining memory consolidation during sleep, focusing on hippocampal theta oscillations and sharp-wave ripples and how they coordinate with cortical patterns. Finally, we highlight how these brain patterns could also sustain sleep-dependent homeostatic processes and evoke several potential future directions for research on the memory function of sleep.
Topics: Animals; Brain Waves; Cerebral Cortex; Hippocampus; Homeostasis; Humans; Memory Consolidation; Neural Pathways; Sleep Stages; Sleep, REM; Theta Rhythm
PubMed: 34709916
DOI: 10.1126/science.abi8370 -
Current Biology : CB Jan 2020For many decades, sleep researchers have sought to determine which species 'have' rapid eye movement (REM) sleep. In doing so, they relied predominantly on a template... (Review)
Review
For many decades, sleep researchers have sought to determine which species 'have' rapid eye movement (REM) sleep. In doing so, they relied predominantly on a template derived from the expression of REM sleep in the adults of a small number of mammalian species. Here, we argue for a different approach that focuses less on a binary decision about haves and have nots, and more on the diverse expression of REM sleep components over development and across species. By focusing on the components of REM sleep and discouraging continued reliance on a restricted template, we aim to promote a richer and more biologically grounded developmental-comparative approach that spans behavioral, physiological, neural, and ecological domains.
Topics: Animals; Humans; Invertebrates; Mammals; Sleep, REM; Vertebrates
PubMed: 31910377
DOI: 10.1016/j.cub.2019.11.045 -
Neurotherapeutics : the Journal of the... Jan 2021Nightmare disorder and recurrent isolated sleep paralysis are rapid eye movement (REM) parasomnias that cause significant distress to those who suffer from them.... (Review)
Review
Nightmare disorder and recurrent isolated sleep paralysis are rapid eye movement (REM) parasomnias that cause significant distress to those who suffer from them. Nightmare disorder can cause insomnia due to fear of falling asleep through dread of nightmare occurrence. Hyperarousal and impaired fear extinction are involved in nightmare generation, as well as brain areas involved in emotion regulation. Nightmare disorder is particularly frequent in psychiatric disorders and posttraumatic stress disorder. Nonmedication treatment, in particular imagery rehearsal therapy, is especially effective. Isolated sleep paralysis is experienced at least once by up to 40% of the general population, whereas recurrence is less frequent. Isolated sleep paralysis can be accompanied by very intense and vivid hallucinations. Sleep paralysis represents a dissociated state, with persistence of REM atonia into wakefulness. Variations in circadian rhythm genes might be involved in their pathogenesis. Predisposing factors include sleep deprivation, irregular sleep-wake schedules, and jetlag. The most effective therapy consists of avoiding those factors.
Topics: Dreams; Humans; Sleep Paralysis; Sleep, REM
PubMed: 33230689
DOI: 10.1007/s13311-020-00966-8 -
Ideggyogyaszati Szemle May 2022We review the literature on REM parasomnias, and their the underlying mechanisms. Several REM parasomnias are consistent with sleep dissociations, where certain elements... (Review)
Review
We review the literature on REM parasomnias, and their the underlying mechanisms. Several REM parasomnias are consistent with sleep dissociations, where certain elements of the REM sleep pattern emerge in an inadequate time (sleep paralysis, hypnagogic hallucinations and cataplexy) or are absent/partial in their normal REM sleep time (REM sleep without atonia, underlying REM sleep behavior disorder). The rest of REM parasomnias (sleep related painful erection, catathrenia) may have other still unclear mechanisms. REM parasomnias deserve attention, because in addition to disturbing sleep and causing injuries, they may shed light on REM sleep functions as well as the heterogeneous etiologies of parasomnias. One of them, REM sleep behavior disorder has special importance as a warning sign of evolving neurodegenerative conditions mainly synucleinopathies (some cases synucleinopathies themselves) and it is a model parasomnia revealing that parasomnias may have by autoimmune, iatrogenic and even psychosomatic etiologies.
Topics: Humans; Parasomnias; REM Sleep Behavior Disorder; Sleep Wake Disorders; Sleep, REM; Synucleinopathies
PubMed: 35819343
DOI: 10.18071/isz.75.0171 -
Arquivos de Neuro-psiquiatria Nov 2019The association between Alzheimer's disease (AD) and sleep disturbances has received increasing scientific attention in the last decades. However, little is known about... (Review)
Review
The association between Alzheimer's disease (AD) and sleep disturbances has received increasing scientific attention in the last decades. However, little is known about the impact of sleep and its disturbances on the development of preclinical AD stages, such as mild cognitive impairment. This review describes the evolution of knowledge about the potential bidirectional relationships between AD and sleep disturbances exploring recent large prospective studies and meta-analyses and studies of the possible mechanisms through which sleep and the neurodegenerative process could be associated. The review also makes a comprehensive exploration of the sleep characteristics of older people, ranging from cognitively normal individuals, through patients with mild cognitive impairment, up to the those with dementia with AD.
Topics: Alzheimer Disease; Cognitive Dysfunction; Electroencephalography; Humans; Polysomnography; Risk Factors; Sleep Wake Disorders; Sleep, REM
PubMed: 31826138
DOI: 10.1590/0004-282X20190149 -
Nature Neuroscience Aug 2022Sleep has a complex micro-architecture, encompassing micro-arousals, sleep spindles and transitions between sleep stages. Fragmented sleep impairs memory consolidation,...
Sleep has a complex micro-architecture, encompassing micro-arousals, sleep spindles and transitions between sleep stages. Fragmented sleep impairs memory consolidation, whereas spindle-rich and delta-rich non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep promote it. However, the relationship between micro-arousals and memory-promoting aspects of sleep remains unclear. In this study, we used fiber photometry in mice to examine how release of the arousal mediator norepinephrine (NE) shapes sleep micro-architecture. Here we show that micro-arousals are generated in a periodic pattern during NREM sleep, riding on the peak of locus-coeruleus-generated infraslow oscillations of extracellular NE, whereas descending phases of NE oscillations drive spindles. The amplitude of NE oscillations is crucial for shaping sleep micro-architecture related to memory performance: prolonged descent of NE promotes spindle-enriched intermediate state and REM sleep but also associates with awakenings, whereas shorter NE descents uphold NREM sleep and micro-arousals. Thus, the NE oscillatory amplitude may be a target for improving sleep in sleep disorders.
Topics: Animals; Arousal; Electroencephalography; Mice; Norepinephrine; Sleep; Sleep Stages; Sleep, REM
PubMed: 35798980
DOI: 10.1038/s41593-022-01102-9 -
Science (New York, N.Y.) Jul 2022In mice, social defeat stress (SDS), an ethological model for psychosocial stress, induces sleep. Such sleep could enable resilience, but how stress promotes sleep is...
In mice, social defeat stress (SDS), an ethological model for psychosocial stress, induces sleep. Such sleep could enable resilience, but how stress promotes sleep is unclear. Activity-dependent tagging revealed a subset of ventral tegmental area γ-aminobutyric acid (GABA)-somatostatin (VTA) cells that sense stress and drive non-rapid eye movement (NREM) and REM sleep through the lateral hypothalamus and also inhibit corticotropin-releasing factor (CRF) release in the paraventricular hypothalamus. Transient stress enhances the activity of VTA cells for several hours, allowing them to exert their sleep effects persistently. Lesioning of VTA cells abolished SDS-induced sleep; without it, anxiety and corticosterone concentrations remained increased after stress. Thus, a specific circuit allows animals to restore mental and body functions by sleeping, potentially providing a refined route for treating anxiety disorders.
Topics: Animals; Corticotropin-Releasing Hormone; Hypothalamic Area, Lateral; Mice; Resilience, Psychological; Sleep; Sleep, REM; Social Defeat; Somatostatin; Stress, Psychological; Ventral Tegmental Area; gamma-Aminobutyric Acid
PubMed: 35771921
DOI: 10.1126/science.abn0853 -
Acta Psychiatrica Scandinavica Jul 2021Narcolepsy is a rare sleep disorder in which psychotic-like symptoms can present diagnostic and therapeutic challenges. We aimed to review the association between, and... (Review)
Review
OBJECTIVE
Narcolepsy is a rare sleep disorder in which psychotic-like symptoms can present diagnostic and therapeutic challenges. We aimed to review the association between, and medical management of, narcolepsy and psychosis in children and adults.
METHODS
We reviewed the full text of 100 papers from 187 identified by a PubMed search on narcolepsy plus any of these keywords: psychosis, schizophrenia, delusion, side effects, safety, and bipolar disorder.
RESULTS
Three relevant groups are described. (i) In typical narcolepsy, psychotic-like symptoms include predominantly visual hallucinations at the sleep-wake transition (experienced as "not real") and dissociation because of intrusion of rapid eye movement (REM) sleep phenomena into wakefulness. (ii) Atypical patients ("the psychotic form of narcolepsy") experience more severe and vivid, apparently REM-related hallucinations or dream/reality confusions, which patients may rationalize in a delusion-like way. (iii) Some patients have a comorbid schizophrenia spectrum disorder with psychotic symptoms unrelated to sleep. Psychostimulants used to treat narcolepsy may trigger psychotic symptoms in all three groups. We analyzed 58 published cases from groups 2 and 3 (n = 17 and 41). Features that were reported significantly more frequently in atypical patients include visual and multimodal hallucinations, sexual and mystical delusions, and false memories. Dual diagnosis patients had more disorganized symptoms and earlier onset of narcolepsy.
CONCLUSION
Epidemiological studies tentatively suggest a possible association between narcolepsy and schizophrenia only for very early-onset cases, which could be related to the partially overlapping neurodevelopmental changes observed in these disorders. We propose a clinical algorithm for the management of cases with psychotic-like or psychotic features.
Topics: Adult; Child; Hallucinations; Humans; Narcolepsy; Psychotic Disorders; Schizophrenia; Sleep, REM
PubMed: 33779983
DOI: 10.1111/acps.13300 -
Journal of Biological Rhythms Aug 2021Acute caffeine intake can attenuate homeostatic sleep pressure and worsen sleep quality. Caffeine intake-particularly in high doses and close to bedtime-may also affect... (Randomized Controlled Trial)
Randomized Controlled Trial
Acute caffeine intake can attenuate homeostatic sleep pressure and worsen sleep quality. Caffeine intake-particularly in high doses and close to bedtime-may also affect circadian-regulated rapid eye movement (REM) sleep promotion, an important determinant of subjective sleep quality. However, it is not known whether such changes persist under chronic caffeine consumption during daytime. Twenty male caffeine consumers (26.4 ± 4 years old, habitual caffeine intake 478.1 ± 102.8 mg/day) participated in a double-blind crossover study. Each volunteer completed a caffeine (3 × 150 mg caffeine daily for 10 days), a withdrawal (3 × 150 mg caffeine for 8 days then placebo), and a placebo condition. After 10 days of controlled intake and a fixed sleep-wake cycle, we recorded electroencephalography for 8 h starting 5 h after habitual bedtime (i.e., start on average at 04:22 h which is around the peak of circadian REM sleep promotion). A 60-min evening nap preceded each sleep episode and reduced high sleep pressure levels. While total sleep time and sleep architecture did not significantly differ between the three conditions, REM sleep latency was longer after daily caffeine intake compared with both placebo and withdrawal. Moreover, the accumulation of REM sleep proportion was delayed, and volunteers reported more difficulties with awakening after sleep and feeling more tired upon wake-up in the caffeine condition compared with placebo. Our data indicate that besides acute intake, also regular daytime caffeine intake affects REM sleep regulation in men, such that it delays circadian REM sleep promotion when compared with placebo. Moreover, the observed caffeine-induced deterioration in the quality of awakening may suggest a potential motive to reinstate caffeine intake after sleep.
Topics: Caffeine; Child, Preschool; Circadian Rhythm; Cross-Over Studies; Electroencephalography; Humans; Male; Sleep; Sleep, REM
PubMed: 34024173
DOI: 10.1177/07487304211013995