scispace - formally typeset
Search or ask a question
Topic

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.


Papers
More filters
Journal ArticleDOI
TL;DR: Self‐reported sleep disturbances are present in over 80% of patients with depression, however, sleep electroencephalography findings, based on overnight polysomnography have not always differentiated depressed patients from healthy individuals.
Abstract: Objective: Self-reported sleep disturbances are present in over 80% of patients with depression. However, sleep electroencephalography (EEG) findings, based on overnight polysomnography have not always differentiated depressed patients from healthy individuals. Method: The present paper will review the findings on sleep EEG studies in depression highlighting how recent technological and methodological advances have impacted on study outcomes. Results: The majority of studies, including our own work, do indicate that sleep homeostasis and sleep EEG rhythms are abnormal in depression, but the sleep disturbances were strongly moderated by gender and age. Melancholic features of depression correlated significantly with low slow-wave activity in depressed men, but not in depressed women. Women with depression showed low temporal coherence of sleep EEG rhythms but the presence or absence of melancholic features did not influence correlations. Conclusion: Diagnostic classification schemas and clinical features of depression may influence sleep EEG findings, but gender may be a more important consideration.

292 citations

Journal ArticleDOI
01 Dec 2007-Sleep
TL;DR: Experimental results from rat cortical depth recordings and human high-density EEG show similar changes in slow-wave parameters with decreasing SWA, suggesting that the underlying mechanism may indeed be a net decrease in synaptic strength.
Abstract: SLOW WAVES ARE A PROMINENT FEATURE OF NON-RAPID EYE MOVEMENT (NREM) SLEEP THAT CAN BE OBSERVED IN THE ELECTROENCEPHALOGRAM (EEG) and local field potentials (LFP). Slow-wave activity (SWA, EEG power 0.5–4.0 Hz) provides a reliable indicator of sleep need, as it increases as a function of prior waking and declines during sleep.1–3 Although the homeostatic regulation of SWA is suggestive of a restorative function of sleep, the underlying mechanisms remain unknown. Different mechanisms can be conceived that might lead to a progressive decline in SWA during sleep, such as an increase in the level of arousal-promoting neuromodulators or a reduction of accumulated metabolites (e.g., adenosine). A recent proposal suggests that the level of SWA may reflect the strength of corticocortical synapses and that a progressive reduction in synaptic strength during sleep would be associated with a corresponding decrease in SWA.4, 5 Mechanistically, stronger cortical connections would produce stronger network synchronization and thus a higher level of SWA, whereas weaker connections would reduce network synchronization and thereby SWA. Connections would become. on average, stronger at the end of a waking day due to synaptic potentiation associated with learning and would weaken during sleep due to sleep-dependent synaptic depression, as suggested by molecular and other evidence.4, 5 Supporting the hypothesis, procedures associated with synaptic potentiation and depression in local cortical areas lead to corresponding changes in sleep SWA. For example, sleep SWA increases over right parietal cortex after a visuomotor learning task6 and decreases over the right sensorimotor cortex after immobilization of the left arm.7 In this paper, we employed a large-scale computer model of the cat thalamocortical system to investigate in detail the relationship between synaptic strength and SWA. The model incorporates key aspects of the neuroanatomic organization of visual thalamocortical circuits, including more than 65,000 integrate-and-fire neurons organized into multiple cortical, thalamic, and reticular areas, and produces physiologically realistic sleep activity patterns.8 Specifically, due to the interaction between several intrinsic and synaptic currents, simulated neurons undergo slow oscillations at around 1 Hz between depolarized periods of activity (up states) and hyperpolarized periods of silence (down states), as observed in intracellular recordings in vivo.9, 10 These single-cell oscillations are synchronized by corticocortical connections and produce realistic slow waves in the calculated LFP. On the basis of this model, we examined the dynamics of single-cell oscillations, cortical synchronization, and LFP slow waves under conditions with a high or low strength of corticocortical connections. We show here that a reduction in cortical synaptic strength leads to a decrease in sleep SWA, a decreased incidence of large-amplitude slow waves, a decrease in their slope, and an increase in the number of multipeak waves. In 2 companion papers, we tested the predictions of the model by examining how slow waves change between early-sleep and late-sleep conditions using LFP recordings in rats11 and high-density EEG recordings in humans.12

292 citations

Journal ArticleDOI
TL;DR: Evaluated the efficacy of bright light exposure in the treatment of sleep maintenance insomnia with the aim of finding an effective non‐drug alternative in the management of age‐related sleep Maintenance insomnia.
Abstract: Objective: Half of the population over 65 suffers from chronic sleep disturbance. As a consequence, almost 40% of hypnotic medications are prescribed to people over age 60. Yet, hypnotics are often of little benefit in this population. As such, an effective non-drug alternative could prove important in the management of age-related sleep maintenance insomnia. The current study sought to evaluate the efficacy of bright light exposure in the treatment of sleep maintenance insomnia. Design: Following baseline sleep and circadian rhythms assessment, subjects with sleep-maintenance insomnia were treated with timed exposure to either bright white light or dim red light for 12 consecutive days. Sleep and circadian rhythms recordings were subsequently obtained and measures of sleep quality were compared to assess efficacy of the treatments. Setting: Baseline and post-treatment sleep and circadian rhythms assessments took place in the Laboratory of Human Chronobiology, Department of Psychiatry, Cornell University Medical College. The treatment phase of the study was conducted in participants' homes. Participants: Sixteen men and women between the ages of 62 and 81 years were studied. All subjects were free of hypnotic medication, and all had experienced sleep disturbance for at least 1 year prior to entering the study. Results: Exposure to bright light resulted in substantial changes in sleep quality. Waking time within sleep was reduced by an hour, and sleep efficiency improved from 77.5% to 90%, without altering time spent in bed. Increased sleep time was in the form of Stage 2 sleep, REM sleep, and slow wave sleep. The effects were remarkably consistent across subjects. Conclusions: The findings demonstrate the effectiveness of timed exposure to bright light in the treatment of age-related sleep maintenance insomnia. With further refinement of treatment regimens, this non-drug intervention may prove useful in a large proportion of sleep disturbed elderly.

292 citations

Journal ArticleDOI
01 Feb 2007-Brain
TL;DR: The restored motor control during REM sleep suggests a transient 'levodopa-like' reestablishment of the basal ganglia loop and parkinsonism may disappear by REM sleep-related disjunction between pyramidal and extrapyramidal systems.
Abstract: Although normal subjects do not move during REM sleep, patients with Parkinson's disease may experience REM sleep behaviour disorder (RBD). The characteristics of the abnormal REM sleep movements in RBD have, however, not been studied. We interviewed one hundred consecutive non-demented patients with Parkinson's disease and their bed partners using a structured questionnaire assessing the presence of RBD. They rated the quality of movements, voice and facial expression during RBD as being better, equal or worse than in awake ON levodopa condition. Night-time sleep and movements were video-monitored during polysomnography in 51 patients to evaluate the presence of bradykinesia, tremor and hypophonia during REM sleep. Fifty-nine patients had clinical RBD with 53/59 bed partners able to evaluate them. All 53 (100%) reported an improvement of at least one component of motor control during RBD. By history, movements were improved in 87% patients (faster, 87%; stronger, 87%; smoother, 51%), speech was better in 77% patients (more intelligible, 77%; louder, 38%; better articulated, 57%) and facial expression was normalized in 47% patients. Thirty-eight per cent of bed partners reported that movements were 'much better', even in the most disabled patients. The video-monitored purposeful movements in REM sleep were also surprisingly fast, ample, coordinated and symmetrical, without obvious sign of parkinsonism. The movements were, however, jerky, violent and often repetitive. While all patients had asymmetrical parkinsonism when awake, most of the time they used the more disabled arm, hand and leg during the RBD (P = 0.04). Movements involved six times as often the upper limbs and the face as the lower limbs (OR: 5.9, P = 0.004). The percentage of time containing tremor EMG activity decreased with sleep stages from 34.9 +/- 15.5% during wakefulness, to 3.6 +/- 5.7% during non-REM sleep stages 1-2, 1.4 +/- 3.0% during non-REM sleep stages 3-4, and 0.06 +/- 0.2% during REM sleep (in this last case, it was subclinical tremor). The restored motor control during REM sleep suggests a transient 'levodopa-like' reestablishment of the basal ganglia loop. Alternatively, parkinsonism may disappear by REM sleep-related disjunction between pyramidal and extrapyramidal systems. We suggest the following model: the movements during the RBD would be generated by the motor cortex and would follow the pyramidal tract bypassing the extrapyramidal system. These movements would eventually be transmitted to lower motor neurons because of brainstem lesions interrupting the pontomedullary pathways which mediate the REM sleep atonia.

290 citations


Network Information
Related Topics (5)
Prefrontal cortex
24K papers, 1.9M citations
82% related
Dopaminergic
29K papers, 1.4M citations
81% related
Dopamine
45.7K papers, 2.2M citations
80% related
Hippocampal formation
30.6K papers, 1.7M citations
80% related
Hippocampus
34.9K papers, 1.9M citations
80% related
Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023229
2022453
2021353
2020283
2019315
2018221