Slow-wave sleep

About: Slow-wave sleep is a research topic. Over the lifetime, 6543 publications have been published within this topic receiving 320663 citations. The topic is also known as: deep sleep.

Sleep homeostasis and cortical synchronization: I. Modeling the effects of synaptic strength on sleep slow waves.

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

Alleviation of Sleep Maintenance Insomnia with Timed Exposure to Bright Light

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.

Restoration of normal motor control in Parkinson's disease during REM sleep

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.

Sleep and morningness-eveningness in the 'middle' years of life (20-59 y).

Abstract: The following four issues were assessed in a group of 110 adults between the age of 20 and 59y: (1) the effect of age (regarded as a continuous variable) on polysomnographic sleep characteristics, habitual sleep-diary patterns, and subjective sleep quality; (2) the effects of age on morningness-eveningness; (3) the effects of morningness-eveningness on sleep, after controlling for the effects of age; and (4) the role of morningness-eveningness as a mediator of the age and sleep relationship. Increasing age was related to earlier habitual waketime, earlier bedtime, less time in bed and better mood and alertness at waketime. In the laboratory, increasing age was associated with less time asleep, increased number of awakenings, decreased sleep efficiency, lower percentages of slow-wave sleep (SWS) and rapid eye movement (REM) sleep, higher percentages of Stage 1 and 2, shorter REM latency and reduced REM activity and density. Increasing age was also associated with higher morningness scores. After controlling for the effects of age, morningness was associated with earlier waketime, earlier bedtime, less time in bed, better alertness at waketime, less time spent asleep, more wake in the last 2 h of sleep, decreased REM activity, less stage REM (min and percentage), more Stage 1 (min and percentage) and fewer minutes of Stage 2. For one set of variables (night time in bed, waketime, total sleep time, wake in the last 2 h of sleep and minutes of REM and REM activity), morningness-eveningness accounted for about half of the relationship between age and sleep. For another set of variables (bedtime, alertness at waketime, percentages of REM and Stage 1), morningness-eveningness accounted for the entire relationship between age and sleep. In conclusion, age and morningness were both important predictors of the habitual sleep patterns and polysomnographic sleep characteristics of people in the middle years of life (20-59 y).