Showing papers on "Non-rapid eye movement sleep published in 2012"
TL;DR: Genetic studies suggest that brain mechanisms controlling waking and NREM sleep are strongly conserved throughout evolution, underscoring their enormous importance for brain function.
Abstract: This review summarizes the brain mechanisms controlling sleep and wakefulness. Wakefulness promoting systems cause low-voltage, fast activity in the electroencephalogram (EEG). Multiple interacting neurotransmitter systems in the brain stem, hypothalamus, and basal forebrain converge onto common effector systems in the thalamus and cortex. Sleep results from the inhibition of wake-promoting systems by homeostatic sleep factors such as adenosine and nitric oxide and GABAergic neurons in the preoptic area of the hypothalamus, resulting in large-amplitude, slow EEG oscillations. Local, activity-dependent factors modulate the amplitude and frequency of cortical slow oscillations. Non-rapid-eye-movement (NREM) sleep results in conservation of brain energy and facilitates memory consolidation through the modulation of synaptic weights. Rapid-eye-movement (REM) sleep results from the interaction of brain stem cholinergic, aminergic, and GABAergic neurons which control the activity of glutamatergic reticular formation neurons leading to REM sleep phenomena such as muscle atonia, REMs, dreaming, and cortical activation. Strong activation of limbic regions during REM sleep suggests a role in regulation of emotion. Genetic studies suggest that brain mechanisms controlling waking and NREM sleep are strongly conserved throughout evolution, underscoring their enormous importance for brain function. Sleep disruption interferes with the normal restorative functions of NREM and REM sleep, resulting in disruptions of breathing and cardiovascular function, changes in emotional reactivity, and cognitive impairments in attention, memory, and decision making.
1,101 citations
TL;DR: Severe circadian sleep/wake disruptions exist despite stability in mood, mental state and newer antipsychotic treatment, and cannot be explained by the individuals' level of everyday function.
Abstract: Sleep disturbances comparable with insomnia occur in up to 80% of people with schizophrenia, but very little is known about the contribution of circadian coordination to these prevalent disruptions.
349 citations
TL;DR: The present review illustrates the story of CAP in the last 25 years, the standardized scoring criteria, the basic physiological properties and how the dimension of sleep instability has provided new insight into pathophysiolology and management of sleep disorders.
313 citations
TL;DR: Overall, Subjective Alertness and Sustained Attention were more affected by both partial and total sleep deprivation than other cognitive domains and tasks including n-back tasks of Working Memory, even when implemented with a high executive load.
Abstract: Cognitive performance deteriorates during extended wakefulness and circadian phase misalignment, and some individuals are more affected than others. Whether performance is affected similarly across cognitive domains, or whether cognitive processes involving Executive Functions are more sensitive to sleep and circadian misalignment than Alertness and Sustained Attention, is a matter of debate.
264 citations
TL;DR: The Hcrt-LC connection is established as a critical integrator-effector circuit that regulates NREM sleep/wake behavior during the inactive period and can be generalized to other hypothalamic integrator nuclei with downstream effector/output populations in the brain.
Abstract: Current models of sleep/wake regulation posit that Hypocretin (Hcrt)-expressing neurons in the lateral hypothalamus promote and stabilize wakefulness by projecting to subcortical arousal centers. However, the critical downstream effectors of Hcrt neurons are unknown. Here we use optogenetic, pharmacological, and computational tools to investigate the functional connectivity between Hcrt neurons and downstream noradrenergic neurons in the locus coeruleus (LC) during nonrapid eye movement (NREM) sleep. We found that photoinhibiting LC neurons during Hcrt stimulation blocked Hcrt-mediated sleep-to-wake transitions. In contrast, when LC neurons were optically stimulated to increase membrane excitability, concomitant photostimulation of Hcrt neurons significantly increased the probability of sleep-to-wake transitions compared with Hcrt stimulation alone. We also built a conductance-based computational model of Hcrt-LC circuitry that recapitulates our behavioral results using LC neurons as the main effectors of Hcrt signaling. These results establish the Hcrt-LC connection as a critical integrator-effector circuit that regulates NREM sleep/wake behavior during the inactive period. This coupling of distinct neuronal systems can be generalized to other hypothalamic integrator nuclei with downstream effector/output populations in the brain.
220 citations
TL;DR: In N1 and N3 sleep, despite spectral EEG differences, the microstate maps and characteristics were surprisingly close to wakefulness, which supports the notion that EEG microstates might reflect a large scale resting state network architecture similar to preserved fMRI resting state connectivity.
190 citations
TL;DR: It is proposed that "instability" of REM sleep contributes to the experience of disrupted and non-restorative sleep and to the explanation of this discrepancy between minor objective alterations in standard parameters of sleep continuity and the profound subjective impairment in patients with insomnia.
Abstract: Chronic insomnia afflicts approximately 10% of the adult population and is associated with daytime impairments and an elevated risk for developing somatic and mental disorders. Current pathophysiological models propose a persistent hyperarousal on the cognitive, emotional and physiological levels. However, the marked discrepancy between minor objective alterations in standard parameters of sleep continuity and the profound subjective impairment in patients with insomnia is unresolved. We propose that "instability" of REM sleep contributes to the experience of disrupted and non-restorative sleep and to the explanation of this discrepancy. This concept is based on evidence showing increased micro- and macro-arousals during REM sleep in insomnia patients. As REM sleep represents the most highly aroused brain state during sleep it seems particularly prone to fragmentation in individuals with persistent hyperarousal. The continuity hypothesis of dream production suggests that pre-sleep concerns of patients with insomnia, i. e., worries about poor sleep and its consequences, dominate their dream content. Enhanced arousal during REM sleep may render these wake-like cognitions more accessible to conscious perception, memory storage and morning recall, resulting in the experience of disrupted and non-restorative sleep. Furthermore, chronic fragmentation of REM sleep might lead to dysfunction in a ventral emotional neural network, including limbic and paralimbic areas that are specifically activated during REM sleep. This dysfunction, along with attenuated functioning in a dorsal executive neural network, including frontal and prefrontal areas, might contribute to emotional and cognitive alterations and an elevated risk of developing depression.
187 citations
TL;DR: A comprehensive and critical account of the research that has been carried out to investigate the association between sleep and ADHD is presented, as well as mechanisms that have been proposed to account for the elusive relationship between sleep disturbances, sleep disorders, and ADHD are discussed.
183 citations
TL;DR: Patients with REM sleep behavior disorder have higher and faster risk for conversion to Parkinson's disease and dementia with Lewy bodies if abnormalities in dopamine transporter imaging, transcranial sonography, olfaction, and color vision are found at baseline, and they constitute a highly specific target for testing neuroprotective agents.
Abstract: Patients with REM sleep behavior disorder (RBD) enact violent dreams during REM sleep in the absence of normal muscle atonia. This disorder is highly frequent in patients with synucleinopathies (60%-100% of patients) and rare in patients with other neurodegenerative disorders. The disorder is detected by interview plus video and sleep monitoring. Abnormal movements expose the patients and bed partners to a high risk of injury and sleep disruption. The disorder is usually alleviated with melatonin and clonazepam. Limb movements are mainly minor, jerky, fast, pseudohallucinatory, and repeated, with a limp wrist during apparently grasping movements, although body jerks and complex violent (fights) and nonviolent culturally acquired behaviors are also observed. Notably, parkinsonism disappears during RBD-associated complex behaviors in patients with Parkinson's disease and with multiple system atrophy, suggesting that the upper motor stream bypasses the basal ganglia during REM sleep. Longitudinal studies show that idiopathic RBD predisposes patients to later develop Parkinson's disease, dementia with Lewy bodies, and, more rarely, multiple system atrophy, with a rate of conversion of 46% within 5 years. During this time window, patients concomitantly develop nonmotor signs (decreased olfaction and color vision, orthostatic hypotension, altered visuospatial abilities, increased harm avoidance) and have abnormal test results (decreased putamen dopamine uptake, slower EEG). Patients with idiopathic RBD have higher and faster risk for conversion to Parkinson's disease and dementia with Lewy bodies if abnormalities in dopamine transporter imaging, transcranial sonography, olfaction, and color vision are found at baseline. They constitute a highly specific target for testing neuroprotective agents.
179 citations
TL;DR: The Reward Activation Model (RAM) for sleep and dreaming is introduced, according to which activation of the ML-DA reward system during sleep contributes to memory processes, to the regulation of rapid-eye movement (REM) sleep, and to the generation and motivational content of dreams.
177 citations
TL;DR: The hypothesis that impaired consciousness during NREM sleep is associated with an increased modularity of brain activity is tested and a modification of the hierarchical organization of large-scale networks into smaller independent modules is revealed.
Abstract: Consciousness is reduced during nonrapid eye movement (NREM) sleep due to changes in brain function that are still poorly understood. Here, we tested the hypothesis that impaired consciousness during NREM sleep is associated with an increased modularity of brain activity. Cerebral connectivity was quantified in resting-state functional magnetic resonance imaging times series acquired in 13 healthy volunteers during wakefulness and NREM sleep. The analysis revealed a modification of the hierarchical organization of large-scale networks into smaller independent modules during NREM sleep, independently from EEG markers of the slow oscillation. Such modifications in brain connectivity, possibly driven by sleep ultraslow oscillations, could hinder the brain's ability to integrate information and account for decreased consciousness during NREM sleep.
TL;DR: During NREM sleep, firing of LC neurons may contribute to the rising phase of the EEG slow wave by providing a neuromodulatory input that increases cortical excitability, thereby promoting plasticity within these circuits.
Abstract: Nonrapid eye movement (NREM) sleep is characterized by periodic changes in cortical excitability that are reflected in the electroencephalography (EEG) as high-amplitude slow oscillations, indicative ofcortical Up/Downstates.These slowoscillations arethoughttobe involved in NREM sleep-dependent memory consolidation. Although thelocuscoeruleus(LC)noradrenergicsystemisknowntoplayarole inoff-linememoryconsolidation(thatmayoccurduringNREMsleep), cortico--coerulear interactions during NREM sleep have not yet been studied in detail. Here, we investigated the timing of LC spikes as a function of sleep-associated slow oscillations. Cortical EEG was monitored,alongwithactivityofLCneuronsrecordedextracellularly, in nonanesthetized naturally sleeping rats. LC spike-triggered averaging of EEG, together with phase-locking analysis, revealed preferential firing of LC neurons along the ascending edge of the EEG slow oscillation, correlating with Down-to-Up state transition. LC neurons were locked best when spikes were shifted forward ~50 ms in time with respect to the EEG slow oscillation. These results suggest that during NREM sleep, firing of LC neurons may contribute to the rising phase of the EEG slow wave by providing a neuromodulatory input that increases cortical excitability, thereby promoting plasticity within these circuits.
TL;DR: A positive association between REM sleep and the selective consolidation of central, negative aspects of complex scenes is shown and suggests that the sleeping brain preserves in long-term memory only what is emotionally salient and perhaps most adaptive to remember.
Abstract: Although we know that emotional events enjoy a privileged status in our memories, we still have much to learn about how emotional memories are processed, stored, and how they change over time. Here we show a positive association between REM sleep and the selective consolidation of central, negative aspects of complex scenes. Moreover, we show that the placement of sleep is critical for this selective emotional memory benefit. When testing occurred 24hr post-encoding, subjects who slept soon after learning (24hr Sleep First group) had superior memory for emotional objects compared to subjects whose sleep was delayed for 16hr post-encoding following a full day of wakefulness (24hr Wake First group). However, this increase in memory for emotional objects corresponded with a decrease in memory for the neutral backgrounds on which these objects were placed. Furthermore, memory for emotional objects in the 24hr Sleep First group was comparable to performance after just a 12hr delay containing a night of sleep, suggesting that sleep soon after learning selectively stabilizes emotional memory. These results suggest that the sleeping brain preserves in long-term memory only what is emotionally salient and perhaps most adaptive to remember.
TL;DR: In this article, Dang-Vu et al. examined the modulation of cerebral responses to tones depending on the presence or absence of sleep spindles and the phase of the slow oscillation.
Abstract: The present study aimed at identifying the neurophysiological responses associated with auditory stimulation during non-rapid eye movement (NREM) sleep using simultaneous electroencephalography (EEG)/functional magnetic resonance imaging (fMRI) recordings. It was reported earlier that auditory stimuli produce bilateral activation in auditory cortex, thalamus, and caudate during both wakefulness and NREM sleep. However, due to the spontaneous membrane potential fluctuations cortical responses may be highly variable during NREM. Here we now examine the modulation of cerebral responses to tones depending on the presence or absence of sleep spindles and the phase of the slow oscillation. Thirteen healthy young subjects were scanned successfully during stage 2–4 NREM sleep in the first half of the night in a 3T scanner. Subjects were not sleep-deprived and sounds were post hoc classified according to (i) the presence of sleep spindles or (ii) the phase of the slow oscillation during (±300 ms) tone delivery. These detected sounds were then entered as regressors of interest in fMRI analyses. Interestingly wake-like responses – although somewhat altered in size and location – persisted during NREM sleep, except during present spindles (as previously published in Dang-Vu et al., 2011) and the negative going phase of the slow oscillation during which responses became less consistent or even absent. While the phase of the slow oscillation did not alter brain responses in primary sensory cortex, it did modulate responses at higher cortical levels. In addition EEG analyses show a distinct N550 response to tones during the presence of light sleep spindles and suggest that in deep NREM sleep the brain is more responsive during the positive going slope of the slow oscillation. The presence of short temporal windows during which the brain is open to external stimuli is consistent with the fact that even during deep sleep meaningful events can be detected. Altogether, our results emphasize the notion that spontaneous fluctuations of brain activity profoundly modify brain responses to external information across all behavioral states, including deep NREM sleep.
TL;DR: In this article, the authors examined EEG spectral power values for standard frequency bands as indices of cortical arousal and sleep protecting mechanisms during sleep in 25 patients with primary insomnia and 29 good sleeper controls.
TL;DR: Breath acetone andIsoprene profiles exhibited pronounced concentration peaks, which were highly specific for leg movements as scored by tibial electromyography, and baseline isoprene concentrations decreased during the transition from the NREM to the REM phase of a complete sleep cycle.
Abstract: This explorative study aims at characterizing the breath behavior of two prototypic volatile organic compounds, acetone and isoprene, during normal human sleep and to possibly relate changes in the respective concentration time courses to the underlying sleep architecture. For this purpose, six normal healthy volunteers (two females, four males, age 20-29 years) were monitored over two consecutive nights (the first one being an adaption night) by combining real-time proton-transfer-reaction mass spectrometry measurements from end-tidal exhalation segments with laboratory-based polysomnographic data. Breath acetone concentrations increased overnight in all measurements, with an average relative change by a factor of up to 4 (median 2.5). Nighttime concentration maxima were usually recorded 2-3 h before lights on. For breath isoprene, a nocturnal increase in baseline concentrations of about 74% was observed, with individual changes ranging from 36-110%. Isoprene profiles exhibited pronounced concentration peaks, which were highly specific for leg movements as scored by tibial electromyography. Furthermore, relative to a linear trend, baseline isoprene concentrations decreased during the transition from the NREM to the REM phase of a complete sleep cycle.
TL;DR: In this paper, the authors examined the cortical arousal responses during sleep to typical hospital noises by sound level and type and sleep stage, and found that sounds in NREM stage 3 were less likely to cause arousals than sounds in non-REM stage 2; however, the probability of arousal to sounds presented in REM sleep varied less by sound type and caused a greater and more sustained elevation of instantaneous heart rate.
Abstract: Background Sleep plays a critical role in maintaining health and well-being; however, patients who are hospitalized are frequently exposed to noise that can disrupt sleep. Efforts to attenuate hospital noise have been limited by incomplete information on the interaction between sounds and sleep physiology. Objective To determine profiles of acoustic disruption of sleep by examining the cortical (encephalographic) arousal responses during sleep to typical hospital noises by sound level and type and sleep stage. Design 3-day polysomnographic study. Setting Sound-attenuated sleep laboratory. Participants Volunteer sample of 12 healthy participants. Intervention Baseline (sham) night followed by 2 intervention nights with controlled presentation of 14 sounds that are common in hospitals (for example, voice, intravenous alarm, phone, ice machine, outside traffic, and helicopter). The sounds were administered at calibrated, increasing decibel levels (40 to 70 dBA [decibels, adjusted for the range of normal hearing]) during specific sleep stages. Measurements Encephalographic arousals, by using established criteria, during rapid eye movement (REM) sleep and non-REM (NREM) sleep stages 2 and 3. Results Sound presentations yielded arousal response curves that varied because of sound level and type and sleep stage. Electronic sounds were more arousing than other sounds, including human voices, and there were large differences in responses by sound type. As expected, sounds in NREM stage 3 were less likely to cause arousals than sounds in NREM stage 2; unexpectedly, the probability of arousal to sounds presented in REM sleep varied less by sound type than when presented in NREM sleep and caused a greater and more sustained elevation of instantaneous heart rate. Limitations The study included only 12 participants. Results for these healthy persons may underestimate the effects of noise on sleep in patients who are hospitalized. Conclusion Sounds during sleep influence both cortical brain activity and cardiovascular function. This study systematically quantifies the disruptive capacity of a range of hospital sounds on sleep, providing evidence that is essential to improving the acoustic environments of new and existing health care facilities to enable the highest quality of care. Primary funding source Academy of Architecture for Health, Facilities Guidelines Institute, and The Center for Health Design.
TL;DR: The results demonstrate altered prediction error signaling during recall of fear extinction after REM sleep deprivation, which may further the understanding of anxiety disorders in which disturbed sleep and impaired fear extinction learning coincide.
Abstract: In a temporal difference learning approach of classical conditioning, a theoretical error signal shifts from outcome deliverance to the onset of the conditioned stimulus. Omission of an expected outcome results in a negative prediction error signal, which is the initial step towards successful extinction and may therefore be relevant for fear extinction recall. As studies in rodents have observed a bidirectional relationship between fear extinction and rapid eye movement (REM) sleep, we aimed to test the hypothesis that REM sleep deprivation impairs recall of fear extinction through prediction error signaling in humans. In a three-day design with polysomnographically controlled REM sleep deprivation, 18 young, healthy subjects performed a fear conditioning, extinction and recall of extinction task with visual stimuli, and mild electrical shocks during combined functional magnetic resonance imaging (fMRI) and skin conductance response (SCR) measurements. Compared to the control group, the REM sleep deprivation group had increased SCR scores to a previously extinguished stimulus at early recall of extinction trials, which was associated with an altered fMRI time-course in the left middle temporal gyrus. Post-hoc contrasts corrected for measures of NREM sleep variability also revealed between-group differences primarily in the temporal lobe. Our results demonstrate altered prediction error signaling during recall of fear extinction after REM sleep deprivation, which may further our understanding of anxiety disorders in which disturbed sleep and impaired fear extinction learning coincide. Moreover, our findings are indicative of REM sleep related plasticity in regions that also show an increase in activity during REM sleep.
TL;DR: The results demonstrate that sleep does in fact stabilize declarative memories, diminishing the negative impact of subsequent wakefulness, and sleep is most beneficial to memory 24 hr later if it occurs shortly after learning.
Abstract: Numerous studies have examined sleep's influence on a range of hippocampus-dependent declarative memory tasks, from text learning to spatial navigation. In this study, we examined the impact of sleep, wake, and time-of-day influences on the processing of declarative information with strong semantic links (semantically related word pairs) and information requiring the formation of novel associations (unrelated word pairs). Participants encoded a set of related or unrelated word pairs at either 9am or 9pm, and were then tested after an interval of 30 min, 12 hr, or 24 hr. The time of day at which subjects were trained had no effect on training performance or initial memory of either word pair type. At 12 hr retest, memory overall was superior following a night of sleep compared to a day of wakefulness. However, this performance difference was a result of a pronounced deterioration in memory for unrelated word pairs across wake; there was no sleep-wake difference for related word pairs. At 24 hr retest, with all subjects having received both a full night of sleep and a full day of wakefulness, we found that memory was superior when sleep occurred shortly after learning rather than following a full day of wakefulness. Lastly, we present evidence that the rate of deterioration across wakefulness was significantly diminished when a night of sleep preceded the wake period compared to when no sleep preceded wake, suggesting that sleep served to stabilize the memories against the deleterious effects of subsequent wakefulness. Overall, our results demonstrate that 1) the impact of 12 hr of waking interference on memory retention is strongly determined by word-pair type, 2) sleep is most beneficial to memory 24 hr later if it occurs shortly after learning, and 3) sleep does in fact stabilize declarative memories, diminishing the negative impact of subsequent wakefulness.
TL;DR: The interrelationships among slow-wave, spindle, and ripple events are defined, indicating that sleep disturbances may be associated with state-dependent decoupling of hippocampal and cortical circuits in psychiatric diseases.
TL;DR: Initial management should focus on decreasing the potential for sleep-related injury followed by treating comorbid sleep disorders, and pharmacotherapy for other parasomnias is less certain, and further investigations are necessary.
TL;DR: It is demonstrated that sleep-related memory consolidation has a higher complexity and more influencing factors than previously assumed and there is a sex and menstrual cycle effect, which seems to be mediated by female hormones and sleep spindles.
TL;DR: The nocturnal polysomnogram and MSLT are useful clinical tools for evaluating pediatric non-respiratory sleep disorders when integrated with the clinical evaluation.
Abstract: Background Although a level 1 nocturnal polysomnogram (PSG) is often used to evaluate children with non-respiratory sleep disorders, there are no published evidence-based practice parameters focused on the pediatric age group. In this report, we present practice parameters for the indications of polysomnography and the multiple sleep latency test (MSLT) in the assessment of non-respiratory sleep disorders in children. These practice parameters were reviewed and approved by the Board of Directors of the American Academy of Sleep Medicine (AASM). Methods A task force of content experts was appointed by the AASM to review the literature and grade the evidence according to the American Academy of Neurology grading system. Recommendations for psg and mslt use PSG is indicated for children suspected of having periodic limb movement disorder (PLMD) for diagnosing PLMD. (STANDARD)The MSLT, preceded by nocturnal PSG, is indicated in children as part of the evaluation for suspected narcolepsy. (STANDARD)Children with frequent NREM parasomnias, epilepsy, or nocturnal enuresis should be clinically screened for the presence of comorbid sleep disorders and polysomnography should be performed if there is a suspicion for sleep-disordered breathing or periodic limb movement disorder. (GUIDELINE)The MSLT, preceded by nocturnal PSG, is indicated in children suspected of having hypersomnia from causes other than narcolepsy to assess excessive sleepiness and to aid in differentiation from narcolepsy. (OPTION)The polysomnogram using an expanded EEG montage is indicated in children to confirm the diagnosis of an atypical or potentially injurious parasomnia or differentiate a parasomnia from sleep-related epilepsy (OPTION)Polysomnography is indicated in children suspected of having restless legs syndrome (RLS) who require supportive data for diagnosing RLS. (OPTION) RECOMMENDATIONS AGAINST PSG USE: Polysomnography is not routinely indicated for evaluation of children with sleep-related bruxism. (STANDARD) CONCLUSIONS: The nocturnal polysomnogram and MSLT are useful clinical tools for evaluating pediatric non-respiratory sleep disorders when integrated with the clinical evaluation.
TL;DR: The results suggest that lack of REM sleep in humans is associated with enhanced emotional reactivity, both at behavioral and neural levels, and thus highlight the specific role of REMSleep in regulating the neural substrates for emotional responsiveness.
Abstract: Converging evidence from animal and human studies suggest that rapid eye movement (REM) sleep modulates emotional processing. The aim of the present study was to explore the effects of selective REM sleep deprivation (REM-D) on emotional responses to threatening visual stimuli and their brain correlates using functional magnetic resonance imaging (fMRI). Twenty healthy subjects were randomly assigned to two groups: selective REM-D, by awakening them at each REM sleep onset, or non-rapid eye movement sleep interruptions (NREM-I) as control for potential non-specific effects of awakenings and lack of sleep. In a within-subject design, a visual emotional reactivity task was performed in the scanner before and 24 h after sleep manipulation. Behaviorally, emotional reactivity was enhanced relative to baseline (BL) in the REM deprived group only. In terms of fMRI signal, there was, as expected, an overall decrease in activity in the NREM-I group when subjects performed the task the second time, particularly in regions involved in emotional processing, such as occipital and temporal areas, as well as in the ventrolateral prefrontal cortex, involved in top-down emotion regulation. In contrast, activity in these areas remained the same level or even increased in the REM-D group, compared to their BL level. Taken together, these results suggest that lack of REM sleep in humans is associated with enhanced emotional reactivity, both at behavioral and neural levels, and thus highlight the specific role of REM sleep in regulating the neural substrates for emotional responsiveness.
TL;DR: Electroencephalographic sigma power and slow‐wave activity were positively correlated with the pre–post‐sleep consolidation of declarative (word list) and procedural (mirror‐tracing) memories, consistent with the view that processes of synaptic strengthening (sleep spindles) and synaptic downscaling (slow‐ wave activity) might act in concert to promote synaptic plasticity and the consolidation of bothDeclarative and procedural memories during sleep.
Abstract: SUMMARY Previous studies suggest that sleep-specific brain activity patterns such as sleep spindles and electroencephalographic slow-wave activity contribute to the consolidation of novel memories. The generation of both sleep spindles and slow-wave activity relies on synchronized oscillations in a thalamo-cortical network that might be implicated in synaptic strengthening (spindles) and downscaling (slow-wave activity) during sleep. This study further examined the association between electroencephalographic power during non-rapid eye movement sleep in the spindle (sigma, 12–16 Hz) and slow-wave frequency range (0.1– 3.5 Hz) and overnight memory consolidation in 20 healthy subjects (10 men, 27.1 ± 4.6 years). We found that both electroencephalographic sigma power and slow-wave activity were positively correlated with the pre–post-sleep consolidation of declarative (word list) and procedural (mirror-tracing) memories. These results, although only correlative in nature, are consistent with the view that processes of synaptic strengthening (sleep spindles) and synaptic downscaling (slow-wave activity) might act in concert to promote synaptic plasticity and the consolidation of both declarative and procedural memories during sleep.
TL;DR: Evidence is provided that there is a clear minimum requirement of sleep continuity in humans to ensure optimal sleep dependent memory processes and important new information is provided about the cognitive impact of obstructive sleep apnea and challenges its current definitions.
Abstract: A growing literature supports a role for sleep after training in long-term memory consolidation and enhancement. Consequently, interrupted sleep should result in cognitive deficits. Recent evidence from an animal study indeed showed that optimal memory consolidation during sleep requires a certain amount of uninterrupted sleep. Sleep continuity is disrupted in various medical disorders. We compared performance on a motor sequence learning task (MST) in relatively young subjects with obstructive sleep apnea (n = 16; apnea-hypopnea index 17.1±2.6/h [SEM]) to a carefully matched control group (n = 15, apnea-hypopnea index 3.7±0.4/h, p<0.001. Apart from AHI, oxygen nadir and arousal index, there were no significant differences between groups in total sleep time, sleep efficiency and sleep architecture as well as subjective measures of sleepiness based on standard questionnaires. In addition performance on the psychomotor vigilance task (reaction time and lapses), which is highly sensitive to sleep deprivation showed no differences as well as initial learning performance during the training phase. However there was a significant difference in the primary outcome of immediate overnight improvement on the MST between the two groups (controls = 14.7±4%, patients = 1.1±3.6%; P = 0.023) as well as plateau performance (controls = 24.0±5.3%, patients = 10.1±2.0%; P = 0.017) and this difference was predicted by the arousal index (p = 0.02) rather than oxygen saturation (nadir and time below 90% saturation. Taken together, this outcome provides evidence that there is a clear minimum requirement of sleep continuity in humans to ensure optimal sleep dependent memory processes. It also provides important new information about the cognitive impact of obstructive sleep apnea and challenges its current definitions.
TL;DR: Objective indices of sleep continuity, depth, and sleep disordered breathing are significant correlates of the metabolic syndrome in midlife women, independent of race, menopausal status and other factors that might otherwise account for these relationships.
Abstract: Study objectives We evaluated associations among subjective and objective measures of sleep and the metabolic syndrome in a multi-ethnic sample of midlife women. Design Cross-sectional study. Setting Participants' homes. Participants Caucasian (n = 158), African American (n = 125), and Chinese women (n = 57); mean age = 51 years. Age range = 46-57 years. Interventions None. Measurements and results Metabolic syndrome was measured in the clinic and sleep quality was assessed by self-report. Indices of sleep duration, continuity/fragmentation, depth, and sleep disordered breathing were assessed by in-home polysomnography (PSG). Covariates included sociodemographics, menopausal status, use of medications that affect sleep, and self-reported health complaints and health behaviors known to influence metabolic syndrome risk. Logistic regression was used to test the hypothesis that the metabolic syndrome would be associated with increased subjective sleep complaints and PSG-assessed sleep disturbances. In univariate analyses, the metabolic syndrome was associated with decreased sleep duration and efficiency and increased NREM beta power and apnea-hypopnea index (AHI). After covariate adjustment, sleep efficiency (odds ratio [OR] = 2.06, 95% confidence interval [CI]: 1.08-3.93), NREM beta power (OR = 2.09, 95% CI: 1.09-3.98), and AHI (OR = 1.86, 95% CI: 1.40-2.48) remained significantly associated with the metabolic syndrome (odds ratio values are expressed in standard deviation units). These relationships did not differ by race. Conclusions Objective indices of sleep continuity, depth, and sleep disordered breathing are significant correlates of the metabolic syndrome in midlife women, independent of race, menopausal status and other factors that might otherwise account for these relationships.
TL;DR: It is proposed that age-related reduction in sleep-dependent memory consolidation may be due in part to changes in NREM sleep oscillations.
Abstract: The human electroencephalogram (EEG) during non-rapid eye movement sleep (NREM) is characterized mainly by high-amplitude (>75 μV), slow-frequency ( 025 s) These NREM oscillations play a crucial role in brain plasticity, and importantly, NREM sleep oscillations change considerably with aging This review discusses the association between NREM sleep oscillations and cerebral plasticity as well as the functional impact of age-related changes on NREM sleep oscillations We propose that age-related reduction in sleep-dependent memory consolidation may be due in part to changes in NREM sleep oscillations
TL;DR: These data provide a demonstration of a temporal relation between puberty and an electrophysiological marker of adolescent brain development that can guide research into whether the neuroendocrine events of puberty are mechanistically linked to cortical maturation or whether, instead, the two maturational processes are parallel but independent programs of human ontogenesis.
Abstract: The steep adolescent decline in the slow wave (delta, 1–4 Hz) electroencephalogram (EEG) of nonrapid eye movement (NREM) sleep is a dramatic maturational change in brain electrophysiology thought to be driven by cortical synaptic pruning. A perennial question is whether this change in brain electrophysiology is related to sexual maturation. Applying Gompertz growth models to longitudinal data spanning ages 9–18 y, we found that the timing of the delta decline was significantly (P < 0.0001) linked to timing of pubertal maturation. This timing relation remained significant when sex differences in the timing of the delta decline were statistically controlled. Sex differences and the relation to the timing of puberty jointly explained 67% of the between-subject variance in the timing of the delta decline. These data provide a demonstration of a temporal relation between puberty and an electrophysiological marker of adolescent brain development. They can guide research into whether the neuroendocrine events of puberty are mechanistically linked to cortical maturation or whether, instead, the two maturational processes are parallel but independent programs of human ontogenesis.
TL;DR: In this article, the nonsynonymous c.22G>A polymorphism (rs73598374) of adenosine deaminase (ADA) was found to reduce the conversion of adenoine to inosine and predicts baseline differences in sleep slow-wave oscillations.
Abstract: Homeostatically regulated slow-wave oscillations in non-rapid eye movement (REM) sleep may reflect synaptic changes across the sleep-wake continuum and the restorative function of sleep. The nonsynonymous c.22G>A polymorphism (rs73598374) of adenosine deaminase (ADA) reduces the conversion of adenosine to inosine and predicts baseline differences in sleep slow-wave oscillations. We hypothesized that this polymorphism affects cognitive functions, and investigated whether it modulates electroencephalogram (EEG), behavioral, subjective, and biochemical responses to sleep deprivation. Attention, learning, memory, and executive functioning were quantified in healthy adults. Right-handed carriers of the variant allele (G/A genotype, n = 29) performed worse on the d2 attention task than G/G homozygotes (n = 191). To test whether this difference reflects elevated homeostatic sleep pressure, sleep and sleep EEG before and after sleep deprivation were studied in 2 prospectively matched groups of G/A and G/G genotype subjects. Deep sleep and EEG 0.75- to 1.5-Hz oscillations in non-REM sleep were significantly higher in G/A than in G/G genotype. Moreover, attention and vigor were reduced, whereas waking EEG alpha activity (8.5-12 Hz), sleepiness, fatigue, and α-amylase in saliva were enhanced. These convergent data demonstrate that genetic reduction of ADA activity elevates sleep pressure and plays a key role in sleep and waking quality in humans.