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While previous work has shown a positive relationship between cognitive performance and lifestyle factors in younger adults, evidence for this relationship among middle-aged and older adults has been mixed. The current study aimed to further test the relationship among physical activity, sleep quality, and memory performance in middle-aged and older adults, and to test whether this relationship holds up during the COVID-19 pandemic. Our results showed that physical activity was associated with better sleep quality and better working memory performance, and better sleep quality was associated with better working memory and self-perceptions of everyday memory abilities. Additionally, we found that the effects of physical activity on working memory were partially mediated by sleep quality. While these effects were small and only correlational in nature, they lend further support to the notion that sleep quality and physical activity are beneficial to memory later in life, even during a global pandemic.

It has become clear that sleep after learning has beneficial effects on the later retrieval of newly acquired memories. The neural mechanisms underlying these effects are becoming increasingly clear as well, particularly those of non-REM sleep. However, much is still unknown about the sleep and memory relationship: the sleep state or features of sleep physiology that associate with memory performance often vary by task or experimental design, and the nature of this variability is not entirely clear. This paper describes pertinent features of sleep physiology and provides a detailed review of the scientific literature indicating beneficial effects of post-learning sleep on memory retrieval. This paper additionally introduces a hypothesis which attributes these beneficial effects of post-learning sleep to separable processes of memory reinforcement and memory refinement whereby reinforcement supports one's ability to retrieve a given memory and refinement supports the precision of that memory retrieval in the context of competitive alternatives. It is observed that features of non-REM sleep are involved in a post-learning substantiation of memory representations that benefit memory performance; thus, memory reinforcement is primarily attributed to non-REM sleep. Memory refinement is primarily attributed to REM sleep given evidence of bidirectional synaptic plasticity in REM sleep and findings from studies of selective REM sleep deprivation., Competing Interests: Conflicts of interest The authors do not have any conflicts of interest to disclose., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Study Objectives: This study investigated the role of pubertal status and hormones in the association between sleep satisfaction and self-reported emotion functioning in 256 children and adolescents aged 8-15., Methods: Self-report data was provided on sleep duration, sleep satisfaction, and emotion reactivity and regulation, and a saliva sample was obtained for hormone measures. A subset of children also wore an Actigraph watch to measure sleep for a week., Results: Latent-class analysis revealed three classes of sleepers: Satisfied, Moderately Satisfied, and Dissatisfied. Dissatisfied sleepers reported more difficulties with emotion regulation and greater emotion reactivity than Satisfied sleepers. High difficulties with emotion regulation was associated with shorter objective sleep duration, and high emotion reactivity was associated with lower sleep efficiency. For girls, Dissatisfied sleepers reported being further through pubertal development than Satisfied sleepers. There were also significant correlations between pubertal development and shorter sleep duration and longer sleep latency in girls, and shorter and more irregular sleep in boys. Finally, pubertal development in girls was a significant moderator in the relationship between sleep satisfaction and difficulties with emotion regulation in Dissatisfied sleepers, such that being further through puberty and having unsatisfactory sleep resulted in the highest emotion regulation difficulties., Conclusions: This study expands on previous literature by considering the role of sleep satisfaction and the interaction with puberty development on emotion function. Specifically, a role for pubertal development was identified in the association between unsatisfactory sleep and emotion regulation in girls., (© The Author(s) 2021. Published by Oxford University Press on behalf of Sleep Research Society.)

Despite complaints of difficulties in waking socioemotional functioning by individuals with insomnia, only a few studies have investigated emotion processing performance in this group. Additionally, the role of sleep in socioemotional processing has not been investigated extensively nor using quantitative measures of sleep. Individuals with insomnia symptoms ( n = 14) and healthy good sleepers ( n = 15) completed two nights of at-home polysomnography, followed by an afternoon of in-lab performance testing on tasks measuring the processing of emotional facial expressions. The insomnia group self-reported less total sleep time, but no other group differences in sleep or task performance were observed. Greater beta EEG power throughout the night was associated with higher intensity ratings of happy, fearful and sad faces for individuals with insomnia, yet blunted sensitivity and lower accuracy for good sleepers. Thus, the presence of hyperarousal differentially impacted socioemotional processing of faces in individuals with insomnia symptoms and good sleepers.

Few studies have experimentally manipulated sleep to study its effect on aggressive behavior. The current study examined how reactive aggression was affected by having sleep restricted to 4-hours on a single night, a level of disruption commonly experienced. Both rested and sleep-restricted participants completed the Point Subtraction Aggression Paradigm (PSAP), a laboratory task in which participants seek to earn points, are provoked by a fictitious opponent stealing their points, and may choose to steal points in response. Logistic mixed-effect models were used to investigate the effect of sleep restriction and the role of sex hormones on the odds of choosing to steal. For men, and women in the luteal phase of the menstrual cycle, sleep restriction did not result in significant changes reactive aggression, although the patterns of aggressive behavior appeared less reactive and retaliatory in nature. For women in the follicular phase of the menstrual cycle, sleep restriction was associated with higher levels of reactive aggression. For both men and women in the luteal phase, sleep restriction disrupted an association between hormone change over the task (testosterone and estradiol, respectively) and reactive aggression that was observed in their control participants. In addition, higher testosterone before the PSAP in men was associated with maintaining a high level of stealing over the task. These results indicate a complex dynamic in which sex hormones and sleep interact to predict aggressive behavior in response to provocation., (© 2018 Wiley Periodicals, Inc.)

We explored changes in multiscale brain signal complexity and power-law scaling exponents of electroencephalogram (EEG) frequency spectra across several distinct global states of consciousness induced in the natural physiological context of the human sleep cycle. We specifically aimed to link EEG complexity to a statistically unified representation of the neural power spectrum. Further, by utilizing surrogate-based tests of nonlinearity we also examined whether any of the sleep stage-dependent changes in entropy were separable from the linear stochastic effects contained in the power spectrum. Our results indicate that changes of brain signal entropy throughout the sleep cycle are strongly time-scale dependent. Slow wave sleep was characterized by reduced entropy at short time scales and increased entropy at long time scales. Temporal signal complexity (at short time scales) and the slope of EEG power spectra appear, to a large extent, to capture a common phenomenon of neuronal noise, putatively reflecting cortical balance between excitation and inhibition. Nonlinear dynamical properties of brain signals accounted for a smaller portion of entropy changes, especially in stage 2 sleep., (© 2018 Wiley Periodicals, Inc.)

Working memory (WM) is impaired following sleep loss and may be improved after a nap. The goal of the current study was to better understand sleep-related WM enhancement by: (1) employing a WM task that assesses the ability to hold and report visual representations as well as the fidelity of the reports on a fine scale, (2) investigating neurophysiological properties of sleep and WM capacity as potential predictors or moderators of sleep-related enhancement, and (3) exploring frontal and occipital event-related delay activity to index the neural processing of stimuli in WM. In a within-subjects design, 36 young adults (M age = 20, 20 men, 16 women) completed a 300-trial, continuous-report task of visual WM following a 90-min nap opportunity and an equivalent period of wakefulness. Mixed-effect models were used to estimate the odds of successful WM reports and the fidelity of those reports. The odds of a successful report were approximately equal between nap and wake conditions for the start of the task, but by the end, the odds of success were 1.26 times greater in the nap condition. Successful WM reports were more accurate after a nap, independent of the time on task. Neither WM capacity nor any of the sleep variables measured were found to significantly moderate the nap effect on WM. Lastly, napping resulted in amplitude changes for frontal and occipital delay activity relative to the wake condition. The findings are discussed in relation to contemporary models of visual WM and the role of sleep in sustained attention.

This systematic review examined the associations between sleep and brain functions and structures in children and adolescents aged 1-17 ys. Included studies (n = 24) were peer-reviewed and met the a priori determined population (apparently healthy children and adolescents aged 1 y to 17 ys), intervention/exposure/comparator (various sleep characteristics including duration, architecture, quality, timing), and outcome criteria (brain functions and/or brain structures, excluding cognitive function outcomes). Collectively, the reviewed studies report some relationships between inadequate sleep and resultant differences in brain functions or structures. Although the research presented supports and offers more insight into the importance of sleep for the developing brain of children and adolescents, no firm conclusions that apply broadly may be drawn from these results, particularly because of the diversity of the sleep variables and outcomes. However, it is clear that sleeping habits in the pediatric population should be prioritized. Health care providers should continue to recommend healthy sleep practices and adequate time for sleep, as they are essential for overall health, including brain health., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

The central aim of this study was to investigate hormones as a predictor of individual vulnerability or resiliency on emotion processing tasks following one night of sleep restriction. The restriction group was instructed to sleep 3 a.m.-7 a.m. (13 men, 13 women in follicular phase, 10 women in luteal phase of menstrual cycle), and a control group slept 11 p.m.-7 a.m. (12 men, 12 follicular women, 12 luteal women). Sleep from home was verified with actigraphy. Saliva samples were collected on the evening prior to restriction, and in the morning and afternoon following restriction, to measure testosterone, estradiol, and progesterone. In the laboratory, event-related potentials (ERPs) were recorded during presentation of images and faces to index neural processing of emotional stimuli. Compared to controls, sleep-restricted participants had a larger amplitude Late Positive Potential (LPP) ERP to positive vs neutral images, reflecting greater motivated attention towards positive stimuli. Sleep-restricted participants were also less accurate categorizing sad faces and exhibited a larger N170 to sad faces, reflecting greater neural reactivity. Sleep-restricted luteal women were less accurate categorizing all images compared to control luteal women, and progesterone was related to several outcomes. Morning testosterone in men was lower in the sleep-restricted group compared to controls; lower testosterone was associated with lower accuracy to positive images, a greater difference between positive vs neutral LPP amplitude, and lower accuracy to sad and fearful faces. In summary, women higher in progesterone and men lower in testosterone were more vulnerable to the effects of sleep restriction on emotion processing tasks. This study highlights a role for sex and sex hormones in understanding individual differences in vulnerability to sleep loss.

Both sleep and future relevance influence memory consolidation; however, limited research has investigated their role in memory reconsolidation. We manipulated the future relevance of both stable and labile memories in need of reconsolidation. Two groups learned two blocks of syllable pairs on one evening and were told they would be tested on one of the blocks later. On the second evening, one group (Labile) received reminders designed to return their memories of syllable pairs to a labile state, while a second group (Stable) received reminders designed to leave these memories in a stable state. No significant differences in memory retention were found between blocks or groups the following morning. Frontal delta (0.5-4 Hz) electroencephalographic power during Stage 2 sleep correlated positively with retention of future-relevant material exclusively in the Labile group. Central theta (4-8 Hz) electroencephalographic power during rapid eye movement (REM) sleep correlated positively with the extent to which the Labile group selectively retained future-relevant material. These relationships suggest that sleep-dependent processes are involved in an economical reprocessing of memories beyond the initial stages of consolidation., (© 2016 European Sleep Research Society.)

Sleep deprivation impacts subjective mood states, but very little research has examined the impact on processing emotional information. In the current study, we investigated the impact of total sleep deprivation on neural responses to emotional facial expressions as well as the accuracy and speed with which these faces were categorized. Forty-nine participants completed two tasks in which they were asked to categorize emotional facial expressions as Happy, Sad, Angry, or Fearful. They were shown the 'full' expression of the emotions in one task and more subtle expressions in a second task in which expressions were 'morphed' with neutral faces so that the intensity of emotion varied. It was expected that sleep deprivation would lead to greater reactivity (indexed by larger amplitude N170 event-related potentials), particularly for negative and more subtle facial expressions. In the full face task, sleep-deprived (SD) participants were significantly less accurate than controls (C) at identifying Sad faces and slower to identify all emotional expressions. P1 was smaller and N170 was larger for the SD compared to C group, but for all emotions, indicating generalized impairment in low-level visual processing. In the more difficult morphed face task, SD participants were less accurate than C participants for Sad faces; as well, the group difference in reaction time was greatest for Sad faces. For the SD group, N170 increased in amplitude with increasing perceptual difficulty for the Fearful and Angry faces, but decreased in amplitude with increasing difficulty for Sad faces. These data illustrate that sleep deprivation led to greater neural reactivity for the threat-related negative emotions as they became more subtle; however, there was a failure to engage these perceptual resources for the processing of Sad faces. Sleep loss preferentially impacted the processing of Sad faces; this has widespread implications for sleep-deprived groups.

There is a need to understand the neural basis of performance deficits that result from sleep deprivation. Performance monitoring tasks generate response-locked event-related potentials (ERPs), generated from the anterior cingulate cortex (ACC) located in the medial surface of the frontal lobe that reflect error processing. The outcome of previous research on performance monitoring during sleepiness has been mixed. The purpose of this study was to evaluate performance monitoring in a controlled study of experimental sleep deprivation using a traditional Flanker task, and to broaden this examination using a response inhibition task. Forty-nine young adults (24 male) were randomly assigned to a total sleep deprivation or rested control group. The sleep deprivation group was slower on the Flanker task and less accurate on a Go/NoGo task compared to controls. General attentional impairments were evident in stimulus-locked ERPs for the sleep deprived group: P300 was delayed on Flanker trials and smaller to Go-stimuli. Further, N2 was smaller to NoGo stimuli, and the response-locked ERN was smaller on both tasks, reflecting neurocognitive impairment during performance monitoring. In the Flanker task, higher error rate was associated with smaller ERN amplitudes for both groups. Examination of ERN amplitude over time showed that it attenuated in the rested control group as error rate increased, but such habituation was not apparent in the sleep deprived group. Poor performing sleep deprived individuals had a larger Pe response than controls, possibly indicating perseveration of errors. These data provide insight into the neural underpinnings of performance failure during sleepiness and have implications for workplace and driving safety., (Copyright © 2013 Elsevier B.V. All rights reserved.)

The role of sleep deprivation in aggressive behavior has not been systematically investigated, despite a great deal of evidence to suggest a relationship. We investigated the impact of 33 h of sleep loss on endocrine function and reactive aggression using the Point Subtraction Aggression Paradigm (PSAP) task. PSAP performance was assessed in 24 young men and 25 women who were randomly assigned to a sleep deprivation or control condition. Sleep deprivation lowered reactive aggression and testosterone (but not cortisol) in men, and disrupted the positive relationship between a pre-post PSAP increase in testosterone and aggression that was evident in rested control men. While women increased aggression following provocation as expected, no influence of sleep deprivation was found. This is the first experimental study to demonstrate that sleep deprivation lowers reactive aggression in men. Testosterone, but not cortisol, played a role in the relationship between sleep and reactive aggression in men., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Accuracy for a second target (T2) is reduced when it is presented within 500 ms of a first target (T1) in a rapid serial visual presentation (RSVP) - an attentional blink (AB). There are reliable individual differences in the magnitude of the AB. Recent evidence has shown that the attentional approach that an individual typically adopts during a task or in anticipation of a task, as indicated by various measures, predicts individual differences in the AB deficit. It has yet to be observed whether indices of attentional approach when not engaged in a goal-directed task are also relevant to individual differences in the AB. The current studies investigated individual differences in the AB by examining their relationship with attention at rest using quantitative measures of EEG. Greater levels of alpha at rest were associated with larger AB magnitudes, where greater levels of beta at rest were associated with smaller AB magnitudes. Furthermore, individuals with more beta than alpha demonstrated a smaller AB effect than individuals with more alpha than beta. Our results suggest that greater attentional engagement at rest, when not engaged in a goal-directed task, is associated with smaller AB magnitudes., (Copyright © 2012 Elsevier Inc. All rights reserved.)

To examine whether anticipatory attention or expectancy is a cognitive process that is automatic or requires conscious control, we employed a paired-stimulus event-related potential (ERP) paradigm during the transition to sleep. The slow negative ERP wave observed between two successive stimuli, the Contingent Negative Variation (CNV), reflects attention and expectancy to the second stimulus. Thirteen good sleepers were instructed to respond to the second stimulus in a pair during waking sessions. In a non-response paradigm modified for sleep, participants then fell asleep while tones played. As expected, N1 decreased and P2 increased in amplitude systematically with the loss of consciousness at sleep onset; the CNV was increasingly more positive. Sleep onset latency was correlated with the amplitude of the CNV. The systematic attenuation of the CNV waveform at sleep onset and its absence in sleep indicates that anticipatory attention requires endogenous conscious control., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Event-related potentials may be applied to directly measure information-processing deficits associated with the problem of insomnia. This study is a systematic investigation of cortical hyperarousal during the sleep-onset period in participants with sleep-onset insomnia complaints. Thirteen poor sleepers and twelve good sleepers (GS) were administered an oddball task while awake in the morning and evening and during repeated sleep-onset attempts. Participants signaled detection of a higher pitch target tone as they fell asleep. P2 amplitude was significantly smaller for poor sleepers compared to GS, following standard stimuli at all fronto-central sites, in the pre-sleep waking period at sleep onset. Groups did not differ for N1, N350, or P300 in wake, Stage 1, or Stage 2. The smaller P2 indicates that poor sleepers failed to inhibit the irrelevant standard stimuli. This hyper-attentiveness may explain chronic problems with sleep initiation and could be the target of behavioral and pharmaceutical treatment strategies.

Few studies have investigated waking electrophysiological measures of arousal during sleep restriction. This study examined electroencephalogram (EEG) activity and performance during a 96-hour laboratory protocol where participants slept a baseline night (8 h), were randomly assigned to 3-, 5-, or 8-hour sleep groups for the next two nights sleep restriction (SR1, SR2), and then slept a recovery night (8 h). There were dose-dependent deficits on measures of mood, sleepiness, and reaction time that were apparent during this short-term bout of sleep restriction. The ratio of alpha to theta EEG recorded at rest indicated dose-dependent changes in CNS arousal. At 9:00 hours, both the 3- and 5-hour groups showed EEG slowing (sleepiness) during restriction, with the 3-hour group exhibiting greater deficits. Later in the day at 13:00 hours, the 5-hour group no longer exhibited EEG slowing, but the extent of slowing was more widespread across the scalp for the 3-hour group. High-frequency EEG, a measure of effort, was greater on the mornings following sleep restriction. The 5-hour group had increased beta EEG at central-parietal sites following both nights of restriction, whereas the 3-hour group had increased beta and gamma EEG at occipital regions following the first night only. Short-term sleep restriction leads to deficits in performance as well as EEG slowing that correspond to the amount and duration of sleep loss. High-frequency EEG may be a marker of effort or compensation.

Napping is a cross-cultural phenomenon which occurs across the lifespan. People vary widely in the frequency with which they nap as well as the improvements in alertness and well-being experienced. The systematic study of daytime napping is important to understand the benefits in alertness and performance that may be accrued from napping. This review paper investigates factors that affect the benefits of napping such as duration and temporal placement of the nap. In addition, the influence of subject characteristics such as age and experience with napping is examined. The focus of the review is on benefits for healthy individuals with regular sleep/wake schedules rather than for people with sleep or medical disorders. The goal of the review is to summarize the type of performance improvements that result from napping, critique the existing studies, and make recommendations for future research.

The neurocognitive model of insomnia predicts information processing deficits in poor sleepers. There is some evidence for deficits in later cognitive processing, but earlier sensory processing remains to be investigated. Paired-click stimuli were delivered to good and poor sleepers in a single night. P50 amplitude to stimuli provided an index of sensory gating in presleep wake, rapid eye movement sleep and stage 2 sleep. Poor sleepers exhibited sensory gating impairments during wake. For both groups, gating was intact in rapid eye movement sleep but absent in stage 2 sleep. These data show that poor sleepers experience enhanced sensory processing in the waking period before sleep. Further study is needed to explore sensory gating in chronic primary insomnia, sleep maintenance insomnia, and across multiple recording nights.

Waking brain physiology underlying deficits from continuous sleep restriction (CSR) is not well understood. Fourteen good sleepers participated in a 21-day protocol where they slept their usual amount in a baseline week, had their time in bed restricted by 33% in a CSR week, and slept the desired amount in a recovery week. Participants slept at home, completing diaries and wearing activity monitors to verify compliance. Each day participants completed an RT task and mood and sleepiness ratings every 3 h. Laboratory assessment of electrophysiology and performance took place at the end of baseline, three times throughout the CSR week, and at the beginning of recovery. Participants reported less sleep during CSR which was confirmed by activity monitors. Correspondingly, well-being and neurobehavioural performance was impaired. Quantitative EEG analysis revealed significantly reduced arousal between the 1st and 7th days of restriction and linear effects at anterior sites (Fp2, Fz, F8, T8). At posterior sites (P4, P8), reductions occurred only later in the week between the 4th and 7th nights of restriction. Both the immediate linear decline in arousal and precipitous drop later in the week were apparent at central sites (C4, Cz). Thus, frontal regions were affected immediately, while parietal regions showed maintenance of function until restriction was more severe. The P300 ERP component showed evidence of reduced attention by the 7th day of restriction (at Pz, P4). EEG and ERPs deficits were more robust in the right-hemisphere, which may reflect greater vulnerability to sleep loss in the non-dominant hemisphere.

Sleep spindles and rapid eye movements have been found to increase following an intense period of learning on a combination of procedural memory tasks. It is not clear whether these changes are task specific, or the result of learning in general. The current study investigated changes in spindles, rapid eye movements, K-complexes and EEG spectral power following learning in good sleepers randomly assigned to one of four learning conditions: Pursuit Rotor (n=9), Mirror Tracing (n=9), Paired Associates (n=9), and non-learning controls (n=9). Following Pursuit Rotor learning, there was an increase in the duration of Stage 2 sleep, spindle density (number of spindles/min), average spindle duration, and an increase in low frequency sigma power (12-14Hz) at occipital regions during SWS and at frontal regions during Stage 2 sleep in the second half of the night. These findings are consistent with previous findings that Pursuit Rotor learning is consolidated during Stage 2 sleep, and provide additional data to suggest that spindles across all non-REM stages may be a mechanism for brain plasticity. Following Paired Associates learning, theta power increased significantly at central regions during REM sleep. This study provides the first evidence that REM sleep theta activity is involved in declarative memory consolidation. Together, these findings support the hypothesis that brain plasticity during sleep does not involve a unitary process; that is, different types of learning have unique sleep-related memory consolidation mechanisms that act in dissociable brain regions at different times throughout the night.

The number of sleep spindles remains relatively stable within individuals from night to night. However, there is little explanation for the large interindividual differences in spindles. The authors investigated the relationship between spindles and intelligence quotient (IQ) in 3 separate studies. The number of spindles and sigma power were positively correlated with performance IQ (PIQ), but not verbal IQ (VIQ). The perceptual/analytical skills measured by the PIQ Picture Completion subscale accounted for most of the interindividual differences in spindles. Furthermore, there was a relationship between the rapid eye movements (REMs) of REM sleep and VIQ in individuals with higher IQ scores. A similar pattern was observed between spindles and PIQ. It was hypothesized that high-IQ individuals have more spindles that can support more complex cortical networks underlying perceptual/analytical abilities., (Copyright (c) 2007 APA, all rights reserved.)

The effect of napping on motor performance was examined in habitual and non-habitual nappers who were randomly assigned to a nap or reading condition. Motor procedural learning and auditory discrimination tasks were administered pre- and post-condition. Both groups reported improved alertness post-nap, but not post-reading. Non-habitual nappers fell asleep faster and tended to have greater sleep efficiency, but did not differ from habitual nappers on other sleep architecture variables. Habitual nappers had greater alpha and theta EEG power in stage 1, and greater delta, alpha and sigma power in stage 2 sleep. Motor performance deteriorated for non-habitual nappers who napped, but improved for all others. The number of sleep spindles and sigma power (13.5-15 Hz) significantly predicted motor performance following the nap, for habitual nappers only. Results indicate that motor learning was consolidated in a brief nap and was associated with stage 2 spindles, but only for those who habitually take naps.

Electroencephalogram (EEG) alpha (8-12 Hz) asymmetries were collected from the mid-frontal and central regions during presleep wakefulness and Stage 1, Stage 2, and rapid eye movement (REM) sleep in 11 healthy right-handed participants who were free of psychiatric, neurological, and sleep problems. The authors found significant correlations between presleep wakefulness and different stages of sleep in the frontal, but not central, EEG alpha asymmetry measure. The strongest correlation was between presleep waking and REM sleep, replicating and extending relation earlier work to a normal population. The high degree of association between presleep waking and REM sleep may be a result of high cortical activation common to these states and may reflect a predisposition to different styles of emotional reactivity.

Study Objectives: Experimental sleep fragmentation involves inducing arousals by administering intrusive auditory stimuli throughout the night. It is intended to model the frequent and periodic disruption experienced in common sleep disorders. Sleep fragmentation leads to daytime sleepiness, although evidence of performance impairment has been inconsistent. The purpose of this study was to investigate brain physiology associated with this level of sleep disruption. Specifically, quantitative analysis of electroencephalography was carried out, and auditory event-related potentials were recorded during daytime performance assessment following sleep fragmentation in good sleepers., Design: Participants spent 4 consecutive 24-hour periods in the laboratory. On nights 2 and 3, sleep was fragmented using auditory stimuli that were delivered with increasing intensity until an arousal was noted. This design aimed to investigate the cumulative effects of sleep fragmentation on daytime functioning., Setting: Data were collected in a sleep research laboratory during a 96-hour protocol., Participants: Eight healthy adults (mean age = 33.25) with no sleep complaints., Measurements and Results: During the day, participants performed a 40-minute computerized test battery at 2-hour intervals (9:00 am -7:00 pm). The battery was presented in a fixed order and included measures of mood, sleepiness, reaction time, and serial addition or subtraction. Results indicated that subjective sleepiness and mood were impaired following sleep-fragmentation nights, compared to both baseline and recovery conditions. No performance deficits were apparent. The alpha:theta ratio, reflecting relative slowing of the electroencephalogram, was dramatically reduced following the second night of sleep fragmentation. Reductions in N1 amplitude of the event-related potentials indicated that attention was impaired with respect to early encoding processes following sleep fragmentation., Conclusions: Electroencephalographic and event-related potentials data illustrate impairment in information-processing capabilities associated with reduced arousal elicited by experimental sleep fragmentation. This subtle degree of sleep disruption, where total sleep time is not reduced, leads to sustained impairment in alertness and attention.

During the waking state, a late component of the auditory event-related potential, P300, is elicited when subjects detect a rare 'target' stimulus. It is usually not elicited when subjects either ignore or fail to detect the stimulus. The presence of P300 is therefore thought to reflect conscious processing of the stimulus. Since P300 has been shown to be an attention-dependent cognitive component in wakefulness, one might suppose that it would be absent during sleep-a time in which information processing of external stimuli is commonly thought to be inhibited. This review examines the presence or absence of P300 in studies employing auditory odd-ball paradigms in sleep. Research to date indicates that P300 can be recorded during the transition to sleep and then reappears in REM sleep. Stimuli that are rare and intrusive are more likely to elicit the classic parietal P300 in REM sleep. There is, however, little or no positivity at frontal sites. This is consistent with brain imaging studies that show frontal deactivation is characteristic of REM sleep. These findings indicate that while sleepers may be able to detect stimulus deviance in stage 1 and REM, the frontal contribution to consciousness may be lost. In non-REM sleep, a later positive wave at 450 ms does not vary according to experimental manipulation in the same way as the waking and REM P300s. This non-REM sleep-related positivity may therefore underlie mechanism distinct from the waking P300.

Although repeated selective rapid eye movement (REM) sleep deprivation by awakenings during nighttime has shown that the number of sleep interruptions required to prevent REM sleep increases within and across consecutive nights, the underlying regulatory processes remained unspecified. To assess the role of circadian and homeostatic factors in REM sleep regulation, REM sleep was selectively deprived in healthy young adult males during a daytime sleep episode (7-15 h) after a night without sleep. Circadian REM sleep propensity is known to be high in the early morning. The number of interventions required to prevent REM sleep increased from the first to the third 2-h interval by a factor of two and then leveled off. Only a minor REM sleep rebound (11.6%) occurred in the following undisturbed recovery night. It is concluded that the limited rise of interventions during selective daytime REM sleep deprivation may be due to the declining circadian REM sleep propensity, which may partly offset the homeostatic drive and the sleep-dependent disinhibition of REM sleep.

Event-related potentials (ERPs) and behavioral responsiveness were investigated during the transition from wakefulness to sleep. Ten participants were presented with an auditory oddball task during repeated sleep onset periods. The EEG was recorded from 29 different scalp sites. A 1500-Hz tone pip was presented infrequently (p = .04) within a series of lower pitch 1000-Hz "standard" stimuli (p = .96). Participants were required to button press upon detection of the rare "target" stimulus. During wakefulness, almost all targets were detected. A large amplitude P300 was observed to these detected targets. This P300 was maximum over parietal areas of the scalp. During stage 1 sleep, subjects continued to respond on 47% of trials. The parietal P300 amplitude remained large to these detected targets. It was, however, much attenuated at frontal sites. When the participant failed to detect the target in either stage 1 or 2, no P300 was visible. P300 is thus associated with behavioral detection of the target stimulus, whether in wakefulness or stage 1 "sleep." Trials were also sorted by reaction time (RT), in which bins 1-3 represented increasingly long RT. In the waking state, P300 amplitude did not significantly vary across the different bins. Although mean RT latency varied by 512 ms from bin 1 to bin 3, P300 latency varied by only 25 ms. Differences in RT are thus probably due to response-related processes rather than stimulus classification time.

Study Objectives: A cognitive evoked potential, labelled "P300," is elicited when an observer attends to and detects an infrequently delivered "target" stimulus. It is not typically present if the target is ignored or undetected. P300 is therefore thought to reflect some aspect of consciousness of the stimulus. There has been much controversy concerning whether P300 can be recorded in sleep, a state in which information processing of external events is presumably reduced. The present study investigated the effects of both pitch and intensity stimuli on information processing, in order to determine whether a more salient stimulus might elicit a P300 in sleep that is comparable to the waking P300., Design: A true P300 will have a parietal maximum peak following a rare stimulus, and its amplitude will vary inversely with the probability of stimulus delivery. Participants were thus randomly assigned to one of three probability groups, in which the deviant was presented on 20%, 10%, or 5% of trials., Setting: Data were collected in the Human Neurophysiology Laboratory at the University of Ottawa., Participants: Twenty-four young adults., Interventions: N/A., Measurements and Results: During wakefulness, a parietal P300 was apparent following both pitch and intensity deviants when participants were asked to detect deviant stimuli. A P300 was also apparent following the intensity deviant when participants were instructed to ignore the stimuli. During non-REM sleep, no P300 could be identified. In REM sleep, very rare (p=.05) loud deviants elicited a parietal P300. This P300 was attenuated relative to the waking ignore condition. Moreover, the frontal dispersion of the peak was absent., Conclusions: These data provide evidence that participants are conscious (parietal P300) of very rare and intrusive stimuli during REM sleep, although the frontal aspects associated with this consciousness may be absent.

The aim of the study was to investigate whether the electromagnetic field (EMF) emitted by digital radiotelephone handsets affects brain physiology. Healthy, young male subjects were exposed for 30 min to EMF (900 MHz; spatial peak specific absorption rate 1 W/kg) during the waking period preceding sleep. Compared with the control condition with sham exposure, spectral power of the EEG in non-rapid eye movement sleep was increased. The maximum rise occurred in the 9.75-11.25 Hz and 12.5-13.25 Hz band during the initial part of sleep. These changes correspond to those obtained in a previous study where EMF was intermittently applied during sleep. Unilateral exposure induced no hemispheric asymmetry of EEG power. The present results demonstrate that exposure during waking modifies the EEG during subsequent sleep. Thus the changes of brain function induced by pulsed high-frequency EMF outlast the exposure period.

Sleep spindles are 12-14 Hz oscillations in EEG, which are thought to inhibit or 'gate' information processing. Event-related potentials may be employed to probe the extent of information processing during sleep. Previous research indicates that event-related potentials elicited by moderate intensity stimuli show increased positivity (or further removal of negativity) when stimuli are presented concurrent with spindles. However, the effectiveness of spindles to inhibit the processing of much louder stimuli remains unknown. The purpose of the present study was to investigate the extent of this gating, by using a range of stimuli including those that are loud and intrusive. Eight good sleepers were recorded during a single night. Auditory stimuli were delivered randomly at 0, 60, 80 or 100 dB SPL. Trials were sorted off-line by sleep stage, stimulus intensity and spindle characteristic (i.e. spindle absent, spindle present). During the sleep-onset period, the often-reported changes in event-related potentials were observed - N1 decreased and P2 increased in amplitude. In Stage 2 sleep, P2 was affected by the presence of spindles, particularly when stimulus intensity was loud. Its amplitude was greatest when spindles occurred following the onset of the stimulus. Scalp-recorded spindles might, therefore, be a consequence of the prior thalamic inhibition of information processing, especially when confronted by loud, intrusive external stimuli.

During NREM sleep a very large amplitude wave-form, known as the K-complex, may be elicited upon presentation of an external stimulus. The present study compared the scalp distribution of a prominent negative wave peaking at about 550 ms and a later positive wave peaking between 900 and 1300 ms in stage 2 and slow wave sleep (SWS). Nine subjects spent a single night in the laboratory. They were presented with an 80 dB SPL 2000 Hz auditory tone pip every 15 s. The EEG was recorded from 29 electrode sites and referenced to the nose. A K-complex was elicited on 34% of trials in stage 2 and on 46% of trials in SWS. A negative wave peaking at 330 ms was larger on trials in which the K-complex was elicited than on trials in which it was not. The large amplitude N550 was readily observable on trials in which the K-complex was elicited but could not be observed on trials in which it was not. The N550 was bilaterally symmetrical and was maximum over fronto-central areas of the scalp in both stage 2 and SWS. It inverted in polarity at the mastoid and inferior parietal regions. The scalp distribution of N550 significantly differed between stage 2 and SWS. It showed a sharper decline in amplitude over parietal and posterior-inferior areas of the scalp in stage 2 compared to SWS. A later P900 was maximum over centro-frontal areas of the scalp and was also bilaterally symmetrical. It showed a significantly sharper decline in amplitude over widespread inferior areas during SWS. Because the scalp maps of the N550 and P900 are different in stage 2 and SWS, their intracranial sources must also be different.

Event-related potentials (ERPs) are often used to measure the extent of information processing during sleep. Previous studies have indicated that a late positive wave, P300, can be elicited during REM sleep if stimuli are very rare and/or very loud. The present study examined the role of stimulus intensity in eliciting a P300 during REM sleep. Eight subjects were presented with auditory tone pips with an intensity of either 0, 60, 80 or 100 dB SPL. Stimuli were delivered at random with equal probability. Trials were sorted by stage of sleep, stimulus intensity, and presence or absence of rapid eye movements in REM sleep. During the waking state, when subjects read a book, the loud 100 dB stimulus elicited short (P3a) and long latency (P300) positive waves (peaking at 293 and 373 ms respectively). In stage of 2 non-REM sleep, N1 decreased to baseline level while P2 increased in amplitude compared to the waking state. A P300 could not be observed in stage 2 sleep regardless of the level of stimulus intensity. During REM sleep, a late P300 (latency 363 ms) was elicited by the 100 dB stimulus. The earlier positive peak (i.e. P3a) was not apparent. The P300 was reduced in amplitude compared to the waking state. Its amplitude did not differ between phasic and tonic states of REM sleep. A late parietal negative slow wave (SW) was also apparent during REM. Although the SW was larger during phasic compared to tonic REM, the difference was not significant. These data suggest that stimuli which are sufficiently intrusive to elicit a P300 in the waking state continue to do so in REM sleep.

Objectives: The P300 component of the auditory event-related potential (ERP) is a large amplitude positive wave peaking at approximately 300 ms following detection of a rare significant stimulus. Although P300 is typically only evoked when the subject attends to the stimulus, it may also be elicited in an awake, inattentive subject if the stimulus is sufficiently intrusive. We therefore employed an oddball task to determine if high intensity stimuli would elicit the P300 during sleep., Methods: A loud 90 dB SPL tone pip was presented infrequently (P = 0.05) in a train of lower intensity 70 dB SPL standard stimuli. A multiple channel EEG was recorded from 8 good sleepers during a single night., Results: A large amplitude parieto-central P300, peaking at 321 ms, was apparent in REM sleep to the loud deviant stimulus. In stage two non-REM sleep, a later positive wave, peaking at 446 ms, was apparent even after K-Complexes were removed from the average. This non-REM P450 was however maximum over occipito-parietal areas of the scalp., Conclusion: The presence of a P300 in REM sleep following a loud, rare stimulus indicates that sensory discrimination capabilities remain intact during this state. This may be associated with either pre- or conscious processing of relevant stimuli.