The effects of sleep deprivation in humans: topographical electroencephalogram changes in non‐rapid eye movement (NREM) sleep versus REM sleep

Studies on homeostatic aspects of sleep regulation have been focussed upon non‐rapid eye movement (NREM) sleep, and direct comparisons with regional changes in rapid eye movement (REM) sleep are sparse. To this end, evaluation of electroencephalogram (EEG) changes in recovery sleep after extended waking is the classical approach for increasing homeostatic need. Here, we studied a large sample of 40 healthy subjects, considering a full‐scalp EEG topography during baseline (BSL) and recovery sleep following 40 h of wakefulness (REC). In NREM sleep, the statistical maps of REC versus BSL differences revealed significant fronto‐central increases of power from 0.5 to 11 Hz and decreases from 13 to 15 Hz. In REM sleep, REC versus BSL differences pointed to significant fronto‐central increases in the 0.5–7 Hz and decreases in the 8–11 Hz bands. Moreover, the 12–15 Hz band showed a fronto‐parietal increase and that at 22–24 Hz exhibited a fronto‐central decrease. Hence, the 1–7 Hz range showed significant increases in both NREM sleep and REM sleep, with similar topography. The parallel change of NREM sleep and REM sleep EEG power is related, as confirmed by a correlational analysis, indicating that the increase in frequency of 2–7 Hz possibly subtends a state‐aspecific homeostatic response. On the contrary, sleep deprivation has opposite effects on alpha and sigma activity in both states. In particular, this analysis points to the presence of state‐specific homeostatic mechanisms for NREM sleep, limited to <2 Hz frequencies. In conclusion, REM sleep and NREM sleep seem to share some homeostatic mechanisms in response to sleep deprivation, as indicated mainly by the similar direction and topography of changes in low‐frequency activity.     

Developmental changes in the sleep electroencephalogram of adolescent boys and girls

The sleep electroencephalogram (EEG) changes across adolescence; however, there are conflicting data as to whether EEG changes are regionally specific, are evident in non‐rapid eye movement (NREM) and rapid eye movement (REM) sleep, and whether there are sex differences. The present study seeks to resolve some of these issues in a combined cross‐sectional and longitudinal analysis of sleep EEG in adolescents. Thirty‐three healthy adolescents (18 boys, 15 girls; 11–14 years) were studied on two occasions 6–8 months apart. Cross‐sectional analysis of data from the initial visit revealed significantly less slow‐wave sleep, delta (0.3 to <4 Hz) and theta (4 to <8 Hz) power in both NREM and REM sleep with advancing age. The age–delta power relationship was significant at the occipital site, with age accounting for 26% of the variance. Longitudinal analysis revealed that NREM delta power declined significantly from the initial to follow‐up visit, in association with declining delta amplitude and incidence (P < 0.01), with the effect being greatest at the occipital site. REM delta power also declined over time in association with reduced amplitude (P < 0.01). There were longitudinal reductions in theta, alpha and sigma power in NREM and REM sleep evident at the occipital site at follow‐up (P < 0.01). No sex differences were apparent in the pattern of change with age for NREM or REM sleep. Declines in sleep EEG spectral power occur across adolescence in both boys and girls, particularly in the occipital derivation, and are not state‐specific, occurring in both NREM and REM sleep.     

Sleep spindle dynamics during NREM and REM sleep following distinct general anaesthesia in control rats and in a rat model of Parkinson’s disease cholinopathy

On the basis of our previous studies and the important role of the thalamo‐cortical network in states of unconsciousness, such as anaesthesia and sleep, and in sleep spindles generation, we investigated sleep spindles (SS) and high‐voltage sleep spindle (HVS) dynamics during non‐rapid eye movement (NREM) and rapid eye movement (REM) sleep following different types of general anaesthesia in both physiological controls and in a rat model of Parkinson's disease (PD) cholinopathy, to follow the impact of anaesthesia on post‐anaesthesia sleep at the thalamo‐cortical level through an altered sleep spindle dynamics. We recorded 6 hr of spontaneous sleep in all rats, both before and 48 hr after ketamine/diazepam or pentobarbital anaesthesia, and we used 1 hr of NREM or REM sleep from each to validate visually the automatically detected SS or HVS for their extraction and analysis. In the controls, SS occurred mainly during NREM, whereas HVS occurred only during REM sleep. Ketamine/diazepam anaesthesia promoted HVS, prolonged SS during NREM, induced HVS of increased frequency during REM, and increased SS/HVS densities during REM versus NREM sleep. Pentobarbital anaesthesia decreased the frequency of SS during NREM and the HVS density during REM sleep. Although the pedunculopontine tegmental nucleus lesion prolonged SS only during NREM sleep, in these rats, ketamine/diazepam anaesthesia suppressed HVS during both sleep states, whereas pentobarbital anaesthesia promoted HVS during REM sleep. The different impacts of two anaesthetic regimens on the thalamo‐cortical regulatory network are expressed through their distinct sleep spindle generation and dynamics that are dependent on the NREM and REM state regulatory neuronal substrate.     

Sleep deprivation suppresses the increase of rapid eye movement density across sleep cycles

We investigated the association between rapid eye movement (REM) density (REMd) and electroencephalogram (EEG) activity during non‐rapid eye movement (NREM) and REM sleep, within the re‐assessment, in a large sample of normal subjects, of the reduction of oculomotor activity in REM sleep after total sleep deprivation (SD). Coherently with the hypothesis of a role of homeostatic sleep pressure in influencing REMd, a negative correlation between changes in REMd and slow‐wave activity (SWA) was expected. A further aim of the study was to evaluate if the decreased REMd after SD affects ultradian changes across sleep periods. Fifty normal subjects (29 male and 21 female; mean age = 24.3 ± 2.2 years) were studied for four consecutive days and nights. Sleep recordings were scheduled in the first (adaptation), second (baseline) and fourth night (recovery). After awakening from baseline sleep, a protocol of 40 h SD started at 10:00 hours. Polysomnographic measures, REMd and quantitative EEG activity during NREM and REM sleep of baseline and recovery nights were compared. We found a clear reduction of REMd in the recovery after SD, due to the lack of REMd changes across cycles. Oculomotor changes positively correlated with a decreased power in a specific range of fast sigma activity (14.75–15.25 Hz) in NREM, but not with SWA. REMd changes were also related to EEG power in the 12.75–13.00 Hz range in REM sleep. The present results confirm the oculomotor depression after SD, clarifying that it is explained by the lack of changes in REMd across sleep cycles. The depression of REMd can not simply be related to homeostatic mechanisms, as REMd changes were associated with EEG power changes in a specific range of spindle frequency activity, but not with SWA.     

Time‐varying correlations between delta EEG power and heart rate variability in midlife women: The SWAN Sleep Study

No studies have evaluated the dynamic, time‐varying relationship between delta electroencephalographic (EEG) sleep and high frequency heart rate variability (HF‐HRV) in women. Delta EEG and HF‐HRV were measured during sleep in 197 midlife women (M_age = 52.1, SD = 2.2). Delta EEG–HF‐HRV correlations in nonrapid eye movement (NREM) sleep were modeled as whole‐night averages and as continuous functions of time. The whole‐night delta EEG–HF‐HRV correlation was positive. The strongest correlations were observed during the first NREM sleep period preceding and following peak delta power. Time‐varying correlations between delta EEG–HF‐HRV were stronger in participants with sleep‐disordered breathing and self‐reported insomnia compared to healthy controls. The dynamic interplay between sleep and autonomic activity can be modeled across the night to examine within‐ and between‐participant differences including individuals with and without sleep disorders.     

Effects of sleep restriction on the sleep electroencephalogram of adolescents

Study ObjectivesThis report describes findings from an ongoing longitudinal study of the effects of varied sleep durations on wake and sleep electroencephalogram (EEG) and daytime function in adolescents. Here, we focus on the effects of age and time in bed (TIB) on total sleep time (TST) and nonrapid eye movement (NREM) and rapid eye movement (REM) EEG.MethodsWe studied 77 participants (41 male) ranging in age from 9.9 to 16.2 years over the 3 years of this study. Each year, participants adhered to each of three different sleep schedules: four consecutive nights of 7, 8.5, or 10 h TIB.ResultsAltering TIB successfully modified TST, which averaged 406, 472 and 530 min on the fourth night of 7, 8.5, and 10 h TIB, respectively. As predicted by homeostatic models, shorter sleep durations produced higher delta power in both NREM and REM although these effects were small. Restricted sleep more substantially reduced alpha power in both NREM and REM sleep. In NREM but not REM sleep, sleep restriction strongly reduced both the all-night accumulation of sigma EEG activity (11–15 Hz energy) and the rate of sigma production (11–15 Hz power).ConclusionsThe EEG changes in response to TIB reduction are evidence of insufficient sleep recovery. The decrease in sigma activity presumably reflects depressed sleep spindle activity and suggests a manner by which sleep restriction reduces waking cognitive function in adolescents. Our results thus far demonstrate that relatively modest TIB manipulations provide a useful tool for investigating adolescent sleep biology.     

Effects of a lifestyle intervention on REM sleep‐related OSA severity in obese individuals with type 2 diabetes

The aim of this study was to determine if an intensive lifestyle intervention (ILI) reduces the severity of obstructive sleep apnea (OSA) in rapid‐eye movement (REM) sleep, and to determine if longitudinal changes in glycaemic control are related to changes in OSA severity during REM sleep over a 4‐year follow‐up. This was a randomized controlled trial including 264 overweight/obese adults with type 2 diabetes (T2D) and OSA. Participants were randomized to an ILI targeted to weight loss or a diabetes support and education (DSE) control group. Measures included anthropometry, apnea–hypopnea index (AHI) during REM sleep (REM‐AHI) and non‐REM sleep (NREM‐AHI) and glycated haemoglobin (HbA1c) at baseline and year 1, year 2 and year 4 follow‐ups. Mean baseline values of REM‐AHI were significantly higher than NREM‐AHI in both groups. Both REM‐AHI and NREM‐AHI were reduced significantly more in ILI versus DSE, but these differences were attenuated slightly after adjustment for weight changes. Repeated‐measure mixed‐model analyses including data to year 4 demonstrated that changes in HbA1c were related significantly to changes in weight, but not to changes in REM‐AHI and NREM‐AHI. Compared to control, the ILI reduced REM‐AHI and NREM‐AHI during the 4‐year follow‐up. Weight, as opposed to REM‐AHI and NREM‐AHI, was related to changes in HbA1c. The findings imply that weight loss from a lifestyle intervention is more important than reductions in AHI for improving glycaemic control in T2D patients with OSA.     

Effects of signal artefacts on electroencephalography spectral power during sleep: quantifying the effectiveness of automated artefact‐rejection algorithms

Electroencephalography (EEG) recordings during sleep are often contaminated by muscle and ocular artefacts, which can affect the results of spectral power analyses significantly. However, the extent to which these artefacts affect EEG spectral power across different sleep states has not been quantified explicitly. Consequently, the effectiveness of automated artefact‐rejection algorithms in minimizing these effects has not been characterized fully. To address these issues, we analysed standard 10‐channel EEG recordings from 20 subjects during one night of sleep. We compared their spectral power when the recordings were contaminated by artefacts and after we removed them by visual inspection or by using automated artefact‐rejection algorithms. During both rapid eye movement (REM) and non‐REM (NREM) sleep, muscle artefacts contaminated no more than 5% of the EEG data across all channels. However, they corrupted delta, beta and gamma power levels substantially by up to 126, 171 and 938%, respectively, relative to the power level computed from artefact‐free data. Although ocular artefacts were infrequent during NREM sleep, they affected up to 16% of the frontal and temporal EEG channels during REM sleep, primarily corrupting delta power by up to 33%. For both REM and NREM sleep, the automated artefact‐rejection algorithms matched power levels to within ~10% of the artefact‐free power level for each EEG channel and frequency band. In summary, although muscle and ocular artefacts affect only a small fraction of EEG data, they affect EEG spectral power significantly. This suggests the importance of using artefact‐rejection algorithms before analysing EEG data.     

Can spectral power predict subjective sleep quality in healthy individuals?

The aim of this study was to assess the relationship between electroencephalogram (EEG) power spectral density and subjective sleep quality in healthy individuals. The sample was selected from the archival database of the Sleep Center at the Department for Psychiatry and Psychotherapy, Medical Center ‐ University of Freiburg, and consisted of 206 healthy adults aged 19–73 years (85 male, 121 female) who underwent a polysomnographic examination for two consecutive nights. A multivariate analysis of variance (MANOVA ) with spectral power variables of different frequency bands as dependent variables and subjective sleep quality, night number, age and gender as independent variables was statistically significant for subjective sleep quality, age and gender, but not for night number. In subsequent separate ANOVAs, higher subjective sleep quality was significantly related to decreased non‐rapid eye movement (NREM) stage 2 sigma 2 and rapid eye movement ( REM ) delta 1; however, the relation between REM delta 1 and sleep quality did not remain significant when REM duration was accounted for. The effect sizes of the correlations between sleep quality and spectral power were small (r = ?0.1). In contrast to common assumptions, the amount of variance in subjective sleep quality that can be explained through EEG power spectral density variables is small. This finding indicates that subjective and objective sleep are different constructs, the interrelations of which are not yet well understood.     

Rapid eye movement sleep parasympathetic activity predicts wake hyperarousal symptoms following a traumatic event

Heart rate variability (HRV) can be used to assess changes in output of the parasympathetic nervous system (PNS). Considering that patients with post-traumatic stress disorder (PTSD) often experience disturbances in sleep, arousal, and autonomic functioning, we sought to explore the association of PNS activity during sleep with hyperarousal symptoms of PTSD. Because a broad literature supports the importance of rapid eye movement (REM) sleep in PTSD, REM-sleep features were specifically examined as predictors of PTSD symptom severity. A total of 90 participants, primarily civilian and female, aged 18–40 years who had experienced a traumatic event in the last 2 years, underwent an ambulatory polysomnography (PSG) acclimation night followed by a second PSG night from which sleep physiological measures were computed. Participants underwent an ambulatory polysomnography (PSG) acclimation night followed by a second PSG night from which sleep physiological measures were computed. PTSD severity was measured using the PTSD Checklist for the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (PCL-5). Dependent variables were total PCL-5 score as well as its hyperarousal symptom subscore. Predictors included REM latency, percentage, density, segment length, and an index of parasympathetic tone (root mean square of the successive differences in the R–R interval or RMSSD). Hierarchical regression models were conducted to analyse the association of REM features with PCL-5 total and hyperarousal subscales. Using hierarchical regression, REM-sleep RMSSD accounted for a significant proportion of the variation in outcome variables, even when accounting for other REM-sleep features. The present findings support hypothesised relationships between PTSD symptomatology and REM-sleep physiology and, specifically, that lowered parasympathetic tone in REM may be an important associate of the hyperarousal symptom cluster in PTSD.     

Age effects on spectral electroencephalogram activity prior to dream recall

Ageing is associated with marked changes in sleep timing, structure and electroencephalographic (EEG) activity. Older people exhibit less slow-wave and spindle activity during non-rapid eye movement (NREM) sleep, together with attenuated levels of rapid eye movement (REM) sleep as compared to young individuals. However, the extent to which these age-related changes in sleep impact on dream processing remains largely unknown. Here we investigated NREM and REM sleep EEG activity prior to dream recall and no recall in 17 young (20-31 years) and 15 older volunteers (57-74 years) during a 40 h multiple nap protocol. Dream recall was assessed immediately after each nap. During NREM sleep prior to dream recall, older participants displayed higher frontal EEG delta activity (1-3 Hz) and higher centro-parietal sigma activity (12-15 Hz) than the young volunteers. Conversely, before no recall, older participants had less frontal-central delta activity and less sigma activity in frontal, central and parietal derivations than the young participants. REM sleep was associated to age-related changes, such that older participants had less frontal-central alpha (10-12 Hz) and beta (16-19 Hz) activity, irrespective of dream recall and no recall. Our data indicate that age-related differences in dream recall seem to be directly coupled to specific frequency and topography EEG patterns, particularly during NREM sleep. Thus, the spectral correlates of dreaming can help to understand the cortical pathways of dreaming.     

NREM‐related parasomnias in Machado–Joseph disease: clinical and polysomnographic evaluation

Spinocerebellar ataxias (SCA) are autosomal dominant neurodegenerative disorders that affect the cerebellum and its connections, and have a marked clinical and genetic variability. Machado–Joseph disease (MJD) or spinocerebellar ataxia type 3 (SCA3)—MJD/SCA3—is the most common SCA worldwide. MJD/SCA3 is characterized classically by progressive ataxia and variable other motor and non‐motor symptoms. Sleep disorders are common, and include rapid eye movement (REM) sleep behaviour disorder (RBD), restless legs syndrome (RLS), insomnia, excessive daytime sleepiness, excessive fragmentary myoclonus and sleep apnea. This study aims to focus upon determining the presence or not of non‐REM (NREM)‐related parasomnias in MJD/SCA 3, using data from polysomnography (PSG) and clinical evaluation. Forty‐seven patients with clinical and genetic diagnosis of MJD/SCA3 and 47 control subjects were evaluated clinically and by polysomnography. MJD/SCA3 patients had a higher frequency of arousals from slow wave sleep (P < 0.001), parasomnia complaints (confusional arousal/sleep terrors, P = 0.001; RBD, P < 0.001; and nightmares, P < 0.001), REM sleep without atonia (P < 0.001), periodic limb movements of sleep index (PLMSi) (P < 0.001), percentage of N3 sleep (P < 0.001) and percentage of N1 sleep (P < 0.001). These data show that NREM‐related parasomnias must be included in the spectrum of sleep disorders in MJD/SCA3 patients.     

Rapid eye movement fragmentation,not slow‐wave sleep,predicts neutral declarative memory consolidation in posttraumatic stress disorder

Individuals diagnosed with posttraumatic stress disorder (PTSD) experience disruption at both slow‐wave sleep (SWS) and rapid‐eye movement (REM) sleep stages and demonstrate marked memory impairment. A small group of studies suggests that, within the disorder, there is a mechanistic relation between these sleep and memory impairments. This study sought to extend that literature by examining whether, in PTSD‐diagnosed individuals, memory‐retention deficits are present after a sleep‐filled (but not after a wake‐filled) delay (i.e., whether memory deficits can be traced to interruptions of sleep‐dependent memory consolidation). Moreover, we investigated whether SWS‐ or REM‐based disturbances, or both, contribute to retention deficits. We recruited participants into three groups: PTSD (n = 21), trauma‐exposed non‐PTSD (TE; n = 19) and healthy control (HC; n = 20). Using a crossover design, we assessed memory recall before and after an 8‐hr period of polysomnography‐monitored sleep and an 8‐hr period of regular waking activity. PTSD‐diagnosed participants retained less information than controls over the sleep‐filled (but not wake‐filled) delay. Furthermore, increased REM fragmentation predicted postsleep memory retention in PTSD‐diagnosed individuals only. No SWS parameter was associated with or predictive of the amount of information retained postsleep. We conclude that specific REM‐related changes in PTSD‐diagnosed individuals affected sleep‐dependent neutral declarative memory consolidation. Generally, these findings extend the literature suggesting that the co‐occurrence of sleep and memory difficulties in PTSD is not accidental, but that these two symptom clusters are meaningfully related. Specifically, the study illustrates that subtle REM‐related disruptions contribute most strongly to memory impairment in PTSD.     

REM Sleep Interruption: Experimental Shortening of REM Period Duration

This experiment concerns itself with the extent to which psychological factors can influence normal sleep patterns. After 4 baseline nights of uninterrupted sleep, each of 4 Ss was awakened in the course of 2 nights during every REM period about 10 min following each REM onset. Ss, however, were not REM deprived. The interruption nights were followed by a recovery night of uninterrupted sleep. All nights were consecutive. The results show that during recovery nights all Ss continued to have significantly shorter than normal REM periods by going into NREM sleep at about the time they would have been awakened during the interruption nights. These shortened REM periods occurred even during early morning hours, when REM periods normally become longer. Arguments are advanced that this finding may best be explained in terms of a conditioned avoidance response.     

Increased EEG sigma and beta power during NREM sleep in primary insomnia

The hyperarousal model of primary insomnia suggests that a deficit of attenuating arousal during sleep might cause the experience of non-restorative sleep. In the current study, we 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. Patients with primary insomnia demonstrated significantly elevated spectral power values in the EEG beta and sigma frequency band during NREM stage 2 sleep. No differences were observed in other frequency bands or during REM sleep. Based on prior studies suggesting that EEG beta activity represents a marker of cortical arousal and EEG sleep spindle (sigma) activity is an index of sleep protective mechanisms, our findings may provide further evidence for the concept that a simultaneous activation of wake-promoting and sleep-protecting neural activity patterns contributes to the experience of non-restorative sleep in primary insomnia.     

Influence of the menopausal transition on polysomnographic sleep characteristics: a longitudinal analysis

Study ObjectivesTo evaluate how change in menopausal status related to spectral analysis and polysomnographic measures of sleep characteristics.MethodsThe Study of Women’s Health Across the Nation (SWAN) Ancillary Sleep Study evaluated sleep characteristics of 159 women who were initially pre- or early perimenopausal and repeated the assessment about 3½ years later when 38 were pre- or early perimenopausal, 31 late perimenopausal, and 90 postmenopausal. Participants underwent in-home ambulatory polysomnography for two to three nights. Average EEG power in the delta and beta frequency bands was calculated during NREM and REM sleep, and sleep duration, wake after sleep onset (WASO), and apnea hypopnea index (AHI) were based on visually-scored sleep.ResultsThe women who transitioned to postmenopause had increased beta NREM EEG power at the second assessment, compared to women who remained pre-or early premenopausal; no other sleep measures varied by change in menopausal status. In multivariate models the associations remained; statistical controls for self-reported hot flashes did not explain findings. In secondary analysis, NREM beta power at the second assessment was greater among women who transitioned into the postmenopause after adjustments for initial NREM beta power.ConclusionsSleep duration and WASO did not vary by menopause transition group across assessments. Consistent with prior cross-sectional analysis, elevated beta EEG power in NREM sleep was apparent among women who transitioned to postmenopause, suggesting that independent of self-reported hot flashes, the menopausal transition is associated with physiological hyperarousal during sleep.     

Increased EEG sigma and beta power during NREM sleep in primary insomnia

The hyperarousal model of primary insomnia suggests that a deficit of attenuating arousal during sleep might cause the experience of non-restorative sleep. In the current study, we 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. Patients with primary insomnia demonstrated significantly elevated spectral power values in the EEG beta and sigma frequency band during NREM stage 2 sleep. No differences were observed in other frequency bands or during REM sleep. Based on prior studies suggesting that EEG beta activity represents a marker of cortical arousal and EEG sleep spindle (sigma) activity is an index of sleep protective mechanisms, our findings may provide further evidence for the concept that a simultaneous activation of wake-promoting and sleep-protecting neural activity patterns contributes to the experience of non-restorative sleep in primary insomnia.     

Cortical activation patterns herald successful dream recall after NREM and REM sleep

Dreaming pertains to both REM and NREM sleep. However, frequency and regional specific differences in EEG activity remains controversial. We investigated NREM and REM sleep EEG power density associated with and without dream recall in 17 young subjects during a 40-h multiple nap protocol under constant routine conditions. NREM sleep was associated with lower EEG power density for dream recall in the delta range, particularly in frontal derivations, and in the spindle range in centro-parietal derivations. REM sleep was associated with low frontal alpha activity and with high alpha and beta activity in occipital derivations. Our data indicate that specific EEG frequency- and topography changes underlie differences between dream recall and no recall after both NREM and REM sleep awakening. This dual NREM-REM sleep modulation holds strong implications for the mechanistic understanding of this complex ongoing cognitive process.     

The spectrum of the non‐rapid eye movement sleep electroencephalogram following total sleep deprivation is trait‐like

The sleep electroencephalogram (EEG) spectrum is unique to an individual and stable across multiple baseline recordings. The aim of this study was to examine whether the sleep EEG spectrum exhibits the same stable characteristics after acute total sleep deprivation. Polysomnography (PSG) was recorded in 20 healthy adults across consecutive sleep periods. Three nights of baseline sleep [12 h time in bed (TIB)] following 12 h of wakefulness were interleaved with three nights of recovery sleep (12 h TIB) following 36 h of sustained wakefulness. Spectral analysis of the non‐rapid eye movement (NREM) sleep EEG (C3LM derivation) was used to calculate power in 0.25 Hz frequency bins between 0.75 and 16.0 Hz. Intraclass correlation coefficients (ICCs) were calculated to assess stable individual differences for baseline and recovery night spectra separately and combined. ICCs were high across all frequencies for baseline and recovery and for baseline and recovery combined. These results show that the spectrum of the NREM sleep EEG is substantially different among individuals, highly stable within individuals and robust to an experimental challenge (i.e. sleep deprivation) known to have considerable impact on the NREM sleep EEG. These findings indicate that the NREM sleep EEG represents a trait.