Sleep EEG Spectral Power Research Articles

The Difference in Spectral Power Density in Sleep Electroencephalography According to the Estimation of Total Sleep Time

Objective: The discrepancy between self-reported subjective sleep time and objective sleep time varies from person to person, and the mechanism that can explain this discrepancy is unclear. This study aimed to investigate the difference in the spectral power of sleep electroencephalography (EEG) according to the estimation of total sleep time (TST).Methods: Of the 4,080 participants in the Sleep Heart Health Study, 2,363 participants with complete data from polysomnography, morning sleep survey, and spectral power of sleep EEG were included in the analysis. The participants were classified as normo-estimators (estimation of TST <±60 min), under-estimators (underestimation of TST ≤60 min), or over-estimators (overestimation of TST ≥60 min). A fast Fourier transformation was used to calculate the EEG power spectrum for total sleep duration within contiguous 30-s epochs of sleep. The sleep EEG spectral power was compared among the groups after adjusting for potential confounding factors, such as age, sex, proportion of participants with insomnia, apnea-hypopnea index, and TST.Results: Of the 2,363 participants, 1,507 (63.8%), 412 (17.4%), and 444 (18.8%) were assigned to the normo-, under-, and over-estimator groups, respectively. The power spectra during total sleep differed significantly among the groups in the delta (p=0.008) and theta bands (p=0.017) after controlling for potential confounders.Conclusion: Higher delta and theta powers were found in the under-estimators than in the over-estimators. This study suggests that differences exist in the microstructures of polysomnography-derived sleep EEG between these two groups. This study suggests that differences exist in the microstructures of polysomnography-derived sleep EEG based on differences in sleep time estimation.

Associations of Baseline Sleep Microarchitecture with Cognitive Function After 8 Years in Middle-Aged and Older Men from a Community-Based Cohort Study.

Prospective studies examining associations between baseline sleep microarchitecture and future cognitive function recruited from small samples with predominantly short follow-up. This study examined sleep microarchitecture predictors of cognitive function (visual attention, processing speed, and executive function) after 8 years in community-dwelling men. Florey Adelaide Male Ageing Study participants (n=477) underwent home-based polysomnography (2010-2011), with 157 completing baseline (2007-2010) and follow-up (2018-2019) cognitive assessments (trail-making tests A [TMT-A] and B [TMT-B] and the standardized mini-mental state examination [SMMSE]). Whole-night F4-M1 sleep EEG recordings were processed following artifact exclusion, and quantitative EEG characteristics were obtained using validated algorithms. Associations between baseline sleep microarchitecture and future cognitive function (visual attention, processing speed, and executive function) were examined using linear regression models adjusted for baseline obstructive sleep apnoea, other risk factors, and cognition. The final sample included men aged (mean [SD]) 58.9 (8.9) years at baseline, overweight (BMI 28.5 [4.2] kg/m2), and well educated (75.2% ≥Bachelor, Certificate, or Trade), with majorly normal baseline cognition. Median (IQR) follow-up was 8.3 (7.9, 8.6) years. In adjusted analyses, NREM and REM sleep EEG spectral power was not associated with TMT-A, TMT-B, or SMMSE performance (all p>0.05). A significant association of higher N3 sleep fast spindle density with worse TMT-B performance (B=1.06, 95% CI [0.13, 2.00], p=0.026) did not persist following adjustment for baseline TMT-B performance. In this sample of community-dwelling men, sleep microarchitecture was not independently associated with visual attention, processing speed, or executive function after 8 years.

Sleep-EEG Spectral Power Predicts Next-Day Pain In Long-Term Opioid Users With Chronic Low-Back Pain

Sleep-EEG Spectral Power Predicts Next-Day Pain In Long-Term Opioid Users With Chronic Low-Back Pain

Season is related to the slow wave and sigma activity of infants and toddlers

Objective/BackgroundSlow wave activity (SWA) and sigma frequency activity (SFA) are hallmarks of NREM sleep EEG and important indicators of neural plasticity, development of the central nervous system, and cognition. However, little is known about the factors that modulate these sleep EEG activities, especially in small children. Patients/methodsWe analyzed the power spectral densities of SWA (1–4 Hz) and SFA range (10–15 Hz) from six EEG derivations of 56 infants (8 months) and 60 toddlers (24 months) during their all-night sleep and during the first and the last half of night sleep. The spectral values were compared between the four seasons. ResultsIn the spring group of infants, compared with the darker seasons, SFA was lower in the centro-occipital EEG derivations during both halves of the night. The SWA findings of the infants were restricted to the last half of the night (SWA2) and frontally, where SWA2 was higher during winter than spring. The toddlers presented less frontal SWA2 during winter compared with autumn. Both age groups showed a reduction in both SWA and SFA towards the last half of the night. ConclusionsThe sleep EEG spectral power densities are more often associated with seasons in infants’ SFA range. The results might stem from seasonally changing light exposure, but the exact mechanism warrants further study. Moreover, contrary to the adult-like increment of SFA, the SFA at both ages was lower at the last part of the night sleep. This suggests different regulation of spindle activity in infants and toddlers.

0024 ARC Genotype Modulates EEG Spectral Power Following Total Sleep Deprivation

Abstract Introduction Sleep homeostasis is manifested by a robust increase in slow wave sleep (SWS) following acute total sleep deprivation (TSD), with concomitant changes in spectral power of the non-REM (NREM) sleep EEG marked by substantial interindividual differences. We previously found that a single nucleotide polymorphism of the activity-regulated cytoskeleton associated protein (ARC) gene modulates SWS rebound following TSD. Here we sought to determine whether ARC genotype is also associated with interindividual differences in spectral power of the NREM sleep EEG. Methods 50 healthy adults (27.3±4.9 years; 28 females) participated in one of two in-laboratory studies. Each participant had a 10h baseline sleep opportunity (22:00–08:00), 38h TSD, and a 10h recovery sleep opportunity (22:00–08:00). Sleep periods were recorded polysomnographically and visually scored according to AASM criteria. Genomic DNA was assayed for the ARC c.*742 + 58C>T non-coding SNP, rs35900184. Log-transformed NREM sleep EEG spectral power (C3-M3 derivation) over 0.2 Hz frequency bins in each of four frequency bands – delta (0.8–4.0 Hz), theta (4.2–8.0 Hz), alpha (8.2–12.0 Hz), and beta (12.2–16.0 Hz) – was analyzed by band using mixed-effects ANOVA with fixed effects for ARC genotype, night (baseline, recovery), frequency bin, and their interactions. Analyses included study and age as covariates and a random effect over subjects on the intercept. Results The genotype distribution in this sample was 33 C/C homozygotes, 11 C/T heterozygotes, and 6 T/T homozygotes. There was a significant ARC by night interaction in the theta (F2,1833=5.94, p=0.003) and alpha (F2,1833=8.58, p<0.001) bands. Compared to baseline sleep, during recovery sleep C/C homozygotes had 18.9% more theta power and 8.7% more alpha power, C/T heterozygotes had 17.9% more theta power and 7.6% more alpha power, and T/T homozygotes had 20.0% more theta power and 15.1% more alpha power. Conclusion Our results show that ARC genotype mediates the NREM sleep EEG response to TSD; compared to C allele carriers, homozygosity for the T allele is associated with a much more pronounced increase in alpha power, as well as a larger increase in theta power. The functional implications of this ARC effect remain to be determined. Support (If Any) ONR N00014-13-1-0302, NIH R21CA167691, and USAMRDC W81XWH-18-1-0100.

Higher sleep EEG spectral power in beta and delta bands during nrem sleep in OSA group than in simple snoring group

Higher sleep EEG spectral power in beta and delta bands during nrem sleep in OSA group than in simple snoring group

0971 Sleep EEG Spectral Power Is Correlated With Subjective-objective Discrepancy Of Sleep Onset Latency In Major Depressive Disorder

0971 Sleep EEG Spectral Power Is Correlated With Subjective-objective Discrepancy Of Sleep Onset Latency In Major Depressive Disorder

0710 Sleep EEG Spectral Power Characteristics According to Age and Gender in Middle-to-Late Adulthood

0710 Sleep EEG Spectral Power Characteristics According to Age and Gender in Middle-to-Late Adulthood

Sleep EEG spectral power is correlated with subjective-objective discrepancy of sleep onset latency in major depressive disorder

We aimed to identify the sleep electroencephalography (EEG) spectral power correlates of the subjective-objective discrepancy (SOD) of sleep onset latency (SOL) in major depressive disorder (MDD), primary insomnia (PI), and normal sleeping control (NSC) groups. We examined relative power values in standard frequency bands of the EEG spectra during the first Non-Rapid Eye Movement (NREM) sleep period as correlates of SOD of SOL between sleep diary and polysomnography in MDD (n = 36), PI (n = 19), and NSC (n = 23) groups. We also compared the relative spectral power of sleep EEG among MDD (n = 40), PI (n = 19), and NSC (n = 23) groups. SOD of SOL in MDD patients was positively correlated with relative sigma (r = 0.622, p corrected < 0.001), beta power (r = 0.559, p corrected = 0.002), and alpha power (r = 0.469, p corrected = 0.024) in the first NREM sleep period. There was no significant difference of sleep EEG power spectra among the three groups. SOD was positively correlated with high frequency EEG in MDD. High frequency EEG power is thought to be associated with hyperarousal and memory consolidation, and future larger-scale studies may further elucidate the neurophysiological mechanisms underlying SOD of sleep onset duration.

Adenosine deaminase polymorphism affects sleep EEG spectral power in a large epidemiological sample.

Slow wave oscillations in the electroencephalogram (EEG) during sleep may reflect both sleep need and intensity, which are implied in homeostatic regulation. Adenosine is strongly implicated in sleep homeostasis, and a single nucleotide polymorphism in the adenosine deaminase gene (ADA G22A) has been associated with deeper and more efficient sleep. The present study verified the association between the ADA G22A polymorphism and changes in sleep EEG spectral power (from C3-A2, C4-A1, O1-A2, and O2-A1 derivations) in the Epidemiologic Sleep Study (EPISONO) sample from São Paulo, Brazil. Eight-hundred individuals were subjected to full-night polysomnography and ADA G22A genotyping. Spectral analysis of the EEG was carried out in all individuals using fast Fourier transformation of the signals from each EEG electrode. The genotype groups were compared in the whole sample and in a subsample of 120 individuals matched according to ADA genotype for age, gender, body mass index, caffeine intake status, presence of sleep disturbance, and sleep-disturbing medication. When compared with homozygous GG genotype carriers, A allele carriers showed higher delta spectral power in Stage 1 and Stages 3+4 of sleep, and increased theta spectral power in Stages 1, 2 and REM sleep. These changes were seen both in the whole sample and in the matched subset. The higher EEG spectral power indicates that the sleep of individuals carrying the A allele may be more intense. Therefore, this polymorphism may be an important source of variation in sleep homeostasis in humans, through modulation of specific components of the sleep EEG.

Developmental Changes in the Human Sleep EEG During Early Adolescence

To use time-frequency analysis to characterize developmental changes in the human sleep electroencephalogram (EEG) across early adolescence. Sleep EEG was recorded when children were 9/10 years old and 1 to 3 years later after sleeping at home on a fixed schedule for at least one week. A 4-bed sleep laboratory. Fourteen (5 girls) healthy children ages 9/10 (mean = 10.13, SD = +/- 0.51) years at initial and 11 to 13 (mean = 12.28, SD = +/- 0.62) years at follow-up. N/A. All-night polysomnography was performed at each assessment and sleep stages were scored with Rechtschaffen and Kales criteria. Slow wave sleep minutes decreased from the initial to the follow-up session by 29%, while minutes of stage 2 increased by 17%. NREM and REM sleep EEG spectra from two central and two occipital leads were examined for developmental changes. All-night analyses showed a significant decrease of EEG power from the initial to follow-up session across a range of frequencies during NREM and REM sleep. This decline occurred across leads and states in the delta/theta bands (3.8 - 7 Hz). Time-frequency analyses indicated that this effect was consistent across the night. The decline in power with age was most pronounced in the left central and right occipital leads. The frequency of greatest power in the sigma band (11 - 16 Hz) was significantly higher at follow-up. This longitudinal analysis highlights asymmetrical frequency-specific declines in sleep EEG spectral power with early adolescent maturation, which may reflect early signs of the cortical synaptic pruning in the healthy adolescent.

Early-night serial awakenings as a new paradigm for studies on NREM dreaming

A new experimental paradigm called “Early-Night Serial Awakenings” (ENSA) was explored to find out its strengths and weaknesses for psychophysiological studies of NREM sleep dreaming. Five participants spent 20 experimental nights in the sleep laboratory, and were serially awakened with approximately 24-minute intervals during Stages 2 and 3 of NREM sleep. As a total, 164 awakenings were conducted during the sessions that lasted on average 193 min. Altogether, 30% of NREM sleep awakenings led to dream reports, 39% to reports of white dreaming, and 31% to reports of dreamless sleep. Results also show that sleep EEG spectral power, dream recall frequency as well as dream complexity remained stable throughout the serial awakening sessions. We conclude that, as ENSA dreams appeared to be static and very limited in content, the paradigm we identified could be used in future studies to reveal the psychophysiological mechanisms of relatively simple forms of early-night NREM sleep dreaming.

Spectral analysis of sleep EEG in patients with restless legs syndrome

Objective Conventional analyses of sleep EEG recordings according to standard criteria indicate severe sleep disturbances in patients with restless legs syndrome (RLS). Spectral analysis of sleep EEG may be a sensitive tool to detect functional alterations of sleep mechanisms beyond the visual scoring of polysomnographic records. We analysed sleep EEG spectral power differences between RLS patients and healthy subjects. Furthermore, we studied the relationship of sleep EEG spectral power to the occurrence of periodic leg movements in sleep (PLMS) and arousal events. Methods Sleep EEGs from 20 patients with idiopathic RLS and of 20 age and sex matched healthy subjects were investigated. The spectral analysis was carried out on the same 30 s epochs for which sleep stages had been determined. As a first step, whole-night spectral power excluding epochs with an arousal or with a PLMS was compared separately for REM and NREM sleep between RLS and healthy subjects. In a second step, we evaluated the spectral effects of PLMS, PLMS with associated arousals and isolated arousals relative to epochs of sleep without such events in both groups. In this part of the analysis, we only included the epochs of sleep stage 2 (the main and most stable non-REM sleep stage) and of REM sleep. Results Spectral power of all sleep epochs (excluding arousals and PLMS) did not differ between patients with RLS and healthy subjects. As expected, arousals and PLMS-associated arousals resulted in a significant increase in higher-frequency activity (alpha, beta1, beta2 and gamma bands) in both groups. Spectral power in epochs with PLMS alone did not significantly differ from spectral power in epochs without PLMS and without arousal in any of the groups. Conclusions We found no evidence for an altered cortical activity in sleep stage 2 and REM sleep epochs in RLS patients compared to that in healthy controls if epochs with arousals were not considered. Furthermore, while PLMS associated with an arousal have a high impact on EEG spectra, the effect of a PLMS without arousal seems to be minor and transient. Significance Our data suggest that RLS related symptoms may intermittently disrupt sleep but do not appear to involve a persistent disturbance of the basic sleep generating patterns.

Increased delta power and discrepancies in objective and subjective sleep measurements in borderline personality disorder

Background Previous studies have shown depression-like sleep abnormalities in borderline personality disorder (BPD). However, findings in BPD are not unequivocal for REM dysregulation, as well as for a decrement of slow wave sleep and sleep continuity disturbances. Earlier findings in sleep EEG abnormalities in BPD may have been confounded by concomitant depressive symptoms. Methods Twenty unmedicated female BPD patients without current comorbid major depression and 20 sex- and age-matched control subjects entered the study. Conventional polysomnographic parameters and for the first time sleep EEG spectral power analysis was performed on two sleep laboratory nights. Subjective sleep parameters were collected by sleep questionnaires in order to assess the relationship between objective and subjective sleep measurements. Results BPD patients showed a tendency for shortened REM latency and significantly decreased NonREM sleep (stage 2). Spectral EEG analysis showed increased delta power in total NREM sleep as well as in REM sleep in BPD patients. Subjective ratings documented drastically impaired sleep quality in BPD patients for the two weeks before the study and during the two laboratory nights. Conclusion Not-depressed BPD patients only showed tendencies for depression-like REM sleep abnormalities. Surprisingly, BPD patients displayed higher levels of delta power in the sleep EEG in NREM sleep than healthy control subjects. There was a marked discrepancy between objective and subjective sleep measurements, which indicates an altered perception of sleep in BPD. The underlying psychological and neurobiological mechanisms of these alterations are still unclear and need to be clarified in future studies including interventions on a pharmacological and cognitive-behavioral level.

Endotoxin Enhances EEG Alpha and Beta Power in Human Sleep

Endotoxin, a lipopolysaccharide (0.4 or 0.8 ng/kg body weight), was injected at 1900 hours in 17 healthy men in a single-blind, placebo-controlled experiment. The administration was followed by a 4-hour period of quiet wakefulness in bed (light intensity < 200 lux). Unlimited sleep was allowed after 2300 hours (lights off) until the next morning. The electroencephalogram (EEG), electromyogram, electrooculogram, electrocardiogram and rectal temperature were recorded throughout the experimental session. Standard sleep stages were assessed, and the EEG was submitted to a state-specific, serial spectral analysis. Endotoxin administration induced a rise of body temperature and heart rate, which started approximately 2 hours after the injection and persisted through most of the sleep period. Sleep latency remained unchanged, whereas rapid eye movement (REM) sleep latency increased from 60.3 to 89.0 minutes (paired t test; p = 0.06) compared to control values. Stage 2 sleep was elevated from 45.5 to 49.0% of time in bed (p < 0.05), and total nonrapid eye movement (NREM) sleep from 64.2 to 69.1% (p < 0.05). No significant change could be observed in slow-wave sleep (SWS, stages 3 and 4). During the first 4 hours of the sleep period, NREM sleep EEG spectral power was distinctly and markedly increased between 8 and 12 Hz (alpha) and 15 and 20 Hz (beta) (p < 0.05), whereas at the same time EEG power between 1 and 8 Hz (delta, theta) was not significantly changed. We conclude that in humans the primary host response induced by endotoxin initially suppresses REM sleep and increases stage 2 NREM sleep, but does not affect SWS. No clear modification of sleep EEG delta activity could be observed after endotoxin injection, despite marked endocrinological and physiological changes such as the elevation of body temperature. Numerous factors related to the human primary host response may be responsible for the EEG intensification of the alpha and beta range.