Lower Delta Power Research Articles

Resting-State EEG Signature of Early Consciousness Recovery in Comatose Patients with Traumatic Brain Injury.

Resting-state electroencephalography (rsEEG) is usually obtained to assess seizures in comatose patients with traumatic brain injury (TBI). We aim to investigate rsEEG measures and their prediction of early recovery of consciousness in patients with TBI. This is a retrospective study of comatose patients with TBI who were admitted to a trauma center (October 2013 to January 2022). Demographics, basic clinical data, imaging characteristics, and EEGs were collected. We calculated the following using 10-min rsEEGs: power spectral density, permutation entropy (complexity measure), weighted symbolic mutual information (wSMI, global information sharing measure), Kolmogorov complexity (Kolcom, complexity measure), and heart-evoked potentials (the averaged EEG signal relative to the corresponding QRS complex on electrocardiography). We evaluated the prediction of consciousness recovery before hospital discharge using clinical, imaging, and rsEEG data via a support vector machine. We studied 113 of 134 (84%) patients with rsEEGs. A total of 73 (65%) patients recovered consciousness before discharge. Patients who recovered consciousness were younger (40 vs. 50years, p = 0.01). Patients who recovered also had higher Kolcom (U = 1688, p = 0.01), increased beta power (U = 1,652 p = 0.003) with higher variability across channels (U = 1534, p = 0.034) and epochs (U = 1711, p = 0.004), lower delta power (U = 981, p = 0.04), and higher connectivity across time and channels as measured by wSMI in the theta band (U = 1636, p = 0.026; U = 1639, p = 0.024) than those who did not recover. The area under the receiver operating characteristic curve for rsEEG was higher than that for clinical data (using age, motor response, pupil reactivity) and higher than that for the Marshall computed tomography classification (0.69 vs. 0.66 vs. 0.56, respectively; p < 0.001). We describe the rsEEG signature in recovery of consciousness prior to discharge in comatose patients with TBI. rsEEG measures performed modestly better than the clinical and imaging data in predicting recovery.

Sleep Delta power, age, and sex effects in treatment-resistant depression

Electroencephalographic (EEG) deficits in slow wave activity or Delta power (0.5–4 Hz) indicate disturbed sleep homeostasis and are hallmarks of depression. Sleep homeostasis is linked to restorative sleep and potential antidepressant response via non-rapid eye movement (NREM) slow wave sleep (SWS) during which neurons undergo essential repair and rejuvenation. Decreased Low Delta power (0.5–2 Hz) was previously reported in individuals with depression. This study investigated power levels in the Low Delta (0.5-<2 Hz), High Delta (2–4 Hz), and Total Delta (0.5–4 Hz) bands and their association with age, sex, and disrupted sleep in treatment-resistant depression (TRD). Mann-Whitney U tests were used to compare the nightly progressions of Total Delta, Low Delta, and High Delta in 100 individuals with TRD and 24 healthy volunteers (HVs). Polysomnographic parameters were also examined, including Total Sleep Time (TST), Sleep Efficiency (SE), and Wake after Sleep Onset (WASO). Individuals with TRD had lower Delta power during the first NREM episode (NREM1) than HVs. The deficiency was observed in the Low Delta band versus High Delta. Females with TRD had higher Delta power than males during the first NREM1 episode, with the most noticeable sex difference observed in Low Delta. In individuals with TRD, Low Delta power correlated with WASO and SE, and High Delta correlated with WASO. Low Delta power deficits in NREM1 were observed in older males with TRD, but not females. These results provide compelling evidence for a link between age, sex, Low Delta power, sleep homeostasis, and non-restorative sleep in TRD.

0783 Sleep Continuity and Quality in Adolescents with Functional Abdominal Pain

Abstract Introduction Functional Abdominal Pain Disorders (FAPD), in which chronic abdominal pain occurs independently of organic pathology, are common in adolescents. FAPD can lead to significant impairment in daytime function and may overlap with sleep disorders. Though several studies have explored the nature of sleep disturbances experienced by adolescents with FAPD, none have characterized differences in sleep architecture in this population. Methods Adolescents (age 11-18 years) with FAPD and age/gender-matched controls were prospectively recruited to undergo polysomnography (PSG). PSG was performed according to AASM guidelines, scored by a registered sleep technologist, and interpreted by a board-certified sleep physician. The first four hours of artifact-free NREM sleep were analyzed using fast Fourier transformation with Welch tapered windows of 1024 samples (and 50% overlap) averaged over 30-second epochs. Total power was calculated for very low (0.3 – 1 Hz), delta (1 – 4 Hz), theta (4 – 8 Hz), and alpha (8-12 Hz) frequencies. Comparisons between groups were made using Wilcoxon rank sum tests or t-tests for non-normal and normal data, respectively. Results A total of 41 subjects were recruited (FAPD n=21, control n=20). The FAPD group had a greater arousal index and a lower percentage of NREM 3 sleep when compared to the control group (FAPD arousals: mean=10.08/min ± 4.89 min, control arousals mean=7.31/min ± 3.61/min, p = 0.046), FAPD NREM 3: mean=20.13% ± 5.47%, control NREM 3: mean=24.77% ± 6.94%, p =0.023). Delta power was significantly lower in the FAPD group compared to controls (FAPD Delta mean=488.67 µV2 ± 282.82 µV2, control Delta mean=1193.14 µV2 ± 663.89 µV2, p &amp;lt; 0.001). Conclusion This study demonstrates significant differences in sleep architecture of adolescents with FAPD compared to their peers. In particular, decreased proportions of NREM 3 sleep and lower Delta power are indicative of diminished slow wave sleep (SWS). Reductions in SWS may be indicative of common neurotransmitter pathways shared between sleep and chronic pain syndromes, or secondary to sleep disruption associated with pain. Further research is indicated. Support (if any) This research is supported by the Cincinnati Children’s Research Foundation and the Summer Medical Student Respiratory Research Fellowship program at Cincinnati Children’s.

The association between sleep microarchitecture and cognitive function in middle-aged and older men: a community-based cohort study.

Sleep microarchitecture parameters determined by quantitative power spectral analysis of electroencephalograms have been proposed as potential brain-specific markers of cognitive dysfunction. However, data from community samples remain limited. This study examined cross-sectional associations between sleep microarchitecture and cognitive dysfunction in community-dwelling men. Florey Adelaide Male Ageing Study participants (n = 477) underwent home-based polysomnography (2010-2011). All-night electroencephalogram recordings were processed using quantitative power spectral analysis following artifact exclusion. Cognitive testing (2007-2010) included the inspection time task, Trail-Making Tests A and B, and Fuld object memory evaluation. Complete case cognition, polysomnography, and covariate data were available in 366 men. Multivariable linear regression models controlling for demographic, biomedical, and behavioral confounders determined cross-sectional associations between sleep microarchitecture and cognitive dysfunction overall and by age-stratified subgroups. In the overall sample, worse Trail-Making Test A performance was associated with higher rapid eye movement (REM) theta and alpha and non-REM theta but lower delta power (all P < .05). In men ≥ 65 years, worse Trail-Making Test A performance was associated with lower non-REM delta but higher non-REM and REM theta and alpha power (all P < .05). Furthermore, in men ≥ 65 years, worse Trail-Making Test B performance was associated with lower REM delta but higher theta and alpha power (all P < .05). Sleep microarchitecture parameters may represent important brain-specific markers of cognitive dysfunction, particularly in older community-dwelling men. Therefore, this study extends the emerging community-based cohort literature on a potentially important link between sleep microarchitecture and cognitive dysfunction. The utility of sleep microarchitecture for predicting prospective cognitive dysfunction and decline warrants further investigation. Parker JL, Appleton SL, Melaku YA, etal. The association between sleep microarchitecture and cognitive function in middle-aged and older men: a community-based cohort study. J Clin Sleep Med. 2022;18(6):1593-1608.

Sleep macro- and microstructure in breast cancer survivors

Complaints of sleep disturbance are prevalent among breast cancer (BC) patients and are predictors of quality of life. Still, electrophysiological measures of sleep are missing in patients, which prevents from understanding the pathophysiological consequences of cancer and its past treatments. Using polysomnography, sleep can be investigated in terms of macro- (e.g. awakenings, sleep stages) and micro- (i.e. cortical activity) structure. We aimed to characterize sleep complaints, and macro- and microstructure in 33 BC survivors untreated by chemotherapy and that had finished radiotherapy since at least 6 months (i.e. out of the acute effects of radiotherapy) compared to 21 healthy controls (HC). Compared to HC, BC patients had a larger number of awakenings (p = 0.008); and lower Delta power (p < 0.001), related to sleep deepening and homeostasis; greater both Alpha (p = 0.002) and Beta power (p < 0.001), related to arousal during deep sleep; and lower Theta power (p = 0.004), related to emotion regulation during dream sleep. Here we show that patients have increased cortical activity related to arousal and lower activity related to sleep homeostasis compared to controls. These results give additional insights in sleep pathophysiology of BC survivors and suggest sleep homeostasis disruption in non-advanced stages of BC.

Sleep Quality and Electroencephalogram Delta Power.

Delta activity on electroencephalogram (EEG) is considered a biomarker of homeostatic sleep drive. Delta power is often associated with sleep duration and intensity. Here, we reviewed the literature to explore how sleep quality was influenced by changes in delta power. However, we found that both the decrease and increase in delta power could indicate a higher sleep quality due to the various factors below. First, the differences in changes in delta power in patients whose sleep quality is lower than that of the healthy controls may be related to the different diseases they suffered from. We found that the patients mainly suffered from borderline personality disorder, and Rett syndrome may have a higher delta power than healthy individuals. Meanwhile, patients who are affected by Asperger syndrome, respiratory failure, chronic fatigue, and post-traumatic stress disorder have lower delta power. Second, if the insomnia patients received the therapy, the difference may be caused by the treatment method. Cognitive or music therapy shows that a better therapeutic effect is associated with decreased delta power, whereas in drug treatment, there is an opposite change in delta power. Last, for healthy people, the difference in delta change may be related to sleep stages. The higher sleep quality is associated with increased delta power during the NREM period, whereas a deceased delta change accompanies higher sleep quality during the REM period. Our work summarizes the effect of changes in delta power on sleep quality and may positively impact the monitoring and intervention of sleep quality.

Impairment of recognition of facial expressions in different types of dementia

AbstractBackgroundImpairment of facial expression recognition in dementia is one of the cognitive deficits that could affect the social life of dementia patients. The severity of the facial expression recognition in different types of dementia has not been fully addressed. Previous studies showed that EEG event‐related oscillation (ERO) studies could reveal the brain dynamics during successful facial expression recognition. Furthermore, the impairment of facial recognition in Alzheimer's disease patients were represented with abnormal EROs (Güntekin et al., 2019). The present study aims to compare the impaired facial expression recognition between different types of dementia by analysis of event‐related delta responses. The role of delta responses in facial expression and emotional paradigms was reported previously by several researchers (Güntekin and Başar, 2014).Method25 Healthy elderly controls (HC), 25 Mild Cognitive Impairment patients (MCI), 25 patients with Alzheimer's disease (AD), 15 patients with Parkinson's disease with Mild Cognitive Impairment (PDMCI) and 16 patients with Parkinson's disease Dementia (PDD) were included in the study. The electroencephalographic activity was recorded during the perception of the facial expression recognition task (Angry, Happy, Neutral). Delta power and phase‐locking were computed for each facial recognition stimuli and compared among the groups (ANOVA, p&lt;0.05).ResultBoth delta power and delta phase locking were lower in dementia groups than healthy controls being worst in PDD. Figure 1 shows the grand average of delta power in all groups for the right occipital location. PDD (p&lt;0.0001) and AD (p&lt;0.05) had lower delta power than the healthy controls, the reduction of delta responses in PDD and AD were especially found over occipital locations. MCI and PDMCI subjects were found less impaired facial expression recognition compared to AD and PDMCI.ConclusionThe present study showed that dementia patients had severe facial recognition deficits that increased cognitive impairment. Event‐related delta responses successfully showed the impaired recognition of facial expression in different types of dementia groups. Among all dementia subjects, PDD patients had the most reduced delta responses that could be an electrophysiological biomarker of impaired facial expression recognition. Acknowledgments: This work (grant number 218S314) was supported by TUBITAK.

Impact of smoking on sleep macro– and microstructure

ObjectivesExisting data suggest that smoking may be associated with sleep disturbances. This study aimed to determine the association between smoking and both subjective and objective sleep quality. MethodsCross-sectional analysis of sleep characteristics in 3233 participants from the population-based CoLaus-HypnoLaus cohort (52.2% women, mean age 56.6 ± 10.2 years) who completed questionnaires on sleep quality, of whom 1489 (46%) had a full polysomnography. Smoking data were self-reported; participants were classified by smoking status as current, former or never smokers. Primary outcomes were subjective sleep quality assessed by sleep questionnaires, and objective sleep quality based on polysomnography (sleep macrostructure), including power spectral analysis of the electroencephalogram on C4 electrode (sleep microstructure), quantifying the relative amount of delta power (1–4 Hz), a marker of sleep depth, and arousal-associated alpha power (8–12 Hz). ResultsCurrent smokers had a shift toward faster sleep electroencephalogram activity with lower delta power in non-REM sleep compared with former and never smokers (−2.8 ± 0.4% and −2.4 ± 0.4%, respectively; both p < 0.001) and higher alpha power (+0.8 ± 0.2%; p < 0.001) compared with never smokers. There was a dose-dependent negative association between electroencephalogram delta power and smoking intensity (r2 = −1.2 [–1.9, −0.5]; p = 0.001). Additionally, mean nocturnal oxygen saturation was lower in current smokers. ConclusionsCurrent smokers had decreased objective sleep quality, with a dose-dependent association between smoking intensity and decrease in electroencephalogram delta power during non-REM sleep, in addition to an increase in alpha power. Considering the importance of sleep quality for wellbeing and health, these results provide further data to support smoking cessation.

Oscillatory neuronal dynamics during L2 sentence comprehension: the effects of sensory enrichment and semantic incongruency

ABSTRACT Given the association between multisensory information and inner attention, the quality of multisensory information is hypothesised to modulate the neuronal activity associated with language comprehension. To verify, we investigated the interaction effect between multisensory quality (sensory enrichment) and semantic (in)congruency during L2 sentence comprehension. English words were selected for the subjects to learn according to the sensory-based emotioncy model. The words were embedded in an acceptability judgment task with 216 sentences under congruent and semantically incongruent conditions. Twenty-two subjects performed the task while their EEG was being recorded. Based on the time–frequency analysis results, in the 300–850 ms window, only lower delta power (1.7–2.2 Hz) showed an enhanced increase after sentences with semantic incongruency. This increase was more pronounced in the sentences with limited multisensory quality. To make up for the insufficient multisensory knowledge and maintain concentration, irrelevant cortical areas were deactivated as a result of lower delta wave synchronisation.

0869 Slow Wave Sleep Is Associated With Decreased Risk Of Gestational Diabetes Mellitus

Abstract Introduction Pregnancy is associated with disrupted slow-wave sleep (SWS) and a high prevalence of sleep disordered breathing (SDB), which may further exacerbate the decrease of deep sleep. Reduced slow wave sleep may impair glucose homeostasis, contributing to Gestational Diabetes Mellitus (GDM). Studies investigating EEG markers of deep and light sleep, and their associations with SDB and GDM are lacking. In this study, we measured associations of EEG Delta-power with objective SDB measures assessed in late-pregnancy to determine if changes in these bands are associated with GDM risk. Methods 74 women (24-36 weeks pregnancy) underwent overnight polysomnography. Spectral profiles for Delta relative power were created for NREM and REM sleep after removing epochs with movements or muscle artifacts. The association of Delta power with SDB, assessed by the Apnea Hypopnea-Index (AHI) and AHI-based SDB severity (none, mild, moderate, severe) was tested by multivariate linear regression including demographic variables with bivariate correlations (p&amp;lt;0.2) versus Delta-power. Conditional-regression was used to explore relationships between Delta-power and GDM, controlling for covariates. Results Obstructive Sleep Apnea (OSA, AHI&amp;gt;5) was present in 14% of subjects (8 GDM-cases and 3 controls). In bivariate analyses, AHI, AHI-severity categories and OSA were associated with Delta-power in NREM (all p&amp;lt;0.2) and AHI was associated with Delta relative-power in REM (p=0.18). However, these associations did not remain significant after adjusting for covariates. Delta relative-power in NREM was significantly associated with decreased risk of GDM (OR:0.50, 95%CI-0.25,0.91), but, in REM sleep, was not associated with GDM risk (OR:1.25, 95%CI-0.79,1.97). Conclusion These analyses failed to demonstrate an association between OSA or OSA severity and EEG Delta power. However, lower levels of SWS, characterized by low Delta power were associated with increased GDM risk. Support NIH-R00-NR013187

EEG evidence of compensatory mechanisms in preclinical Alzheimer's disease.

Early biomarkers are needed to identify individuals at high risk of preclinical Alzheimer's disease and to better understand the pathophysiological processes of disease progression. Preclinical Alzheimer's disease EEG changes would be non-invasive and cheap screening tools and could also help to predict future progression to clinical Alzheimer's disease. However, the impact of amyloid-β deposition and neurodegeneration on EEG biomarkers needs to be elucidated. We included participants from the INSIGHT-preAD cohort, which is an ongoing single-centre multimodal observational study that was designed to identify risk factors and markers of progression to clinical Alzheimer's disease in 318 cognitively normal individuals aged 70-85 years with a subjective memory complaint. We divided the subjects into four groups, according to their amyloid status (based on 18F-florbetapir PET) and neurodegeneration status (evidenced by 18F-fluorodeoxyglucose PET brain metabolism in Alzheimer's disease signature regions). The first group was amyloid-positive and neurodegeneration-positive, which corresponds to stage 2 of preclinical Alzheimer's disease. The second group was amyloid-positive and neurodegeneration-negative, which corresponds to stage 1 of preclinical Alzheimer's disease. The third group was amyloid-negative and neurodegeneration-positive, which corresponds to 'suspected non-Alzheimer's pathophysiology'. The last group was the control group, defined by amyloid-negative and neurodegeneration-negative subjects. We analysed 314 baseline 256-channel high-density eyes closed 1-min resting state EEG recordings. EEG biomarkers included spectral measures, algorithmic complexity and functional connectivity assessed with a novel information-theoretic measure, weighted symbolic mutual information. The most prominent effects of neurodegeneration on EEG metrics were localized in frontocentral regions with an increase in high frequency oscillations (higher beta and gamma power) and a decrease in low frequency oscillations (lower delta power), higher spectral entropy, higher complexity and increased functional connectivity measured by weighted symbolic mutual information in theta band. Neurodegeneration was associated with a widespread increase of median spectral frequency. We found a non-linear relationship between amyloid burden and EEG metrics in neurodegeneration-positive subjects, either following a U-shape curve for delta power or an inverted U-shape curve for the other metrics, meaning that EEG patterns are modulated differently depending on the degree of amyloid burden. This finding suggests initial compensatory mechanisms that are overwhelmed for the highest amyloid load. Together, these results indicate that EEG metrics are useful biomarkers for the preclinical stage of Alzheimer's disease.

Cortical activation during sleep predicts dream experience in narcolepsy.

ObjectiveNarcolepsy type 1 widely affects the architecture of sleep with frequent fast transition to REM sleep at both nighttime and daytime sleep onset. The occurrence of repeated sleep onset REM periods over the Multiple Sleep Latency Test offers a unique opportunity to identify EEG patterns predictive of successful dream recall after short periods composed of only REM or NREM sleep. It also permits to disentangle state‐ from trait‐like differences in dream recall, by using a within‐subjects design.MethodsA consecutive series of 115 first‐diagnosed drug‐free adult narcolepsy‐type 1 patients underwent Multiple Sleep Latency Tests and were asked after each nap opportunity if they had or had not a dream experience. Scalp EEG power and a specific index of cortical activation (delta/beta power ratio), obtained from naps of 43 patients with both presence and absence of dream recall in the same sleep stage, were compared separately for REM and NREM sleep.ResultsSuccessful dream recall was associated with an increased EEG desynchronization in both REM and NREM over partially overlapping cortical areas. Compared to unsuccessful recall, it showed (1) lower delta power over centro‐parietal areas during both stages, (2) higher beta power in the same cortical areas during NREM, and (3) lower values in the delta/beta ratio during NREM in most scalp locations.InterpretationA more activated electrophysiological milieu in both REM and NREM sleep promotes dream recall, strengthening the notion that the parietal areas are crucial not only in generating dream experience, as shown in brain‐damaged patients, but also in the memory processing leading to recall.

Sleep disturbance by pramipexole is modified by Meis1 in mice.

Meis homeobox 1 (Meis1) is a transcription factor functioning in the development of the nervous system and the cardiovascular system. Both common and rare variants within the gene have been associated with restless legs syndrome (RLS), while its association with symptoms of insomnia has also been discovered recently. RLS is associated with sleep disturbances, and while Meis1 haploinsufficiency is one of the most promising strategies for an RLS animal model, sleep phenotyping of Meis1 knockout mice has never been conducted. We report a detailed sleep analysis of heterozygous Meis1 knockout mice and challenge it with pramipexole, a dopamine agonist used in the treatment of RLS. At baseline, the Meis1-haploinsufficient mice had a trend towards lower delta power in the electroencephalogram (EEG) during sleep compared to the wild-type littermates, possibly indicating reduced sleep quality, but not sleep fragmentation. Pramipexole had a sleep disrupting effect in both genotype groups. In addition, it exerted differential effects on the EEG power spectra of the two mouse lines, remarkably elevating thetheta power of the mutant mice during recovery more than that of the wild-types. In conclusion, Meis1 haploinsufficiency seems to have only a modest effect on sleep, but the gene may interact with the sleep-disrupting effect of dopamine agonists.

EEG ultradian rhythmicity differences in disorders of consciousness during wakefulness.

Temporal fluctuations of cognitively-mediated behaviors in minimally conscious state (MCS) have been linked to changes of awareness, but the time-pattern of these variations remains ill-described. We analyzed 4-h EEG recordings from 12 patients with disorders of consciousness (6 MCS and 6 vegetative state/unresponsive wakefulness syndrome, VS/UWS). Relative powers (delta, theta, alpha, beta1 and beta2 bands) and spectral entropy were estimated (Fz, Cz and Pz derivations). Spectral entropy time-courses were then analyzed. MCS patients had higher theta and alpha and lower delta power when compared to VS/UWS. They showed higher spectral entropy mean value and higher time variability. MCS patients were characterized by spectral entropy fluctuations with periodicities of 70min (range 57-80 min). Notably, these periodicities closely resemble those described in awake healthy subjects, which were hypothesized to be related to fluctuation in vigilance/attention. No significant periodicity was observed for VS/UWS. The spectral entropy periodicity found in MCS patients could reflect the fluctuation of awareness responsible for the inconsistency of MCS manifestation of cognitively-mediated behaviors. The presence of a 70min periodicity in spectral entropy could permit clinicians to better choose their time-window when performing a clinical assessment of consciousness. It could also permit to monitor fluctuations in cognitive performance (i.e., response to command) during complementary testing by passive or active electrophysiological or functional neuroimaging paradigms or in resting state conditions.

Delta rhythm in wakefulness: evidence from intracranial recordings in human beings.

A widely accepted view is that wakefulness is a state in which the entire cortical mantle is persistently activated, and therefore desynchronized. Consequently, the EEG is dominated by low-amplitude, high-frequency fluctuations. This view is currently under revision because the 1-4 Hz delta rhythm is often evident during "quiet" wakefulness in rodents and nonhuman primates. Here we used intracranial EEG recordings to assess the occurrence of delta rhythm in 18 awake human beings. Our recordings reveal rhythmic delta during wakefulness at 10% of all recording sites. Delta rhythm could be observed in a single cortical lobe or in multiple lobes. Sites with high delta could flip between high and low delta power or could be in a persistently high delta state. Finally, these sites were rarely identified as the sites of seizure onset. Thus rhythmic delta can dominate the background operation and activity of some neocortical circuits in awake human beings.

The human leucocyte antigen DQB1*0602 allele is associated with electroencephelograph differences in individuals with obstructive sleep apnoea syndrome

Human leucocyte antigen (HLA) DQB1*0602 allele, a well-known genetic risk factor for narcolepsy, has been associated with sleep parameters in healthy subjects. We aimed to assess the association of this allele with daytime sleepiness and altered sleep electroencephalogram characteristics in the general population and in patients with obstructive sleep apnoea syndrome (OSAS). Eight hundred and ninety-four individuals from the Epidemiologic Study of Sleep were genotyped for the HLA DQB1*0602 allele. Full-night polysomnography was performed, and daytime sleepiness was analysed according to the Epworth Sleepiness Scale. HLA-DQB1*0602 allele-positive and -negative subjects in the general population, as well as in patients with OSAS, exhibited similar sleep parameters and levels of daytime sleepiness. However, spectral analysis showed that allele-positive individuals with OSAS exhibited higher theta power during sleep Stage 1 (P<0.05) in occipital derivations, and lower delta power during sleep Stages 1 and 2 (P<0.01) compared with individuals negative for the allele, even after correction for potential confounders as age, sex, body mass index and European ancestry. No significant differences in the electroencephalogram variables were found in individuals without OSAS. The data highlight the HLA-DQB1*0602 as a potential genetic factor influencing sleep physiology in individuals diagnosed with OSAS.

Progressive changes in cortical state before and after spontaneous arousals from sleep in elderly and middle-aged women

Arousals are often considered to be events which have an abrupt onset and offset, indicating abrupt changes in the state of the cortex. We hypothesized that cortical state, as reflected in electroencephalograph (EEG) signals, exhibits progressive systematic changes before and after a spontaneous, isolated arousal and that the time courses of the spectral components of the EEG before and after an arousal would differ between healthy middle-aged and elderly subjects. We analyzed the power spectrum and Sample Entropy of the C3A2 EEG before and after isolated arousals from 20 middle-aged (47.2±2.0 years) and 20 elderly (78.4±3.8 years) women using polysomnograms from the Sleep Heart Health Study database. In middle-aged women, all EEG spectral band powers <16 Hz exhibited a significant increase relative to baseline at some time in the 21 s before an arousal, but only low- (0.2–2.0 Hz) and high-frequency (2.0–4.0 Hz) delta increased in elderly and only during the last 7 s pre-arousal. Post-arousal, all frequency bands below 12 Hz transiently fell below pre-arousal baseline in both age groups. Consistent with these findings, Sample Entropy decreased steadily before an arousal, increased markedly during the arousal, and remained above pre-arousal baseline levels for ∼30 s after the arousal. In middle-aged, but not in elderly, women the presence of early pre-arousal low delta power was associated with shorter arousals. We propose that this attenuation of the effect of the arousing stimulus may be related to the slow (<1 Hz) cortical state oscillation, and that prolonged alterations of cortical state due to arousals may contribute to the poor correlation between indices of arousals and indices of sleepiness or impaired cognitive function.

Sleepwalking and night terrors: Psychopathological and psychophysiological correlates

Sleepwalking and night terrors are considered to be manifestations of the same nosologic continuum. It has been proposed that a sudden arousal from non-rapid eye movement (NREM) sleep is the cause of these disorders. Benign forms of NREM arousal parasomnias occur frequently in childhood and attenuate in teen years; however, they can persist into or begin in adulthood. The available literature documents high levels of psychopathology in adult patients. Sleepwalking and night terrors are most likely to manifest during the first episode of slow wave sleep, but may also appear any time during NREM sleep. The hypersynchronous delta activity, previously considered to be a hallmark of somnambulism, has proven to be unspecific. Post-arousal EEG activity reveals altered consciousness during sleepwalking and sleep terror episodes. Pathophysiology of NREM arousal parasomnias consists of predisposing factors, which may be a genetically determined tendency for deep sleep, facilitating factors which deepen sleep and increase slow wave sleep, and triggering factors which increase sleep fragmentation, such as stress, environmental or endogenous stimuli, and stimulants. Recently published data on low delta power in the first sleep cycle and slow decline of delta power in successive sleep cycles suggest a chronic inability to sustain slow wave sleep.

EEG delta power during sleep in young and old rats

Delta EEG power density, which has been viewed as a measure of intensity of NREM sleep, declines across the lifetime in humans, cats, and hamsters, but data in rats have been unclear. It is also uncertain whether older rats differ from younger animals in the degree of change in delta power during recovery sleep following short-term sleep deprivation. We have examined delta power density in NREM sleep under baseline conditions and following 48 h of sleep deprivation in young (3 months), middle-aged (12 months), and older (24 months) rats. The presence or absence of age effects was highly dependent on the method of normalizing the data. When expressed as a fraction of total NREM EEG power, there was no age effect on baseline delta power density, or on the change from baseline to recovery conditions. When expressed as a multiple of delta power in REM under the same condition, the younger rats had higher delta power density than the middle-aged and older rats. For all the ages combined, there was an increase in delta power density in the recovery condition. When examined by age, the younger rats (which started from a higher level of delta power density than the other groups) did not have an increase in delta during recovery; the middle-aged rats tended to, and the older rats (which started from lower baseline levels) significantly increased delta power density in the recovery condition. This suggests that the lower delta power seen during baseline in older rats is not due to decreased ability to generate delta activity.