Modulation of Sleep Architecture by Whole-Body Static Magnetic Exposure: A Study Based on EEG-Based Automatic Sleep Staging

A steady increase in sleep problems has been observed along with the development of society. Overnight exposure to a static magnetic field has been found to improve sleep quality; however, such studies were mainly based on subjective evaluation. Thus, the presented data cannot be used to infer sleep architecture in detail. In this study, the subjects slept on a magneto-static mattress for four nights, and self-reported scales and electroencephalogram (EEG) were used to determine the effect of static magnetic field exposure (SMFE) on sleep. Machine learning operators, i.e., decision tree and supporting vector machine, were trained and optimized with the open access sleep EEG dataset to automatically discriminate the individual sleep stages, determined experimentally. SMEF was found to decrease light sleep duration (N2%) by 3.51%, and sleep onset latency (SOL) by 15.83%, while it increased deep sleep duration (N3%) by 8.43%, compared with the sham SMFE group. Further, the overall sleep efficiency (SE) was also enhanced by SMFE. It is the first study, to the best of our knowledge, where the change in sleep architecture was explored by SMFE. Our findings will be useful in developing a non-invasive sleep-facilitating instrument.

Validation Study of a Contactless Monitoring Device for Vital Signs During Sleep and Sleep Architecture in Adults With Sleep-Disordered Breathing

Background and Objective Few clinical studies have investigated the accuracy of non-contact monitoring devices for vital signs during sleep and sleep architecture in adults with sleep-disordered breathing (SDB). The purpose of this study was to assess the accuracy of a contactless monitoring device for 1) heart rate, respiratory rate, and body temperature during sleep and 2) sleep architecture in adults with SDB.Methods Thirty-five consecutive adults, who visited a tertiary university hospital due to suspected SDB, underwent a complete physical examination and standard (level 1) polysomnography plus body temperature measurement with a contactless monitoring device (HoneyCube System).Results A total of 30 subjects (mean age = 46.43 ± 12.9 years; male: female = 22: 8) were finally included, and five subjects were excluded due to inadequate data in this study. The intraclass correlation coefficient values of heart rate, respiratory rate, and body temperature measured using the contactless monitoring device were 0.91 (95% confidence interval [CI]: 0.892, 0.928), 0.937 (95% CI: 0.919, 0.954), and 0.918 (95% CI: 0.895, 0.941), respectively. The mean kappa value for sleep architecture was 0.562 (95% CI: 0.529, 0.596).Conclusions The contactless monitoring device showed good (almost perfect) agreement in terms of heart rate, respiratory rate, and body temperature and moderate agreement in sleep architecture with contact measurements. These results suggest that the HoneyCube System is a good candidate device for sleep monitoring at home and in multiple accommodations.

The Association between Insomnia-like Sleep Pattern Changes and Cognitive Dysfunction: Possible Mechanism and Therapeutic Strategy

: The prevalence of sleep disorders and cognitive dysfunction has overwhelmingly increased, with insomnia and Alzheimer’s disease (AD) being the most common form. A multitude of studies have linked the alterations in sleep continuity or sleep architecture with cognitive impairment bilaterally, but the management of disrupted sleep patterns in preclinical AD could be more beneficial since there is no cure for AD. This review mainly focuses on the altered sleep patterns in insomnia, and summarizes potential pathways underlying the relationship between insomnia and cognitive impairment, aiming to establish certain sleep pattern changes as biomarkers for cognitive decline and explore potential therapeutic targets based on evidence from research advances.

Disturbances of the Gut Microbiota, Sleep Architecture, and mTOR Signaling Pathway in Patients with Severe Obstructive Sleep Apnea-Associated Hypertension

Intermittent hypoxia and sleep fragmentation are pathophysiological processes involved in obstructive sleep apnea (OSA) which affect gut microbiota, sleep architecture, and mTOR signaling pathway. However, the involvement of these elements in the pathogenesis mechanism of OSA-associated hypertension remains unclear. Therefore, this study investigated whether the OSA-associated hypertension mechanism is regulated by the gut microbiota and mTOR signaling pathway. Patients were diagnosed by polysomnography; their fecal samples were obtained and analyzed for their microbiome composition by 16S ribosomal RNA pyrosequencing and bioinformatics analysis. Transcript genes on fasting peripheral blood mononuclear cells (PBMCs) were examined using Illumina RNA-sequencing analysis. Totally, we enrolled 60 patients with severe OSA [without hypertension (n = 27) and with hypertension (n = 33)] and 12 controls (neither OSA nor hypertension). Results revealed that severe-OSA patients with hypertension had an altered gut microbiome, decreased short-chain fatty acid-producing bacteria P < 0.05 , and reduced arginine and proline metabolism pathways P = 0.001 , compared with controls; also, they had increased stage N1 sleep and reduced stages N2 and N3 sleep accompanied by repeated arousals P < 0.05 . Analysis of PBMCs using the Kyoto Encyclopedia of Genes and Genomes database showed that the mTOR signaling pathway P = 0.006 was the most important differential gene-enriched pathway in severe-OSA patients with hypertension. Our findings extend prior work and suggest a possibility that the regulation of the mTOR signaling pathway is involved in developing OSA-associated hypertension through its interaction with the disturbance of the gut microbiome and sleep architecture.

Preliminary Study on Changes of Sleep EEG Power and Plasma Melatonin in Male Patients With Major Depressive Disorder After 8 Weeks Treatment

Objective: To clarify the effects of escitalopram on sleep EEG power in patients with Major depressive disorder (MDD).Method: Polysomnography (PSG) was detected overnight, and blood samples were collected at 4 h intervals over 24 h from 13 male healthy controls and 13 male MDD patients before and after treatment with escitalopram for 8 weeks. The outcome measures included plasma melatonin levels, sleep architecture, and the sleep EEG power ratio.Results: Compared with healthy controls, MDD patients presented abnormalities in the diurnal rhythm of melatonin secretion, including peak phase delayed 3 h and a decrease in plasma melatonin levels at night and an increase at daytime, accompanied by sleep disturbances, a decrease in low-frequency bands and an increase in high-frequency bands, and the dominant right-side brain activity. Several of these abnormalities (abnormalities in the diurnal rhythm of melatonin secretion, partial sleep architecture parameters) persisted for at least the 8-week testing period.Conclusions: Eight weeks of treatment with escitalopram significantly improved subjective sleep perception and depressive symptoms of patients with MDD, and partially improved objective sleep parameters, while the improvement of circadian rhythm of melatonin was limited.

NREM sleep signatures of memory disruption and psychiatric symptoms in young people with 22q11.2 deletion syndrome

Background Young people with 22q11.2 Deletion Syndrome (22q11.2DS) are at increased risk of schizophrenia, intellectual disability, Attention-Deficit Hyperactivity Disorder (ADHD) and autism spectrum disorder. In common with these conditions, 22q11.2DS is also associated with sleep problems. We investigated whether abnormal sleep or sleep-dependent network activity in 22q11.2DS may reflect convergent, early signatures of neural circuit disruption also evident in associated neurodevelopmental conditions. Methods We recorded high-density sleep EEG in young people (6-20 years) with 22q11.2DS (n=28) and their unaffected siblings (n=17), quantifying the associations between sleep architecture, EEG oscillations (spindles and slow-waves) and psychiatric symptoms. We also measured performance on a memory task before and after sleep. Results 22q11.2DS was associated with significant alterations in sleep architecture, including a greater proportion of N3 sleep and lower proportions of N1 and REM sleep than in siblings. During NREM sleep, deletion carriers showed increased power in slow delta and sigma oscillations, increased slow-wave and spindle amplitudes, and altered coupling between spindles and slow-waves. Spindle and slow-wave amplitudes correlated positively with overnight memory in controls, but negatively in 22q11.2DS. Mediation analyses indicated that increased slow-wave amplitude in 22q11.2DS was statistically mediated via ADHD symptoms. Conclusions This first study of sleep EEG in 22q11.2DS highlights several alterations in EEG signatures of NREM sleep, some of which were associated with ADHD symptoms. ADHD symptoms have previously been associated with incident psychotic symptoms in 22q11.2DS; our findings may therefore reflect delayed or compromised neurodevelopmental processes which precede, and may be biomarkers for, psychotic disorders.