Sleep assessment using EEG-based wearables - A systematic review.

Polysomnography (PSG) is the reference standard of sleep measurement, but is burdensome for the participant and labor intensive. Affordable electroencephalography (EEG)-based wearables are easy to use and are gaining popularity, yet selecting the most suitable device is a challenge for clinicians and researchers. In this systematic review, we aim to provide a comprehensive overview of available EEG-based wearables to measure human sleep. For each wearable, an overview will be provided regarding validated population and reported measurement properties. A systematic search was conducted in the databases OVID MEDLINE, Embase.com and CINAHL. A machine learning algorithm (ASReview) was utilized to screen titles and abstracts for eligibility. In total, 60 papers were selected, covering 34 unique EEG-based wearables. Feasibility studies indicated good tolerance, high compliance, and success rates. The 42 included validation studies were conducted across diverse populations and showed consistently high accuracy in sleep staging detection. Therefore, the recent advancements in EEG-based wearables show great promise as alternative for PSG and for at-home sleep monitoring. Users should consider factors like user-friendliness, comfort, and costs, as these devices vary in features and pricing, impacting their suitability for individual needs.

Effects of surgery and general anaesthesia on sleep-wake timing: CLOCKS observational study.

Surgery and general anaesthesia have the potential to disturb the body's circadian timing system, which may affect postoperative outcomes. Animal studies suggest that anaesthesia could induce diurnal phase shifts, but clinical research is scarce. We hypothesised that surgery and general anaesthesia would result in peri-operative changes in diurnal sleep-wake patterns in patients. In this single-centre prospective cohort study, we recruited patients aged ≥18 years scheduled for elective surgery receiving ≥30 min of general anaesthesia. The Munich Chronotype Questionnaire and Pittsburgh Sleep Quality Index were used to determine baseline chronotype, sleep characteristics and sleep quality. Peri-operative sleeping patterns were logged. Ninety-four patients with a mean (SD) age of 52 (17) years were included; 56 (60%) were female. The midpoint of sleep (SD) three nights before surgery was 03.33 (55 min) and showed a phase advance of 40 minutes to 02.53 (67 min) the night after surgery (p < 0.001). This correlated with the midpoint of sleep three nights before surgery and was not associated with age, sex, duration of general anaesthesia or intra-operative dexamethasone use. Peri-operatively, patients had lower subjective sleep quality and worse sleep efficiency. Disruption started from one night before surgery and did not normalise until 6 days after surgery. We conclude that there is a peri-operative phase advance in midpoint of sleep, confirming our hypothesis that surgery and general anaesthesia disturb the circadian timing system. Patients had decreased subjective sleep quality, worse sleep efficiency and increased daytime fatigue.

Hypothalamic-pituitary-adrenal axis abnormalities in response to deletion of 11beta-HSD1 is strain-dependent.

Inter-individual differences in hypothalamic-pituitary-adrenal (HPA) axis activity underlie differential vulnerability to neuropsychiatric and metabolic disorders, although the basis of this variation is poorly understood. 11beta-Hydroxysteroid dehydrogenase type 1 (11beta-HSD1) has previously been shown to influence HPA axis activity. 129/MF1 mice null for 11beta-HSD1 (129/MF1 HSD1(-/-)) have greatly increased adrenal gland size and altered HPA activity, consistent with reduced glucocorticoid negative feedback. On this background, concentrations of plasma corticosterone and adrenocorticotrophic hormone (ACTH) were elevated in unstressed mice, and showed a delayed return to baseline after stress in HSD1-null mice with reduced sensitivity to exogenous glucocorticoid feedback compared to same-background genetic controls. In the present study, we report that the genetic background can dramatically alter this pattern. By contrast to HSD1(-/-) mice on a 129/MF1 background, HSD1(-/-) mice congenic on a C57Bl/6J background have normal basal plasma corticosterone and ACTH concentrations and exhibit normal return to baseline of plasma corticosterone and ACTH concentrations after stress. Furthermore, in contrast to 129/MF1 HSD1(-/-) mice, C57Bl/6J HSD1(-/-) mice have increased glucocorticoid receptor expression in areas of the brain involved in glucocorticoid negative feedback (hippocampus and paraventricular nucleus), suggesting this may be a compensatory response to normalise feedback control of the HPA axis. In support of this hypothesis, C57Bl/6J HSD1(-/-) mice show increased sensitivity to dexamethasone-mediated suppression of peak corticosterone. Thus, although 11beta-HSD1 appears to contribute to regulation of the HPA axis, the genetic background is crucial in governing the response to (and hence the consequences of) its loss. Similar variations in plasticity may underpin inter-individual differences in vulnerability to disorders associated with HPA axis dysregulation. They also indicate that 11beta-HSD1 inhibition does not inevitably activate the HPA axis.