Changes In Sleep Architecture Research Articles

Melinjo (Gnetum gnemon L.) seed extract for treatment of sleep/wake fragmentation in diet-induced obese mice.

Dietary supplementation with melinjo (Gnetum gnemon L.) seed extract (MSE) has been an integral part of an anti-obesity therapeutic regimen. To examine the relationship between anti-obesity and sleep, we explored the effect of MSE on sleep structure in high-fat diet (HFD)-induced obese mice. Although HFD did not alter the total amount of daily sleep, it significantly reduced the average duration of non-rapid eye movement (NREM) sleep and wakefulness episodes and significantly increased the number of these episodes. These findings indicate fragmented NREM sleep due to repeated brief awakenings in the HFD-fed mice. When 1% (w/v) MSE was given to HFD-fed mice, their weight or sleep structure were comparable to those of ND-fed mice, proving that dietary MSE completely hindered HFD-induced weight gain and sleep/wake fragmentation. Our data provide compelling evidence that MSE is a novel and promising dietary supplement that restores obesity-induced sleep architecture changes in mice.

The first-night effect of sleep occurs over nonconsecutive nights in unfamiliar and familiar environments.

The first night in an unfamiliar environment is marked by reduced sleep quality and changes in sleep architecture. This so-called first-night effect (FNE) is well established for two consecutive nights and lays the foundation for including an adaptation night in sleep research to counteract FNEs. However, adaptation nights rarely happen immediately before experimental nights, which raises the question of how sleep adapts over nonconsecutive nights. Furthermore, it is yet unclear, how environmental familiarity and hemispheric asymmetry of slow-wave sleep (SWS) contribute to the explanation of FNEs. To address this gap, 45 healthy participants spent two weekly separated nights in the sleep laboratory. In a separate study, we investigated the influence of environmental familiarity on 30 participants who spent two nonconsecutive nights in the sleep laboratory and two nights at home. Sleep was recorded by polysomnography. Results of both studies show that FNEs also occur in nonconsecutive nights, particularly affecting wake after sleep onset, sleep onset latency, and total sleep time. Sleep disturbances in the first night happen in both familiar and unfamiliar environments. The degree of asymmetric SWS was not correlated with the FNE but rather tended to vary over the course of several nights. Our findings suggest that nonconsecutive adaptation nights are effective in controlling for FNEs, justifying the current practice in basic sleep research. Further research should focus on trait- and fluctuating state-like components explaining interhemispheric asymmetries.

Exploring the Evolution of Sleep Patterns From Infancy to Adolescence.

Sleep is a critical component of healthy development, particularly during the formative years from infancy through adolescence. Sleep undergoes continuous change throughout life characterized by frequent awakenings and a high proportion of rapid eye movement (REM) sleep during infancy, changes in sleep architecture, an increase in non-rapid eye movement (NREM) sleep during adolescence, and an eventual decrease in REM sleep in old age. Adequate sleep is therefore essential for cognitive development, especially between ages 10 and 16. Sleep deprivation may negatively affect academic performance, attention regulation, and emotional well-being. Biological factors, such as hormonal changes during puberty, significantly influence sleep patterns, leading to later bedtimes and a tendency for chronic sleep deprivation in adolescents. Environmental factors, including light exposure and screen time, also play a critical role in regulating sleep. This paper examines the evolution of sleep patterns across infancy and adolescence, describing changes in sleep architecture, timing, and regulation. The influence of biological, environmental, and socio-cultural factors on sleep is explored, highlighting how these factors collectively shape sleep behaviors and health outcomes. It also addresses the profound role sleep plays in cognitive development, brain maturation, and emotional well-being. The importance of understanding sleep patterns and their developmental trajectories to address sleep-related issues is emphasized. Promoting healthy sleep from an early age can enhance cognitive and emotional outcomes, contributing to better academic performance and overall well-being in children and adolescents. The findings advocate for further standardized sleep intervention programs globally to prioritize sleep health and support optimal development.

Sleep and Neuroaffective Development From Early to Late Adolescence

Sleep is fundamental to human existence—especially during periods of extensive neurodevelopment such as adolescence. Importantly, poor sleep health in the transition into puberty can impact developing neural systems, contributing to the onset and maintenance of emotional disorders such as anxiety and depression. This review explores the complex interplay between sleep and neuroaffective development in adolescence, when changes in sleep architecture, circadian rhythms, and hormonal fluctuations interact with ongoing brain maturation to impact cognitive and emotional functioning. By synthesizing extant literature and charting future directions for research and intervention, this review elucidates the bidirectional associations between sleep and neuroaffective processes during puberty and highlights how sleep architecture and neurophysiology can inform our understanding of adolescent brain development. Ultimately, this article argues that promoting sleep health and addressing sleep-related challenges, especially in early adolescence, are promising strategies for enhancing well-being and fostering positive neurodevelopmental outcomes across both healthy and clinical populations.

Adenotonsillectomy outcomes in children with down syndrome and obstructive sleep apnea: a single center study.

This study aimed to evaluate polysomnographic (PSG) outcomes of tonsillectomy and adenoidectomy (T&A) in children with Down Syndrome (DS) and OSA, and the difference in PSG outcomes of T&A between children with DS and age- and gender-matched normally developing (non-DS) children. This was a single center retrospective study that included children with DS and OSA who underwent T&A and had pre-operative and post-operative PSG. The baseline and the differences of pre- and post-operative PSG variables were compared with those of an age- and gender-matched group of non-DS children. Forty-eight children with DS were included in the study; the median age was 5 years (IQR 5.5), 58% were males, and the median BMI was 18.2 (IQR 3.3). There was statistically significant improvement noted between pre-operative and post-operative OAHI 17.9 ± 26.7 vs. 9.1 ± 13.6 (p = 0.022) and non-REM AHI 13.9 ± 19.7 vs. 6.9 ± 14.2 (p = 0.027). However, there were no significant changes in sleep architecture, oxygen desaturation nadir, or CO2 levels. 54.2% of the DS children continued to have moderate to severe OSA after T&A. Univariate logistic regression showed that for every 1% increase in oxygen desaturation nadir, the odds of having residual moderate or severe OSA decreased by 28% (p = 0.002) compared to the cured and mild OSA groups. There was no significant pre- and post-operative differences in PSG variables noted in 16 children with DS compared to age- and gender-matched non-DS children. Despite the overall significant reduction of OAHI in children with DS and OSA who underwent T&A, there was a residual moderate to severe OSA in about half of the included children. Oxygen desaturation nadir was a predicting factor for persistent moderate to severe OSA. There were no significant pre- and post-operative PSG differences in between DS children compared to non-DS children.

The impact of cannabis use proximal to sleep and cannabinoid metabolites on sleep architecture.

Cannabis is a common sleep aid, however the effects of its use prior to sleep are poorly understood. This study aims to determine the impact of non-medical whole plant cannabis use three hours prior to sleep and measured cannabis metabolites on polysomnogram measures. This is a cross-sectional study of 177 healthy adults who provided detailed cannabis use history, underwent a one-night home sleep test (HST) and had measurement of eleven plasma and urinary cannabinoids, quantified using mass spectroscopy, the morning after the HST. Multivariable models were used to assess the relationship between cannabis use proximal to sleep, which was defined as use three hours before sleep, and individual HST measurements. Correlation between metabolite concentrations and polysomnogram measures were assessed. In adjusted models, cannabis use proximal to sleep was associated with increased wake after sleep onset (median 60.5 versus 45.8 minutes), rate ratio 1.59 (1.22, 2.05), and increased proportion of stage one sleep (median 15.2% versus 12.3%), effect estimate 0.16 (0.06, 0.25). Compared to non-users, frequent cannabis users (>20 days per month) also had increased wake after sleep onset and stage one sleep, in addition to increased REM latency and decreased percent sleep efficiency. Delta-9 tetrahydrocannabinol metabolites correlated with these HST measures. Cannabis use proximal to sleep was associated with minimal changes in sleep architecture. Its use wasn't associated with measures of improved sleep including increased sleep time or efficiency and may be associated with poor quality sleep through increase wake onset and stage 1 sleep.

Effectiveness of multi-modal home-based videoconference interventions on sleep in older adults: study protocol for a randomized controlled trial.

Aging is characterized by substantial changes in sleep architecture that negatively impact fitness, quality of life, mood, and cognitive functioning. Older adults often fail to reach the recommended level of physical activity to prevent the age-related decline in sleep function, partly because of geographical barriers. Implementing home-based interventions could surmount these obstacles, thereby encouraging older adults to stay active, with videoconference administration emerging as a promising solution. Increasing the availability of biological rhythms synchronizers, such as physical activity, light exposure, or vestibular stimulation, represents a viable non-pharmacological strategy for entraining circadian rhythms and potentially fortifying the sleep-wake cycle, thereby enhancing sleep in aging. This study aims to (1) assess the impact of remote physical exercise training and its combination with bright light exposure, and (2) investigate the specific contribution of galvanic vestibular stimulation, to sleep quality among healthy older adults with sleep complaints. One hundred healthy older adults aged 60-70 years with sleep complaints will be randomly allocated to one of four groups: a physical exercise training group (n = 25), a physical exercise training combined with bright light exposure group (n = 25), a galvanic vestibular stimulation group (n = 25) or a control group (i.e., health education) (n = 25). While physical exercise training and health education will be supervised via videoconference at home, bright light exposure (for the physical exercise training combined with bright light exposure group) and vestibular stimulation will be self-administered at home. Pre-and post-tests will be conducted to evaluate various parameters, including sleep (polysomnography, subjective questionnaires), circadian rhythms (actigraphy, temperature), fitness (physical: VO2 peak, muscular function; and motor: balance, and functional mobility), cognition (executive function, long-term memory), quality of life and mood (anxiety and depression). The findings will be anticipated to inform the development of recommendations and non-pharmaceutical preventive strategies for enhancing sleep quality in older adults, potentially leading to improvements in fitness, cognition, quality of life, and mood throughout aging.

Distinct lateral hypothalamic CaMKIIα neuronal populations regulate wakefulness and locomotor activity

For nearly a century, evidence has accumulated indicating that the lateral hypothalamus (LH) contains neurons essential to sustain wakefulness. While lesion or inactivation of LH neurons produces a profound increase in sleep, stimulation of inhibitory LH neurons promotes wakefulness. To date, the primary wake-promoting cells that have been identified in the LH are the hypocretin/orexin (Hcrt) neurons, yet these neurons have little impact on total sleep or wake duration across the 24-h period. Recently, we and others have identified other LH populations that increase wakefulness. In the present study, we conducted microendoscopic calcium imaging in the LH concomitant with EEG and locomotor activity (LMA) recordings and found that a subset of LH neurons that express Ca2+/calmodulin-dependent protein kinase IIα (CaMKIIα) are preferentially active during wakefulness. Chemogenetic activation of these neurons induced sustained wakefulness and greatly increased LMA even in the absence of Hcrt signaling. Few LH CaMKIIα-expressing neurons are hypocretinergic or histaminergic while a small but significant proportion are GABAergic. Ablation of LH inhibitory neurons followed by activation of the remaining LH CaMKIIα neurons induced similar levels of wakefulness but blunted the LMA increase. Ablated animals showed no significant changes in sleep architecture but both spontaneous LMA and high theta (8 to 10 Hz) power during wakefulness were reduced. Together, these findings indicate the existence of two subpopulations of LH CaMKIIα neurons: an inhibitory population that promotes locomotion without affecting sleep architecture and an excitatory population that promotes prolonged wakefulness even in the absence of Hcrt signaling.

Prior knowledge benefits older adults' tonal consolidation through talker generalization

Recent research indicated that post-training sleep facilitates memory consolidation and talker generalization in young adults' tone learning. For instance, a nap study showed the newly learned tonal contrast that relates to prior knowledge consolidated more rapidly than that does not after daytime naps. Notably, older adults' declarative memory consolidation is impaired with age-related changes in sleep architecture. The current study examines whether prior (contour-tone) knowledge benefits Mandarin-speaking older adults' Cantonese tone learning. Mandarin employs pitch contours (falling versus rising) to cue tones in signaling word identity. Besides pitch contours, Cantonese also utilizes pitch heights (higher versus lower) in level tones to encode word meanings. In the pilot phase (60 Mandarin-speaking older adults will be recruited with data collection ongoing), participants were trained to learn Cantonese contour-level and level-level contrasts in the evening or the morning. A novel word-object identification task was used in the training, followed by three tone identification tasks: a posttest immediately after training, a 12-h delayed posttest (a trained talker), and another delayed posttest (a novel talker). Aligned with the nap study, preliminary results suggested overnight sleep might enhance seniors' tone-related memory by promoting generalization across talkers in learning contour-level contrast owing to their prior contour-tone knowledge.

Effects of periodic breathing on sleep at high altitude: a randomized, placebo-controlled, crossover study using inspiratory CO2.

Hypoxia at high altitude facilitates changes in ventilatory control that can lead to nocturnal periodic breathing (nPB). Here, we introduce a placebo-controlled approach to prevent nPB by increasing inspiratory CO2 and used it to assess whether nPB contributes to the adverse effects of hypoxia on sleep architecture. In a randomized, single-blinded, crossover design, 12 men underwent two sojourns (three days/nights each, separated by 4weeks) in hypobaric hypoxia corresponding to 4000m altitude, with polysomnography during the first and third night of each sojourn. During all nights, subjects' heads were encompassed by a canopy retaining exhaled CO2 , and CO2 concentration in the canopy (i.e. inspiratory CO2 concentration) was controlled by adjustment of fresh air inflow. Throughout the placebo sojourn inspiratory CO2 was ≤0.2%, whereas throughout the other sojourn it was increased to 1.76% (IQR, 1.07%-2.44%). During the placebo sojourn, total sleep time (TST) with nPB was 54.3% (37.4%-80.8%) and 45.0% (24.5%-56.5%) during the first and the third night, respectively (P=0.042). Increased inspiratory CO2 reduced TST with nPB by an absolute 38.1% (28.1%-48.1%), the apnoea-hypopnoea index by 58.1/h (40.1-76.1/h), and oxygen desaturation index ≥3% by 56.0/h (38.9.1-73.2/h) (all P<0.001), whereas it increased the mean arterial oxygen saturation in TST by 2.0% (0.4%-3.5%, P=0.035). Increased inspiratory CO2 slightly increased the percentage of N3sleep during the third night (P=0.045), without other effects on sleep architecture. Increasing inspiratory CO2 effectively prevented hypoxia-induced nPB without affecting sleep macro-architecture, indicating that nPB does not explain the sleep deterioration commonly observed at high altitudes. KEY POINTS: Periodic breathing is common during sleep at high altitude, and it is unclear how this affects sleep architecture. We developed a placebo-controlled approach to prevent nocturnal periodic breathing (nPB) with inspiratory CO2 administration and used it to assess the effects of nPB on sleep in hypobaric hypoxia. Nocturnal periodic breathing was effectively mitigated by an increased inspiratory CO2 fraction in a blinded manner. Prevention of nPB did not lead to relevant changes in sleep architecture in hypobaric hypoxia. We conclude that nPB does not explain the deterioration in sleep architecture commonly observed at high altitude.

Polysomnographic features associated with clonazepam and melatonin treatment in isolated REM sleep behavior disorder: Time for new therapeutic approaches?

Although clonazepam (CLO) and melatonin (MLT) are the most frequently used treatments for REM sleep behavior disorder, the polysomnographic features associated with their use are little known. The aim of this study was to evaluate polysomnographic and clinical parameters of patients with idiopathic/isolated REM sleep behavior disorder (iRBD) treated chronically with CLO, sustained-release MLT, alone or in combination, and in a group of drug-free iRBD patients. A total of 96 patients were enrolled: 43 drug-free, 21 with CLO (0.5-2 mg), 20 with sustained-release MLT (1-4 mg), and 12 taking a combination of them (same doses). Clinical variables and polysomnography were collected. Although clinical improvement was reported in all groups, MLT impacted sleep architecture more than the other treatments, with significant and large increase in N3 stage, moderate reduction in N2 and REM sleep, and moderate increase in REM latency. CLO moderately increased the percentage of both REM sleep and especially N2, while reducing N1 and wakefulness. Patients treated with both CLO and MLT did not show major changes in sleep architecture. These results suggest that the administration of MLT or CLO impacts (positively) on sleep parameters of iRBD patients. However, there is a need to better stratify patients, in order to treat them in a targeted manner, depending on the patient's individual sleep architecture and expected differential effects of these agents.

The Interplay between Disordered Sleep and Alzheimer’s Disease: Exploring the Bidirectional Relationship

The debilitating neurodegenerative condition referred to as Alzheimer’s Disease (AD), results in severe cognitive deterioration, including deficits in memory, confusion, and abnormal behaviour. Sleep plays a crucial role in sustaining cognitive health, as it supports brain repair and performs memory consolidation. Complaints of consistently disrupted sleeping habits, such as reduced quality and fragmented sleep, are increasingly recognized as potential risk factors for AD. The fundamental elements of healthy sleep: its structure, oscillations and benefits- then considering how changes in sleep architecture, including alterations in REM and NREM stages, are associated with cognitive decline. Another significant concept is the finding that sleep deprivation is often correlated with increased levels of amyloid beta (Aβ) and tau proteins in the brain, which are two biomarkers of AD pathology and accumulate with disease progression. This review examines the connection between unhealthy sleep patterns during aging and AD development, emphasizing the need for continued research into how improving sleep hygiene could potentially moderate the effects of cognitive deterioration.

INVESTIGATING DREAMING IN COGNITIVELY DIVERSE OLDER ADULTS

Abstract Dreaming changes across the lifespan. While our understanding of how dreaming relates to aging and well-being has developed with respect to early and middle phases of the lifespan, the dreams of older adults remain under-studied. Reviews of the literature suggest decreases in dream recall and the emotionality of dream content that often precede age-related changes in sleep architecture, with few changes in dreaming occurring between ages 45-75, after which dream recall declines steeply. However, these findings are based on relatively few studies. This point is underscored when considering the effects of secondary aging on dreaming, where virtually no literature exists on the dreams of older adults experiencing mild cognitive impairment. Studying the dreams of older adults experiencing cognitive impairment may seem trivial when compared to other processes implicated in secondary aging, but recent studies examining the relationship between frequency of negative dream content and the increased risk of onset and acceleration of cognitive decline beg a closer examination of how dreaming contributes to a broader understanding of health and functioning across the lifespan. The scoping review of sleep, dreams, well-being and cognition across the lifespan, and the subsequent proposed study design seeks to employ the Hall and Van de Castle Coding System of content analysis to contribute to the literature on the dream frequency and content of cognitively typical older adults while also exploring the feasibility and methodological considerations of studying the dream content of older adults with mild cognitive impairment.

An acute bout of high-intensity exercise affects nocturnal sleep and sleep-dependent memory consolidation.

Acute exercise has been shown to affect long-term memory and sleep. However, it is unclear whether exercise-induced changes in sleep architecture are associated with enhanced memory. Recently, it has been shown that exercise followed by a nap improved declarative memory. Whether these effects transfer to night sleep and other memory domains has not yet been studied. Here, we investigate the influence of exercise on nocturnal sleep architecture and associations with sleep-dependent procedural and declarative memory consolidation. Nineteen subjects (23.68 ± 3.97 years) were tested in a balanced cross-over design. In two evening sessions, participants either exercised (high-intensity interval training) or rested immediately after encoding two memory tasks: (1) a finger tapping task and (2) a paired-associate learning task. Subsequent nocturnal sleep was recorded by polysomnography. Retrieval was conducted the following morning. High-intensity interval training lead to an increased declarative memory retention (p = 0.047, d = 0.40) along with a decrease in REM sleep (p = 0.012, d = 0.75). Neither procedural memory nor NREM sleep were significantly affected. Exercise-induced changes in N2 showed a positive correlation with procedural memory retention which did not withstand multiple comparison correction. Exploratory analyses on sleep spindles and slow wave activity did not reveal significant effects. The present findings suggest an exercise-induced enhancement of declarative memory which aligns with changes in nocturnal sleep architecture. This gives additional support for the idea of a potential link between exercise-induced sleep modifications and memory formation which requires further investigation in larger scaled studies.

Sleep Disorders and Aging in Women.

Women of advancing age can suffer from an array of sleep disorders. We review the changes in sleep architecture, the impact of hormonal changes on sleep, and the various sleep disorders in women of advancing age. A focused history in this population should include the temporal relation to menopause and comorbid conditions. Treatment options should involve patient preference and review of current medications and comorbid conditions to optimize sleep in this population.

Altered sleep architecture in children and adolescents with Down syndrome.

Children with Down syndrome (DS) may experience changes in sleep architecture (i.e., different sleep stages) that then affect waketime functioning, including learning, mood, and disruptive behavior. For designing and testing interventions, it is important to document any differences in sleep architecture in children with DS with and without co-occurring diagnoses, including neuropsychiatric diagnoses and obstructive sleep apnea (OSA). A retrospective cohort study was performed at Massachusetts General Hospital for children and adolescents with DS who underwent polysomnography (PSG) between August 2016 and July 2022. Patient data collected from the electronic medical record included diagnoses, age at PSG, and PSG report. Statistical analysis included unpaired T tests to test hypotheses about differences in sleep architecture within age groups, and differences between children with DS and a co-occurring diagnosis. One way ANOVA was used to determine statistical significance of OSA severity within patients with DS. When compared by age group, those with DS had negative changes in sleep architecture (e.g., less sleep and more wake) when compared to normative data. Within this cohort, having a co-occurring diagnosis of autism resulted in further, negative effects on sleep architecture. 89% of those with DS had diagnosed OSA but only those with severe OSA experienced negative effects on sleep architecture. Age is an important covariate when studying the sleep of children with DS and neurotypical children. Studies are needed to test whether minimizing the observed differences in sleep architecture will translate to improved learning, mood, and behavioral outcomes, and how treating OSA affects sleep architecture.

Effect of obstructive sleep apnea syndrome on sleep architecture: comparative study between geriatrics and middle-aged adult patients

Abstract Background Obstructive sleep apnea (OSA) is a prevalent sleep disordered breathing in geriatrics but still frequently undiagnosed. Sleep architecture changes with ageing. Geriatrics spend more time in the N1, N2 than in N3, REM. Also, there are more frequent awakenings, arousals and sleep stage shifts. This leads to decrease in sleep efficiency. Geriatric patients with OSA have more affected sleep architecture than middle-aged adults. The aim This work aimed to assess and compare sleep architecture changes in geriatrics versus middle-aged adult patients with OSA syndrome. Patients and methods This comparative study conducted in chest department Menoufia University Hospitals included 50 patients divided to two equal groups; geriatric group age 65 years old or more and middle-aged adult group aged from 18 to 50 years old. All patients were complaining of symptoms suggestive of OSA. All patients underwent sleep questionnaires and Polysomnography using model; Philipsrespironic alice6. Results There was no statistically significant difference between the studied groups regarding sex, smoking, co morbidities, BMI and symptoms. Regarding changes in sleep architecture, geriatric group showed a significantly higher Sleep latency and wakefulness after sleep onset in comparison to middle-aged adults (P=0.004 and 0.039, respectively) versus significantly lower Sleep efficiency, N3%, REM% (P=0.009,0.011 and 0.001, respectively). The median Total Apnea-Hypopnea index was 40.2 (/h sleep) in geriatric group and 35.4 in middle-aged adult group. Regarding severity of OSA; geriatric group showed mild OSA in five (20%) patients, moderate in five (20%) patient and severe in 15 (60%) patients. Middle-aged adults showed mild OSA in 10 (40%) patients, moderate in two (8%) patients, and severe in 13 (52%) patients. Conclusions Sleep architecture is affected in all OSA patients, but these changes are more obvious in geriatric patients. Geriatric patients have higher wakefulness after sleep onset and sleep latency. On the other hand, they have a lower N3%, REM% and sleep efficiency.

Influence of sex hormone use on sleep architecture in a transgender cohort.

Sex differences in sleep architecture are well-documented, with females experiencing longer total sleep time, more slow wave sleep (SWS), and shorter Rapid Eye Movement (REM) sleep duration than males. Although studies imply that sex hormones could affect sleep, research on exogenous sex hormones on sleep architecture is still inconclusive. This study examined sleep architecture changes in transgender individuals after 3 months of gender-affirming hormone therapy (GAHT). We assessed sleep architecture in 73 transgender individuals: 38 transmasculine participants who started using testosterone and 35 transfeminine participants who started using estrogens and antiandrogens. Sleep architecture was measured before GAHT and after 3 months of GAHT for 7 nights using an ambulatory single-electrode sleep EEG device. Changes in sleep architecture were analyzed using linear mixed models, and non-normally distributed outcomes were log-transformed and reported as percentages. In transmasculine participants, SWS decreased by 7 minutes (95% CI: -12; -3) and 1.7% (95% CI: -3%; -0.5%), REM sleep latency decreased by 39% (95% CI: -52%; -22%) and REM sleep duration increased by 17 minutes (95% CI: 7; 26) after 3 months of GAHT. In transfeminine participants, sleep architecture showed no significant changes after 3 months of GAHT. Sleep architecture changes after 3 months of masculinizing GAHT in line with sleep in cisgender males, while it shows no changes after feminizing GAHT. The sex-specific nature of these changes raises new questions about sex hormones and sleep. Future research should focus on studying possible underlying neural mechanisms and clinical consequences of these changes.

Moving time zones in a flash with light therapy during sleep

In humans, exposure to continuous light is typically used to change the timing of the circadian clock. This study examines the efficiency of a sequence of light flashes (“flash therapy”) applied during sleep to shift the clock. Healthy participants (n = 10) took part in two 36-h laboratory stays, receiving a placebo (goggles, no light) during one visit and the intervention (goggles, 2-ms flashes broad-spectrum light for 60 min, delivered every 15 s, starting 30 min after habitual sleep onset) during the other. Circadian phase shift was assessed with changes in salivary dim light melatonin onset (DLMO). Sleep, measured with polysomnography, was analyzed to assess changes in sleep architecture and spectral power. After 1 h of flashes, DLMO showed a substantial delay (1.13 ± 1.27 h) compared to placebo (12 ± 20 min). Two individuals exhibited very large shifts of 6.4 and 3.1 h. There were no substantive differences in sleep architecture, but some evidence for greater instability in sleep. 1 h of flash therapy during sleep evokes large changes in circadian timing, up to 6 h, and does so with only minimal, if any, impact on sleep. Flash therapy may offer a practical option to delay the circadian clock in shift workers and jet travelers.

Accelerometer-derived sleep measures in idiopathic dystonia: A UK Biobank cohort study.

Sleep disturbance is an increasingly recognized non-motor trait in dystonia, with varying findings reported to date. Here, we examine sleep in a UK Biobank derived dystonia cohort using subjective self-reported sleep symptoms and objective accelerometer-derived sleep measures, with comparison to a control population. A total of 241 dystonia cases were compared to 964 matched controls in analysis of self-reported sleep symptoms and changes in sleep architecture using wrist-worn triaxial accelerometers. Dystonia participants had poorer self-reported sleep patterns compared to controls. Accelerometery measurements demonstrated later sleep times, reduced time in bed, and shifts in circadian rhythm. No association was observed with pain, and only limited relationships with psychiatric symptoms. This study demonstrates the utility of accelerometers in longer term evaluation of sleep in dystonia, for measurement of disturbance and response to treatment. Compared to controls, altered sleep and circadian rhythm were more common in dystonia patients which may contribute to the clinical phenotype.