Alterations In Sleep Architecture Research Articles

Sleep is associated with telomere shortening: A population-based longitudinal study.

As the chronological age increases, there is a decrease in the telomere length (TL). Associations between TL and age-related diseases have been described. Since the major pathophysiological factors related to inadequate sleep (including sleep complaints and sleep disorders) contribute to the exacerbation of inflammation and oxidative stress, an association of sleep and TL has been proposed. The aim of this study was to evaluate the association between sleep-related variables with TL in a longitudinal framework. We used data derived from the EPISONO cohort, which was followed over 8 years. All individuals answered sleep-related questionnaires, underwent a full-night polysomnography (PSG), and had their blood collected for DNA extraction. The TL was measured through a quantitative real time polymerase chain reaction. Age, sex, body mass index (BMI), smoking, physical activity status, and the 10 principal components (ancestry estimate) were considered covariables. Of the 1042 individuals in the EPISONO cohort, 68.3% agreed to participate in the follow-up study (n = 712). Baseline SpO2 (ß = 0.008, p = 0.007), medium SpO2 (ß = 0.013, p = 0.013), and total sleep time <90% (ß = -0.122, p = 0.012) had an effect on TL from the follow-up. The 8 year TL attrition was inversely associated with total sleep time, sleep efficiency, sleep architecture variables, wake after sleep onset, arousal index, oxygen-related variables baseline, and the presence of obstructive sleep apnea (OSA). We conclude that individuals with worse sleep quality, alterations in sleep architecture, and OSA had greater TL attrition over the 8 years. Using a longitudinal approach, these findings confirm previous cross-sectional evidence linking sleep with accelerated biological ageing.

Long-term night-shift work is associated with accelerates brain aging and worsens N3 sleep in female nurses

BackgroundShift work disrupts circadian rhythms and alters sleep patterns, resulting in various health problems. To quantitatively assess the impact of shift work on brain health, we evaluated the brain age index (BAI) derived from sleep electroencephalography (EEG) results in night-shift workers and compared it with that in daytime workers. MethodsWe studied 45 female night shift nurses (mean age: 28.2 ± 3.3 years) and 44 female daytime workers (30.5 ± 4.7 years). Sleep EEG data were analyzed to calculate BAI. The BAI of night shift workers who were asleep during the daytime with those of daytime workers who were asleep at night were statistically compared to explore associations between BAI, duration of shift work, and sleep quality. ResultsNight-shift workers exhibited significantly higher BAI (2.14 ± 6.04 vs. 0 ± 5.35), suggesting accelerated brain aging and altered sleep architecture, including reduced delta and sigma wave frequency activity during non-rapid eye movement sleep than daytime workers. Furthermore, poor deep sleep quality, indicated by a higher percentage of N1, lower percentage of N3, and higher arousal index, was associated with increased BAI among shift workers. Additionally, a longer duration of night-shift work was correlated with increased BAI, particularly in older shift workers. ConclusionNight-shift work, especially over extended periods, may be associated with accelerated brain aging, as indicated by higher BAI and alterations in sleep architecture. Interventions are necessary to mitigate the health impacts of shift work. Further research on the long-term effects and potential strategies for sleep improvement and mitigating brain aging in shift workers is warranted.

Clinical and Polysomnographic Profile of Patients with Sleep Disordered Breathing in a Tertiary Care Hospital

Background: Obstructive Sleep Apnea (OSA) is a prevalent sleep disorder associated with various health complications, yet it often remains undiagnosed. Understanding its clinical and polysomnographic profiles is crucial for effective management. Objective: To investigate the clinical characteristics, including demographic factors and comorbidities, of patients diagnosed with Obstructive Sleep Apnea (OSA). To analyze the polysomnographic profiles of individuals with OSA, focusing on respiratory events, sleep architecture alterations, and cardio metabolic parameters, to provide insights into the severity and manifestations of the disorder. Methodology: Data were collected from patients who underwent Level 1 polysomnography at a Sleep Laboratory in Bangalore Medical College And Research Institute from January 2021 to September 2023. Clinical profiles and polysomnographic data were analyzed using IBM SPSS software. Results: The study included 112 patients with a median age of 52 years and a high median BMI of 33.29. Polysomnographic analysis revealed a mean AHI of 36.709, indicating severe OSA. Respiratory events during REM and NREM sleep showed variations in apnea and hypopnea occurrences. Cardio metabolic parameters indicated potential subclinical cardiac dysfunction and dyslipidemia. Conclusion: In conclusion, our study demonstrates a strong correlation between Obstructive Sleep Apnea (OSA) and cardiovascular health, characterized by respiratory disturbances and obesity. Notably, elevated Pulmonary Artery Systolic Pressure (PASP) highlights the potential risk of pulmonary hypertension in this population, warranting close monitoring and targeted therapies. The findings underscore the importance of multidisciplinary management approaches in addressing OSA and its associated health conditions to improve patient outcomes and quality of life.

Polysomnographic Characteristics of Sleep Architecture in Children With Obstructive Sleep Apnea.

The conventional measure of sleep fragmentation is via polysomnographic evaluation of sleep architecture. Adults with OSA have disruption in their sleep cycles and spend less time in deep sleep stages. However, there is no available evidence to suggest that this is also true for children and published results have been inconclusive. To determine polysomnographic characteristics of sleep architecture in children with OSA and investigate effects relative to OSA severity. Overnight polysomnograms (PSG) of children referred for suspected OSA were reviewed. Subjects were classified by apnea hypopnea index (AHI). PSG parameters of sleep architecture were recorded and analyzed according to OSA severity. Two hundred and eleven children were studied (median age of 7.0 years, range 4-10 years) Stage N1 sleep was longer while stage N2 sleep and REM sleep was reduced in the OSA group when compared to those without OSA (6.10 vs 2.9, P < .001; 42.0 vs 49.7, P < .001; 14.0 vs 15.9, P = .05). The arousal index was also higher in the OSA group (12.9 vs 8.2, P < .001). There was a reduction in sleep efficiency and total sleep time and an increase in wake after sleep onset noted in the OSA group (83.90 vs 89.40, P = .003; 368.50 vs 387.25, P = .001; 40.1 ± 35.59 vs 28.66 ± 24.14, P = .007; 29.00 vs 20.50; P = .011). No significant difference was found in N3 sleep stage (33.60 vs 30.60, P = .14). We found evidence that children with OSA have a disturbance in their sleep architecture. The changes indicate greater sleep fragmentation and more time spent in lighter stages of sleep. Future research is needed and should focus on more effective methods to measure alterations in sleep architecture.

Структурная организация сна у пациентов в раннем восстановительном периоде ишемического и геморрагического инсульта

Aim – to identify the differences in sleep architecture of patients in the early recovery period after ischemic and hemorrhagic stroke. Methods. The study involved 143 patients in their early post-stroke recovery period, the patients’ average age was 59.6 ± 7.4 years. Among subjects there were 69 males (48.2%) and 74 females (51.8%). A total of 62% (89 patients) had ischemic lesions, 38% (54 patients) had hemorrhagic lesions. Patients with insomnia were identified based on the results of preliminary questionnaire survey involving the use of the screening assessment scale of subjective sleep characteristics. Objective assessment of the night sleep architecture features was performed by polysomnography. Results. Comparative assessment of sleep architecture showed that the majority of surveyed patients had a combination of phenomenological sleep disorder types, however, predominance of presomnic disorders was reported in patients after ischemic stroke, while patients after hemorrhagic stroke showed predominance of intrasomnic disorders. The sleep stage duration alterations (larger share of superficial sleep and smaller share of deep sleep) were typical for both types of cerebrovascular disease, they were slightly more prominent in patients after ischemic stroke, which could be due to the brain tissue necrosis, cystic-gliotic changes in the affected area. Conclusions. The differences in sleep architecture identified are consistent with the papers by domestic and foreign researchers on the impaired structure and lower effectiveness of sleep in post-stroke patients. To date, the cause of significant alterations of sleep architecture in patients after ischemic stroke is poorly understood and requires further research in this area.

Effects of Vortioxetine on Sleep Architecture of Adolescents with Major Depressive Disorder.

The relationship between depression and insomnia is bidirectional and both conditions need to be treated adequately, especially in a vulnerable neurodevelopmental stage of adolescence. This study aimed to evaluate the effects of antidepressant treatment using vortioxetine (VOR) on the sleep architecture of depressed adolescents by using video-polysomnography (v-PSG), which has not been researched before. The v-PSG was performed on 30 adolescent in-patients (mean age of 15.0 years ± 1.5 SD, 21 girls) treated with VOR (dosage of 10/15/20 mg/day) administered orally once a day, before and after VOR treatment. The evaluated parameters were conventional sleep parameters, sleep fragmentation parameters, and selected spectral power indices. Symptoms of depression and insomnia before and after the treatment period were evaluated using valid and reliable questionnaires (the Children´s Depression Inventory and the Athens Insomnia Scale). Depressed adolescents showed higher REM latency and decreased REM sleep percentage after treatment than before the treatment period (p = 0.005, p = 0.009, respectively). Our study revealed REM suppression (increased REM latency and reduced REM sleep percentage), indicating altered sleep architecture as a potential result of VOR treatment, which seems to be dose-dependent.

FRI636 Sleep Architecture In Diabetic Patients With Sleep Apnea On Metformin

Abstract Disclosure: M. Varma: None. M. Eghbali: None. D. Hung: None. A. Sahai: None. Background: Metformin, commonly used medication to treat Type II Diabetes Mellitus (DM) improves insulin sensitivity, reduces glucose production in liver and absorption by intestines. Type II DM patients often have higher BMI with increased incidence of sleep apnea. Metformin consuming patients sometimes report insomnia. Blood glucose levels affect sleep duration; therefore Metformin-related changes in blood glucose levels may affect sleep. Metformin prescriptions grew from 40 million in 2004 to 90 million in 2020. This has improved long term vascular complications outcomes in diabetics. Coincidentally the number of patients using sleeping aids has increased. Melatonin sales have doubled since 2004, approximating 821 million USD in sales in 2020. With diabetes and Metformin each causing significant changes in sleep, we aimed to examine sleep architecture in known diabetic patients on Metformin presenting with excessive daytime sleepiness and fatigue. Hypothesis: We hypothesize that Metformin affects sleep and influences sleep architecture in diabetic patients. Methods: Sleep architecture in 29 Type II DM patients taking Metformin, with symptoms of excessive daytime sleepiness, snoring, and fatigue was examined. Patients underwent overnight polysomnography which included six channel EEG, Electrooculogram, Electromyogram EKG, and pulse oximetry, respiratory and flow monitoring in a sleep lab. Sleep staging done using AASM guidelines. Data on age, gender, BMI, medications and sleep stages N1, N2, N3 and REM was collected. Data analyzed and shown as mean + SD, t test p&amp;lt;0.05 significant. Results: All patients had OSA diagnoses per AASM guidelines. The average age of patients with DM and OSA on Metformin therapy was 63 years, average BMI was 36. AASM stage distribution was N1 2.69 % + 0.02, N2 59.31% + 0.15, N3 12.22 % + 0.09, (Normal 25%) with 5.71% +0.06 REM sleep (normal 25%). All stages of sleep were reduced with significant reduction in deep sleep (N3) and REM sleep. Conclusion: Diabetic patients on Metformin had alterations in sleep architecture with significantly reduced restorative phases of deep and REM sleep. Sleep apnea reduces N3 and REM sleep, but diabetic pts had a more significant decrease. Although Metformin improves long term outcomes in diabetes associated complications, it alters sleep patterns. Altered sleep patterns further modify insulin release and over prolonged periods worsen glycemic control. Often patients on Metformin need additional medication like insulin for metabolic control. In part the progression of insulin resistance can be from altered sleep. Better understanding the effects of Metformin on sleep is needed to prevent long-term deteriorating effects on sleep while maintaining effective metabolic control. Presentation: Friday, June 16, 2023

Melatonin-related dysfunction in chronic restraint stress triggers sleep disorders in mice.

Stress may trigger sleep disorders and are also risk factors for depression. The study explored the melatonin-related mechanisms of stress-associated sleep disorders on a mouse model of chronic stress by exploring the alteration in sleep architecture, melatonin, and related small molecule levels, transcription and expression of melatonin-related genes as well as proteins. Mice undergoing chronic restraint stress modeling for 28days showed body weight loss and reduced locomotor activity. Sleep fragmentation, circadian rhythm disorders, and insomnia exhibited in CRS-treated mice formed sleep disorders. Tryptophan and 5-hydroxytryptamine levels were increased in the hypothalamus, while melatonin level was decreased. The transcription and expression of melatonin receptors were reduced, and circadian rhythm related genes were altered. Expression of downstream effectors to melatonin receptors was also affected. These results identified sleep disorders in a mice model of chronic stress. The alteration of melatonin-related pathways was shown to trigger sleep disorders.

Functional recovery after ischemic stroke: Impact of different sleep health parameters.

Sleep disturbances after ischaemic stroke include alterations of sleep architecture, obstructive sleep apnea, restless legs syndrome, daytime sleepiness and insomnia. Our aim was to explore their impacts on functional outcomes at month 3 after stroke, and to assess the benefit of continuous positive airway pressure in patients with severe obstructive sleep apnea. Ninety patients with supra-tentorial ischaemic stroke underwent clinical screening for sleep disorders and polysomnography at day 15 ± 4 after stroke in a multisite study. Patients with severe obstructive apnea (apnea-hypopnea index ≥ 30 per hr) were randomized into two groups: continuous positive airway pressure-treated and sham (1:1 ratio). Functional independence was assessed with the Barthel Index at month 3 after stroke in function of apnea-hypopnea index severity and treatment group. Secondary objectives were disability (modified Rankin score) and National Institute of Health Stroke Scale according to apnea-hypopnea index. Sixty-one patients (71.8 years, 42.6% men) completed the study: 51 (83.6%) had obstructive apnea (21.3% severe apnea), 10 (16.7%) daytime sleepiness, 13 (24.1%) insomnia, 3 (5.7%) depression, and 20 (34.5%) restless legs syndrome. Barthel Index, modified Rankin score and Stroke Scale were similar at baseline and 3 months post-stroke in the different obstructive sleep apnea groups. Changes at 3 months in those three scores were similar in continuous positive airway pressure versus sham-continuous positive airway pressure patients. In patients with worse clinical outcomes at month 3, mean nocturnal oxygen saturation was lower whereas there was no association with apnea-hypopnea index. Poorer outcomes at 3 months were also associated with insomnia, restless legs syndrome, depressive symptoms, and decreased total sleep time and rapid eye movement sleep.

Alteration of sleep architecture in children with obstructive sleep apnea syndrome.

Alteration of sleep architecture in children with obstructive sleep apnea syndrome.

The relations of circulating agouti-related peptide and leptin with altered sleep architecture in patients with active Cushing's disease: a pilot study.

To evaluate sleep architecture of patients with Cushing's disease (CD) and to explore whether agouti-related peptide (AgRP) and/or leptin play a permissive role in sleep alterations in patients with active CD. We performed polysomnography on 26 patients with active CD and age 26 age- and sex-matched control subjects. Blood samples were obtained from all participants for the analyzes of AgRP and leptin. The laboratory and sleep-related parameters were compared. The groups were similar in age, gender, and body mass index. The CD group had reduced sleep efficiency (71.6 ± 12.1% vs. 78.8 ± 12.6%, p = 0.042) and increased wake after sleep onset (WASO%) (24.7 ± 13.1% vs. 17.4 ± 11.6%, p = 0.040) as compared to control group. Seventeen patients with CD (65.4%) and 18 control subjects (69.2%) had obstructive sleep apnea. Serum AgRP (13.2 ± 7.4pg/ml vs. 9 ± 3.1, p = 0.029), leptin (59.5 mcg/l, [IQR] 32.6-94.6 vs. 25.3 mcg/l, [IQR] 12.9-57.5, p = 0.007) were higher in CD group. AgRP and leptin correlated negatively with total sleep time, sleep efficiency, stage N2 sleep (%), and positively with WASO%. In multiple regression analyses, serum cortisol (ß = - 0.359, p = 0.042) and AgRP (ß = - 0.481, p = 0.01) were significant predictor of sleep efficiency. AgRP was also significant predictor of WASO% (ß = 0.452 and p < 0.05). Active CD carries an increased risk of impaired sleep efficiency and continuity which may worsen health-related quality of life. Elevated circulating AgRP and, to a lesser extent, leptin may be associated with decreased sleep efficiency and continuity in patients with CD. Patients with CD who have subjective sleep symptoms should be screened with polysomnography.

The relationship between cortisol and sleep architecture in perimenopausal and postmenopausal women

Objectives: Women report worse sleep quality during and after the menopausal transition than in premenopause, but null or minimal alterations in sleep architecture have been found. Concentrations of cortisol seem to increase temporally during perimenopause. However, the associations between cortisol and sleep architecture in women around the menopausal transition have not been examined in detail to date.

Sepsis-Induced Changes in Spectral Segregation and Kinetics of Hippocampal Oscillatory States in Rats.

Sepsis-associated encephalopathy (SAE) is a frequent severe complication of sepsis and the systemic inflammatory response syndrome, associated with high mortality and long-term neurologic consequences in surviving patients. One of the main clinical signs of SAE are discontinuous sleep periods that are fragmented by frequent awakenings. Although this brain state fragmentation strongly impacts the functionality of the nervous and other systems, its underlying network mechanisms are still poorly understood. In this work, we therefore aim to characterize the properties and dynamics of brain oscillatory states in response to SAE in an acute rat model of sepsis induced by high-dose lipopolysaccharide (LPS; 10 mg/kg). To focus on intrinsically generated brain state dynamics, we used a urethane model that spares oscillatory activity in rapid eye movement (REM)-like and nonrapid eye movement (NREM)-like sleep states. Intraperitoneal LPS injection led to a robust instability of both oscillatory states resulting in several folds more state transitions. We identified opposing shifts in low-frequency oscillations (1-9 Hz) in REM and NREM-like states under influence of LPS. This resulted in increased similarity between both states. Moreover, the state-space jitter in both states increased as well, pointing to higher within-state instability. The reduction of interstate spectral distances in 2-D state space, combined with increased within-state jitter might represent a key factor in changing the energy landscape of brain oscillatory state attractors, and hence lead to altered sleep architecture. Their emergence during sepsis might point to a mechanism underlying severe sleep fragmentation as described both in sepsis patients and SAE animal models.

Effects of emerging alcohol use on developmental trajectories of functional sleep measures in adolescents.

Adolescence is characterized by significant brain development, accompanied by changes in sleep timing and architecture. It also is a period of profound psychosocial changes, including the initiation of alcohol use; however, it is unknown how alcohol use affects sleep architecture in the context of adolescent development. We tracked developmental changes in polysomnographic (PSG) and electroencephalographic (EEG) sleep measures and their relationship with emergent alcohol use in adolescents considering confounding effects (e.g. cannabis use). Adolescents (n = 94, 43% female, age: 12-21 years) in the National Consortium on Alcohol and Neurodevelopment in Adolescence (NCANDA) study had annual laboratory PSG recordings across 4-years. Participants were no/low drinkers at baseline. Linear mixed effect models showed developmental changes in sleep macrostructure and EEG, including a decrease in slow wave sleep and slow wave (delta) EEG activity with advancing age. Emergent moderate/heavy alcohol use across three follow-up years was associated with a decline in percentage rapid eye movement (REM) sleep over time, a longer sleep onset latency (SOL) and shorter total sleep time (TST) in older adolescents, and lower non-REM delta and theta power in males. These longitudinal data show substantial developmental changes in sleep architecture. Emergent alcohol use during this period was associated with altered sleep continuity, architecture, and EEG measures, with some effects dependent on age and sex. These effects, in part, could be attributed to the effects of alcohol on underlying brain maturation processes involved in sleep-wake regulation.

Distinct Sleep Alterations in Alcohol Use Disorder Patients with and without Korsakoff's Syndrome: Relationship with Episodic Memory.

Alcohol Use Disorder (AUD) results in sleep disturbances that may have deleterious impacts on cognition, especially on memory. However, little is known about the sleep architecture in patients with Korsakoff's syndrome (KS). This study aims at characterizing sleep disturbances in KS compared to AUD without KS and at specifying the relationships with cognitive impairments. Twenty-nine AUD patients (22 without KS and 7 with KS) and 15 healthy controls underwent a neuropsychological assessment and a polysomnography. The severity of sleep-disordered breathing and sleep fragmentation was similar in AUD and KS patients compared to controls. Sleep architecture differed between both patient groups: the proportion of slow-wave sleep was reduced in AUD patients only, while a lower proportion of rapid-eye movement (REM) sleep was specifically observed in KS patients. The proportion of REM sleep correlated with the severity of episodic memory deficits when AUD and KS were examined together. These data provide evidence for both similarities and specificities regarding sleep alterations in AUD patients with and without KS. They also indicate that altered sleep architecture may contribute to the pathophysiology of alcohol-related memory disorders.

Correlations between sleep architecture and sleep-related masseter muscle activity in children with sleep bruxism.

Sleep bruxism (SB) occurring during No-REM (nREM) sleep and increase in microarousals per hour have been described in adults, but not in children. To assess the correlation between sleep architecture and masseter muscle activity related to sleep bruxism (SB/MMA) in children. Forty-three children aged 7-12 years (mean age: 9.4 ± 1.3) with confirmed SB underwent a two-night polysomnographic (PSG) study in a sleep laboratory, for accommodation (first night) and data collection (second night). Data on sleep architecture (total sleep duration (TSD), sleep efficiency (SE), sleep onset latency (SOL), REM and nREM sleep duration and proportion and microarousals/hour during REM and nREM sleep) and episodes/hour of SB/MMA were recorded. Single and multiple-variable linear regression analyses were performed to assess the correlation between data on sleep architecture (predictors) and SB/MMA (dependent variable). Shorter TSD, REM and nREM stage 1 sleep duration,longerSOLand more microarousals/hour during REM and nREM sleep were found to be positive predictors of SB/MMA in children in the multiple-variable regression analysis (R2 =0.511). Within the limitations of this study, it can be concluded that SB/MMA is correlated with altered sleep architecture in children (shorter total sleep duration (TSD), shorter nREM and REM sleep and higher microarousals during REM and nREM sleep). Nevertheless, the clinical significance of these findings need to be demonstrated in future studies.

Sleep EEG in young people with 22q11.2 deletion syndrome: A cross-sectional study of slow-waves, spindles and correlations with memory and neurodevelopmental symptoms.

Young people living with 22q11.2 Deletion Syndrome (22q11.2DS) are at increased risk of schizophrenia, intellectual disability, attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). 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 reflects convergent, early signatures of neural circuit disruption also evident in associated neurodevelopmental conditions. In a cross-sectional design, we recorded high-density sleep EEG in young people (6-20 years) with 22q11.2DS (n=28) and their unaffected siblings (n=17), quantifying 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. 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 sleep, deletion carriers showed broadband increases in EEG power with increased slow-wave and spindle amplitudes, increased spindle frequency and density, and stronger 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 genotype effects on anxiety, ADHD and ASD were partially mediated by sleep EEG measures. This study provides a detailed description of sleep neurophysiology in 22q11.2DS, highlighting alterations in EEG signatures of sleep which have been previously linked to neurodevelopment, some of which were associated with psychiatric symptoms. Sleep EEG features may therefore reflect delayed or compromised neurodevelopmental processes in 22q11.2DS, which could inform our understanding of the neurobiology of this condition and be biomarkers for neuropsychiatric disorders. This research was funded by a Lilly Innovation Fellowship Award (UB), the National Institute of Mental Health (NIMH 5UO1MH101724; MvdB), a Wellcome Trust Institutional Strategic Support Fund (ISSF) award (MvdB), the Waterloo Foundation (918-1234; MvdB), the Baily Thomas Charitable Fund (2315/1; MvdB), MRC grant Intellectual Disability and Mental Health: Assessing Genomic Impact on Neurodevelopment (IMAGINE) (MR/L011166/1; JH, MvdB and MO), MRC grant Intellectual Disability and Mental Health: Assessing Genomic Impact on Neurodevelopment 2 (IMAGINE-2) (MR/T033045/1; MvdB, JH and MO); Wellcome Trust Strategic Award 'Defining Endophenotypes From Integrated Neurosciences' Wellcome Trust (100202/Z/12/Z MO, JH). NAD was supported by a National Institute for Health Research Academic Clinical Fellowship in Mental Health and MWJ by a Wellcome Trust Senior Research Fellowship in Basic Biomedical Science (202810/Z/16/Z). CE and HAM were supported by Medical Research Council Doctoral Training Grants (C.B.E. 1644194, H.A.M MR/K501347/1). HMM and UB were employed by Eli Lilly & Co during the study; HMM is currently an employee of Boehringer Ingelheim Pharma GmbH & Co KG. The views and opinions expressed are those of the author(s), and not necessarily those of the NHS, the NIHR or the Department of Health funders.

Cognitive alterations in patients with alterations in sleep architecture in a court of Colombian patients

Cognitive alterations in patients with alterations in sleep architecture in a court of Colombian patients

Studying the Effect of Long COVID-19 Infection on Sleep Quality Using Wearable Health Devices: Observational Study.

BackgroundPatients with COVID-19 have increased sleep disturbances and decreased sleep quality during and after the infection. The current published literature focuses mainly on qualitative analyses based on surveys and subjective measurements rather than quantitative data.ObjectiveIn this paper, we assessed the long-term effects of COVID-19 through sleep patterns from continuous signals collected via wearable wristbands.MethodsPatients with a history of COVID-19 were compared to a control arm of individuals who never had COVID-19. Baseline demographics were collected for each subject. Linear correlations among the mean duration of each sleep phase and the mean daily biometrics were performed. The average duration for each subject’s total sleep time and sleep phases per night was calculated and compared between the 2 groups.ResultsThis study includes 122 patients with COVID-19 and 588 controls (N=710). Total sleep time was positively correlated with respiratory rate (RR) and oxygen saturation (SpO2). Increased awake sleep phase was correlated with increased heart rate, decreased RR, heart rate variability (HRV), and SpO2. Increased light sleep time was correlated with increased RR and SpO2 in the group with COVID-19. Deep sleep duration was correlated with decreased heart rate as well as increased RR and SpO2. When comparing different sleep phases, patients with long COVID-19 had decreased light sleep (244, SD 67 vs 258, SD 67; P=.003) and decreased deep sleep time (123, SD 66 vs 128, SD 58; P=.02).ConclusionsRegardless of the demographic background and symptom levels, patients with a history of COVID-19 infection demonstrated altered sleep architecture when compared to matched controls. The sleep of patients with COVID-19 was characterized by decreased total sleep and deep sleep.

Polysomnography Following Traumatic Brain Injury: A Systematic Review and Meta-Analysis

IntroductionSleep disturbances are common following traumatic brain injury (TBI) worsening morbidity and other neuropsychiatric symptoms. Post-TBI alterations in sleep architecture require further study.Objectives(1) To evaluate polysomnographic measures of sleep architecture in participants with history of TBI compared to controls and as meta-analyses of pooled means. (2) To evaluate effects of timing and severity of TBI on polysomnographic outcomes.MethodsPRISMA compliant systematic review was conducted of MEDLINE, PsycINFO, EMBASE and Scopus. Inclusion criteria: 1) reporting polysomnography in the context of TBI and 2) operationalizing TBI using clear/formalized criteria. Data were pooled in random-effects meta-analyses with outcomes expressed as mean differences (MD).ResultsIn participants with TBI, sleep was comprised of 19.39% REM sleep, 8.13% N1, 51.18% N2, and 17.53% N3, as determined by meta-analyses of single means. Total sleep time was reduced in chronic (&gt;6 months) TBI compared to acute-intermediate TBI (&lt;6 months) (p=0.01). Compared to controls, participants with TBI differed with increased N1 sleep (MD=0.64%; 95%CI=0.02,1.25; p=0.04), reduced sleep efficiency (MD=-1.65%; 95%CI=-3.18,-0.12; p=0.03), and reduced sleep latency on the multiple sleep latency test (MD=-5.90mins; 95%CI=-10.09,-1.72; p&lt;0.01). On sub-group analyses, participants with mild TBI differed from controls with reduced total sleep time (MD=-29.22mins, 95%CI=-54.16,-4.27; p=0.02). Similarly, participants with acute-intermediate TBI exhibited increased sleep latency compared to controls (MD=8.96mins; 95%CI=4.07,13.85; p&lt;0.01) and differed significantly from participants with chronic TBI (X2(1,N=608)=6.54; p=0.01).ConclusionsSleep architecture is altered following TBI with potential implications regarding functional outcomes and recovery. These alterations appear to differ based on severity of injury and time since injury.DisclosureNo significant relationships.