Differences In Sleep Architecture Research Articles

0986 Inter-Individual Differences in Sleep Architecture of Patients Receiving Methadone for Opioid Use Disorder

0986 Inter-Individual Differences in Sleep Architecture of Patients Receiving Methadone for Opioid Use Disorder

Gender differences in sleep architecture of diabetic patients on metformin with sleep apnea: an analysis of polysomnography studies

Gender differences in sleep architecture of diabetic patients on metformin with sleep apnea: an analysis of polysomnography studies

Inflammatory Markers and Sleep Architecture in Sleep Bruxism—A Case-Control Study

Background: Sleep bruxism (SB) is a common sleep-related movement behavior with a multifaceted etiology and a deficiently understood pathophysiology. A recent hypothesis suggests a link between SB and systemic inflammation. The scope of the study was to determine whether bruxers have altered sleep structure and different levels of inflammatory parameters compared to nonbruxers. Methods: A total of 83 adults underwent full-night polysomnography. The polysomnograms were evaluated using the American Academy of Sleep Medicine (AASM) guidelines. Then, the blood samples were obtained from the participants by venipuncture and the analyses were performed. The study group was divided based on bruxism episode index (BEI) into two groups: BEI ≤ 4 and BEI > 4. Results: In comparison with nonbruxers, the oxygen desaturation index (ODI) was significantly higher in severe bruxers (7.5 ± 11.08 vs. 3.33 ± 5.75, p < 0.005), as well as the arousal parameters (7.77 ± 4.68 vs. 4.03 ± 2.97, p < 0.001), and the mean oxygen desaturation (3.49 ± 0.69 vs. 3.01 ± 0.67, p < 0.05). Moreover, the differences in sleep architecture and deprivation of the deep sleep phase were observed, the non-REM sleep stage 3 was significantly shorter in severe bruxers (p < 0.03). Differences were also noted in non-REM sleep stage 1 and REM sleep phase. In the investigated group, there were no statistical differences in inflammatory cytokines levels between bruxers and nonbruxers. Conclusions: Sleep bruxism is associated with sleep structure alterations and may be associated with deep sleep phase deprivation. The inflammatory markers are not linearly correlated with the severity of sleep bruxism expressed as BEI.

Sex Differences in Sleep Architecture After Traumatic Brain Injury: Potential Implications on Short-Term Episodic Memory and Recovery.

Sleep-wake disturbances (SWDs) are common after TBI and often extend into the chronic phase of recovery. Such disturbances in sleep can lead to deficits in executive functioning, attention, and memory consolidation, which may ultimately impact the recovery process. We examined whether SWDs post-TBI were associated with morbidity during the post-acute period. Particular attention was placed on the impact of sleep architecture on learning and memory. Because women are more likely to report SWDs, we examined sex as a biological variable. We also examined subjective quality of life, depression, and disability levels. Data were retrospectively analyzed for 57 TBI patients who underwent an overnight polysomnography. Medical records were reviewed to determine cognitive and functional status during the period of the sleep evaluation. Consideration was given to medications, owing to the fact that a high number of these are likely to have secondary influences on sleep characteristics. Women showed higher levels of disability and reported more depression and lower quality of life. A sex-dependent disruption in sleep architecture was observed, with women having lower percent time in REM sleep. An association between percent time in REM and better episodic memory scores was found. Melatonin utilization had a positive impact on REM duration. Improvements in understanding the impact of sleep-wake disturbances on post-TBI outcome will aid in defining targeted interventions for this population. Findings from this study support the hypothesis that decreases in REM sleep may contribute to chronic disability and underlie the importance of considering sex differences when addressing sleep.

Sex differences in sleep architecture in a mouse model of Huntington's disease.

Sleep and circadian rhythm disturbances are common features of Huntington's disease (HD). HD is an autosomal dominant neurodegenerative disorder that affects men and women in equal numbers, but some epidemiological studies as well as preclinical work indicate there may be sex differences in disease presentation and progression. Since sex differences in HD could provide important insights to understand cellular and molecular mechanism(s), we used the bacterial artificial chromosome transgenic mouse model of HD (BACHD) to examine whether sex differences in sleep/wake cycles are detectable in an animal model of the disease. Electroencephalography/electromyography (EEG/EMG) was used to measure sleep/wake states and polysomnographic patterns in young adult (12-week-old) male and female wild-type and BACHD mice. Our findings show that male, but not female, BACHD mice exhibited increased variation in phases of the rhythms as compared to age- and sex-matched wild-types. For both rapid-eye movement (REM) and non-rapid eye movement (NREM) sleep, genotypic and sex differences were detected. In particular, the BACHD males spent less time in NREM sleep and exhibited a more fragmented sleep than the other groups. Finally, in response to 6 h of sleep deprivation, both genotypes and sexes displayed the predicted homeostatic responses to sleep loss. These findings suggest that females are relatively protected early in disease progression in this HD model.

EEG Power Spectral Density in NREM Sleep is Associated with the Degree of Hypoxia in Patients with Obstructive Sleep Apnea.

Obstructive sleep apnea (OSA) is a prevalent sleep-related breathing disorder. Research conducted on patients with OSA using electroencephalography (EEG) has revealed a noticeable shift in the overnight polysomnography (PSG) power spectrum. To better quantify the effects of OSA on brain function and to identify the most reliable predictors of pathological cortical activation, this study quantified the PSG power and its association with the degree of hypoxia in OSA patients. This retrospective study recruited 93 patients with OSA. OSA patients were divided into three groups based on their apnea-hypopnea index (AHI) scores. The clinical characteristics and sleep macrostructure of these patients were examined, followed by an analysis of PSG signals. Power spectral density (PSD) in five frequency bands was analyzed during nonrapid eye movement (NREM) sleep, rapid eye movement (REM) sleep, and wakefulness. Finally, correlation analysis was conducted to assess the relationships among PSD, PSG parameters, and serum levels of S100β and uric acid. Obstructive sleep apnea occurred during both the NREM and REM sleep phases. Except for a decrease in the duration of N2 sleep and an increase in the microarousal index, there were no significant differences in sleep architecture based on disease severity. Compared to the mild OSA group, the theta and alpha band PSD in the frontal and occipital regions during NREM sleep and wakefulness were significantly decreased in the moderate and severe OSA groups. Correlation analysis revealed that theta PSD in N1 and N3 stages were negatively correlated the AHI, oxygen desaturation index, SaO2<90% and microarousal index. These findings imply that patients with more severe OSA exhibited considerable NREM hypoxia and abnormal brain activity in the frontal and occipital regions. Therefore, sleep EEG oscillation may be a useful neurophysiological indicator for assessing brain function and disease severity in patients with OSA.

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.

Polysomnographic profile in children diagnosed with celiac disease before starting on a gluten free diet

Study aimsThe study assessed the presence of sleep abnormalities in children who had recently been diagnosed with celiac disease (CD) and not started a gluten free diet (GFD). The children's polysomnographic profiles were also characterized and further compared with healthy children of the same age. MethodsThis prospective cross-sectional study involved 46 pediatric subjects (aged 1–19 years) who had recently been diagnosed with CD and not started a GFD. The control group consisted of 32 healthy children (aged 2–17 years). All children underwent anthropometric measurement, laboratory testing and standard overnight observation with in-laboratory video-PSG. The study and control group were divided into subgroups according to the subjects’ median ages (8.1 years): celiac children aged less than 8.1 years (n = 23) and more than 8.1 years (n = 23), healthy children less aged than 8.1 years (n = 16) and more than 8.1 years (n = 16). ResultsNo significant differences in the basic demographic and anthropometric parameters between the celiac and control group were observed. Significantly prolonged sleep latency (SOL) was evident in the celiac subjects (21.89 ± 20.77 min. vs. 10.99 ± 7.94 min, p = 0.02), with a probability of prolonged SOL of 4.23-fold greater (OR = 4.23; 95 % CI 1.1–16.22) than the healthy controls, especially in the subgroup of older celiac patients. No significant differences in the sleep period time (SPT), total sleep time (TST), wake during sleep (WASO), sleep efficiency (SE) and sleep stage distribution and cyclization were found. The respiratory rates during sleep indicated a significantly greater incidence of the central apnea-hypopnea index (CAHI) (0.54 ± 0.78 vs. 0.18 ± 0.24, p = 0.03) with a 3.16-fold greater probability of pathological CAHI (OR = 3.16; 95 % CI 1.02–9.77) than the control group. An increased incidence of CSA in the subgroup of younger celiac patients compared to younger healthy controls was especially evident. ConclusionsThe findings of our study suggest a difference in sleep architecture and an increased incidence of CSA in children with untreated CD, but additional research is required to verify the results.

Comparing Sleep Patterns and Clinical Features between Preschool and School-Age Children with OSA.

This study aimed to evaluate sleep patterns and investigate differences in clinical features among young individuals with snoring and obstructive sleep apnea (OSA). Data from 213 children and adolescents who underwent polysomnography (PSG) for primary snoring or OSA were collected between July 2017 and December 2021. To analyze differences in sleep architecture, hypoxia levels, and other clinical features, the participants were divided into two age groups: a preschool group and a school-age group. The school-age group had significantly higher apnea-hypopnea index, obstructive apnea index, oxygen desaturation index, and body mass index than the preschool group. Both the lowest and average oxygen saturation levels were lower in the school-age group. Adenoid hypertrophy was more prevalent in the preschool group. The rate of overweight or obesity was 35.6% in the preschool group and even 94.2% in the school-age group. There were higher percentages of N1 and N2 sleep stages, and lower percentages of N3 and REM sleep stages in the school-age group. The groups exhibiting moderate to severe OSA demonstrated significant alterations in the difference between sleeping and waking diastolic blood pressure. There is a higher frequency of respiratory events among school-age children compared with their preschool peers. Moreover, alterations in sleep structure are more prominent in the school-age group. Adenoid hypertrophy may serve as the primary instigator of OSA in preschool children, whereas the predominant causes in school-age children may be obesity or excessive weight. Retrospective chart review, 3 Laryngoscope, 134:1472-1478, 2024.

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.

Altered sleep architecture in diabetes and prediabetes: findings from the Baependi Heart Study.

People with diabetes and prediabetes are more likely to have sleep-disordered breathing (SDB), but few studies examined sleep architecture in people with diabetes or prediabetes in the absence of moderate-severe SDB, which was the aim of our cross-sectional study. This cross-sectional sample is from the Baependi Heart Study, a family-based cohort of adults in Brazil. About 1074 participants underwent at-home polysomnography (PSG). Diabetes was defined as fasting glucose >125 mg/dL or HbA1c > 6.4 mmol/mol or taking diabetic medication, and prediabetes was defined as HbA1c ≥ 5.7 & <6.5 mmol/mol or fasting glucose ≥ 100 & ≤125 mg/dl. We excluded participants with an apnea-hypopnea index (AHI) ≥ 30 in primary analyses and ≥ 15 in secondary analysis. We compared sleep stages among the 3 diabetes groups (prediabetes, diabetes, neither). Compared to those without diabetes, we found shorter REM duration for participants with diabetes (-6.7 min, 95%CI -13.2, -0.1) and prediabetes (-5.9 min, 95%CI -10.5, -1.3), even after adjusting for age, gender, BMI, and AHI. Diabetes was also associated with lower total sleep time (-13.7 min, 95%CI -26.8, -0.6), longer slow-wave sleep (N3) duration (+7.6 min, 95%CI 0.6, 14.6) and higher N3 percentage (+2.4%, 95%CI 0.6, 4.2), compared to those without diabetes. Results were similar when restricting to AHI < 15. People with diabetes and prediabetes had less REM sleep than people without either condition. People with diabetes also had more N3 sleep. These results suggest that diabetes and prediabetes are associated with differences in sleep architecture, even in the absence of moderate-severe sleep apnea.

0796 Safety and efficacy of the combination of atomoxetine and oxybutynin for OSA treatment in children with Down Syndrome

Abstract Introduction Children with Down syndrome (DS) are at very high risk for obstructive sleep apnea (OSA), with a prevalence of OSA of 50-79%. Current OSA treatments for children with DS have limited effectiveness, as positive airway pressure therapy is poorly tolerated and adenotonsillectomy is not curative in most children with DS. The combination of atomoxetine and oxybutynin (ato-oxy) is a promising OSA treatment in adults. Ato-oxy has been shown to improve upper airway hypotonia, a key feature of OSA in children with DS, thus it may be particularly effective for OSA in children with DS. Methods We performed a randomized, double-blind, crossover pilot trial examining the short-term efficacy of ato-oxy in 15 children aged 6 to 17 years with DS and OSA. Participants received 4 weeks of low dose (0.5 mg/kg atomoxetine and 5 mg oxybutynin) as well as 4 weeks of high dose (1.2 mg/kg atomoxetine and 5 mg oxybutynin) in random order. Participants underwent polysomnography as well as parent-reported health-related quality of life assessment using the OSA-18 at baseline and at the end of each dosing period. The primary study endpoint was reduction in obstructive apnea-hypopnea index (oAHI) from baseline. Paired t-tests were used to compare baseline to low and high dose ato-oxy. Results 15 participants qualified for randomization and 11 participants had complete data at all points. Baseline oAHI was 7.4 ± 3.7 (mean ± standard deviation), oAHI with low dose ato-oxy was 3.6 ± 3.3 (p=0.001 vs baseline) and oAHI with high dose ato-oxy was 3.9 ± 2.8 (p=0.003 vs baseline). There were no differences in sleep architecture or sleep efficiency between baseline and either dose of ato-oxy. OSA-18 total score was 51.5 ± 18.5 at baseline; improved to 44.6 ± 17.0 (p=0.09) at the end of 4-weeks of low dose ato-oxy; and improved to 45.5 ± 15.7 (p=0.37) at the end of high-dose ato-oxy therapy. The most common adverse effects were irritability and fatigue, and these were generally mild. Conclusion Ato-oxy is a promising treatment for OSA in children with DS. Support (if any) Funding provided by NIH (HL151254 and HD109777) as well as the Lumind-IDSC foundation.

Sleep architecture is associated with core symptom severity in autism spectrum disorder: a few methodological observations.

Dear Editor, We have read the article by Kawai et al. [1] in your esteemed journal with great academic and clinical interest and found that it has enhanced the knowledge regarding sleep architecture in Autism spectrum disorder (ASD) and has attempted to throw light upon the differences in sleep architecture between ASD and typically developing controls. We would like to make a few observations about the current study. The cases for the study appear to have been recruited in a consecutive fashion from the Stanford Autism Clinic; however, the Inclusion and Exclusion criteria for the recruitment have not been explicitly mentioned. If the same had been done, it would have painted a clearer picture for the readers of the sample being analyzed. The study mentions that 22 cases out of the total of 53, were already on various medications, which included antidepressants, Selective Serotonin Reuptake Inhibitors, antipsychotics, antiepileptic medications, benzodiazepines, and stimulants. There is ample evidence pointing to the fact that such medications themselves have an independent influence on sleep architecture [2–4]. Hence, the results of this study might be ridden with confounders that would compromise the impact which autism would have had in isolation, on the sleep architecture in the present study.

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.

Developmental changes in obstructive sleep apnea and sleep architecture in Down syndrome.

Down syndrome (DS, also known as Trisomy 21) is a condition associated with abnormal neurodevelopment and a higher risk for sleep apnea. Our study sought to better understand and characterize the age-related developmental differences in sleep architecture and obstructive sleep apnea (OSA) severity in children with DS compared to euploid individuals. Retrospective review of polysomnograms in over 4151 infants, children, and adolescents in the pediatric sleep center at Children's National Hospital in Washington D.C. (0-18 years) including 218 individuals with DS. The primary findings of our study are that: (1) severe OSA (obstructive apnea-hypopnea index ≥ 10/h) was more prevalent in the DS group (euploid 18% vs. DS 34%, p < 0.001) with the highest OSA severity being present in young children (<3 years old) and adolescents (>10 years old), (2) abnormalities in sleep architecture in children with DS were characterized by a prolonged rapid-eye movement (REM) sleep onset latency (SOL) (euploid 119 min vs. DS 144 min, p < 0.001) and greater arousal indexes (euploid 10.7/h vs. DS 12.2/h, p < 0.001), (3) developmental changes in the amount of REM sleep or slow wave sleep were not different in DS individuals relative to euploid children, (4) multivariate analyses showed that OSA and REM sleep latency differences between DS and euploid individuals were still present after adjusting by age, biological sex, and body mass index. Severe OSA is highly prevalent in children with DS and follows an age-dependent "U" distribution with peaks in newborns/infants and children >10 years of age. Children with DS also have disturbances in sleep architecture characterized by a longer REM SOL and elevated arousal indexes. As sleep cycle generation and continuity play crucial roles in neuroplasticity and cognitive development, these findings offer clinically relevant insights to guide anticipatory guidance for infants, children, and adolescents with DS.

The first-night effect and the consistency of short sleep in insomnia disorder.

The nature and degree of objective sleep impairments in insomnia disorder remain unclear. This issue is complicated further by potential changes in sleep architecture on the first compared with subsequent nights in the laboratory. Evidence regarding differential first-night effects in people with insomnia disorder and controls is mixed. Here, we aimed to further characterize insomnia- and night-related differences in sleep architecture. A comprehensive set of 26 sleep variables was derived from two consecutive nights of polysomnography in 61 age-matched patients with insomnia and 61 good sleeper controls. People with insomnia expressed consistently poorer sleep than controls on several variables during both nights. While poorer sleep during the first night was observed in both groups, there were qualitative differences regarding the specific sleep variables expressing a first-night effect. Short sleep (total sleep time < 6 hr) was more likely during the first night and in insomnia, although approximately 40% of patients with insomnia presenting with short sleep on night 1 no longer met this criterion on night 2, which is important given the notion of short-sleeping insomnia as a robust subtype.

Long-term ear-EEG monitoring of sleep - A case study during shift work.

The interest in sleep as a potential clinical biomarker is growing, but the standard method of sleep assessment, polysomnography, is expensive, time consuming, and requires a lot of expert assistance for both set-up and interpretation. To make sleep analysis more available both in research and in the clinic, there is a need for a reliable wearable device for sleep staging. In this case study, we test ear-electroencephalography. A wearable, where electrodes are placed in the outer ear, as a platform for longitudinal at-home recording of sleep. We explore the usability of the ear-electroencephalography in a shift work case with alternating sleep conditions. We find the ear-electroencephalography platform to be reliable both in terms of showing substantial agreement to polysomnography after long-time use (with an overall agreement, using Cohen's kappa, of 0.72) and by being unobtrusive enough to wear during night shift conditions. We find that fractions of non-rapid eye movement sleep and transition probability between sleep stages show great potential as sleep metrics when exploring quantitative differences in sleep architecture between shifting sleep conditions. This study shows that the ear-electroencephalography platform holds great potential as a reliable wearable for quantifying sleep "in the wild", pushing this technology further towards clinical adaptation.

Contribution of obstructive sleep apnea to disrupted sleep in a large clinical cohort of patients with suspected obstructive sleep apnea.

The response of sleep depth to CPAP in patients with OSA is unpredictable. The odds-ratio-product (ORP) is a continuous index of sleep depth and wake propensity that distinguishes different sleep depths within sleep stages, and different levels of vigilance during stage wake. When expressed as fractions of time spent in different ORP deciles, nine distinctive patterns are found. Only three of these are associated with OSA. We sought to determine whether sleep depth improves on CPAP exclusively in patients with these three ORP patterns. ORP was measured during the diagnostic and therapeutic components of 576 split-night polysomnographic (PSG) studies. ORP architecture in the diagnostic section was classified into one of the nine possible ORP patterns and the changes in sleep architecture were determined on CPAP for each of these patterns. ORP architecture was similarly determined in the first half of 760 full-night diagnostic PSG studies and the changes in the second half were measured to control for differences in sleep architecture between the early and late portions of sleep time in the absence of CPAP. Frequency of the three ORP patterns increased progressively with the apnea-hypopnea index. Sleep depth improved significantly on CPAP only in the three ORP patterns associated with OSA. Changes in CPAP in the other six patterns, or in full diagnostic PSG studies, were insignificant or paradoxical. ORP architecture types can identify patients in whom OSA adversely affects sleep and whose sleep is expected to improve on CPAP therapy.

Variations in Sleep Architecture among Different Subtypes of Schizophrenia: A Cross-sectional Study

Introduction: Schizophrenia is a severe mental disorder characterised by positive symptoms such as delusions and hallucinations, as well as negative symptoms including anhedonia, asociality, avolition, and affective blunting. It may also be associated with cognitive deficits. Sleep disturbances are commonly encountered in schizophrenia, and there may be variations in sleep patterns among its different subtypes. These differences in sleep patterns could have prognostic implications for the various subtypes of schizophrenia. Effective management of sleep disturbances could contribute to the recovery and wellbeing of individuals diagnosed with schizophrenia. Aim: To compare the differences in sleep architecture between the various subtypes of schizophrenia and to compare them with socio-demographically matched healthy volunteers. Materials and Methods: A cross-sectional study was conducted at the Institute of Psychiatry-Centre of Excellence, Kolkata, West Bengal, India over a duration of one year (May 2016 to June 2017). The study included 60 medication-naïve patients diagnosed with schizophrenia according to International Classification of Diseases (ICD)-10 criteria, and a control group of 30 demographically matched healthy volunteers. All study participants were aged between 18 and 60 years and free from any co-morbid illnesses. Patients with schizophrenia were further classified into four groups based on the ICD-10 subtypes: paranoid, hebephrenic, catatonic, and undifferentiated. Overnight polysomnography was performed to assess sleep parameters, including total record time, total sleep time, sleep onset latency, Rapid Eye Movement (REM), sleep latency, sleep efficiency, durations of Total Non Rapid Eye Movement (NREM) Sleep, Total REM sleep, and the different phases of NREM sleep. Statistical analysis was performed using Statistical Package for the Social Sciences (SPSS) version 20.0. Analysis of Variance (ANOVA), Chi-square, and t-test were used as applicable, with a p-value &lt;0.05 considered statistically significant. Results: The results showed a decrease in sleep efficiency, total sleep time, and shorter duration of mean N1, N2, and N3 sleep in schizophrenia patients compared to the control group. There was a significant difference in N3 sleep duration, reduced duration of total NREM and REM sleep, reduced REM latency, increased sleep onset latency, and the number of awakenings during sleep in schizophrenia patients. Statistically significant differences (p-values &lt;0.05) were also noted in some sleep parameters among the various subtypes of schizophrenia. The paranoid subtype had the shortest REM latency, while the catatonic subtype had the longest. The hebephrenic subtype had the lowest percentage of REM sleep and sleep efficiency, while the catatonic subtype had the highest. The duration of Slow Wave Sleep (SWS) was lowest in the undifferentiated subtype and highest in the catatonic subtype. Conclusion: This study reveals significant differences in sleep patterns between patients with schizophrenia and the control group, as well as among the various subtypes of schizophrenia. These distinctions provide insight into the relationship between schizophrenia subtypes, sleep irregularities, and clinical consequences. Further investigation is necessary to explore differences in sleep architecture among the various subtypes of schizophrenia and yield clinically meaningful results.