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to prospectively assess sleep and sleep disorders during pregnancy and postpartum in a large cohort of women. multicenter prospective Life-ON study, recruiting consecutive pregnant women at a gestational age between 10 and 15 weeks, from the local gynecological departments. The study included home polysomnography performed between the 23rd and 25th week of pregnancy and sleep-related questionnaires at 9 points in time during pregnancy and 6 months postpartum. 439 pregnant women (mean age 33.7 ± 4.2 yrs) were enrolled. Poor quality of sleep was reported by 34% of women in the first trimester of pregnancy, by 46% of women in the third trimester, and by as many as 71% of women in the first month after delivery. A similar trend was seen for insomnia. Excessive daytime sleepiness peaked in the first trimester (30% of women), and decreased in the third trimester, to 22% of women. Prevalence of restless legs syndrome was 25%, with a peak in the third trimester of pregnancy. Polysomnographic data, available for 353 women, revealed that 24% of women slept less than 6 h, and 30.6% of women had a sleep efficiency below 80%. Sleep-disordered breathing (RDI≥5) had a prevalence of 4.2% and correlated positively with BMI. The Life-ON study provides the largest polysomnographic dataset coupled with longitudinal subjective assessments of sleep quality in pregnant women to date. Sleep disorders are highly frequent and distributed differently during pregnancy and postpartum. Routine assessment of sleep disturbances in the perinatal period is necessary to improve early detection and clinical management. • Sleep disorders are very frequent during pregnancy and puerperium. • Sleepiness peaks in the first trimester of pregnancy. • Insomnia and low sleep quality peak in the immediate post-partum period. • Multiparity is a risk factor for insomnia and low quality of sleep. • 25% of women reported restless legs syndrome during pregnancy. [ABSTRACT FROM AUTHOR]

INTRODUCTION: The clinical importance of obstructive sleep apnea (OPSA), which can be prevalent during rapid eye movement (REM) sleep, is unclear. This study aimed to explore possible differences between patients with REM-related OSA and non-REM-related OSA. METHODS: This retrospective study consisted of two groups of OSA patients, matched in age, gender and body mass index, who were examined at a Greek tertiary hospital; 147 patients with REM-related OSA were compared with 147 patients with non-REM-related OSA. RESULTS: Respiratory events occurred predominantly during REM sleep in REM-related OSA patients (p<0.001) and during non-rapid eye movement sleep (NREM) in the control group (p<0.001). The majority of REM-related OSA patients had mild OSA, while the majority of the control group had severe OSA. REM-related OSA patients had lower Arousal Index (p<0.001), lower Oxygen Desaturation Index (p<0.001), lower percent of recording time, spent at oxyhemoglobin saturation below 90% (p<0.001) and shorter mean event duration (p<0.001). The average SatO2% and the minimum SatO2% oxyhemoglobin saturation during sleep, were significantly higher, compared to the control group (p=0.002 and p=0.005, respectively). When comparing the anthropometric characteristics, the majority of the clinical features and the reported comorbidities, no significant differences were found between the two groups. However, REM-related OSA patients reported less frequently, excessive daytime sleepiness (p<0.001). Also, a positive correlation was found between reported insomnia and the minimum SatO2% in them. CONCLUSIONS: Our results show that REM-related OSA patients, despite their milder polysomnographic phenotype, they do not carry a lighter comorbidity load, when compared to non-REM-related OSA patients. [ABSTRACT FROM AUTHOR]

Background and objective: Existing research has confirmed the link between childhood trauma and poor sleep quality in adulthood. This study focused on the relationship between childhood trauma and hypersomnia specifically, which is understudied. Additionally, childhood maltreatment has been related to mentalizing deficits. The current study examined the role of mentalizing deficits as mediators between childhood trauma and hypersomnia. Method: The study sample of this cross‐sectional study consisted of 496 individuals, who participated in the online survey, which contained the following measures: Persian version of the Mini Sleep Questionnaire, Reflective Functioning Questionnaire (RFQ‐8), and Childhood Trauma Questionnaire (CTQ). Results: The results from structural equation modeling indicated that emotional abuse positively predicts hypersomnia. Mediation analysis confirmed that hypo‐mentalizing partially mediates the association between emotional abuse and hypersomnia. Conclusion: The present study provides primary evidence that experiencing emotional abuse during childhood is associated with hypersomnia in adulthood. This association underlines the importance of prevention. The result from mediation analysis suggests addressing mentalizing impairments in patients with hypersomnia and a history of emotional abuse may be helpful. [ABSTRACT FROM AUTHOR]

The study aimed to evaluate the mid-term effect of MDO in children with Robin sequence (RS). In this case series, 13 patients with RS who underwent MDO were followed up for more than 5 years. Data were collected using clinical history and physical examination. Polysomnography was performed and endoscopic evaluations of the airway was performed if patients still presented obstructive signs of upper airways and/or dysphagia. The patients' clinical signs improved in the mid-term after versus before MDO (inspiratory noise, 92,3% vs 30,8%; apnea, 84,6% vs 7,7%; cyanosis, 76,9% vs 0%; desaturations, 69,2% vs 0%; and suprasternal/intercostal retractions, 61,5% vs 0%; p < 0.05). Statistically significant improvement was noted in the following polysomnographic parameters evaluated in the pre and postoperative mid-term: apnea-hypopnea index, total sleep time and desaturation index (p < 0.05). Within the limitations of the study it seems that MDO is an effective surgical option for children with RS, not only in the short term as previously demonstrated, but also in the mid-term. [ABSTRACT FROM AUTHOR]

Background: Digital cognitive behavioral therapy for insomnia (dCBTi) is an effective intervention for treating insomnia. The findings regarding its efficacy compared to face-to-face cognitive behavioral therapy for insomnia are inconclusive but suggest that dCBTi might be inferior. The lack of human support and low treatment adherence are believed to be barriers to dCBTi achieving its optimal efficacy. However, there has yet to be a direct comparative trial of dCBTi with different types of coaching support. Objective: This study examines whether adding chatbot-based and human coaching would improve the treatment efficacy of, and adherence to, dCBTi. Methods: Overall, 129 participants (n=98, 76% women; age: mean 34.09, SD 12.05 y) whose scores on the Insomnia Severity Index [ISI] were greater than 9 were recruited. A randomized controlled comparative trial with 5 arms was conducted: dCBTi with chatbot-based coaching and therapist support (dCBTi-therapist), dCBTi with chatbot-based coaching and research assistant support, dCBTi with chatbot-based coaching only, dCBTi without any coaching, and digital sleep hygiene and self-monitoring control. Participants were blinded to the condition assignment and study hypotheses, and the outcomes were self-assessed using questionnaires administered on the web. The outcomes included measures of insomnia (the ISI and the Sleep Condition Indicator), mood disturbances, fatigue, daytime sleepiness, quality of life, dysfunctional beliefs about sleep, and sleep-related safety behaviors administered at baseline, after treatment, and at 4-week follow-up. Treatment adherence was measured by the completion of video sessions and sleep diaries. An intention-to-treat analysis was conducted. Results: Significant condition-by-time interaction effects showed that dCBTi recipients, regardless of having any coaching, had greater improvements in insomnia measured by the Sleep Condition Indicator (P=.003; d=0.45) but not the ISI (P=.86; d=-0.28), depressive symptoms (P<.001; d=-0.62), anxiety (P=.01; d=-0.40), fatigue (P=.02; d=-0.35), dysfunctional beliefs about sleep (P<.001; d=-0.53), and safety behaviors related to sleep (P=.001; d=-0.50) than those who received digital sleep hygiene and self-monitoring control. The addition of chatbot-based coaching and human support did not improve treatment efficacy. However, adding human support promoted greater reductions in fatigue (P=.03; d=-0.33) and sleep-related safety behaviors (P=.05; d=-0.30) than dCBTi with chatbot-based coaching only at 4-week follow-up. dCBTi-therapist had the highest video and diary completion rates compared to other conditions (video: 16/25, 60% in dCBTi-therapist vs <3/21, <25% in dCBTi without any coaching), indicating greater treatment adherence. Conclusions: Our findings support the efficacy of dCBTi in treating insomnia, reducing thoughts and behaviors that perpetuate insomnia, reducing mood disturbances and fatigue, and improving quality of life. Adding chatbot-based coaching and human support did not significantly improve the efficacy of dCBTi after treatment. However, adding human support had incremental benefits on reducing fatigue and behaviors that could perpetuate insomnia, and hence may improve long-term efficacy. [ABSTRACT FROM AUTHOR]

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Background/Aim: Restless legs syndrome (RLS) is a chronic neurological disease that impairs sleep quality, causes emotional stress and affects daily activities. While the association between disease severity and low iron and ferritin levels is known, the magnesium (Mg) results are contradictory. This study aimed to investigate the influence of low Mg and ferritin levels on the severity of the disease and sleep quality. Methods: A case-control study included 50 RLS patients aged 18-78 years and 50 healthy control patients. Mg and ferritin levels were measured, considering values below <1.8 mg/dL and 75 ng/mL as low. Both groups completed the International Restless Legs Syndrome Study Group score (IRLSSG score) to assess the severity of RLS, as well as the Pittsburgh Sleep Quality Index (PSQI) and the Epworth Sleepiness Scale (ESS) to evaluate subjective sleep quality. Results: The mean age of RLS patients and the control group was 47.06 (13.35) years and 43.30 (15.43) years, respectively (P=0.196). The RLS patients had an IRLSSG score of 25.16 (6.85). The PSQI total scores, subscale scores, and ESS scores of RLS patients were significantly higher than those of the control group. However, no significant difference was observed in the IRLSSG score, PSQI, and ESS scores based on Mg and ferritin levels. Sleep latency was found to be shorter in individuals with Mg deficiency. Conclusion: Sleep disorders are prevalent among RLS patients. No correlation was found between Mg and ferritin levels and disease severity or sleep disorders. Furthermore, Mg deficiency did not appear to exacerbate the IRLSSG score or sleep disorder scores. [ABSTRACT FROM AUTHOR]

The objectives of this study were: (1) to identify subjects with hyperprolactinemia in a clinical sample of patients; (2) to compare the neurologic, psychiatric, and sleep conditions found in patients subgrouped by excessive daytime sleepiness (EDS) and hyperprolactinemia; and (3) to identify patients with hyperprolactinemia and EDS not supported by the presence of any other neurologic, psychiatric, or sleep disorder, or substance/medication use. A retrospective chart review of inpatients was carried out in order to identify all patients in whom the prolactin (PRL) serum levels were determined. A total of 130 subjects were retrieved: 55 had increased levels of PRL, while the remaining 75 participants had normal PRL levels. EDS was reported by 32 (58.2%) participants with increased PRL and 34 (45.3%) with normal PRL. Obstructive sleep apnea or other sleep or neurologic/psychiatric conditions could explain EDS in all participants with normal PRL. Among subjects with increased PRL, eight had no other neurologic/psychiatric or sleep disorder (or drug) potentially causing EDS; these participants, at polysomnography, had time in bed, sleep period time, and total sleep time longer than those with EDS associated to another condition. These findings can be considered as a preliminary indication of a role of hyperprolactinemia in EDS and represent a basis for future controlled studies able to test this hypothesis in a reliable, objective, and methodologically more appropriate way.

Annelies Santschi,1,&ast; David R Schreier,1,&ast; Anneke Hertig-Godeschalk,1 Samuel EJ Knobel,1 Uli S Herrmann,1 Jelena Skorucak,2 Wolfgang J Schmitt,3 Johannes Mathis1,4 1Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland; 2University Children’s Hospital Zurich, Zurich, Switzerland; 3University Hospital of Psychiatry, University of Bern, Bern, Switzerland; 4Sleep Medicine, Neurozentrum Bern, Bern, Switzerland&ast;These authors contributed equally to this workCorrespondence: David R Schreier, Department of Neurology, Inselspital, Bern University Hospital, Freiburgstrasse 16, Bern, CH-3010, Switzerland, Tel +41 31 632 21 11, Email david.r.schreier@gmail.comPurpose: Differential diagnosis of central disorders of hypersomnolence remains challenging, particularly between idiopathic (IH) and nonorganic hypersomnia (NOH). We hypothesized that eyelid closure behavior in the maintenance of wakefulness test (MWT) could be a valuable biomarker.Patients and Methods: MWT recordings of patients with IH, NOH, narcolepsy-cataplexy (NC), and healthy sleep-deprived controls (H) were retrospectively analyzed (15 individuals per group). For each MWT trial, visual scoring of face videography for partial (50– 80%) and full eyelid closure (≥ 80%) was performed from “lights off” to the first microsleep episode (≥ 3 s).Results: In all groups, the frequency and cumulative duration of periods with partial and full eyelid closure gradually increased toward the first microsleep episode. On the group level, significant differences occurred for the latency to the first microsleep episode (IH 21 min (18– 33), NOH 23 min (17– 35), NC 11 min (7– 19), H 10 min (6– 25); p = 0.009), the ratio between partial and full eyelid closure duration (IH 2.2 (0.9– 3.1), NOH 0.5 (0– 1.2), NC 2.8 (1.1– 5), H 0.7 (0.4– 3.3); p = 0.004), and the difference between full and partial eyelid closure duration in the five minutes prior to the first microsleep episode (∆full – partial eyelid closure duration: IH − 16 s (− 35 to 28); NOH 46 s (9– 82); NC − 6 s (− 26 to 5); H 10 s (− 4 to 18); p = 0.007). IH and NOH significantly differed comparing the ratio between partial and full eyelid closure (p = 0.005) and the difference between ∆full – partial eyelid closure duration in the five minutes prior to the first microsleep episode (p = 0.006).Conclusion: In the MWT, eyelid closure behavior (∆full – partial) in the period prior to the first microsleep episode could be of value for discriminating NOH from other etiologies of excessive daytime sleepiness, particularly IH.Keywords: hypersomnia, hypersomnia associated with psychiatric disorders, excessive daytime sleepiness, vigilance test, central disorders of hypersomnolence, microsleep

Abstract Background and objective Existing research has confirmed the link between childhood trauma and poor sleep quality in adulthood. This study focused on the relationship between childhood trauma and hypersomnia specifically, which is understudied. Additionally, childhood maltreatment has been related to mentalizing deficits. The current study examined the role of mentalizing deficits as mediators between childhood trauma and hypersomnia. Method The study sample of this cross‐sectional study consisted of 496 individuals, who participated in the online survey, which contained the following measures: Persian version of the Mini Sleep Questionnaire, Reflective Functioning Questionnaire (RFQ‐8), and Childhood Trauma Questionnaire (CTQ). Results The results from structural equation modeling indicated that emotional abuse positively predicts hypersomnia. Mediation analysis confirmed that hypo‐mentalizing partially mediates the association between emotional abuse and hypersomnia. Conclusion The present study provides primary evidence that experiencing emotional abuse during childhood is associated with hypersomnia in adulthood. This association underlines the importance of prevention. The result from mediation analysis suggests addressing mentalizing impairments in patients with hypersomnia and a history of emotional abuse may be helpful.

Background: Excessive daytime sleepiness (EDS) is a frequent nonmotor symptoms of Parkinson's disease (PD), which seriously affects the quality of life of PD patients and exacerbates other nonmotor symptoms. Previous studies have used static analyses of these resting-state functional magnetic resonance imaging (rs-fMRI) data were measured under the assumption that the intrinsic fluctuations during MRI scans are stationary. However, dynamic functional network connectivity (dFNC) analysis captures time-varying connectivity over short time scales and may reveal complex functional tissues in the brain. Purpose: To identify dynamic functional connectivity characteristics in PD-EDS patients in order to explain the underlying neuropathological mechanisms. Methods: Based on rs-fMRI data from 16 PD patients with EDS and 41 PD patients without EDS, we applied the sliding window approach, k-means clustering and independent component analysis to estimate the inherent dynamic connectivity states associated with EDS in PD patients and investigated the differences between groups. Furthermore, to assess the correlations between the altered temporal properties and the Epworth sleepiness scale (ESS) scores. Results: We found four distinct functional connectivity states in PD patients. The patients in the PD-EDS group showed increased fractional time and mean dwell time in state IV, which was characterized by strong connectivity in the sensorimotor (SMN) and visual (VIS) networks, and reduced fractional time in state I, which was characterized by strong positive connectivity intranetwork of the default mode network (DMN) and VIS, while negative connectivity internetwork between the DMN and VIS. Moreover, the ESS scores were positively correlated with fraction time in state IV. Conclusion: Our results indicated that the strong connectivity within and between the SMN and VIS was characteristic of EDS in PD patients, which may be a potential marker of pathophysiological features related to EDS in PD patients. [ABSTRACT FROM AUTHOR]

Dim light melatonin onset (DLMO) is considered the most reliable marker of the circadian rhythm phase in humans. DLMO may moderately correlate with sleep onset and sleep offset time. There are no sufficient data about the correlations between DLMO and clinical scales assessing sleep quality and daytime symptoms of poor night sleep. The aim of the study was to determine the association between DLMO and basic sleep parameters from actigraphy and sleep diaries, as well as the association between DLMO and the following insomnia clinical scales: the Athens Insomnia Scale (AIS), Insomnia Severity Index (ISI), Epworth Sleepiness Scale (ESS), and chronotype questionnaires: Morningness–Eveningness Questionnaire (MEQ) and Composite Scale of Morningness (CSM). Participants of the study were healthy volunteers. Sleep parameters were measured by sleep diaries and actigraphy, and the following clinical scales: the AIS, ISI, and ESS, and chronotype questionnaires: MEQ and CSM. DLMO was calculated based on plasma melatonin concentration. The blood samples were collected hourly at five time points between 20:00 and 00:00 during the session in dim red light (<50 lux). Melatonin concertation was determined by LC-MS/MS. Twenty-one volunteers participated in the study. DLMO was calculated in 12 participants. There was a significant correlation between DLMO and ISI (r = 0.60, p = 0.038) and ESS (r = 0.61, p = 0.034). The correlation coefficient between the DLMO and the AIS was also high, however insignificant (r = 0.57, p = 0.054). There were no significant correlations between DLMO and chronotype scales MEQ and CSM. DLMO did not correlate with sleep onset and sleep offset; however, DLMO correlated with the Sleep Fragmentation Index (SFI) (r = 0.67, p = 0.017). DLMO is associated with poorer sleep maintenance, a stronger feeling of insomnia, and sleepiness during the day. Simultaneously, chronotype pattern and circadian rhythm parameters do not correlate with DLMO. Biological circadian rhythm does not reflect the real-life sleep–wake rhythm, indicating that the lifestyle is more often disconnected from the biological clock. [ABSTRACT FROM AUTHOR]

Background: Protein-rich element binding protein A (PURA) syndrome is a genetic neurodevelopmental disorder that results in profound neurodevelopmental delay and intellectual disability. Few cases of PURA syndrome have been recognized in neonatal life, partly due to heterogenous clinical presentation, low clinical suspicion, and symptom progression that results in a more thorough workup later in life. Case Presentation: We report the case of a newborn who presented with hypotonia, feeding difficulties, and respiratory distress within the first hours of birth. Neonatal screening, infectious workup, and imaging were unremarkable. Clinical exome sequencing revealed de-novo, a pathogenic variant in the PURA gene. The patient received comprehensive rehabilitative care and social support. At one-year follow-up, the patient continued to experience feeding difficulties and apneic events and demonstrated significant neurodevelopmental delay. Conclusion: This report documents the consideration and diagnosis of PURA syndrome in the neonatal period and describes the implications of early diagnosis on prompt symptomatic management and patient outcomes at 1-year follow-up. [ABSTRACT FROM AUTHOR]

Harriet Tubman, a hero of the abolitionist movement and early civil rights advocate, suffered a head injury in childhood and subsequently developed sleep attacks associated with visions that were extensively documented in historical accounts. Her contemporaries perceived these visions together with unpredictable and unavoidable urges to sleep as manifestations of her deep faith, rather than as symptoms of an illness. While religious perspectives remain crucial to understanding Tubman's sleep-related experiences, some may consider them insufficient in view of modern medical advances. We propose the parallel explanation that her sleep attacks, usually attributed to temporal lobe epilepsy, actually represent a hypersomnia that is most consistent with the modern diagnosis of post-traumatic narcolepsy. Using historical analysis as well as current understandings of sleep medicine, we aim to shed light on this under-recognized aspect of Tubman's life. In addition, this case study allows us to review the potential long-term effects of severe traumatic brain injuries; consider a differential for excessive daytime sleepiness and hypnagogic hallucinations; and familiarize readers with the pathophysiology, diagnosis, and treatment of narcolepsy. Whether her symptoms are viewed through the lens of the past or measured against current biomedical standards, Tubman demonstrated an inspiring ability to persevere despite intrusive sleep episodes and to realize her dreams for the betterment of others. [ABSTRACT FROM AUTHOR]

Introduction: Idiopathic/isolated rapid eye movement (REM) sleep behavior disorder (iRBD) is considered the prodromal stage of alpha‐synucleinopathies. Thus, iRBD patients are the ideal target for disease‐modifying therapy. The risk FActoRs PREdictive of phenoconversion in iRBD Italian STudy (FARPRESTO) is an ongoing Italian database aimed at identifying risk factors of phenoconversion, and eventually to ease clinical trial enrollment of well‐characterized subjects. Methods: Polysomnography‐confirmed iRBD patients were retrospectively and prospectively enrolled. Baseline harmonized clinical and nigrostriatal functioning data were collected at baseline. Nigrostriatal functioning was evaluated by dopamine transporter‐single‐photon emission computed tomography (DaT‐SPECT) and categorized with visual semi‐quantification. Longitudinal data were evaluated to assess phenoconversion. Cox regressions were applied to calculate hazard ratios. Results: 365 patients were enrolled, and 289 patients with follow‐up (age 67.7 ± 7.3 years, 237 males, mean follow‐up 40 ± 37 months) were included in this study. At follow‐up, 97 iRBD patients (33.6%) phenoconverted to an overt synucleinopathy. Older age, motor and cognitive impairment, constipation, urinary and sexual dysfunction, depression, and visual semi‐quantification of nigrostriatal functioning predicted phenoconversion. The remaining 268 patients are in follow‐up within the FARPRESTO project. Conclusions: Clinical data (older age, motor and cognitive impairment, constipation, urinary and sexual dysfunction, depression) predicted phenoconversion in this multicenter, longitudinal, observational study. A standardized visual approach for semi‐quantification of DaT‐SPECT is proposed as a practical risk factor for phenoconversion in iRBD patients. Of note, non‐converted and newly diagnosed iRBD patients, who represent a trial‐ready cohort for upcoming disease‐modification trials, are currently being enrolled and followed in the FARPRESTO study. New data are expected to allow better risk characterization. [ABSTRACT FROM AUTHOR]

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 <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 <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. [ABSTRACT FROM AUTHOR]

Objectives: Rapid eye movement (REM) sleep behavior disorder (RBD) is proposed as an early diagnostic marker in Parkinson's disease (PD). We investigated the frequency of RBD during the progression of PD in the advanced stages and identified potential risk factors for developing RBD earlier or later. Patients and Methods: We performed a retrospective analysis and determined the frequency of RBD in all PD in‐patients (Hoehn and Yahr stages ≥3) with motor fluctuations who had undergone video‐polysomnography (vPSG) for a sleep complaint or daytime sleepiness. To correct for selection bias, we analyzed the prevalence of RBD in PD patients from the DeNoPa cohort. PD patients with RBD were compared with PD without RBD. To identify potential risk factors, we performed multiple regression modeling. Results: A total of 504 PD patients had vPSG. 37 were excluded due to missing REM or artifacts during REM. RBD was present in 406/467 (86.9%) PD patients. PD + RBD patients were older than PDnonRBD (69 ± 7.7 vs. 64 ± 9.2 years, P < 0.01), were more likely to have postural instability [234 (59.1%) vs. 19 (33.9%), P < 0.01], and were treated more often with antidepressants (other than SSRIs) [141 (34.7%) vs. 7 (13%), P < 0.01]. Multiple regression modeling identified predictors of RBD with an AUC of 0.78. Conclusion: The prevalence of RBD in patients with advanced PD is high and increases with disease severity, motor deficits, postural instability, orthostatic symptoms, and age. This suggests RBD is a progression marker of PD in patients with sleep complaints. [ABSTRACT FROM AUTHOR]

This study examines the (dis)agreement between objective and subjective sleep and their prospective changes in a randomized controlled trial of bright light therapy (BLT) in patients with major depressive disorder (MDD) and eveningness. A total of 93 adults were randomized to receive either 30-min daily of 10,000 lux BLT or 50lux placebo dim red light therapy (DRL group) for a total of 5 weeks. Actigraphic data were collected at the baseline and during the last week of treatment. (Dis)Concordance of diary and actigraphic sleep parameters were assessed by partial correlations and Bland-Altman plots, and the associations between these discrepancies to depression severity was assessed by linear regression models. Changes of sleep parameters were assessed by linear mixed models. Significant correlations were found between subjective sleep timings and chronotype to actigraphic parameters. Discrepancies between diary- and actigraphic-measures were observed, and patients with more severe depressive symptoms were associated with a greater under-estimation of total sleep time (TST). A greater advance in the diary-based time to fall sleep and rise time were achieved in the BLT group as compared to the DRL group, while diary-based wake after sleep onset (WASO), TST and sleep efficiency (SE) comparably improved with time in both groups. There was no significant difference between the two groups in the actigraphic parameters after treatment. In this study, we found that depression severity influenced subjective report of sleep. BLT led to a greater advance in subjective sleep timings when compared to the placebo group. • In this study, subjective sleep timings and circadian preference strongly correlated with actigraphic timings. • Patients with more severe depressive symptoms were associated with a greater under-estimation of total sleep time. • Bright light therapy was superior in advancing the subjective sleep timing than placebo. [ABSTRACT FROM AUTHOR]

Excessive daytime sleepiness is common with obstructive sleep apnoea and can persist despite efforts to optimise primary airway therapy. The literature lacks recommendations regarding differential diagnosis and management of excessive daytime sleepiness in obstructive sleep apnoea. This study sought to develop expert consensus statements to bridge the gap between existing literature/guidelines and clinical practice. A panel of 10 international experts was convened to undertake a modified Delphi process. Statements were developed based on available evidence identified through a scoping literature review, and expert opinion. Consensus was achieved through 3 rounds of iterative, blinded survey voting and revision to statements until a predetermined level of agreement was met (≥80 % voting "strongly agree" or "agree with reservation"). Consensus was achieved for 32 final statements. The panel agreed excessive daytime sleepiness is a patient-reported symptom. The importance of subjective/objective evaluation of excessive daytime sleepiness in the initial evaluation and serial management of obstructive sleep apnoea was recognised. The differential diagnosis of residual excessive daytime sleepiness in obstructive sleep apnoea was discussed. Optimizing airway therapy (eg, troubleshooting issues affecting effectiveness) was addressed. The panel recognised occurrence of residual excessive daytime sleepiness in obstructive sleep apnoea despite optimal airway therapy and the need to evaluate patients for underlying causes. Excessive daytime sleepiness in patients with obstructive sleep apnoea is a public health issue requiring increased awareness, recognition, and attention. Implementation of these statements may improve patient care, long-term management, and clinical outcomes in patients with obstructive sleep apnoea. • Excessive daytime sleepiness (EDS) is common in obstructive sleep apnea (OSA). • EDS can persist despite optimal airway therapy; EDS is a public health burden. • Residual EDS should be addressed; no guidelines exist for managing EDS in OSA. • Comprehensive evaluation of EDS in the management of OSA may improve outcomes. • Pharmacotherapy may benefit some patients along with primary airway therapy. [ABSTRACT FROM AUTHOR]

Obstructive sleep apnea (OSA) is associated with atrial fibrillation (AF) in cardiac cohorts. Less is known regarding the magnitude of this association in a sleep clinic cohort with vs. without excessive daytime sleepiness (EDS). To explore the association of OSA severity with AF in a sleep clinic cohort stratified by EDS. All consecutive adults (n = 3814) admitted to the Skaraborg Hospital, Sweden between Jan 2005 and December 2011 were registered in a local database, and the follow-up ended in December 2018. OSA was defined as an apnea-hypopnea index (AHI) ≥5 events/h. Mild OSA was defined as AHI ≥5 & AHI<15 events/h; moderate OSA as AHI ≥15 & AHI<30 events/h; and severe OSA as AHI ≥30 events/h. EDS was defined as an Epworth Sleepiness Scale score ≥11. We conducted cross-sectional analyzes of the prevalent AF across the OSA severity categories and logistic regression analyzes stratified by EDS. In all, 202 patients (5.3%) had AF at baseline, 1.6% in no-OSA, 3.9% in mild OSA, 5.2% in moderate OSA, and 7.6% in severe OSA, respectively (p < 0.001). The stratified analyzes revealed that patients with severe OSA without EDS had an increased risk for prevalent AF (OR 2.54, 95% CI 1.05–6.16; p = 0.039) independent of the confounding factors. There was an independent dose-response relationship between OSA and prevalent AF among the non-sleepy phenotype in this sleep clinic cohort. Since adherence to OSA treatment is challenging in the absence of EDS, these patients may have increased risk for adverse cardiovascular outcomes. • OSA is associated with AF, which is confounded by common risk factors and congestive heart failure in cardiac cohorts. • Less is known regarding of this association in a sleep clinic cohort with vs. without excessive daytime sleepiness. • There was an independent linear relationship between OSA and AF among the non-sleepy in this large sleep clinic cohort. • OSA treatment is challenging in the absence of symptoms, so, these patients may have an increased risk for adverse outcomes. [ABSTRACT FROM AUTHOR]

This research targeted to understand the impact of clinical findings, non-motor symptoms, white matter hyperintensities (WMHs), and metabolic features on cognition in Parkinson's disease patients with mild cognitive impairment (PD-MCI). Sixty-one PD patients sundered into two groups: PD-MCI and normal cognition (PD-NC). We assessed cognition using Montreal Cognitive Assessment-TR (MoCA-TR) and Frontal Assessment Battery (FAB). We used the modified Hoehn&Yahr staging scale (mH&Y), Unified Parkinson's Disease Rating Scale (UPDRS), Freezing of Gait questionnaire, Beck Depression Inventory, Parkinson's disease sleep scale-2, Pittsburgh sleep quality index, Epworth sleepiness scale, and Non-motor symptoms questionnaire to evaluate all patients. We used the Fazekas scale to evaluate the WMHs and also investigated all laboratory parameters affecting cognitive functions. Duration of disease, UPDRS-Motor part, age, disease stage, and daytime sleepiness were dramatically higher in the PD-MCI group than in PD-NC (p < 0.05). WMHs and homocysteine were higher in the PD-MCI group than in the controls (p = 0.016 and p < 0.001, respectively). There was a negative correlation between cognition and duration of disease, age, disease stage, UPDRS-Motor scale, daytime drowsiness, WMHs and homocysteine levels. Homocysteine was negatively related to visuospatial/executive functions (r=-0.303, p = 0.021). WMHs were correlated with global cognition (p =.000 r =.-542), language (p =.001, r = -.434), and delayed recall (p =.011, r = -.332). Mild cognitive impairment is a widespread clinical situation of PD patients and often presents before the motor symptoms. Revealing curable causes that affect cognition before the development of PD-related dementia is crucial in controlling motor findings and reducing the burden of the caretakers. [ABSTRACT FROM AUTHOR]

Purpose: This study aimed to (1) evaluate in patients with multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) the presence of sleep disorders such as hypersomnia, fatigue, risk of apnea, and the presence of restless legs syndrome/Willis-Ekbom disease (RLS/WED); (2) evaluate quality of sleep in patients with MS and NMOSD; and (3) correlate them with clinical and imaging data. Methods: The study was cross-sectional and was carried out in the sector of demyelinating diseases of the neurology service of HUGV-UFAM, Manaus, Brazil, from January 2017 to December 2020. Results: Our sample consisted of 60 patients, 41 with MS and 19 with NMOSD. We found that patients with MS and NMOSD have poor sleep quality (65%) and hypersomnia (53% in MS; 47% in NMOSD), but low risk of apnea by STOP-BANG. The frequency of RLS/WE found was 14% in MS, and 5% in NMOSD. No correlation existed between sleep quality, number of relapses, and sleep quality for the Expanded Disability Status Scale (EDSS), i.e., fatigue/illness duration. Conclusion: Patients with MS and NMOSD have poor sleep quality, excessive sleepiness, and are at low risk for OSA, yet the frequency of RLS/WED is like that of the general population. There does not seem to be a significant difference between these sleep disorders in these demyelinating diseases of the CNS. [ABSTRACT FROM AUTHOR]

Objectives: Sleep disorders are a frequent health problem in older patients with diabetes mellitus (DM). There has been no study investigating the factors associated with excessive daytime sleepiness (EDS) in older diabetic patients. We aimed to investigate the prevalence and associated factors of EDS. Methods: We performed a retrospective cross-sectional study in older diabetic patients. The Epworth Sleepiness Scale score of ≥ 11 points indicated EDS. All patients underwent comprehensive geriatric assessment including demographic characteristics, blood pressures, comorbid diseases, cognitive and nutritional states, basic and instrumental daily living activity indexes, lower urinary tract symptoms, and laboratory values. Results: Of 227 patients, 73.1% were females, with a mean age of 78.8 ± 6.5. The prevalence of EDS was 19.8%. Patients with EDS were mostly males with dementia and used significantly more medication with more anticholinergic drug burden, falls, urge incontinence, and nocturia (p < 0.05). They had higher SARC-F and lower Barthel index, Lawton-Brodie, Tinetti, MMSE scores, and high-density lipoprotein than the patients without EDS (p < 0.05). After adjusting for age, sex, and dementia, all parameters that were significant in univariate analysis remained associated with EDS, except for falls, and MMSE scores. Conclusion: The EDS was found in one in five older diabetic patients. There was a significant relationship between EDS and drug use, anticholinergic drug burden, impaired excretory functions, sarcopenia, decreased functional capacity, falls, gait-balance disorder, and cognitive dysfunction. The recognization of EDS and the implementation of interventions may be helpful in the management of geriatric syndromes. [ABSTRACT FROM AUTHOR]

We present a case of an adult female diagnosed with Delayed Sleep-Wake Phase Disorder (DSWPD) and Optic Nerve Hypoplasia (ONH), with a confirmed delayed Dim Light Melatonin Onset (DLMO), who reports the inability to fall asleep at their desired bedtime and obtain adequate sleep nightly, despite the ability to have a full night's sleep when not required to be up at a specific time for societal requirements. The participant was enrolled in an 11-month Open-Label Extension (OLE) following the randomized portion of a clinical study and was successfully treated with tasimelteon. DSWPD symptoms were resolved, and their previously delayed sleep-wake cycle was advanced. Clinical trial registration: https://clinicaltrials.gov/ct2/show/NCT04652882, identifier NCT04652882. [ABSTRACT FROM AUTHOR]

Background: The progression of sleep disturbances remains unclear in patients with early multiple system atrophy (MSA). We aimed to explore the frequency, severity, and coexistence of 2-year longitudinal changes of sleep disturbances including REM sleep behavior disorder (RBD), excessive daytime sleepiness (EDS), and Parkinson's disease-related sleep problems (PD-SP) in early MSA. Methods: MSA patients with a disease duration < 3 years were enrolled to complete a 2-year follow-up visit. Sleep disturbances including RBD, EDS, and PD-SP were assessed using the RBD Screening Questionnaire, Epworth sleepiness scale, and PD sleep scale-2, respectively. Results: A total of 220 patients with MSA enrolled in the study and 90 patients completed the 2-year follow-up visit. The score of all three sleep disturbances significantly increased over the 2-year follow-up in MSA and MSA with the predominant parkinsonism group (all p < 0.05). The frequency of PD-SP (from 14.5 to 26.7%) and EDS (from 17.7 to 37.8%) was progressively increased (all p < 0.05) except for RBD (from 51.8 to 65.6%, p = 0.152) over the 2-year follow-up in MSA. The frequency of coexistence of two or three sleep disturbances also increased over time. The most common sleep disturbance was RBD, followed by EDS and PD-SP over the 2-year follow-up. Conclusions: The present study demonstrated that the frequency of different types of sleep disturbances progressively increased except for RBD and the coexistence of two or three sleep disturbances became more common over time in early MSA. Our study suggested that the assessment and management of sleep disturbances should begin early in MSA. [ABSTRACT FROM AUTHOR]

Background: Both lower urinary tract symptoms (LUTS) and excessive daytime sleepiness (EDS) could negatively impair the patients' quality of life, increasing the sensitivity to psychological distress that results in mental health disorders. The relationships of both urinary and respiratory domains with psychological distress in obstructive sleep apnea patients is still underestimated. Methods: This study was a post hoc analysis of a web-based Italian survey, which included 1998 participants. Three hierarchical multiple linear regression analyses with psychological distress as dependent variable were performed on the study of 1988 participants enrolled in the final analysis. Cohen's f2 was used for the assessment of the effect size. Results: From the hierarchical multiple linear regression analyses, it emerged that the final statistical model (including sociodemographic characteristics, comorbidities, perceived urinary function, and excessive daytime sleepiness) for all dimensions accounted for 16.7% of the variance in psychological distress, with a medium effect size (f2 = 0.15). Conclusions: People reported psychological distress was impaired by the presence of LUTS and EDS. Specifically, our study showed that higher levels of distress were scored especially in young women exhibiting urinary symptoms and with high values of daytime sleepiness. [ABSTRACT FROM AUTHOR]

Introduction: Cognitive decline is common in Parkinson's disease (PD). Calculating personalized risk of cognitive decline in PD would allow for appropriate counseling, early intervention with available treatments, and inclusion in diseasemodifying trials. Methods: Data were from the Parkinson's Progression Markers Initiative de novo cohort. Baseline scores were calculated for Lifestyle for Brain Health (LIBRA) and the Montreal Parkinson Risk of Dementia Scale (MoPaRDS) per prior literature and preliminary Parkinson's disease Risk Estimator for Decline In Cognition Tool (pPREDICT) by attributing a point for fourteen posited risk factors. Baseline and 5-year follow-up composite cognitive scores (CCSs) were calculated from a neuropsychological battery and used to define cognitive decliners (PD-decline) versus maintainers (PD-maintain). Results: The PD-decline group (n = 44) had higher LIBRA (6.76 ± 0.57, p < 0.05), MoPaRDS (2.45 ± 1.41, p < 0.05) and pPREDICT (4.52 ± 1.66, p < 0.05) scores compared to the PD-maintain group (n = 263; LIBRA 4.98 ± 0.20, MoPaRDS 1.68 ± 1.16, pPREDICT 3.38 ± 1.69). Area-under-the-curve (AUC) for LIBRA was 0.64 (95% confidence interval [CI], 0.55-0.73), MoPaRDS was 0.66 (95% CI, 0.58-0.75) and for pPREDICT was 0.68 (95% CI, 0.61-0.76). In linear regression analyses, LIBRA (p < 0.05), MoPaRDS (p < 0.05) and pPREDICT (p < 0.05) predicted change in CCS. Only age stratified by sex (p < 0.05) contributed significantly to the model for LIBRA. Age and presence of hallucinations (p < 0.05) contributed significantly to the model for MoPaRDS. Male sex, older age, excessive daytime sleepiness, and moderate-severe motor symptoms (all p < 0.05) contributed significantly to the model for pPREDICT. Conclusion: Although MoPaRDS is a PD-specific tool for predicting cognitive decline relying on only clinical features, it does not focus on potentially modifiable risk factors. LIBRA does focus on potentially modifiable risk factors and is associated with prediction of all-cause dementia in some populations, but pPREDICT potentially demonstrates improved performance in cognitive decline risk calculation in individuals with PD and may identify actionable risk factors. As pPREDICT incorporates multiple potentially modifiable risk factors that can be obtained easily in the clinical setting, it is a first step in developing an easily assessable tool for a personalized approach to reduce dementia risk in people with PD. [ABSTRACT FROM AUTHOR]

Background: Depression is associated with metabolic alterations including lipid dysregulation, whereby associations may vary across individual symptoms. Evaluating these associations using a network perspective yields a more complete insight than single outcome-single predictor models. Methods: We used data from the Netherlands Study of Depression and Anxiety (N = 2498) and leveraged networks capturing associations between 30 depressive symptoms (Inventory of Depressive Symptomatology) and 46 metabolites. Analyses involved 4 steps: creating a network with Mixed Graphical Models; calculating centrality measures; bootstrapping for stability testing; validating central, stable associations by extra covariate-adjustment; and validation using another data wave collected 6 years later. Results: The network yielded 28 symptom-metabolite associations. There were 15 highly-central variables (8 symptoms, 7 metabolites), and 3 stable links involving the symptoms Low energy (fatigue), and Hypersomnia. Specifically, fatigue showed consistent associations with higher mean diameter for VLDL particles and lower estimated degree of (fatty acid) unsaturation. These remained present after adjustment for lifestyle and health-related factors and using another data wave. Conclusions: The somatic symptoms Fatigue and Hypersomnia and cholesterol and fatty acid measures showed central, stable, and consistent relationships in our network. The present analyses showed how metabolic alterations are more consistently linked to specific symptom profiles. [ABSTRACT FROM AUTHOR]

Background: Sleep abnormalities have been reported in Charcot–Marie–Tooth disease (CMT), but data are scanty. We investigated their presence and correlation in a large CMT patients' series. Methods: Epworth Sleepiness Scale (ESS) and Pittsburgh Sleep Quality Index (PSQI) were administered to CMT patients of the Italian registry and controls. ESS score > 10 indicated abnormal daytime somnolence, PSQI score > 5 bad sleep quality. We analyzed correlation with disease severity and characteristics, Hospital Anxiety and Depression Scale (HADS), Modified Fatigue Impact Scale (MFIS), Body Mass Index, drug use. Results: ESS and PSQI questionnaires were filled by 257 and 253 CMT patients, respectively, and 58 controls. Median PSQI score was higher in CMT patients than controls (6 vs 4, p = 0.006), with no difference for ESS score. Abnormal somnolence and poor sleep quality occurred in 23% and 56% of patients; such patients had more frequently anxiety/depression, abnormal fatigue, and positive sensory symptoms than those with normal ESS/PSQI. Moreover, patients with PSQI score > 5 had more severe disease (median CMT Examination Score, CMTES, 8 vs 6, p = 0.006) and more frequent use of anxiolytic/antidepressant drugs (29% vs 7%, p < 0.001). Conclusions: Bad sleep quality and daytime sleepiness are frequent in CMT and correlated with anxiety, depression and fatigue, confirming that different components affect sleep. Sleep disorders, such as sleep apnea and restless leg syndrome, not specifically investigated here, are other factors known to impact on sleep quality and somnolence. CMT patients' management must include sleep behavior assessment and evaluation of its correlated factors, including general distress and fatigue. [ABSTRACT FROM AUTHOR]

Disrupted sleep and post-traumatic stress disorder (PTSD) are bi-directionally linked and have been found to mutually reinforce each other on a day-to-day basis. However, most of the previous research has focused on subjective measures of sleep only. Here, we investigated the temporal relationship between sleep and PTSD symptoms using both subjective (sleep diary) and objective measures of sleep (actigraphy). Forty-one non-treatment seeking, trauma exposed young adults (age M = 24.68, SD = 8.15) with a range of PTSD symptom severities (PTSS, 0–53 on PCL-5) were recruited. Participants completed two surveys per day over four weeks to measure day-time PTSD symptoms (i.e. PTSS and number of intrusions) and night-time sleep subjectively, while wearing an actigraphy watch to measure sleep objectively. Linear mixed models revealed that subjectively reported sleep disruptions were associated with elevated next-day PTSS and increasing number of intrusive memories both within and between participants. Similar results were found for daytime PTSD symptoms on night-time sleep. However, these associations were not found using objective sleep data. Exploratory moderator analyses including sex (male vs. female) found that these associations differed in strength between sexes but were generally in the same direction. These results were in line with our hypothesis with regards to the sleep diary (subjective sleep), but not actigraphy (objective sleep). Several factors which have implications on both PTSD and sleep, such as the COVID-19 pandemic and/ or sleep-state misperception, may be potential reasons behind those discrepancies. However, this study had limited power and needs to be replicated in larger samples. Nonetheless, these results add to the current literature about the bi-directional relationship between sleep and PTSD and have clinical implications for treatment strategies. Elevated day-time PTSD symptom severity (PTSS) and more frequent intrusive memories were generally associated with subjectively reported disruptions in sleep and vice versa, but not with objective measures of sleep. While longer subjective sleep duration predicted reductions in PTSS and shorter sleep onset latency predicted reduced numbers of intrusions the next day, reduced daytime PTSS was only associated with reductions in distress associated with nightmares during the following night. Exploratory analyses showed that sex (men vs. women) moderated the bi-directional relationships between night-time sleep and day-time PTSD symptoms with longer sleep onset latency and lower sleep efficiency being related to worse PTSD symptoms the next day in women, but was not associated with men. [ABSTRACT FROM AUTHOR]

Major depressive disorder (MDD) is associated with profound sleep architectural alterations including reduced slow wave activity, increased delta sleep ratio, REM sleep disinhibition, shortened REM onset latency, and increased REM density. Antidepressants, though mitigating depressive symptoms, often disrupt sleep patterns, highlighting the delicate balance between treatment benefits and sleep-related impacts. Comprehensive assessment and management of insomnia is pivotal due to its significant implications for effective clinical management and treatment outcomes in MDD. Nonpharmacological treatments, notably cognitive-behavioral therapy for insomnia (CBTi), and digital CBTi (dCBTi) should be considered. CBTi unravels maladaptive sleep beliefs and behaviors, yielding improvements in both insomnia and MDD symptoms. Digital CBTi platforms extend accessibility, offering potential relief to a broader demographic. Sedating antidepressants, nonbenzodiazepine hypnotics, and atypical antipsychotics address insomnia within MDD, with cautious consideration for side effects. A combination of pharmacotherapy with CBTi might yield augmented outcomes in patients with MDD and comorbid insomnia. Ketamine, electroconvulsive therapy (ECT), repetitive transcranial magnetic stimulation (rTMS), vagal nerve stimulation (VNS), and deep brain stimulation (DBS) explore novel dimensions in treating treatment-resistant depression, potentially influencing sleep disruptions. [Psychiatr Ann. 2023;53(11):502–507.] [ABSTRACT FROM AUTHOR]

Background: There is a high prevalence of sleep disorders in Japan, and they are a factor in a decreased quality of life. The main objective of this study was to clarify the background factors of sleep disorders that affect sleep duration, such as subjective symptoms and working hours. Methods: We performed a cross-sectional study on the Japanese national statistics data. Answers from a household questionnaire were used to analyze risk factors for decreases in sleep duration. The subjects were a total of 3972 men and women aged 40–59 years, the age group that forms the core of the working population. For the analysis, a univariate analysis (contingency table) between sleep duration (two groups: sleep duration ≥ 6 h and <6 h) and 42 subjective symptoms was carried out. A multivariate analysis (binomial logistic regression) was conducted using sleep duration and subjective health assessment as objective variables, and odds ratios (ORs) adjusted for sex, working hours, and other factors were obtained. Results: The univariate analysis by subjective symptom showed significant ORs for eight symptoms, including poor sleep quality (OR: 2.24), constipation (OR: 2.24), and dizziness (OR: 1.77). In the multivariate analysis, the model with sleep duration as the objective variable showed significantly adjusted ORs for four variables, including constipation (1.72) and poor sleep quality (1.66). The model with subjective health assessment as the objective variable showed significantly adjusted ORs for eight variables, including dizziness (4.18), while poor sleep quality (1.45) was not significant. Conclusions: The present results suggest the presence of subjective symptoms that may be inferred to be related to decreases in sleep duration. [ABSTRACT FROM AUTHOR]

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Background: The association between sleep-related disorders and inflammation has been demonstrated in previous studies. The systemic immune-inflammation index (SII) is a novel inflammatory index based on leukocytes, but its relationship with sleep-related disorder is unclear. We aimed to investigate the relationship between sleep-related disorder and SII in a nationally representative nonhospitalized sample. Methods: Data were obtained from the 2005–2008 National Health and Nutrition Examination Survey (NHANES). Exposure variables included self-reported sleep-related disorders, such as sleep duration, sleep problems, high risk of OSA, and daytime sleepiness. SII and other traditional markers of inflammation were considered as outcome variables, including platelet-to-lymphocyte ratio (PLR) and neutrophil-to-lymphocyte ratio (NLR). Multiple linear regression models were employed to examine the correlation between sleep-related disorders and inflammatory markers. Subgroup interactions were analyzed using likelihood ratio tests, and nonlinear relationships were explored by fitting restricted cubic splines. Results: A total of 8,505 participants were enrolled in this study. Overall, sleep-related disorders were found to have a stronger association with SII compared to the PLR and NLR. The results of multiple linear regression analysis revealed that participants who experienced sleep problems (β: 21.421; 95% CI 1.484, 41.358), had symptoms of OSA (β: 23.088; 95% CI 0.441, 45.735), and reported daytime sleepiness (β: 30.320; 95% CI 5.851, 54.789) exhibited a positive association with higher SII. For the analysis of other inflammatory markers, we only found that daytime sleepiness was associated with increased NLR levels (β: 0.081; 95% CI 0.002, 0.159). Conclusion: Sleep problems, symptoms of OSA, and daytime sleepiness were found to have a positive association with the SII in US adults. However, further prospective studies are necessary to establish whether there is a causal relationship between these factors. [ABSTRACT FROM AUTHOR]

The odds ratio product (ORP) is a continuous metric of sleep depth that ranges from 0 (very deep sleep) to 2. 5 (full wakefulness). Its advantage over the conventional method recommended by AASM is that it discloses different levels of stage wake (sleep propensity) and different sleep depths within the same sleep stage. As such, it can be used to identify differences in sleep depth between subjects, and in the same subjects under different circumstances, when differences are not discernible by conventional staging. It also identifies different sleep depths within stage rapid-eye-movement sleep, with possible implications to disorders during this stage. Epoch-by-epoch ORP can be displayed graphically across the night or as average values in conventional sleep stages. In addition, ORP can be reported as % of recording time in specific ORP ranges (e.g., deciles of the total ORP range) where it produces distinct distribution patterns (ORP-architecture) that have been associated with different clinical disorders and outcomes. These patterns offer unique research opportunities to identify different mechanisms and potential therapy for various sleep complaints and disorders. In this reviewI will discuss howORP ismeasured, its validation, differences fromdelta power, and the various phenotypes, and their postulated mechanisms, identified by ORP architecture and the opportunities for research to advance management of sleep-disordered breathing, insomnia and idiopathic hypersomnia. [ABSTRACT FROM AUTHOR]

Rationale: Sleep disturbances (insomnia and nightmare symptoms) are the most sensitive and persistent symptoms of pediatric post-traumatic stress disorder (PTSD). Untreated, these sleep disturbances (SD) associated with PTSD are predictive of PTSD persistence and increased psychiatric complications. The aim of this study was to evaluate sleep and circadian rhythms in children with PTSD under both laboratory and ecological conditions in comparison with a control population and to test for the first time the hypothesis that SD and circadian rhythms are positively correlated with PTSD severity and its comorbidities. Method: This prospective pilot study evaluated PTSD, SD (insomnia, nightmares), and sleep-wake rhythms in 11 children with PTSD (aged 3–18), compared with the age and sex-matched control groups. Assessment of PTSD and subjective and objective measures of sleep and sleep-wake rhythms (questionnaires, 24-h in-laboratory video-polysomnography, 15-day at-home actigraphy recording) were performed between 1 and 6 months after the traumatic event. Results: Children with PTSD had higher sleep fragmentation (increased wake-after-sleep onset, increased number of sleep stage changes) compared to controls, with a change in sleep microarchitecture (micro-arousal index at 14.8 versus 8.2, p = 0.039). Sleep fragmentation parameters correlated with PTSD symptomatology, insomnia, and post-traumatic nightmare severity. The within-group comparison revealed a better sleep architecture in the controlled (sleep laboratory) than in the ecological condition (at home) (total sleep time 586 versus 464 min, p = 0.018). Conclusions: Sleep and rhythm disturbances are strongly associated with PTSD in children. The assessment of SD in children with PTSD should be carried out systematically and preferentially under ecological conditions, and management of SD should integrate the environment (environmental design, psycho-education for the children and their parents) more fully into therapy focused on sleep and trauma. [ABSTRACT FROM AUTHOR]

Asthma and obstructive sleep apnea are highly prevalent conditions with a high cost burden. In addition to shared risk factors, existing data suggest a bidirectional relationship between asthma and OSA, where each condition can impact the other. Patients with asthma often complain of sleep fragmentation, nocturnal asthma symptoms, daytime sleepiness, and snoring. The prevalence of OSA increases with asthma severity, as evidenced by multiple large studies. Asthma may lower the threshold for arousal in OSA, resulting in the hypopnea with arousal phenotype. Epidemiologic studies in adults have shown that OSA is associated with worse asthma severity, increased frequency of exacerbation, and poor quality of life. The current literature assessing the relationship among OSA, asthma, and CPAP therapy is heavily dependent on observational studies. There is a need for randomized controlled trials to minimize the interference of confounding shared risk factors. [ABSTRACT FROM AUTHOR]

Background: Soluble amyloid-beta oligomers (Aβo) begin to accumulate in the human brain one to two decades before a clinical diagnosis of Alzheimer's disease (AD). The literature supports that soluble Aβo are implicated in synapse and neuronal losses in the brain regions such as the hippocampus. This region importantly contributes to explicit memory, the first type of memory affected in AD. During AD preclinical and prodromal stages, people are also experiencing wake/sleep alterations such as insomnia (e.g., difficulty initiating sleep, decreased sleep duration), excessive daytime sleepiness, and sleep schedule modifications. In addition, changes in electroencephalographic (EEG) activity during wake and sleep have been reported in AD patients and animal models. However, the specific contribution of Aβo to wake/sleep alterations is poorly understood and was investigated in the present study. Methods: Chronic hippocampal injections of soluble Aβo were conducted in male rats and combined with EEG recording to determine the progressive impact of Aβ pathology specifically on wake/sleep architecture and EEG activity. Bilateral injections were conducted for 6 consecutive days, and EEG acquisition was done before, during, and after Aβo injections. Immunohistochemistry was used to assess neuron numbers in the hippocampal dentate gyrus (DG). Results: Aβo injections did not affect the time spent in wakefulness, slow wave sleep (SWS), and paradoxical sleep but altered EEG activity during wake and SWS. More precisely, Aβo increased slow-wave activity (SWA; 0.5–5 Hz) and low-beta activity (16–20 Hz) during wake and decreased theta (5–9 Hz) and alpha (9–12 Hz) activities during SWS. Moreover, the theta activity/SWA ratio during wake and SWS was decreased by Aβo. These effects were significant only after 6 days of Aβo injections and were found with alterations in neuron counts in the DG. Conclusions: We found multiple modifications of the wake and SWS EEG following Aβo delivery to the hippocampus. These findings expose a specific EEG signature of Aβ pathology and can serve the development of non-invasive and cost-effective markers for the early diagnosis of AD or other amyloid-related diseases. [ABSTRACT FROM AUTHOR]

Objective: Obesity is one of the most important risk factors and also consequences of obstructive sleep apnea (OSA). Weight loss and positive airway pressure therapy are the main approaches in the treatment of OSA. In this study, it was aimed to evaluate the prevalence of OSA in obesity patients scheduled for bariatric surgery. Methods: In the University Hospital Obesity Center, 141 consecutive patients who were candidates for bariatric surgery in 2015 were clinically evaluated preoperatively for sleep-related respiratory disorders. Preoperative polysomnographic examination was recommended to all cases. Results: Of 141 bariatric surgery candidates with a mean age of 37±10 years, and 103 (73%) were female. The mean body mass index of the cases was 46.9±6.4 kg/m2. Among the major symptoms of OSA, snoring was present in 119 (84.4%), daytime sleepiness in 63 (44.7%) and witnessed apnea in 49 (34.8%) patients. OSA was detected because AHI>5/hour was found in 75.7% (84/111) of the patients who accepted the polysomnographic evaluation. 24.3% (27/111) of the cases who underwent polysomnography had non OSA, 29.7% (33/111) mild OSA, 17.1% (19/111) moderate OSA, and 28.8% (32 /111), severe OSA was detected. AHI was positively correlated with age (p=0.003), neck and waist diameter (p<0.001), and negatively correlated with percent of the forced vital capacity (p<0.001). In polysomnographic controls performed an average of 9 months after bariatric surgery, an average of 41.2% improvement in AHI was observed, compared to an average of 22.8% decrease in BMI. Conclusions: OSA prevalence was found to be very high in bariatric surgery candidates. It was thought that polysomnographic examination should be performed before bariatric surgery not only in symptomatic cases but also in all cases. Bariatric surgery can help improve OSA. [ABSTRACT FROM AUTHOR]

Kleine–Levin Syndrome is a rare neurological disorder with onset typically during adolescence that is characterized by recurrent episodes of hypersomnia, behavioral changes, and cognitive abnormalities, in the absence of structural changes in neuroimaging. As for many functional brain disorders, the exact disease mechanism in Kleine-Levin Syndrome is presently unknown, preventing the development of specific treatment approaches or protective measures. Here we review the pathophysiology and genetics of this functional brain disorder and then present a specific working hypothesis. A neurodevelopmental mechanism has been suspected based on associations with obstetric complications. Recent studies have focused on genetic factors whereby the first genome-wide association study (GWAS) in Kleine–Levin Syndrome has defined a linkage at the TRANK1 locus. A Gene x Environment interaction model involving obstetric complications was proposed based on concepts developed for other functional brain disorders. To stimulate future research, we here performed annotations of the genes under consideration for Kleine–Levin Syndrome in relation to factors expected to be associated with obstetric complications. Annotations used data-mining of gene/protein lists related to for hypoxia, ischemia, and vascular factors and targeted literature searches. Tentative links for TRANK1, four additional genes in the TRANK1 locus, and LMOD3-LMO2 are described. Protein interaction data for TRANK1 indicate links to CBX2, CBX4, and KDM3A, that in turn can be tied to hypoxia. Taken together, the neurological sleep disorder, Kleine-Levin Syndrome, shows genetic and mechanistic overlap with well analyzed brain disorders such as schizophrenia, autism spectrum disorder and ADHD in which polygenic predisposition interacts with external events during brain development, including obstetric complications. Gene x Environment interaction (G x E) model for the sleep disorder, Kleine-Levin Syndrome (KLS). This hypothesis-generating study proposes that perturbations during neurodevelopment affect the formation of neural circuits for sleep regulation in KLS. Thereby, genetic factors linked to KLS interact ("x") with obstetric complications as environmental factors. A subset of genes may mediate between the risk for KLS and hypoxia, ischemia, or vascular changes during obstetric complications. [ABSTRACT FROM AUTHOR]

This systematic review and meta-analysis aimed to assess the effectiveness of internet-delivered cognitive behavioral therapy for insomnia (ICBT-I) in the short and long term. We searched five electronic databases for studies published from June 2000 to May 2022. Our analysis included 27 studies with 8,728 participants, of which 4394 were in the experimental group and 4334 were in the control group. ICBT-I significantly improved the sleep scores of the experimental group by reducing the intensity of insomnia (ISI) (−4.32) in the post-intervention (I2 = 94%) (95% CI −6.15 to −2.48, p < 0.0001, g = 0.760) and follow-up phases (−2.92) (I2 = 95%) (95% CI −4.87 to −0.97, p < 0.0003, g = 0.622). This therapy also effectively improves short-term and long-term insomnia symptoms, including sleep onset latency, wake after sleep onset, night awakenings, sleep efficiency, and total sleep time. That holds the potential for extensive utilization across diverse populations suffering from insomnia, surpassing the limitations associated with conventional in-person therapeutic methods. [ABSTRACT FROM AUTHOR]

Objective: Major neurocognitive Disorder (NCD) is a largely heterogeneous condition with numerous etiological possibilities. Most diagnosed cases have unspecified origins. As such, Fahr's syndrome (FS) is a rare neurodegenerative condition that clinically presents with varying neurologic, neuropsychiatric, and movement disorder features. FS is characterized by bilateral basal ganglia calcifications secondary to other conditions (e.g., endocrine and metabolic disorders, infectious diseases). This case will expand upon the literature of rare and poly-etiological presentations of NCD. Method: A 75-year-old White male underwent neuropsychological evaluation due to concerns from his wife regarding sudden onset of diminished mood, anhedonia, hypersomnia, disinhibition, and idiosyncratic motor movements two years prior which worsened after contracting COVID-19. Patient has multiple co-morbid medical conditions including hypothyroidism, hypercholesterolemia, intermediate hyperglycemia, prostate cancer (in remission), and history of a syncopal episode. Neuroimaging was remarkable for bilateral basal ganglia calcifications and white matter lesions. Results: At the exam, patient exhibited hypomimia, ataxic gait, alogia, sporadic motor stereotypies, and motor overflow. Overall performance on the Meyers Neuropsychological Battery was Below Average with relative weaknesses in attention, memory, processing speed, mental flexibility, and motor functioning. Patient was diagnosed with Major NCD of unspecified etiology and instructed to continue consultation with neurology. Conclusions: This patient's cognitive difficulties appeared poly-etiological and are likely attributed to the combination of basal ganglia calcification, white matter changes, hypothyroidism, and COVID-19 which suggests the presence of FS. This case exemplifies the importance of considering multiple etiologies, including the implications of COVID-19 during the diagnostic process as more neurologic symptoms of COVID-19 are still being discovered. [ABSTRACT FROM AUTHOR]

Sleep behaviors are potentially modifiable risk factors for common mental disorders and cardiovascular disease (CVD). However, the associations between combined sleep behaviors and common mental disorders among individuals with CVD remain unclear. A total of 18,776 participants with a history of CVD from UK Biobank, who were free of depression or anxiety from 2006 to 2010 were included. A composite healthy sleep score was constructed based on five sleep behaviors (chronotype, sleep duration, insomnia, snoring, and excessive daytime sleepiness). Cox proportional hazard regression models were performed to calculate hazard ratios (HRs) and 95 % confidence intervals (CIs) for incident depression and anxiety. During a median follow-up of 11.8 years, 965 depression and 812 anxiety cases were recorded. The adjusted HRs for participants with a healthy sleep pattern compared with a poor sleep pattern were 0.45 (95 % CI: 0.35–0.57) for depression and 0.77 (95 % CI: 0.58–1.03) for anxiety. There was a linear dose-response association of healthy sleep score with incident depression and anxiety (HR = 0.82, 95 % CI: 0.77–0.87; HR = 0.92, 95 % CI: 0.86–0.99 per 1-score increase, respectively). Likewise, these associations were observed among individuals with coronary heart disease, stroke, heart failure and atrial fibrillation. A healthy sleep pattern is significantly associated with a lower risk of depression among individuals with CVD, highlighting the importance of monitoring and improving sleep health in the prevention of common mental disorders among individuals with CVD. • The adjusted HRs for healthy sleepers versus poor sleepers were 0.45 (95% CI: 0.35-0.57) for depression. • A higher sleep score is associated with a lower risk of depression and anxiety, with a linear dose-response relationship. • Monitoring and improving sleep health is crucial in preventing common mental disorders among CVD patients. [ABSTRACT FROM AUTHOR]

Myotonic dystrophy type 1 is a dominantly inherited multisystemic disease caused by CTG tandem repeat expansions in the DMPK 3′ untranslated region. These expanded repeats are transcribed and produce toxic CUG RNAs that sequester and inhibit activities of the MBNL family of developmental RNA processing factors. Although myotonic dystrophy is classified as a muscular dystrophy, the brain is also severely affected by an unusual cohort of symptoms, including hypersomnia, executive dysfunction, as well as early onsets of tau/MAPT pathology and cerebral atrophy. To address the molecular and cellular events that lead to these pathological outcomes, we recently generated a mouse Dmpk CTG expansion knock-in model and identified choroid plexus epithelial cells as particularly affected by the expression of toxic CUG expansion RNAs. To determine if toxic CUG RNAs perturb choroid plexus functions, alternative splicing analysis was performed on lateral and hindbrain choroid plexi from Dmpk CTG knock-in mice. Choroid plexus transcriptome-wide changes were evaluated in Mbnl2 knockout mice, a developmental-onset model of myotonic dystrophy brain dysfunction. To determine if transcriptome changes also occurred in the human disease, we obtained post-mortem choroid plexus for RNA-seq from neurologically unaffected (two females, three males; ages 50–70 years) and myotonic dystrophy type 1 (one female, three males; ages 50–70 years) donors. To test that choroid plexus transcriptome alterations resulted in altered CSF composition, we obtained CSF via lumbar puncture from patients with myotonic dystrophy type 1 (five females, five males; ages 35–55 years) and non-myotonic dystrophy patients (three females, four males; ages 26–51 years), and western blot and osmolarity analyses were used to test CSF alterations predicted by choroid plexus transcriptome analysis. We determined that CUG RNA induced toxicity was more robust in the lateral choroid plexus of Dmpk CTG knock-in mice due to comparatively higher Dmpk and lower Mbnl RNA levels. Impaired transitions to adult splicing patterns during choroid plexus development were identified in Mbnl2 knockout mice, including mis-splicing previously found in Dmpk CTG knock-in mice. Whole transcriptome analysis of myotonic dystrophy type 1 choroid plexus revealed disease-associated RNA expression and mis-splicing events. Based on these RNA changes, predicted alterations in ion homeostasis, secretory output and CSF composition were confirmed by analysis of myotonic dystrophy type 1 CSF. Our results implicate choroid plexus spliceopathy and concomitant alterations in CSF homeostasis as an unappreciated contributor to myotonic dystrophy type 1 CNS pathogenesis. [ABSTRACT FROM AUTHOR]