Individual stability of daytime sleep structure in subjects without sleep disorders

To identify the most relevant clinical and video-polysomnographic characteristics of patients with sleep-related dissociative disorders (SRDDs) and to propose a framework for new diagnostic criteria. We searched potential SRDD cases from the scientific literature and from a database of patients referred for clinical and video-polysomnographic assessment in a single sleep disorders center for disruptive nocturnal behaviors (n = 731). The most relevant clinical and neurophysiological characteristics of the cases were extracted and a descriptive analysis was performed. Twenty-six SRDD cases (8 new and 18 previously published cases) were reviewed. Almost all cases of SRDDs occurred in a context of past traumatic events or abuse and were associated with at least 1 comorbid psychiatric disorder. We highlighted 4 relevant clinical characteristics of SRDD useful for the differential diagnosis with parasomnias: episodes of long duration of more than 1 hour (90.9%), self-inflicted injuries (83.3%), occurrence while awake close to bedtime (35.7%), and the presence of daytime dissociative symptoms (72.7%). The video-polysomnography documented typical episodes of SRDD with prolonged wakefulness before, during, and after the event in 11/26 cases. New diagnostic criteria for SRDD were proposed, with 3 levels of certainty for the diagnosis based on clinical, video-polysomnographic, and homemade video findings. More than 30 years after its formal identification, SRDD is not currently recognized as an official diagnostic entity. We better delineate the clinical and neurophysiological features of SRDD and propose a framework for its reinstatement in the next revisions of the sleep and psychiatric disorders classifications. Lopez R, Lefevre L, Barateau L, Micoulaud-Franchi J-A, Dauvilliers Y, Schenck CH. A series of 8 cases of sleep-related psychogenic dissociative disorders and proposed updated diagnostic criteria. J Clin Sleep Med. 2022;18(2):563-573.

Purpose of the Study: Sleep problems are frequently encountered in Parkinson's disease (PD), including sleep fragmentation, rapid eye movement (REM) sleep behavior disorder (RBD), excessive daytime sleepiness, and sleep-disordered breathing. In this study, we aimed to examine the relationship between sleep structure and sleep disorders on motor and nonmotor symptoms of PD. Basic Procedures: Seventy-three consecutive patients diagnosed as having PD based on the United Kingdom Brain Bank Criteria were prospectively enrolled. Detailed histories of PD-related symptoms, sleep anamnesis, subjective evaluation of nocturnal sleep, and daytime sleepiness were made. All participants underwent one-night video-polysomnography (PSG) and multiple sleep latency test (MSLT) in a sleep laboratory. Main Findings: A significant correlation was present between female sex and RLS (P = 0.009). Age and body mass index showed no significant correlations with PD-related parameters including Unified Parkinson's Disease Rating Scale (UPDRS) scores and PSG parameters. RLS or RBD showed no significant correlation with PD-related variables. Among PSG parameters, higher REM sleep percentages showed a statistically significant correlation with increased scores of UPDRS part III (P = 0.007). A statistically significant negative correlation was present between apnea–hypopnea index and PD duration (P = 0.005), and the presence of obstructive sleep apnea syndrome (OSAS) was statistically significantly correlated with lower scores of UPDRS part II (P = 0.050). The mean sleep latency in MSLT decreased as the dose of dopaminergic treatment increased (P = 0.016). Principal Conclusions: Our study demonstrated that changes in sleep structure and sleep-related disorders observed in PD could be attributed to intrinsic disease-related properties. The presence of changes in sleep structure as higher REM sleep percentages and sleep-related disorders such as OSAS show correlations with the severity of PD.

Objective: This study was conducted to find out the sleep structure of children hospitalized with epilepsy, and to explore the influencing factors of epilepsy with sleep disorders, in order to provide a reference of interventions to reduce the incidence of sleep disorders in epileptic children, to promote physical and mental healthy development of epileptic children.Methods: 111 patients were diagnosed epilepsy with sleep disorders in Hunan children' s hospital from December 2006 to June 2010, as a case group; while select 89 epileptic children not accompanied sleep disorders as the control group at the same time. Results: 1) The general information description: epilepsy with sleep disorders group (case group) 111 cases, sex ratio was 1.31:1, epileptic children not accompanied sleep disorders (control group) 89cases, sex ratio was 0.31:1. 2) Sleep structure: compared with the control group, case group had significant sleep structure disorder. 3) Those epileptic children who have sleep disturbance, hyperactivity or frequent awakening, difficulty falling asleep, and whose family sleep environment is not quiet were apt to lead sleep disorders. Conclusion: Epilepsy children with sleep disorder have significant changes in sleep structure, the occurrence of sleep disorders affected by many factors. Health education of sleeping should be enhanced. Early monitoring and guidance of sleep can improve the quality of life of epileptic children.

To compare clinical and functional features of the essential tremor (ET) and Parkinson's disease (PD) with- or without rapid eye movement (REM) sleep behavior disorder (RBD). Sixty patients with PD and 52 patients with ET were examined. Cognitive functions, anxiety, asthenia and depression, autonomic disorders and sleep disorders were assessed with scales and questionnaires. All patients underwent polysomnography (PSG). Based on the results of PSG, patients were divided by the presence or absence of parasomnia, known as REM sleep behavior disorder. Patients with PD and ET suffering from RBD were more likely to be overweight, more likely to develop cognitive impairment, obstructive sleep apnea, and emotional disorders. In addition, presence of RBD has adverse effects on the sleep structure. The profile of memory, attention, psychoemotional and sleep disorders in patients with PD and ET had common features, which suggests that it is RPBDH that affects the change in the clinical picture. Presence of RBD aggravates non-motor manifestations of such extrapyramidal diseases as PD and ET. On the one hand it helps to predict the course of the disease, on the other hand let us suspect RBD when we see non-motor symptoms worsening.

Molecular pathways and therapy strategies of sleep disorders and molecular processes of sleep

Children with overweight or obesity are more likely to experience sleep disorders, although the role of weight in pediatric insomnia treatment has not been examined. The current study examined the relationships of high body mass with pretreatment insomnia severity and global sleep problems and the potential moderating impact of weight on changes in insomnia severity following insomnia treatment. Participants included 1,133 youth ages 2-18 years clinically referred for insomnia treatment. The Pediatric Insomnia Severity Index was collected at the initial assessment and throughout treatment as part of routine clinical care. Treatment status was coded as no treatment, early termination, and completed treatment. Secondary measures of global sleep problems at the initial assessment included the Adolescent Sleep Wake Scale, Adolescent Sleep Hygiene Scale, and Children's Sleep Habits Questionnaire. Medical chart review of visits within ± 3 months of baseline was used to obtain age-adjusted and sex-adjusted body mass index Z-score. Among adolescents, regression analyses found that higher body mass index Z-score modestly predicted baseline insomnia severity (P = .021) and worse sleep hygiene (P < .001). For children, higher body mass index Z-score was modestly associated with baseline total sleep problems (P = .006) but not insomnia severity (P = .792). Across ages, body mass index Z-score predicted neither treatment status nor insomnia improvement (P > .05). Findings were similar in categorical analyses comparing patients with overweight/obesity to healthy weight. Although there is evidence that children of higher body mass present for insomnia treatment with greater sleep concerns, body mass does not predict treatment completion or insomnia improvement. Data suggest insomnia treatment is effective irrespective of weight status. Duraccio KM, Simmons DM, Beebe DW, Byars KC. Relationship of overweight and obesity to insomnia severity, sleep quality, and insomnia improvement in a clinically referred pediatric sample. J Clin Sleep Med. 2022;18(4):1083-1091.

We report results of a polysomnographic study carried out with children aged 6 to 12 years with either ADHD or a sleep disorder. The study focussed on whether the sleep structure and architecture of n = 36 ADHD children with and without sleep disorders differed from that of either n=15 children with sleep disorders or n=87 children without sleep disorders. Moreover, we assessed whether there was an increased risk for co-morbid sleep-related breathing disorders among ADHD children. All children underwent polysomnography in a paediatric clinic. Principal variables of the sleep structure and architecture as well as cardiorespirographic measures were analysed. Our findings demonstrate that sleep problems in children with ADHD seem to be unspecific concurrent symptoms since the sleep structure of sleep-disordered ADHD children and children with sleep disorders was similar. Only minor differences were found between non-sleep-disturbed ADHD children and healthy children without sleep problems. We conclude that sleep problems in ADHD are independent co-morbid symptoms without any pathogenetic relationship to vigilance functions in ADHD. The cardiorespirographic analyses showed that a subgroup of ADHD children with sleep problems may be at increased risk for co-morbid sleep-related breathing disorder. This finding is potentially important for differential diagnostic considerations in ADHD.

Objective To analyze the characteristics and influencing factors of sleep disorders and nocturnal hypoxemia of patients with different degrees of obstructive sleep apnea-hypopnea syndrome (OSAHS). Methods Four hundred and twenty-five patients with snoring were scored by Epworth Sleepiness Scale ( ESS), and monitored by polysomnography (PSG). The possible correlations between sleep structure, hypoxia parameters, ESS and clinical features were analyzed and compared in those patients. Results Four hundred and twenty-five patients were divided into 4 groups according to the apnea-hypopnea index (AHI). There were 65 primary snoring patients (15.3%) and 360 OSAHS patients (84. 7% ) including 187 patients (44. 0% ) in severe OSAHS group. ESS was increased as aggravation of OSAHS. There were significant statistical differences in ESS among each group. Compared with primary snoring group, sleep efficiency, NREM1 + 2, oxygen desaturation index ( ODI), time with pulse oxygen saturation below 90% (T(SpO2 <90% ) ) were significantly higher in the OSAHS groups, and NREM3 +4, lowest pulse oxygen saturation level ( LSpO2 ) were lower. ESS was correlated positively with AHI (r= 0. 474,P <0. 01 ). They were both correlated positively with ODI, T (SpO2 <90% ) and NREM1 + 2( ESSr =0. 392, 0. 356,0. 194;AHI r = 0. 714, O. 682, 0. 365, all P < 0. 01 ), and correlated negatively with LSpO2, NREM3 + 4 ( ESS r = - 0. 414, - 0. 196; AHI r = - 0. 740, - 0. 385, both P < 0. 01 ). LSpO2, ODI and T (SpO2 < 90% ) were the primary influencing factors. Common clinical presentations and subjective symptoms were presented including daytime sleepiness, impaired memory, fatigue, dry mouth, oppressive wake and morning headache, etc. Percentage of individuals with daytime sleepiness in the severe OSAHS group was 73. 3% (137/187). These had serious impact on the patients' quality of life, leading to difficulty concentrating, poor memory and cognitive impairment. Conclusions Sleep disorders are found in the patients with different degrees of OSAHS. The excessive daytime sleepiness interrelated partly with the structure of sleep, and totally with hypoxia parameters. The more severity the patients have, the more nocturnal hypoxia, sleep disorders and higher ESS are found. Key words: Sleep apnea,obstructive; Sleep disorders; Lethargy; Severity of illness index

Sleep disorders may cause dysregulation in cerebral glucose metabolism and synaptic functions, as well as alterations in cerebrospinal fluid (CSF) biomarker levels. This study aimed at measuring sleep, CSF Alzheimer's disease (AD) biomarkers, and cerebral glucose consumption in patients with obstructive sleep apnea syndrome (OSAS) and patients with periodic limb movement disorder (PLMD), compared to controls. OSAS and PLMD patients underwent 18F-fluoro-2-deoxy-D-glucose positron emission tomography (18F-FDG PET), polysomnographic monitoring, and lumbar puncture to quantify CSF levels of amyloid-β42 (Aβ42), total tau, and phosphorylated tau. All patients were compared to controls, who were not affected by sleep or neurodegenerative disorders. Twenty OSAS patients, 12 PLMD patients, and 15 controls were included. Sleep quality and sleep structure were altered in both OSAS and PLMD patients when compared to controls. OSAS and PLMD patients showed lower CSF Aβ42 levels than controls. OSAS patients showed a significant increase in glucose uptake in a wide cluster of temporal-frontal areas and cerebellum, as well as a reduced glucose consumption in temporal-parietal regions compared to controls. PLMD patients showed increased brain glucose consumption in the left parahippocampal gyrus and left caudate than controls. Sleep dysregulation and nocturnal hypoxia present in OSAS patients, more than sleep fragmentation in PLMD patients, were associated with the alteration in CSF and 18F-FDG PET AD biomarkers, namely reduction of CSF Aβ42 levels and cerebral glucose metabolism dysregulation mainly in temporal areas, thus highlighting the possible role of sleep disorders in driving neurodegenerative processes typical of AD pathology.

Sleep disturbances in long-term immigrants with chronic mountain sickness: A comparison with healthy immigrants at high altitude

Sleep undergoes changes from birth to adulthood, while sleep disorders are associated with various cognitive deficiencies in childhood. In parallel, prematurity is known to predispose to poor neurodevelopmental outcomes. Our aim is to provide literature data about factors influencing sleep in the premature infants and sleep outcomes in this population. A systematic review was conducted using a variety of health-related databases. Original research papers were considered and no year-of-publication restriction was placed. In total, 22 articles fulfilled our selection criteria. Available studies present remarkable heterogeneity in terms of methodological design. Compared to full term, premature infants exhibit significant differences in sleep structure, which mainly include differences in electroencephalographic spectral values, in total sleep time and in arousal threshold. Furthermore, prematurity seems to be a risk factor of sleep breathing disorders in childhood and adolescence. Data about the effect of methylxanthines and the environment of neonatal intensive care unit is controversial. With regard to the impact of prematurity-related sleep disorders on future neurodevelopment, available research papers are generally few. The alterations in sleep patterns are an outcome of prematurity (immaturity of nervous system) as well as of postnatal factors and comorbidities. Sleep problems in this population of infants seems to be a missing piece of the puzzle of impaired neurodevelopment. Future studies should focus on interventions to improve sleep hygiene and limit neurodevelopmental problems.

ObjectiveThe purpose of this study was to illustrate the electrophysiological features of sleep disturbances in patients with anti-leucine-rich glioma-inactivated protein 1 (anti-LGI1) encephalitis in both active and recovery stages.MethodsRetrospectively filed video electroencephalogram (VEEG) and polysomnography (PSG) data in 24 patients with anti-LGI1 encephalitis were analyzed in comparison with that in 20 individuals without sleep disorders as control group.ResultsSleep efficiency (SE) and total sleep time involving REM and NREM sleep were significantly decreased in patients with anti-LGI1 encephalitis during the active stage compared to that during the recovery stage and in the control group. Imbalanced sleep structure was found, demonstrated by elevated N1, decreased N3 and REM components, as well as abnormal N2 structure characterized with significantly lower spindle duration and density during the active stage. These findings were independent of the presence of nocturnal episodic events or sleep hyperkinetic movements (HMs). HMs were present in 11/23 patients throughout NREM and REM sleep (nonspecific in sleep stages) during the active stage. During the recovery stage, SE and sleep structures were dramatically improved, including the percentage of N3 and REM sleep, spindle duration and density. Ten of 11 patients with HMs were followed up. HMs were totally remitted in 3 patients and still persistent in 1, while evolved into REM sleep behavior disorder (RBD) in 4 with comorbid periodic limb movement syndrome (PLMS) in 3/4, and only PLMS in 2.ConclusionSleep disturbances were remarkable and intrinsic features in active anti-LGI1 encephalitis, marked by overall disruptions of both NREM and REM sleep, as well as the presence of HMs, which tend to evolve into RBD or PLMS during the recovery stage. Long-term follow-up with PSG is needed, especially for those patients with severe sleep disturbances during the active phase.

Background: Sleep disorders may cause dysregulation in cerebral glucose metabolism and synaptic functions, as well as alterations in cerebrospinal fluid (CSF) biomarker levels. Objective: This study aimed at measuring sleep, CSF Alzheimer’s disease (AD) biomarkers, and cerebral glucose consumption in patients with obstructive sleep apnea syndrome (OSAS) and patients with periodic limb movement disorder (PLMD), compared to controls. Methods: OSAS and PLMD patients underwent 18F-fluoro-2-deoxy-D-glucose positron emission tomography (18F-FDG PET), polysomnographic monitoring, and lumbar puncture to quantify CSF levels of amyloid-β42 (Aβ42), total tau, and phosphorylated tau. All patients were compared to controls, who were not affected by sleep or neurodegenerative disorders. Results: Twenty OSAS patients, 12 PLMD patients, and 15 controls were included. Sleep quality and sleep structure were altered in both OSAS and PLMD patients when compared to controls. OSAS and PLMD patients showed lower CSF Aβ42 levels than controls. OSAS patients showed a significant increase in glucose uptake in a wide cluster of temporal-frontal areas and cerebellum, as well as a reduced glucose consumption in temporal-parietal regions compared to controls. PLMD patients showed increased brain glucose consumption in the left parahippocampal gyrus and left caudate than controls. Conclusion: Sleep dysregulation and nocturnal hypoxia present in OSAS patients, more than sleep fragmentation in PLMD patients, were associated with the alteration in CSF and 18F-FDG PET AD biomarkers, namely reduction of CSF Aβ42 levels and cerebral glucose metabolism dysregulation mainly in temporal areas, thus highlighting the possible role of sleep disorders in driving neurodegenerative processes typical of AD pathology.

Patients with Parkinson's disease experience prominent difficulties in maintaining sleep, painful night-time abnormal movements, and daytime sleepiness, sometimes culminating in sleep attacks. Recent insights into the pathophysiology of sleep disorders in PD points to a complex interaction between movement disorders, side-effects of dopamine agents and lesions in sleep-wake regulating systems. Treatment with dopamine agonists provides a twice higher risk of daytime sudden sleep episodes than levodopa, with no difference between ergotic and non ergotic compounds. Insomnia can be improved by a better control of night-time disability, restless legs syndrome and dystonia using subthalamic nucleus stimulation or night-time levodopa. A specific REM sleep disorder contributes to REM sleep behavior disorder and also to hallucinations (suggesting they could be awake dreams) and excessive daytime sleepiness. The management of sleep and alertness problems requires to analyze their potential causes, to monitor night-time and daytime sleep, and to subtly adjust psychotropic and dopaminergic treatment.

This study aims to integrate cross-disease omics data and perform multidimensional analysis to uncover the molecular basis of schizophrenia (SCZ) and sleep disorder (SD) comorbidity and to systematically analyze the potential mechanism of the Hugan Tiaoshen Formula (HGTS) in treating SCZ with SD. Integrate transcriptional data of SCZ and SD from the GEO database, screen disease-shared differential genes. Construct PPI network, identify core targets by topological analysis. Use machine learning algorithms to select cross-disease hub genes. Analyze immune cell infiltration and gene-immune interaction. Conduct molecular docking. Build an SCZ-SD comorbidity mouse model and assess behavioral improvements. Verify key pathway regulatory effects by Western blot and qRT-PCR. Cross-disease analysis identified 25 shared core targets. The constructed "compound-target" network revealed quercetin, β-sitosterol, and ADRB2 as key nodes. The PPI network identified HSPB1, THBS1, and other targets enriched in antigen presentation and PI3K-Akt pathways. Machine learning algorithms highlighted HSPB1, ADRB2, and GZMM as core genes. In SCZ, resting CD4+ memory T cells were positively correlated with HSPB1, while abnormal dendritic cells and low ADRB2 expression were associated with SD. Molecular docking confirmed strong binding between baicalin, β-sitosterol, and the targets. Animal experiments showed that HGTS improved neurological symptoms and sleep structure while regulating the expression of HSPB1, ADRB2, and BDNF. This study reveals shared core targets HSPB1, ADRB2, and GZMM between SCZ and SD. The compound HGTS, through the synergistic action of multiple components such as quercetin and β-sitosterol, improves neurological symptoms and sleep rhythm.