Percentage Of Slow-wave Sleep Research Articles

P001 Sleep disturbance in patients with long-term neurological sequelae of COVID-19

Abstract Introduction Post COVID-19 neurological sequelae (popularly termed “Long COVID”), which include chronic sleep disruption and “brain fog” are widespread; however, studies have not yet comprehensively evaluated the concurrent effects of these disruptions of neurocognitive function and their relationship to sleep disturbance. Methods Participants aged between 40-65, with no more than 2 cardiovascular risk factors were stratified into three groups of ten: Group 1 (pre-pandemic datasets), Group 2 (individuals recovered from COVID-19), and Group 3 (individuals diagnosed with Long COVID under the WHO criteria). Polysomnography (PSG), Multiple Sleep Latency Test (MSLT), participant surveys and neurocognitive testing, among other data, were collected. Results Control group 1 included more participants (70%) with obstructive sleep apnoea (OSA) compared to the Long COVID group, resulting in a markedly greater arousal index (ANOVA p=0.03), but no significant differences in percentage of Slow Wave Sleep (SWS) and Rapid Eye Movement (REM) sleep were observed between all three groups (ANOVA p=0.29). The Long COVID group displayed heightened daytime sleepiness, based on MSLT, Epworth Sleepiness Scores, and fatigue severity scores (Group 2: 28±10 vs Group 3:44±11, unpaired t-test p=0.01). Discussion Initial observations suggest sleep architecture (proportion of SWS and REM sleep) in Long COVID does not differ from controls, however the reduced sleep latency and elevated subjective fatigue suggest dysfunction of sleep in Long COVID which needs to be further explored.

Sleep and Respiratory Parameters After Lung Transplantation in Adult Patients With Cystic Fibrosis.

We aimed to explore the prevalence and predictive factors of sleep-disordered breathing (SDB) in patients with cystic fibrosis (pwCF) after lung transplantation (LTX). We prospectively recruited adult pwCF who underwent LTX in our hospital from 2013 to 2022 and invited them for an attended overnight polysomnography (PSG) 1year after transplantation. The apnea-hypopnea index (AHI) was the primary outcome, and SDB was defined as an AHI≥5. Demographic, anthropometric, cardiometabolic, drug treatment, and pulmonary function variables were compared between pwCF with and without SDB. Multiple regression analysis was used to identify significant predictors of SDB. For a subset of participants who had available PSG before transplantation, sleep parameters were compared pre-post transplantation. Sixty-two pwCF (31 females) were enrolled. Thirty participants had SDB, but only 11 of them had moderate-to-severe SDB (AHI≥15). The average Epworth Sleepiness Scale (ESS) score indicated the absence of excessive daytime sleepiness. Older age (p<0.001), male sex (p<0.001), and smaller thoracic gas volume (p=0.002) significantly predicted higher AHI. Comparison between pre- and post-transplantation polysomnographic data showed a significant increase in the percentage of slow wave sleep (p=0.047), as well as a significant improvement in mean nocturnal oxygen saturation (p=0.007). A statistically significant increase in the AHI was also observed (p=0.047), but its clinical importance is uncertain (p=0.476 for the increase in the ESS score). We may conclude that SDB is prevalent in pwCF after LTX, but its severity is mild. Older male pwCF with greater improvement in lung hyperinflation after transplantation might be at risk for SDB and should be followed for symptoms or signs of sleep apnea.

Objective sleep enhancement in Parkinson's disease: A sham-controlled trial of low-frequency repetitive transcranial magnetic stimulation over the right dorsolateral prefrontal cortex

IntroductionParkinson's disease (PD) is often accompanied by sleep disturbances, impacting patients' quality of life. While repetitive transcranial magnetic stimulation (rTMS) shows promise in improving self-reported sleep quality, its effects on objective sleep architecture in PD remain understudied. Sleep disturbances, including rapid eye movement (REM) and slow-wave sleep disturbances, correlate with cognitive decline and motor symptoms. This study investigated the effect of low-frequency rTMS targeting the right dorsolateral prefrontal cortex (DLPFC) modifying objective sleep architecture and explored symptom improvement mechanisms in PD patients. MethodsIn this randomized, double-blind, sham-controlled trial, 67 PD patients received 10 consecutive days of 1-Hz rTMS over the right DLPFC. Polysomnography assessed sleep microstructure, while electroencephalogram recordings evaluated power spectral density and sleep spindle activity. Clinical scales measured sleep quality, motor symptoms, and cognition at baseline, post-treatment, and 3 months post-rTMS. ResultsThe rTMS group exhibited improvements in sleep quality, motor symptoms, and cognition post-treatment, persisting at the 3-month follow-up. There was a notable increase in the REM sleep proportion post-rTMS. The rTMS group exhibited elevated low-frequency (0.5–2 Hz) slow-wave electroencephalogram spectral density during non-REM sleep. Cognitive enhancement correlated with increased lower delta power, while motor symptom progression correlated with spindle frequency and slow-wave sleep percentage changes. ConclusionLow-frequency rTMS targeting the right DLPFC holds promise for improving clinical symptoms and modulating sleep architecture in PD. These findings suggest a link between symptom improvement and sleep structure enhancement, highlighting the need for further investigation into the therapeutic potential of rTMS in PD management.

The stability of slow-wave sleep and EEG oscillations across two consecutive nights of laboratory polysomnography in cognitively normal older adults.

Laboratory polysomnography provides gold-standard measures of sleep physiology, but multi-night investigations are resource intensive. We assessed the night-to-night stability via reproducibility metrics for sleep macrostructure and electroencephalography oscillations in a group of cognitively normal adults attending two consecutive polysomnographies. Electroencephalographies were analysed using an automatic algorithm for detection of slow-wave activity, spindle and K-complex densities. Average differences between nights for sleep macrostructure, electroencephalography oscillations and sleep apnea severity were assessed, and test-retest reliability was determined using two-way intraclass correlations. Agreement was calculated using the smallest real differences between nights for all measures. Night 2 polysomnographies showed significantly greater time in bed, total sleep time (6.3 hr versus 6.8 hr, p < 0.001) and percentage of rapid eye movement sleep (17.5 versus 19.7, p < 0.001). Intraclass correlations were low for total sleep time, percentage of rapid eye movement sleep and sleep efficiency, moderate for percentage of slow-wave sleep and percentage of non-rapid eye movement 2 sleep, good for slow-wave activity and K-complex densities, and excellent for spindles and apnea-hypopnea index with hypopneas defined according to 4% oxygen desaturation criteria only. The smallest real difference values were proportionally high for most sleep macrostructure measures, indicating moderate agreement, and proportionally lower for most electroencephalography microstructure variables. Slow waves, K-complexes, spindles and apnea severity indices are highly reproducible across two consecutive nights of polysomnography. In contrast, sleep macrostructure measures all demonstrated poor reproducibility as indicated by low intraclass correlation values and moderate agreement. Although there were average differences in percentage of rapid eye movement sleep and total sleep time, these were numerically small and perhaps functionally or clinically less significant. One night of in-laboratory polysomnography is enough to provide stable, reproducible estimates of an individual's sleep concerning measures of slow-wave activity, spindles, K-complex densities and apnea severity.

Worse sleep architecture but not self-reported insomnia and sleepiness is associated with higher cortisol levels in menopausal women

ObjectiveWorsening of sleep quality during menopause is well recognized. However, the underlying hormonal regulation is insufficiently described. In this study, we evaluated associations between sleep and cortisol levels. Study designSeventeen perimenopausal and 18 postmenopausal women were enrolled in a three-night sleep study. Diurnal blood sampling was performed during the third night and the following day. Main outcome measuresSelf-reported insomnia and sleepiness were evaluated with the Basic Nordic Sleep Questionnaire and sleep architecture with all-night polysomnography. Diurnal cortisol samples were collected at 20-min intervals. Correlation analyses and generalized linear models adjusted by age, body mass index, vasomotor symptoms and depressive symptoms were conducted. ResultsIn correlation analyses, self-reported insomnia and sleepiness were not associated with cortisol levels. Lower sleep efficiency, slow-wave sleep and stage 1 percentages, number of slow-wave sleep and of rapid-eye-movement (REM) periods, longer slow-wave sleep latency and higher wake after sleep onset percentage were associated with higher cortisol levels (all p < 0.05). Further, lower slow-wave sleep percentage and longer slow-wave sleep latency correlated with steeper daytime cortisol slope (i.e. day cortisol decrease, both p < 0.05). In adjusted generalized linear models, lower sleep efficiency and number of rapid-eye-movement periods as well as higher wake after sleep onset percentage correlated with higher cortisol levels; lower slow-wave sleep percentage correlated with higher cortisol awakening response. ConclusionsWorse sleep architecture but not worse self-reported insomnia and sleepiness was associated with higher cortisol levels. This is important for understanding sleep in women, especially during the menopausal period.

Sleep Physiology and Neurocognition Among Adolescents With Attention-Deficit/Hyperactivity Disorder

Few studies have characterized the nature of sleep problems among adolescents with attention-deficit/hyperactivity disorder (ADHD) using polysomnography (PSG). Additionally, although adolescents with ADHD and adolescents with sleep disturbances display similar neurocognitive deficits, the role of sleep in contributing to neurocognitive impairment in adolescent ADHD is unknown. This study investigated differences in PSG-measured sleep among adolescents with ADHD compared with non-psychiatric controls and associations with neurocognition. Medication-free adolescents aged 13 to 17 (N = 62, n= 31 with ADHD; mean age= 15.3 years; 50% female) completed a diagnostic evaluation, 3 nights of ambulatory PSG, the Cambridge Neuropsychological Test Automated Battery, and subjective reports of sleep and executive functioning. Linear regressions covarying for age, sex, and pubertal status examined group differences in sleep indices, and partial Pearson correlations assessed relations between sleep and neurocognition. Although adolescents with ADHD did not exhibit differences in PSG-measured sleep duration, awakenings, or latency (ps > .05) compared with non-psychiatric controls, they displayed lower slow wave sleep percentage (β=-.40) and non-rapid eye movement (NREM) electroencephalogram (EEG) delta power (β=-.29). They also exhibited greater stage 2 percentage (β= .41), NREM EEG sigma power (β= .41), and elevated self-reported sleep disturbances (ps< .05). Lower NREM EEG delta power, increased high-frequency power, and slower decline in NREM EEG delta power overnight were associated with poorer neurocognition among adolescents with ADHD. Adolescents with ADHD reported more sleep disturbances than non-psychiatric controls and exhibited differences in sleep stage distribution and NREM sleep EEG frequency. Sleep-EEG spectral indices were associated with impaired neurocognition, suggesting that physiological sleep processes may underlie neurocognitive deficits in ADHD. Future studies may clarify whether sleep plays a causal role in neurocognitive impairments in adolescent ADHD and whether interventions normalizing sleep improve neurocognition. Sleep Dysfunction and Neurocognitive Outcomes in Adolescent ADHD; https://clinicaltrials.gov/; NCT02897362. We worked to ensure sex and gender balance in the recruitment of human participants. We worked to ensure race, ethnic, and/or other types of diversity in the recruitment of human participants. We worked to ensure that the study questionnaires were prepared in an inclusive way. One or more of the authors of this paper self-identifies as a member of one or more historically underrepresented sexual and/or gender groups in science. We actively worked to promote sex and gender balance in our author group. While citing references scientifically relevant for this work, we also actively worked to promote sex and gender balance in our reference list.

Sleep Microbiome: Insights into Probiotics and Sleep Health

Introduction&#x0D; The World Health Organization (WHO) defines probiotics as "live microorganisms that, when administered in adequate amounts, confer health benefits to the host." A number of scientific reports show that their effects extend beyond the immune and gastrointestinal systems, and that poor sleep quality and insomnia are an increasingly important social problem. Studies indicate that 30-50% of adults experience sleep problems. Sleep deficiencies are associated with higher rates of obesity, hypertension, type 2 diabetes, cardiovascular diseases, mental health disorders and increased risk of death. One promising way to help treat sleep problems is through the use of probiotics. Interaction through the gut-brain axis suggests that altering the gut microbiota may become a useful tool for improving sleep quality.&#x0D; Aim of the study&#x0D; The purpose of this study was to investigate the potential effectiveness of probiotics in improving sleep quality and treating insomnia.&#x0D; Materials and Methodology&#x0D; PubMed and Google Scholar databases were analyzed. Articles were searched in English using the following keywords: probiotics; sleep quality.&#x0D; Results &#x0D; Probiotics resulted in a favorable cumulative effect on sleep quality as measured by the PSQI global questionnaire and a statistically significant positive effect on at least one of the components characterizing sleep quality (i.e., sleep latency, sleep length, sleep disturbance, daytime sleepiness). They allow to maintain a high percentage of slow-wave sleep, despite stressors, and indirectly affect sleep quality in athletes by reducing muscle soreness.&#x0D; Conclusion&#x0D; The results of studies to date indicate that probiotics are an effective, safe and clinically sound adjunctive method for improving sleep quality and treating insomnia. However, these studies are at an early stage and require further efforts using larger research groups.

Reduced slow‐wave sleep is associated with greater tau accumulation and reduced cortical thickness in the temporal lobe

AbstractBackgroundSlow wave sleep (SWS) plays an important role in overnight memory consolidation and promotes overnight clearance of amyloid‐β and tau proteins. Reduced SWS has been associated with higher amyloid burden in CSF in preclinical stages of Alzheimer’s disease (AD). However, little is known about the relationship between SWS, tau burden and neurodegeneration in cognitively unimpaired (CU) adults. Thus, we investigated the relationships between slow‐wave sleep, regional tau PET (18F‐flortaucipir; FTP‐PET) and temporal lobe cortical thickness in cognitively unimpaired adults at risk of AD.MethodsThis study included 39 CU adults from the Harvard Aging Brain Study (mean age 74.6 years, 61.5% females) who underwent at‐home polysomnography (PSG; Compumedics Somte), tau PET (FTP‐PET, amyloid PET (PIB‐PET) and MRI (Table 1). We used separate multivariate linear regressions to assess associations between the percentage of slow‐wave sleep (SWS) and tau PET signal in the following ROIs: entorhinal cortex, inferior temporal cortex, and a temporal composite comprised of entorhinal, inferior temporal, middle temporal and fusiform cortices. Primary analyses were adjusted for age and sex. Secondary analyses also adjusted for global amyloid (PiB‐PET) burden. Lastly, we investigated the relationship between SWS and cortical thickness in the same ROIs, assessed using FreeSurfer v6.0.ResultsLower percentage of SWS was associated with greater tau burden in entorhinal (p = 0.036), inferior temporal (p = 0.011), and temporal composite ROIs (p = 0.005). Associations between reduced SWS and greater FTP‐PET signal in the inferior temporal cortex and temporal composite ROI remained after controlling for PiB‐PET (p = 0.028; p = 0.017, respectively; Table 2). Additionally, lower SWS was associated with reduced cortical thickness in the entorhinal (p = 0.031), inferior temporal (p = 0.023) and temporal composite ROIs (p = 0.002) (Table 3).ConclusionsLower SWS in CU adults was associated with higher tau burden in regions of the temporal lobe that are commonly sites of early tau accumulation. These effects were independent of amyloid burden, suggesting disrupted sleep may lead to increased tau accumulation via an amyloid‐independent pathway. Importantly, lower SWS was also associated with reduced cortical thickness in temporal regions, suggesting that disrupted sleep may be tied to early AD‐related neuronal loss in the temporal lobe.

Involvement of orexin type-2 receptors in genetic absence epilepsy rats.

Orexin is a neuropeptide neurotransmitter that regulates the sleep/wake cycle produced by the lateral hypothalamus neurons. Recent studies have shown the involvement of orexin system in epilepsy. Limited data is available about the possible role of orexins in the pathophysiology of absence seizures. This study aims to understand the role of orexinergic signaling through the orexin-type 2 receptor (OX2R) in the pathophysiology of absence epilepsy. The pharmacological effect of a selective OX2R agonist, YNT-185 on spike-and-wave-discharges (SWDs) and the OX2R receptor protein levels in the cortex and thalamus in adult GAERS were investigated. The effect of intracerebroventricular (ICV) (100, 300, and 600 nmol/10 μL), intrathalamic (30 and 40 nmol/500 nL), and intracortical (40 nmol/500 nL) microinjections of YNT-185 on the duration and number of spontaneous SWDs were evaluated in adult GAERS. The percentage of slow-wave sleep (SWS) and spectral characteristics of background EEG were analyzed after the ICV application of 600 nmol YNT-185. The level of OX2R expression in the somatosensory cortex and projecting thalamic nuclei of adult GAERS were examined by Western blot and compared with the non-epileptic Wistar rats. We showed that ICV administration of YNT-185 suppressed the cumulative duration of SWDs in GAERS compared to the saline-administered control group (p < 0.05). However, intrathalamic and intracortical microinjections of YNT-185 did not show a significant effect on SWDs. ICV microinjections of YNT-185 affect sleep states by increasing the percentage of SWS and showed a significant treatment effect on the 1-4 Hz delta frequency band power during the 1-2 h post-injection period where YNT-185 significantly decreased the SWDs. OXR2 protein levels were significantly reduced in the cortex and thalamus of GAERS when compared to Wistar rats. This study investigated the efficacy of YNT-185 for the first time on absence epilepsy in GAERS and revealed a suppressive effect of OX2R agonist on SWDs as evidenced by the significantly reduced expression of OX2R in the cortex and thalamus. YNT-185 effect on SWDs could be attributed to its regulation of wake/sleep states. The results constitute a step toward understanding the effectiveness of orexin neuropeptides on absence seizures in GAERS and might be targeted by therapeutic intervention for absence epilepsy.

Association Between Slow-Wave Sleep Loss and Incident Dementia

Slow-wave sleep (SWS) supports the aging brain in many ways, including facilitating the glymphatic clearance of proteins that aggregate in Alzheimer disease. However, the role of SWS in the development of dementia remains equivocal. To determine whether SWS loss with aging is associated with the risk of incident dementia and examine whether Alzheimer disease genetic risk or hippocampal volumes suggestive of early neurodegeneration were associated with SWS loss. This prospective cohort study included participants in the Framingham Heart Study who completed 2 overnight polysomnography (PSG) studies in the time periods 1995 to 1998 and 2001 to 2003. Additional criteria for individuals in this study sample were an age of 60 years or older and no dementia at the time of the second overnight PSG. Data analysis was performed from January 2020 to August 2023. Changes in SWS percentage measured across repeated overnight sleep studies over a mean of 5.2 years apart (range, 4.8-7.1 years). Risk of incident all-cause dementia adjudicated over 17 years of follow-up from the second PSG. From the 868 Framingham Heart Study participants who returned for a second PSG, this cohort included 346 participants with a mean age of 69 years (range, 60-87 years); 179 (52%) were female. Aging was associated with SWS loss across repeated overnight sleep studies (mean [SD] change, -0.6 [1.5%] per year; P < .001). Over the next 17 years of follow-up, there were 52 cases of incident dementia. In Cox regression models adjusted for age, sex, cohort, positivity for at least 1 APOE ε4 allele, smoking status, sleeping medication use, antidepressant use, and anxiolytic use, each percentage decrease in SWS per year was associated with a 27% increase in the risk of dementia (hazard ratio, 1.27; 95% CI, 1.06-1.54; P = .01). SWS loss with aging was accelerated in the presence of Alzheimer disease genetic risk (ie, APOE ε4 allele) but not hippocampal volumes measured proximal to the first PSG. This cohort study found that slow-wave sleep percentage declined with aging and Alzheimer disease genetic risk, with greater reductions associated with the risk of incident dementia. These findings suggest that SWS loss may be a modifiable dementia risk factor.

The role of the sleep K-complex on the conversion from mild cognitive impairment to Alzheimer's disease.

The present literature points to an alteration of the human K-complex during non-rapid eye movement sleep in Alzheimer's disease. Nevertheless, the few findings on the K-complex changes in mild cognitive impairment and their possible predictive role on the Alzheimer's disease conversion show mixed findings, lack of replication, and a main interest for the frontal region. The aim of the present study was to assess K-complex measures in amnesic mild cognitive impairment subsequently converted in Alzheimer's disease over different cortical regions, comparing them with healthy controls and stable amnesic mild cognitive impairment. We assessed baseline K-complex density, amplitude, area under the curve and overnight changes in frontal, central and parietal midline derivations of 12 amnesic mild cognitive impairment subsequently converted in Alzheimer's disease, 12 stable amnesic mild cognitive impairment and 12 healthy controls. We also assessed delta electroencephalogram power, to determine if K-complex alterations in amnesic mild cognitive impairment occur with modification of the electroencephalogram power in the frequency range of the slow-wave activity. We found a reduced parietal K-complex density in amnesic mild cognitive impairment subsequently converted in Alzheimer's disease compared with stable amnesic mild cognitive impairment and healthy controls, without changes in K-complex morphology and overnight modulation. Both amnesic mild cognitive impairment groups showed decreased slow-wave sleep percentage compared with healthy controls. No differences between groups were observed in slow-wave activity power. Our findings suggest that K-complex alterations in mild cognitive impairment may be observed earlier in parietal regions, likely mirroring the topographical progression of Alzheimer's disease-related brain pathology, and express a frontal predominance only in a full-blown phase of Alzheimer's disease. Consistently with previous results, such K-complex modification occurs in the absence of significant electroencephalogram power changes in the slow oscillations range.

0751 Early Childhood Sleep Associated with Adolescent Sleep Physiology among Youth with ADHD

Abstract Introduction Sleep complaints are prevalent and impairing symptoms among adolescents with ADHD. Our recent work has shown that key aspects of sleep physiology differentiate adolescents with ADHD from healthy controls (HC), including reduced slow-wave sleep percentage (SWS%) and relative delta power (rDelta) and increased stage 2 percentage (N2%) and relative sigma power (rSigma) after accounting for sleep duration. ADHD-related sleep problems may emerge as early as toddlerhood, yet little is known about the trajectory of sleep disturbances over time in ADHD. The current study examines relationships between early childhood sleep problems and adolescent sleep physiology in ADHD and HC. Methods Sixty-two medication-free adolescents (31 with ADHD, mean age=15.3, 50% female) completed a diagnostic interview (Mini International Neuropsychiatric Interview) and 3 nights of at-home polysomnography. Spectral analysis was conducted on a single O1-C3 channel. Caregivers reported on participants’ sleep problems during toddlerhood and preschool (Child Behavior Questionnaire; CBQ). Linear regressions controlling for age, sex, and pubertal status examined relationships between early childhood sleep problems and aspects of sleep physiology implicated in adolescent ADHD (SWS%, rDelta, N2%, rSigma) and whether associations differed between groups. Results Adolescents with ADHD had greater caregiver-reported early childhood sleep problems compared to HC (t(60)=3.71, p&amp;lt;.001). In the full sample, greater caregiver-reported sleep problems in early childhood were associated with reduced SWS% (β=-.28, p=.04) and rDelta (β=-.27, p=.04), and increased rSigma (β=.33, p=.02), in adolescence. An early childhood sleep by group interaction was observed for rDelta (β=1.09, p=.04), such that the association was significantly stronger for adolescents with ADHD than HC. Conclusion The current study found that sleep problems in early development were associated with disruptions in sleep physiology in adolescents, including relatively less time spent in SWS, reduced delta power, and increased sigma power. Results suggest that ADHD-related sleep problems may begin early in life and persist into adolescence. Screening for and treating sleep problems during early development may be important for supporting sleep health among adolescents with ADHD, and future studies should assess this possibility. Future studies employing longitudinal designs may clarify the contribution of sleep disturbances to the onset and persistence of ADHD symptoms across development. Support (if any) K23MH108704; R34MH128440

Sleep in amyotrophic lateral sclerosis: A systematic review and meta-analysis of polysomnographic findings

BackgroundThis study explores the polysomnographic differences between amyotrophic lateral sclerosis (ALS) patients and healthy controls. MethodsAn electronic literature search was conducted in MEDLINE, EMBASE, All EBM databases, Web of Science, and CNKI from inception to Oct 2022. ResultsMeta-analyses revealed significant reductions in sleep efficiency, total sleep time, N2%, slow wave sleep percentage, minimum SpO2, and mean SpO2, and increases in wake time after sleep onset and N1%, sleep latency, rapid eye movement sleep latency, time spent with SpO2 < 90%, oxygen desaturation index, and apnea hypopnea index in ALS patients compared with controls. Sensitivity analyses showed that some heterogeneity was explained by excluding patients taking medications impacting sleep, whether studies employed an adaptation night, and the use of different PSG scoring rules. ConclusionsSignificant polysomnographic abnormalities are present in ALS. Our findings underscore the need for a comprehensive PSG assessment of sleep changes in ALS patients. When performing PSG examinations in ALS, whether the patients are taking medication impacting sleep and the scoring system used should be considered.

Metabolic disturbances in children with narcolepsy: a retrospective study.

To determine the prevalence of metabolic syndrome (MS) in children with narcolepsy and to evaluate their clinical and sleep characteristics according to the different components of MS. This retrospective study consisted of 58 de novo children with narcolepsy (median age: 12.7 years, 48.3% of boys). The recently published MS criteria in a French population of children were used. Clinical and sleep characteristics were compared between groups with different components of MS. MS was present in 17.2% of children with narcolepsy, among whom 79.3% presented with high homeostasis model assessment for insulin resistance (HOMA-IR), 25.9% with high body mass index, 24.1% with low high-density lipoprotein cholesterol (HDL-C), and 12.1% with high triglycerides. Patients with at least two MS components had more night eating behaviors and tended to have lower percentage of slow-wave sleep and more fragmented sleep. On multiple sleep latency test, they had shorter mean sleep latencies to rapid eye movement (REM), non-REM sleep and tended to have more sleep onset REM periods (SOREMPs) than those with less than two MS components. Insulin resistance was found to be the core metabolic disturbance in obese as well as in nonobese children with narcolepsy. Children with narcolepsy with at least two MS components presented a more severe daytime sleepiness and a higher prevalence of night-eating behaviors than those with less than two MS components. Such children might benefit from early evaluation and management in order to prevent future complications.

0192 Effects of emerging alcohol use on developmental trajectories of functional sleep measures in adolescents

Abstract Introduction Adolescence is characterized by developmental changes in sleep timing and architecture as well as alcohol use initiation. While the effects of acute and chronic alcohol use on sleep in adults are well-documented, much less is known in adolescents. We used longitudinal data from the National Consortium on Alcohol and Neurodevelopment in Adolescence (NCANDA) to examine how emerging alcohol use affected sleep architecture in adolescents. Methods Overnight polysomnographic recordings were made each year, for 4 years, in 94 adolescents (12–21 years at baseline, 43% female) from the NCANDA cohort. All participants were no or low (youth adjusted Cahalan score of zero) alcohol users at baseline. These data were used to examine developmental trajectories of sleep macro-architecture and sleep electroencephalographic (EEG) measures using linear mixed effect models (LMMs), considering age, sex, family history of alcohol use, body mass index, ethnicity, and alcohol use class (i.e., no-to-low, moderate or heavy) at each annual assessment. Results There were strong developmental changes in sleep macro-structure and EEG, most notably, a decrease in slow wave sleep percentage and slow wave (delta) EEG activity with advancing age (p=0.02)​. Compared to those who remained no-to-low drinkers, participants who became moderate/heavy drinkers during the follow-up period, had different sleep trajectories, especially those older at baseline at baseline, including higher slow wave activity (p = 0.04), higher REM sleep percentage (p = 0.03), poorer sleep efficiency​ (p=0.003), and longer latency to sustained sleep (p = 0.03). The effects of alcohol use depended on sex, with male heavy drinkers having more REM sleep than female heavy drinkers (p = 0.04). Overall, a positive family history of alcohol use was associated with less NREM sleep and shorter sleep duration. Conclusion Our results present novel findings showing that emerging alcohol use during adolescence exerts complex effects on sleep macro- and micro-structure, over and above normal developmental changes in sleep. These effects could, in part, be alcohol effects on brain maturation processes underlying sleep regulation. Support (If Any) AA021696, AA021690

Subjective-objective sleepiness discrepancy in adult-onset myotonic dystrophy type 1.

Subjective-objective sleepiness discrepancy in adult-onset myotonic dystrophy type 1.

Abnormal sleep physiology in children with 15q11.2-13.1 duplication (Dup15q) syndrome

BackgroundSleep disturbances in autism spectrum disorder (ASD) represent a common and vexing comorbidity. Clinical heterogeneity amongst these warrants studies of the mechanisms associated with specific genetic etiologies. Duplications of 15q11.2-13.1 (Dup15q syndrome) are highly penetrant for neurodevelopmental disorders (NDDs) such as intellectual disability and ASD, as well as sleep disturbances. Genes in the 15q region, particularly UBE3A and a cluster of GABAA receptor genes, are critical for neural development, synaptic protein synthesis and degradation, and inhibitory neurotransmission. During awake electroencephalography (EEG), children with Dup15q syndrome demonstrate increased beta band oscillations (12–30 Hz) that likely reflect aberrant GABAergic neurotransmission. Healthy sleep rhythms, necessary for robust cognitive development, are also highly dependent on GABAergic neurotransmission. We therefore hypothesized that sleep physiology would be abnormal in children with Dup15q syndrome.MethodsTo test the hypothesis that elevated beta oscillations persist in sleep in Dup15q syndrome and that NREM sleep rhythms would be disrupted, we computed: (1) beta power, (2) spindle density, and (3) percentage of slow-wave sleep (SWS) in overnight sleep EEG recordings from a cohort of children with Dup15q syndrome (n = 15) and compared them to age-matched neurotypical children (n = 12).ResultsChildren with Dup15q syndrome showed abnormal sleep physiology with elevated beta power, reduced spindle density, and reduced or absent SWS compared to age-matched neurotypical controls.LimitationsThis study relied on clinical EEG where sleep staging was not available. However, considering that clinical polysomnograms are challenging to collect in this population, the ability to quantify these biomarkers on clinical EEG—routinely ordered for epilepsy monitoring—opens the door for larger-scale studies. While comparable to other human studies in rare genetic disorders, a larger sample would allow for examination of the role of seizure severity, medications, and developmental age that may impact sleep physiology.ConclusionsWe have identified three quantitative EEG biomarkers of sleep disruption in Dup15q syndrome, a genetic condition highly penetrant for ASD. Insights from this study not only promote a greater mechanistic understanding of the pathophysiology defining Dup15q syndrome, but also lay the foundation for studies that investigate the association between sleep and cognition. Abnormal sleep physiology may undermine healthy cognitive development and may serve as a quantifiable and modifiable target for behavioral and pharmacological interventions.

Effects of Organic Light-Emitting Diodes on Circadian Rhythm and Sleep.

ObjectiveOrganic light-emitting diodes (OLEDs) emit less blue light than traditional light-emitting diodes (LEDs), and we previously found that early-night OLED light exposure (LE) delays the melatonin phase by less than LED at a color temperature of 4,000 K. As a follow-up study, we investigated the effects of OLED and LED at a different color temperature (3,000 K) on melatonin profile, sleep, and vigilance. Methods24 healthy subjects (27.5±5.1 years) were exposed to three light conditions [OLED, LED, and dim light (DL)] from 17:30 to 24:00, in a random order and with a 1-week interval. Saliva samples for melatonin were taken every hour from 18:00 to 24:00. Polysomnography (PSG) and a psychomotor vigilance test (PVT) were performed. ResultsMelatonin onset time was significantly delayed under OLED and LED compared with DL, with no significant difference between OLED and LED. The mean melatonin level at 24:00 under LED was lower than that under DL, but there was no significant difference between OLED LE and DL. The percentage of slow wave sleep (N3) in LED was significantly lower than in OLED. ConclusionExposure to light in the evening can suppress melatonin secretion late at night and disturb deep sleep, and those effects are slightly worse under LED than OLED.

062 Sex Differences in Slow Wave Sleep Following Evening Binge Alcohol Consumption

Abstract Introduction Binge alcohol consumption alters normal sleep architecture, often via increased slow wave sleep (SWS) and decreased rapid eye movement (REM) sleep. Women may be more susceptible to the sedative effects of alcohol during blood alcohol content (BAC) decrease as they report higher subjective sleepiness scores prior to bedtime. The purpose of the present study was to examine changes in SWS between men and women following binge alcohol consumption and determine the relation between BAC change at lights out and subsequent sleep architecture. Methods Twenty-three participants (11 men, 12 women) between the ages of 21–45 years were tested twice, once after evening binge alcohol consumption and once after fluid control (randomized, cross-over design). The alcohol dose was based on body weight and sex (1g/kg in men, 0.85g/kg in women) and served as a 4–5 drink equivalent consumed over two hours. Breath alcohol content (BrAC) was monitored in 15-minute increments from first drink consumption to lights out. Overnight polysomnography (PSG) was recorded in each individual and scored by a board-certified sleep physician. Statistical analysis consisted of repeated measures ANOVA and Pearson correlation (p&amp;gt;0.05). Results Age (24±4 vs. 26±6 years) and BMI (27±4 vs. 27±4 kg/m2) were similar between men and women. Peak BrAC (0.10±0.02% vs. 0.10±0.02%) and percent change (-19±11% vs. -19±11%) in BrAC from peak to lights out were also similar between the sexes. Peak BrAC was significantly correlated to the percentage of SWS in women (r=-0.71; p=0.01), but not men (r=-0.25; p=0.45). Similarly, the percent change in BrAC from peak to lights out was significantly correlated to the percentage of SWS in women (r=-0.66; p=0.02), but not men (r=-0.40; p=0.22). The SWS and REM latencies were not associated with either peak or lights out BrAC in both men and women. Conclusion Peak BrAC, and the rate of BrAC clearance prior to lights out, appear to impact SWS differently in men and women. Specifically, women appear to have more SWS in response to high BrAC than their male counterparts, suggesting a stronger depressor impact with regards to SWS in women. Support (if any) National Institutes of Health (AA-024892; U54GM115371; P20GM103474).

The impact of antiseizure medications on polysomnographic parameters: a systematic review and meta-analysis

BackgroundOral antiseizure medications (ASMs) are first-line treatments for patients with epilepsy. However, ASMs may alter sleep architecture, adversely affecting patient outcomes. The meta-analysis aimed to elucidate the effect of ASMs on sleep architecture. MethodsPubMed, Embase, and Cochrane Central database (up to Febrary 2021) were searched for randomized control trials (RCT) with effects of ASMs on polysomnography parameters. A meta-analysis using a random-effects model was performed. We did not set limitation to the participants with underlying diagnosis of epilepsy. ResultsEighteen randomized-controlled trials fulfilled the eligibility criteria. The effects of five main groups of ASMs (sodium channel blockers, calcium channel blockers, GABA enhancers, synaptic vesicle glycoprotein 2A [SV2A] ligand, and broad-spetrum ASMs) on slow-wave sleep (SWS), rapid eye movement (REM) sleep, and sleep efficiency (SE) were analyzed. Compared with placebo, calcium channel blockers and GABA enhancers significantly increased SWS. GABA enhancers also decreased REM sleep percentage, whereas calcium channel blockers significantly increased SE. Sodium channel blockers, SV2A ligand and broad-spectrum ASMs did not affect SWS, REM sleep, or SE. The subgroup analysis revealed that gabapentin, pregabalin, and tiagabine increased the percentage of SWS. Tiagabine also decreased REM sleep, whereas pregabalin increased SE. Finally, levetiracetam did not affect SWS, REM sleep, and SE. ConclusionsThis meta-analysis indicated that ASMs can have a statistically significant effect on sleep parameters; the effect differs between ASMs.