Changes In Sleep Architecture Research Articles

Effectiveness of multi-modal home-based videoconference interventions on sleep in older adults: study protocol for a randomized controlled trial.

Aging is characterized by substantial changes in sleep architecture that negatively impact fitness, quality of life, mood, and cognitive functioning. Older adults often fail to reach the recommended level of physical activity to prevent the age-related decline in sleep function, partly because of geographical barriers. Implementing home-based interventions could surmount these obstacles, thereby encouraging older adults to stay active, with videoconference administration emerging as a promising solution. Increasing the availability of biological rhythms synchronizers, such as physical activity, light exposure, or vestibular stimulation, represents a viable non-pharmacological strategy for entraining circadian rhythms and potentially fortifying the sleep-wake cycle, thereby enhancing sleep in aging. This study aims to (1) assess the impact of remote physical exercise training and its combination with bright light exposure, and (2) investigate the specific contribution of galvanic vestibular stimulation, to sleep quality among healthy older adults with sleep complaints. One hundred healthy older adults aged 60-70 years with sleep complaints will be randomly allocated to one of four groups: a physical exercise training group (n = 25), a physical exercise training combined with bright light exposure group (n = 25), a galvanic vestibular stimulation group (n = 25) or a control group (i.e., health education) (n = 25). While physical exercise training and health education will be supervised via videoconference at home, bright light exposure (for the physical exercise training combined with bright light exposure group) and vestibular stimulation will be self-administered at home. Pre-and post-tests will be conducted to evaluate various parameters, including sleep (polysomnography, subjective questionnaires), circadian rhythms (actigraphy, temperature), fitness (physical: VO2 peak, muscular function; and motor: balance, and functional mobility), cognition (executive function, long-term memory), quality of life and mood (anxiety and depression). The findings will be anticipated to inform the development of recommendations and non-pharmaceutical preventive strategies for enhancing sleep quality in older adults, potentially leading to improvements in fitness, cognition, quality of life, and mood throughout aging.

Distinct lateral hypothalamic CaMKIIα neuronal populations regulate wakefulness and locomotor activity

For nearly a century, evidence has accumulated indicating that the lateral hypothalamus (LH) contains neurons essential to sustain wakefulness. While lesion or inactivation of LH neurons produces a profound increase in sleep, stimulation of inhibitory LH neurons promotes wakefulness. To date, the primary wake-promoting cells that have been identified in the LH are the hypocretin/orexin (Hcrt) neurons, yet these neurons have little impact on total sleep or wake duration across the 24-h period. Recently, we and others have identified other LH populations that increase wakefulness. In the present study, we conducted microendoscopic calcium imaging in the LH concomitant with EEG and locomotor activity (LMA) recordings and found that a subset of LH neurons that express Ca2+/calmodulin-dependent protein kinase IIα (CaMKIIα) are preferentially active during wakefulness. Chemogenetic activation of these neurons induced sustained wakefulness and greatly increased LMA even in the absence of Hcrt signaling. Few LH CaMKIIα-expressing neurons are hypocretinergic or histaminergic while a small but significant proportion are GABAergic. Ablation of LH inhibitory neurons followed by activation of the remaining LH CaMKIIα neurons induced similar levels of wakefulness but blunted the LMA increase. Ablated animals showed no significant changes in sleep architecture but both spontaneous LMA and high theta (8 to 10 Hz) power during wakefulness were reduced. Together, these findings indicate the existence of two subpopulations of LH CaMKIIα neurons: an inhibitory population that promotes locomotion without affecting sleep architecture and an excitatory population that promotes prolonged wakefulness even in the absence of Hcrt signaling.

Effects of periodic breathing on sleep at high altitude: a randomized, placebo-controlled, crossover study using inspiratory CO2.

Hypoxia at high altitude facilitates changes in ventilatory control that can lead to nocturnal periodic breathing (nPB). Here, we introduce a placebo-controlled approach to prevent nPB by increasing inspiratory CO2 and used it to assess whether nPB contributes to the adverse effects of hypoxia on sleep architecture. In a randomized, single-blinded, crossover design, 12 men underwent two sojourns (three days/nights each, separated by 4weeks) in hypobaric hypoxia corresponding to 4000m altitude, with polysomnography during the first and third night of each sojourn. During all nights, subjects' heads were encompassed by a canopy retaining exhaled CO2 , and CO2 concentration in the canopy (i.e. inspiratory CO2 concentration) was controlled by adjustment of fresh air inflow. Throughout the placebo sojourn inspiratory CO2 was ≤0.2%, whereas throughout the other sojourn it was increased to 1.76% (IQR, 1.07%-2.44%). During the placebo sojourn, total sleep time (TST) with nPB was 54.3% (37.4%-80.8%) and 45.0% (24.5%-56.5%) during the first and the third night, respectively (P=0.042). Increased inspiratory CO2 reduced TST with nPB by an absolute 38.1% (28.1%-48.1%), the apnoea-hypopnoea index by 58.1/h (40.1-76.1/h), and oxygen desaturation index ≥3% by 56.0/h (38.9.1-73.2/h) (all P<0.001), whereas it increased the mean arterial oxygen saturation in TST by 2.0% (0.4%-3.5%, P=0.035). Increased inspiratory CO2 slightly increased the percentage of N3sleep during the third night (P=0.045), without other effects on sleep architecture. Increasing inspiratory CO2 effectively prevented hypoxia-induced nPB without affecting sleep macro-architecture, indicating that nPB does not explain the sleep deterioration commonly observed at high altitudes. KEY POINTS: Periodic breathing is common during sleep at high altitude, and it is unclear how this affects sleep architecture. We developed a placebo-controlled approach to prevent nocturnal periodic breathing (nPB) with inspiratory CO2 administration and used it to assess the effects of nPB on sleep in hypobaric hypoxia. Nocturnal periodic breathing was effectively mitigated by an increased inspiratory CO2 fraction in a blinded manner. Prevention of nPB did not lead to relevant changes in sleep architecture in hypobaric hypoxia. We conclude that nPB does not explain the deterioration in sleep architecture commonly observed at high altitude.

Polysomnographic features associated with clonazepam and melatonin treatment in isolated REM sleep behavior disorder: Time for new therapeutic approaches?

Although clonazepam (CLO) and melatonin (MLT) are the most frequently used treatments for REM sleep behavior disorder, the polysomnographic features associated with their use are little known. The aim of this study was to evaluate polysomnographic and clinical parameters of patients with idiopathic/isolated REM sleep behavior disorder (iRBD) treated chronically with CLO, sustained-release MLT, alone or in combination, and in a group of drug-free iRBD patients. A total of 96 patients were enrolled: 43 drug-free, 21 with CLO (0.5-2 mg), 20 with sustained-release MLT (1-4 mg), and 12 taking a combination of them (same doses). Clinical variables and polysomnography were collected. Although clinical improvement was reported in all groups, MLT impacted sleep architecture more than the other treatments, with significant and large increase in N3 stage, moderate reduction in N2 and REM sleep, and moderate increase in REM latency. CLO moderately increased the percentage of both REM sleep and especially N2, while reducing N1 and wakefulness. Patients treated with both CLO and MLT did not show major changes in sleep architecture. These results suggest that the administration of MLT or CLO impacts (positively) on sleep parameters of iRBD patients. However, there is a need to better stratify patients, in order to treat them in a targeted manner, depending on the patient's individual sleep architecture and expected differential effects of these agents.

INVESTIGATING DREAMING IN COGNITIVELY DIVERSE OLDER ADULTS

Abstract Dreaming changes across the lifespan. While our understanding of how dreaming relates to aging and well-being has developed with respect to early and middle phases of the lifespan, the dreams of older adults remain under-studied. Reviews of the literature suggest decreases in dream recall and the emotionality of dream content that often precede age-related changes in sleep architecture, with few changes in dreaming occurring between ages 45-75, after which dream recall declines steeply. However, these findings are based on relatively few studies. This point is underscored when considering the effects of secondary aging on dreaming, where virtually no literature exists on the dreams of older adults experiencing mild cognitive impairment. Studying the dreams of older adults experiencing cognitive impairment may seem trivial when compared to other processes implicated in secondary aging, but recent studies examining the relationship between frequency of negative dream content and the increased risk of onset and acceleration of cognitive decline beg a closer examination of how dreaming contributes to a broader understanding of health and functioning across the lifespan. The scoping review of sleep, dreams, well-being and cognition across the lifespan, and the subsequent proposed study design seeks to employ the Hall and Van de Castle Coding System of content analysis to contribute to the literature on the dream frequency and content of cognitively typical older adults while also exploring the feasibility and methodological considerations of studying the dream content of older adults with mild cognitive impairment.

An acute bout of high-intensity exercise affects nocturnal sleep and sleep-dependent memory consolidation.

Acute exercise has been shown to affect long-term memory and sleep. However, it is unclear whether exercise-induced changes in sleep architecture are associated with enhanced memory. Recently, it has been shown that exercise followed by a nap improved declarative memory. Whether these effects transfer to night sleep and other memory domains has not yet been studied. Here, we investigate the influence of exercise on nocturnal sleep architecture and associations with sleep-dependent procedural and declarative memory consolidation. Nineteen subjects (23.68 ± 3.97 years) were tested in a balanced cross-over design. In two evening sessions, participants either exercised (high-intensity interval training) or rested immediately after encoding two memory tasks: (1) a finger tapping task and (2) a paired-associate learning task. Subsequent nocturnal sleep was recorded by polysomnography. Retrieval was conducted the following morning. High-intensity interval training lead to an increased declarative memory retention (p = 0.047, d = 0.40) along with a decrease in REM sleep (p = 0.012, d = 0.75). Neither procedural memory nor NREM sleep were significantly affected. Exercise-induced changes in N2 showed a positive correlation with procedural memory retention which did not withstand multiple comparison correction. Exploratory analyses on sleep spindles and slow wave activity did not reveal significant effects. The present findings suggest an exercise-induced enhancement of declarative memory which aligns with changes in nocturnal sleep architecture. This gives additional support for the idea of a potential link between exercise-induced sleep modifications and memory formation which requires further investigation in larger scaled studies.

Sleep Disorders and Aging in Women.

Women of advancing age can suffer from an array of sleep disorders. We review the changes in sleep architecture, the impact of hormonal changes on sleep, and the various sleep disorders in women of advancing age. A focused history in this population should include the temporal relation to menopause and comorbid conditions. Treatment options should involve patient preference and review of current medications and comorbid conditions to optimize sleep in this population.

Altered sleep architecture in children and adolescents with Down syndrome.

Children with Down syndrome (DS) may experience changes in sleep architecture (i.e., different sleep stages) that then affect waketime functioning, including learning, mood, and disruptive behavior. For designing and testing interventions, it is important to document any differences in sleep architecture in children with DS with and without co-occurring diagnoses, including neuropsychiatric diagnoses and obstructive sleep apnea (OSA). A retrospective cohort study was performed at Massachusetts General Hospital for children and adolescents with DS who underwent polysomnography (PSG) between August 2016 and July 2022. Patient data collected from the electronic medical record included diagnoses, age at PSG, and PSG report. Statistical analysis included unpaired T tests to test hypotheses about differences in sleep architecture within age groups, and differences between children with DS and a co-occurring diagnosis. One way ANOVA was used to determine statistical significance of OSA severity within patients with DS. When compared by age group, those with DS had negative changes in sleep architecture (e.g., less sleep and more wake) when compared to normative data. Within this cohort, having a co-occurring diagnosis of autism resulted in further, negative effects on sleep architecture. 89% of those with DS had diagnosed OSA but only those with severe OSA experienced negative effects on sleep architecture. Age is an important covariate when studying the sleep of children with DS and neurotypical children. Studies are needed to test whether minimizing the observed differences in sleep architecture will translate to improved learning, mood, and behavioral outcomes, and how treating OSA affects sleep architecture.

Influence of sex hormone use on sleep architecture in a transgender cohort.

Sex differences in sleep architecture are well-documented, with females experiencing longer total sleep time, more slow wave sleep (SWS), and shorter Rapid Eye Movement (REM) sleep duration than males. Although studies imply that sex hormones could affect sleep, research on exogenous sex hormones on sleep architecture is still inconclusive. This study examined sleep architecture changes in transgender individuals after 3 months of gender-affirming hormone therapy (GAHT). We assessed sleep architecture in 73 transgender individuals: 38 transmasculine participants who started using testosterone and 35 transfeminine participants who started using estrogens and antiandrogens. Sleep architecture was measured before GAHT and after 3 months of GAHT for 7 nights using an ambulatory single-electrode sleep EEG device. Changes in sleep architecture were analyzed using linear mixed models, and non-normally distributed outcomes were log-transformed and reported as percentages. In transmasculine participants, SWS decreased by 7 minutes (95% CI: -12; -3) and 1.7% (95% CI: -3%; -0.5%), REM sleep latency decreased by 39% (95% CI: -52%; -22%) and REM sleep duration increased by 17 minutes (95% CI: 7; 26) after 3 months of GAHT. In transfeminine participants, sleep architecture showed no significant changes after 3 months of GAHT. Sleep architecture changes after 3 months of masculinizing GAHT in line with sleep in cisgender males, while it shows no changes after feminizing GAHT. The sex-specific nature of these changes raises new questions about sex hormones and sleep. Future research should focus on studying possible underlying neural mechanisms and clinical consequences of these changes.

Moving time zones in a flash with light therapy during sleep

In humans, exposure to continuous light is typically used to change the timing of the circadian clock. This study examines the efficiency of a sequence of light flashes (“flash therapy”) applied during sleep to shift the clock. Healthy participants (n = 10) took part in two 36-h laboratory stays, receiving a placebo (goggles, no light) during one visit and the intervention (goggles, 2-ms flashes broad-spectrum light for 60 min, delivered every 15 s, starting 30 min after habitual sleep onset) during the other. Circadian phase shift was assessed with changes in salivary dim light melatonin onset (DLMO). Sleep, measured with polysomnography, was analyzed to assess changes in sleep architecture and spectral power. After 1 h of flashes, DLMO showed a substantial delay (1.13 ± 1.27 h) compared to placebo (12 ± 20 min). Two individuals exhibited very large shifts of 6.4 and 3.1 h. There were no substantive differences in sleep architecture, but some evidence for greater instability in sleep. 1 h of flash therapy during sleep evokes large changes in circadian timing, up to 6 h, and does so with only minimal, if any, impact on sleep. Flash therapy may offer a practical option to delay the circadian clock in shift workers and jet travelers.

Accelerometer-derived sleep measures in idiopathic dystonia: A UK Biobank cohort study.

Sleep disturbance is an increasingly recognized non-motor trait in dystonia, with varying findings reported to date. Here, we examine sleep in a UK Biobank derived dystonia cohort using subjective self-reported sleep symptoms and objective accelerometer-derived sleep measures, with comparison to a control population. A total of 241 dystonia cases were compared to 964 matched controls in analysis of self-reported sleep symptoms and changes in sleep architecture using wrist-worn triaxial accelerometers. Dystonia participants had poorer self-reported sleep patterns compared to controls. Accelerometery measurements demonstrated later sleep times, reduced time in bed, and shifts in circadian rhythm. No association was observed with pain, and only limited relationships with psychiatric symptoms. This study demonstrates the utility of accelerometers in longer term evaluation of sleep in dystonia, for measurement of disturbance and response to treatment. Compared to controls, altered sleep and circadian rhythm were more common in dystonia patients which may contribute to the clinical phenotype.

0218 Changes in sleep architecture and topography of sleep EEG slow wave activity following acute wake extension in early adolescence

Abstract Introduction A progression of peak sleep EEG slow wave activity (SWA; EEG power 0.5-4Hz) from posterior to anterior expression reflects brain development. Further, increased EEG SWA after extended wakefulness is a marker of sleep pressure. However, it is unclear whether recovery sleep SWA in later youth is expressed in a similar scalp topography as typical sleep. Using experimental wake-extension, we investigated homeostatic changes in sleep architecture and SWA topography in early adolescence. Methods Twenty-two young adolescents (M±SD: 12.03±1.14y, 12F) participated in two consecutive laboratory stays after at least a week of at-home actigraphy-monitored stabilization (9.5h in bed). A baseline night (BSL; 9.5h 21:00-06:30) was followed by wake-extension (WE) to 02:30 and a 4h recovery sleep opportunity (RS; 02:30-06:30), each monitored by polysomnography including a 25-channel EEG array. The current analyses examined R&amp;K sleep architecture at BSL and RS. SWA in RS was compared to the first 4h of BSL in two ways: (1) absolute NREM power (µV2); (2) an index (TI) of the topographical distribution of midline SWA (FPz-AFz-Fz-FCz-Cz-CPz-Pz-POz-Oz) providing a score of 1 to 9 indicating frontal to occipital peak distribution. Results WE significantly altered RS sleep architecture, including an increase in slow-wave sleep (%TST) versus BSL (M±SD BSL: 26.76±5.69%, RS: 51.65±7.83%, t(21)=-17.09, p&amp;lt;.001, d=-3.65). SWA was also significantly greater in RS (channel-averaged SWA BSL: 11883.50±5142.17 µV2, RS: 18955.82±7451.20 µV2, t(21)=-8.67, p&amp;lt;.001) with 22/25 individual electrodes meeting Bonferroni-corrected significance (ps&amp;lt;.001). Finally, we observed a small frontal shift (t(21)=2.39, p=.027, d=.51) of maximal SWA in RS (TI: 4.46±2.58; i.e., FCz/Cz) compared to BSL (5.32±2.78, i.e., Cz/CPz). Conclusion These data indicate robust sleep homeostasis in young adolescents after wake extension, expressed as increased SWA across the scalp. The findings also add to existing literature by indicating that SWA topography may also be sensitive to homeostatic challenge. Specifically, a baseline centroparietal locus of maximal SWA typical to this age became more frontocentral in recovery sleep. This anterior shift may reflect a homeostatic need over developmentally sensitive prefrontal cortex. Next steps will assess how individual responses may reflect a child’s neurodevelopment (e.g., inattention symptoms) or manifested behavior after wake extension and recovery sleep. Support (if any) K01MH109854, P20GM139743, R01HD103655

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

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

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

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

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

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

Sleep changes during a spontaneous manic episode: PSG assessment in a clinical context

Sleep plays a key role in the pathogenesis and clinical presentation of mood disorders. However, only a few studies have investigated sleep architecture during the manic episodes of Bipolar Disorder (BD) and changes in sleep parameters that follow clinical variations.Twenty-one patients (8 males, 13 females) affected by BD, manic phase, underwent polysomnographic recordings (PSG) at the beginning of the admission in our ward (T0) and after three weeks of hospital treatment (T1). All participants were clinically evaluated using Young Mania Rating Scale (YMRS), Pittsburgh Sleep Quality Index (PSQI) and Morningness-Eveningness Questionnaire (MEQ).During the admission, we observed an increase in both quantity (Total Sleep Time - TST) and quality (Sleep Efficiency - SE) of sleep. In addition, clinical improvement, evaluated with YMRS and PSQI scales, was accompanied by a significant increase in the percentage of REM sleep.According to our findings, the improvement of manic symptoms is accompanied by an increase in "REM pressure" (increase in REM% and REM density, reduction of REM latency).Overall, changes in sleep architecture appear to be markers sensitive to clinical variations during manic phases of Bipolar Disorder.

The Assessment and Management of Insomnia Among Older Adults

As many as 50% of older adults have concerns regarding the initiation or maintenance of sleep. The underdiagnosis or misdiagnosis of sleep disorders can cause significant complications in the elderly, and this symposium aims to provide the geriatric specialist with the knowledge and tools to evaluate and treat common sleep concerns. The session will open with a brief introduction overviewing the epidemiology and significance of insomnia. Dr. Srinivasan will open with a review of the physiologic stages of the sleep cycle. She will also discuss age-related changes in sleep architecture that clinicians should be aware of when conceptualizing sleep in elderly patients.In section 2, Dr. Johnson will review the evaluation of insomnia in older adults, with a focus on differential diagnosis of sleep disorders. Insomnia will be sub-divided into initial, middle, and terminal insomnia and include brief overviews of obstructive sleep apnea, parasomnias including REM sleep behavior disorder, restless legs syndrome, and factors impacting the circadian cycle. Screening tools and scales to assist in the evaluation of sleep disorders will also be discussed.Section 3 will be an overview of non-pharmacological interventions from Dr. Srinivasan. She will review the evidence for Cognitive Behavioral Therapy for Insomnia (CBT-I) and also discuss the core components of CBT-I. While sleep hygiene and behavioral therapies are usually considered first line treatment, pharmacotherapy may be beneficial as adjunctive treatment in patients with persistent insomnia who are unable to pursue cognitive behavioral therapies. According to the medical literature, both treatment modalities have been found to yield similar short-term outcomes, while CBT-I has been shown to yield better long-term outcomes. In the 4th section of the session, Dr. Dix will provide an overview of different classes of pharmacological interventions for insomnia, discussing a variety of treatments and their mechanism of action, dosing, efficacy, risks, and benefits. Prior to allowing time for questions from the audience, Dr. Tampi will briefly discuss the practical application of available evidence in managing insomnia among older adults.

Animal models of human insomnia.

Insomnia disorder (chronic sleep continuity disturbance) is a debilitating condition affecting 5%-10% of the adult population worldwide. To date, researchers have attempted to model insomnia in animals through breeding strategies that create pathologically short-sleeping individuals or with drugs and environmental contexts that directly impose sleeplessness. While these approaches have been invaluable for identifying insomnia susceptibility genes and mapping the neural networks that underpin sleep-wake regulation, they fail to capture concurrently several of the core clinical diagnostic features of insomnia disorder in humans, where sleep continuity disturbance is self-perpetuating, occurs despite adequate sleep opportunity, and is often not accompanied by significant changes in sleep duration or architecture. In the present review, we discuss these issues and then outline ways animal models can be used to develop approaches that are more ecologically valid in their recapitulation of chronic insomnia's natural aetiology and pathophysiology. Conditioning of self-generated sleep loss with these methods promises to create a better understanding of the neuroadaptations that maintain insomnia, including potentially within the infralimbic cortex, a substrate at the crossroads of threat habituation and sleep.

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

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

Effect of obstructive sleep apnea syndrome on sleep architecture: comparative study between geriatrics and middle-aged adult patients

Abstract Background Obstructive sleep apnea (OSA) is a prevalent sleep disordered breathing in geriatrics but still frequently undiagnosed. Sleep architecture changes with ageing. Geriatrics spend more time in the N1, N2 than in N3, REM. Also, there are more frequent awakenings, arousals and sleep stage shifts. This leads to decrease in sleep efficiency. Geriatric patients with OSA have more affected sleep architecture than middle-aged adults. The aim This work aimed to assess and compare sleep architecture changes in geriatrics versus middle-aged adult patients with OSA syndrome. Patients and methods This comparative study conducted in chest department Menoufia University Hospitals included 50 patients divided to two equal groups; geriatric group age 65 years old or more and middle-aged adult group aged from 18 to 50 years old. All patients were complaining of symptoms suggestive of OSA. All patients underwent sleep questionnaires and Polysomnography using model; Philipsrespironic alice6. Results There was no statistically significant difference between the studied groups regarding sex, smoking, co morbidities, BMI and symptoms. Regarding changes in sleep architecture, geriatric group showed a significantly higher Sleep latency and wakefulness after sleep onset in comparison to middle-aged adults (P=0.004 and 0.039, respectively) versus significantly lower Sleep efficiency, N3%, REM% (P=0.009,0.011 and 0.001, respectively). The median Total Apnea-Hypopnea index was 40.2 (/h sleep) in geriatric group and 35.4 in middle-aged adult group. Regarding severity of OSA; geriatric group showed mild OSA in five (20%) patients, moderate in five (20%) patient and severe in 15 (60%) patients. Middle-aged adults showed mild OSA in 10 (40%) patients, moderate in two (8%) patients, and severe in 13 (52%) patients. Conclusions Sleep architecture is affected in all OSA patients, but these changes are more obvious in geriatric patients. Geriatric patients have higher wakefulness after sleep onset and sleep latency. On the other hand, they have a lower N3%, REM% and sleep efficiency.