A Thalamocortical Perspective on Sleep Spindle Alterations in Neurodevelopmental Disorders.

Purpose of Review: Neurodevelopmental disorders are a group of conditions that affect the development and function of the nervous system, typically arising early in life. These disorders can have various genetic, environmental, and/or neural underpinnings, which can impact the thalamocortical system. Sleep spindles, brief bursts of oscillatory activity that occur during NREM sleep, provide a unique in vivo measure of the thalamocortical system. In this manuscript, we review the development of the thalamocortical system and sleep spindles in rodent models and humans. We then utilize this as a foundation to discuss alterations in sleep spindle activity in four of the most pervasive neurodevelopmental disorders-intellectual disability, attention deficit hyperactivity disorder, autism, and schizophrenia. Recent Findings: Recent work in humans has shown alterations in sleep spindles across several neurodevelopmental disorders. Simultaneously, rodent models have elucidated the mechanisms which may underlie these deficits in spindle activity. This review merges recent findings from these two separate lines of research to draw conclusions about the pathogenesis of neurodevelopmental disorders. Summary: We speculate that deficits in the thalamocortical system associated with neurodevelopmental disorders are exquisitely reflected in sleep spindle activity. We propose that sleep spindles may represent a promising biomarker for drug discovery, risk stratification, and treatment monitoring.

The Hierarchy of Coupled Sleep Oscillations Reverses with Aging in Humans.

A well orchestrated coupling hierarchy of slow waves and spindles during slow-wave sleep supports memory consolidation. In old age, the duration of slow-wave sleep and the number of coupling events decrease. The coupling hierarchy deteriorates, predicting memory loss and brain atrophy. Here, we investigate the dynamics of this physiological change in slow wave-spindle coupling in a frontocentral electroencephalography position in a large sample (N = 340; 237 females, 103 males) spanning most of the human life span (age range, 15-83 years). We find that, instead of changing abruptly, spindles gradually shift from being driven by slow waves to driving slow waves with age, reversing the coupling hierarchy typically seen in younger brains. Reversal was stronger the lower the slow-wave frequency, and starts around midlife (age range, ∼40-48 years), with an established reversed hierarchy between 56 and 83 years of age. Notably, coupling strength remains unaffected by age. In older adults, deteriorating slow wave-spindle coupling, measured using the phase slope index (PSI) and the number of coupling events, is associated with blood plasma glial fibrillary acidic protein levels, a marker for astrocyte activation. Data-driven models suggest that decreased sleep time and higher age lead to fewer coupling events, paralleled by increased astrocyte activation. Counterintuitively, astrocyte activation is associated with a backshift of the coupling hierarchy (PSI) toward a "younger" status along with increased coupling occurrence and strength, potentially suggesting compensatory processes. As the changes in coupling hierarchy occur gradually starting at midlife, we suggest there exists a sizable window of opportunity for early interventions to counteract undesirable trajectories associated with neurodegeneration.SIGNIFICANCE STATEMENT Evidence accumulates that sleep disturbances and cognitive decline are bidirectionally and causally linked, forming a vicious cycle. Improving sleep quality could break this cycle. One marker for sleep quality is a clear hierarchical structure of sleep oscillations. Previous studies showed that sleep oscillations decouple in old age. Here, we show that, rather, the hierarchical structure gradually shifts across the human life span and reverses in old age, while coupling strength remains unchanged. This shift is associated with markers for astrocyte activation in old age. The shifting hierarchy resembles brain maturation, plateau, and wear processes. This study furthers our comprehension of this important neurophysiological process and its dynamic evolution across the human life span.

Sleep spindles across youth affected by schizophrenia or anti-N-methyl-D-aspartate-receptor encephalitis.

Background: Sleep disturbances are intertwined with the progression and pathophysiology of psychotic symptoms in schizophrenia. Reductions in sleep spindles, a major electrophysiological oscillation during non-rapid eye movement sleep, have been identified in patients with schizophrenia as a potential biomarker representing the impaired integrity of the thalamocortical network. Altered glutamatergic neurotransmission within this network via a hypofunction of the N-methyl-D-aspartate receptor (NMDAR) is one of the hypotheses at the heart of schizophrenia. This pathomechanism and the symptomatology are shared by anti-NMDAR encephalitis (NMDARE), where antibodies specific to the NMDAR induce a reduction of functional NMDAR. However, sleep spindle parameters have yet to be investigated in NMDARE and a comparison of these rare patients with young individuals with schizophrenia and healthy controls (HC) is lacking. This study aims to assess and compare sleep spindles across young patients affected by Childhood-Onset Schizophrenia (COS), Early-Onset Schizophrenia, (EOS), or NMDARE and HC. Further, the potential relationship between sleep spindle parameters in COS and EOS and the duration of the disease is examined. Methods: Sleep EEG data of patients with COS (N = 17), EOS (N = 11), NMDARE (N = 8) aged 7-21 years old, and age- and sex-matched HC (N = 36) were assessed in 17 (COS, EOS) or 5 (NMDARE) electrodes. Sleep spindle parameters (sleep spindle density, maximum amplitude, and sigma power) were analyzed. Results: Central sleep spindle density, maximum amplitude, and sigma power were reduced when comparing all patients with psychosis to all HC. Between patient group comparisons showed no differences in central spindle density but lower central maximum amplitude and sigma power in patients with COS compared to patients with EOS or NMDARE. Assessing the topography of spindle density, it was significantly reduced over 15/17 electrodes in COS, 3/17 in EOS, and 0/5 in NMDARE compared to HC. In the pooled sample of COS and EOS, a longer duration of illness was associated with lower central sigma power. Conclusions: Patients with COS demonstrated more pronounced impairments of sleep spindles compared to patients with EOS and NMDARE. In this sample, there is no strong evidence that changes in NMDAR activity are related to spindle deficits.

Pediatric sleep: current knowledge, gaps, and opportunities for the future.

This White Paper addresses the current gaps in knowledge, as well as opportunities for future studies in pediatric sleep. The Sleep Research Society's Pipeline Development Committee assembled a panel of experts tasked to provide information to those interested in learning more about the field of pediatric sleep, including trainees. We cover the scope of pediatric sleep, including epidemiological studies and the development of sleep and circadian rhythms in early childhood and adolescence. Additionally, we discuss current knowledge of insufficient sleep and circadian disruption, addressing the neuropsychological impact (affective functioning) and cardiometabolic consequences. A significant portion of this White Paper explores pediatric sleep disorders (including circadian rhythm disorders, insomnia, restless leg and periodic limb movement disorder, narcolepsy, and sleep apnea), as well as sleep and neurodevelopment disorders (e.g. autism and attention deficit hyperactivity disorder). Finally, we end with a discussion on sleep and public health policy. Although we have made strides in our knowledge of pediatric sleep, it is imperative that we address the gaps to the best of our knowledge and the pitfalls of our methodologies. For example, more work needs to be done to assess pediatric sleep using objective methodologies (i.e. actigraphy and polysomnography), to explore sleep disparities, to improve accessibility to evidence-based treatments, and to identify potential risks and protective markers of disorders in children. Expanding trainee exposure to pediatric sleep and elucidating future directions for study will significantly improve the future of the field.

Feasibility, efficacy, and functional relevance of automated auditory closed-loop suppression of slow-wave sleep in humans.

Slow-wave sleep (SWS) is a fundamental physiological process, and its modulation is of interest for basic science and clinical applications. However, automatised protocols for the suppression of SWS are lacking. We describe the development of a novel protocol for the automated detection (based on the whole head topography of frontal slow waves) and suppression of SWS (through closed-loop modulated randomised pulsed noise), and assessed the feasibility, efficacy and functional relevance compared to sham stimulation in 15 healthy young adults in a repeated-measure sleep laboratory study. Auditory compared to sham stimulation resulted in a highly significant reduction of SWS by 30% without affecting total sleep time. The reduction of SWS was associated with an increase in lighter non-rapid eye movement sleep and a shift of slow-wave activity towards the end of the night, indicative of a homeostatic response and functional relevance. Still, cumulative slow-wave activity across the night was significantly reduced by 23%. Undisturbed sleep led to an evening to morning reduction of wake electroencephalographic theta activity, thought to reflect synaptic downscaling during SWS, while suppression of SWS inhibited this dissipation. We provide evidence for the feasibility, efficacy, and functional relevance of a novel fully automated protocol for SWS suppression based on auditory closed-loop stimulation. Future work is needed to further test for functional relevance and potential clinical applications.

Sleep regularity in healthy adolescents: Associations with sleep duration, sleep quality, and mental health.

Current evidence points to the importance of sleep for adolescent physical and mental health. To date, most studies have examined the association between sleep duration/quality and health in adolescence. An emerging line of research suggests that regularity in the timing of sleep may also play an important role in well-being. To address this aspect of sleep, the present study investigated daily variability of sleep, quantified using the sleep regularity index (SRI), in 46 adolescents (M = 12.78 ± 1.07 years) and its association with depressive symptoms/mental health. Sleep was measured during a 6 month period (M = 133.11 ± 36.42 nights) using actigraphs to quantify SRI values calculated for school days, weekends and holidays. Depressive symptoms and general psychopathology were assessed at the beginning (baseline) and end (follow-up) of the actigraphy measurements. Sleep was most regular during school days and associated with a longer total sleep time, shorter sleep onset latency, and higher sleep efficiency. Moreover, a higher SRI on school days was associated with fewer depressive symptoms at follow-up, whereas higher SRI on weekends was associated with less overall psychopathology at follow-up. Furthermore, the change in overall psychopathology, but not depressive symptoms across the two assessments was correlated with sleep regularity index. Our results suggest that regular timing of sleep is associated with sleep that is of longer duration and higher quality and may be protective of adolescent mental health. Therefore, adolescents should be encouraged not only to get enough sleep, but also to retain regular sleeping patterns to promote well-being and mental health.

The relationship between sleep disturbance and self-harming behaviours in high-risk clinical adolescents.

Emerging research has identified sleep disturbance as an important risk factor for predicting self-harming behaviours. However, the temporality of this relationship, particularly in clinical adolescent samples remains poorly understood. This study examines the relationship between sleep disturbance and self-harming behaviours (namely nonsuicidal self-injury and suicide attempts) in clinical adolescents engaging in risk-taking and self-harming behaviours using secondary analyses from a clinical cohort study. Cross-lagged structural equation modelling was used to determine whether baseline sleep disturbance and self-harming behaviours were predictors of each other over a one-year follow-up period in a sample of adolescents (n = 238, 89.5% female) attending and receiving treatment from an outpatient clinic specializing in risk-taking and self-harming behaviours. When controlling for age, sex and depressive symptoms, greater sleep disturbance (p = 0.001) at baseline independently predicted higher numbers of suicide attempts at follow-up. No bidirectional relationship was found when sleep disturbance was modelled with the frequency of nonsuicidal self-injury. This study adds to the growing evidence that sleep disturbance may predict suicidal behaviours. Clinicians should thus regularly assess for sleep disturbances when evaluating suicidal behaviours in high-risk adolescents. Further research and clinical trials should investigate whether sleep-based interventions may be efficacious in reducing the prevalence of suicidal behaviours.

Heritability of REM sleep neurophysiology in adolescence.

Alterations of rapid eye movement (REM) sleep have long been observed in patients with psychiatric disorders and proposed as an endophenotype-a link between behavior and genes. Recent experimental work has shown that REM sleep plays an important role in the emotional processing of memories, emotion regulation, and is altered in the presence of stress, suggesting a mechanism by which REM sleep may impact psychiatric illness. REM sleep shows a developmental progression and increases during adolescence-a period of rapid maturation of the emotional centers of the brain. This study uses a behavioral genetics approach to understand the relative contribution of genes, shared environmental and unique environmental factors to REM sleep neurophysiology in adolescents. Eighteen monozygotic (MZ; n = 36; 18 females) and 12 dizygotic (DZ; n = 24; 12 females) same-sex twin pairs (mean age = 12.46; SD = 1.36) underwent whole-night high-density sleep EEG recordings. We find a significant genetic contribution to REM sleep EEG power across frequency bands, explaining, on average, between 75 to 88% of the variance in power, dependent on the frequency band. In the lower frequency bands between delta and sigma, however, we find an additional impact of shared environmental factors over prescribed regions. We hypothesize that these regions may reflect the contribution of familial and environmental stress shared amongst the twins. The observed strong genetic contribution to REM sleep EEG power in early adolescence establish REM sleep neurophysiology as a potentially strong endophenotype, even in adolescence-a period marked by significant brain maturation.

Sleep and physical activity: results from a long-term actigraphy study in adolescents.

PURPOSE: Research to date suggests that physical activity is associated with improved sleep, but studies have predominantly relied on self-report measures and have not accounted for school day/free day variability. To address these gaps in the literature, the aim of the present study was to (a) quantify physical activity in adolescents using long-term daily actigraphy measurement and (b) to examine the association between actigraphically assessed steps and sleep behavior in a sample of healthy adolescents. To be able to capture intra- and inter-individual differences in the daily physical activity of adolescents, we examined within as well as between subjects effects and its association with sleep. METHODS: Fifty adolescents between 10 and 14 years of age were included in the present study. In total 5989 days of actigraphy measurement (average of 119 ± 40 days per participant; range = 39-195 days) were analyzed. We use multilevel modeling to disentangle the within and between subject effects of physical activity on sleep. In this way, we examine within an individual, the association between steps during the day and subsequent sleep on a day-to-day basis. On the other hand, our between subjects' analysis allows us to ascertain whether individuals with more overall physical activity have better sleep. RESULTS: Within a subject more steps on school and free days were associated with later bed times on school and free days as well as later rise times on school days only. On the other hand, comparing between subjects' effects, more steps were associated with lower sleep efficiency on free and school days. No other significant associations were found for the other sleep variables. CONCLUSION: Our results obtained through objective and long-term measurement of both sleep and number of steps suggest weak or non-significant associations between these measures for most sleep variables. We emphasize the importance of the methodology and the separation of within subject from between subject features when examining the relationship between physical activity and sleep.

Local slow-wave activity over the right prefrontal cortex reveals individual risk preferences.

In everyday life, we have to make decisions under varying degrees of risk. Even though previous research has shown that the manipulation of sleep affects risky decision-making, it remains unknown whether individual, temporally stable neural sleep characteristics relate to individual differences in risk preferences. Here, we collected sleep data under normal conditions in fifty-four healthy adults using a portable high-density EEG at participants' home. Whole-brain corrected for multiple testing, we found that lower slow-wave activity (SWA, an indicator of sleep depth) in a cluster of electrodes over the right prefrontal cortex (PFC) is associated with higher individual risk propensity. Importantly, the association between local sleep depth and risk preferences remained significant when controlling for total sleep time and for time spent in deep sleep, i.e., sleep stages N2 and N3. Moreover, the association between risk preferences and SWA over the right PFC was very similar in all sleep cycles. Because the right PFC plays a central role in cognitive control functions, we speculate that local sleep depth in this area, as reflected by SWA, might serve as a dispositional indicator of self-regulatory ability, which in turn reflects risk preferences.

Sleep: Twitch in tempo.

Sudden bursts of jerky movements during sleep, called twitches, aid early developmental brain wiring in mice. Translating these findings to humans, a new study reveals that quiet sleep twitches increase in early infancy and coordinate with sleep spindles to establish functional connectivity.

Naps not as effective as a night of sleep at dissipating sleep pressure.

The two-process model of sleep posits that two processes interact to regulate sleep and wake: a homeostatic (Process S) and a circadian process (Process C). Process S compensates for sleep loss by increasing sleep duration and intensity. Process C gates the timing of sleep/wake favouring sleep during the circadian night in humans. In this study, we examined whether taking six naps throughout a 24-hr period would result in the same amount of dissipation of homeostatic pressure at the end of the day as a night of sleep, when time in bed is equivalent. Data from 46 participants (10-23 years; mean = 14.5 [±â€…2.9]; 25 females) were analysed. Slow-wave energy, normalized to account for individual differences in slow-wave activity, was used as a measure of sleep homeostasis. In the nap condition, slow-wave energy of six naps distributed equally during a 24-hr period was calculated. In the baseline condition, slow-wave energy was measured after 9-hr time in bed. A paired t-test was used to compare nap and baseline conditions. A linear regression was used to examine whether slow-wave energy varied as a function of age. Slow-wave energy was greater during baseline than the nap condition (p < .001). No association between age and slow-wave energy was found for baseline or nap conditions. Our findings indicate that multiple naps throughout the day are not as effective at dissipating sleep pressure as a night of sleep. This is likely due to the influence of the circadian system, which staves off sleep during certain times of the day.

Sleep neurophysiology in childhood onset schizophrenia.

Altered sleep neurophysiology has consistently been reported in adult patients with schizophrenia. Converging evidence suggests that childhood onset schizophrenia (COS), a rare but severe form of schizophrenia, is continuous with adult onset schizophrenia. The aim of the current study was to characterize sleep neurophysiology in COS. An overnight sleep electroencephalogram (EEG) was recorded in 17 children and adolescents with COS (16 years ± 6.6) and 17 age and gender-matched controls. Non-rapid eye movement (NREM) and rapid eye movement (REM) sleep EEG power and coherence for the frequency bands delta (1.6-4.8 Hz), theta (5-8.4 Hz), alpha (8.6-11 Hz), beta 1 (16.4-20.2 Hz) and beta 2 (20.4-24.2 Hz) were compared between COS patients and controls. COS patients exhibited significant and widespread deficits in beta power during NREM and REM sleep. With regard to coherence, we found increases in COS patients across brain regions, frequency bands and sleep states. This study demonstrates the utility of the sleep EEG for studying vulnerable populations and its potential to aid diagnosis.

Sleep spindle activity in childhood onset schizophrenia: Diminished and associated with clinical symptoms.

Neuroimaging studies of childhood onset schizophrenia (COS), a rare yet severe form of schizophrenia with an onset before the age of 13 years, have shown continuity with adult onset schizophrenia. Previous research in adult patients has shown reduced sleep spindle activity, transient oscillations in the sleep electroencephalogram (EEG) generated through thalamocortical loops. The current study examines sleep spindle activity in patients with COS. Seventeen children and adolescents with COS (16 years ±6.6) underwent overnight sleep EEG recordings. Sleep spindle activity was compared between patients with COS and age and gender matched controls and correlated with clinical symptom severity. We found pronounced deficits in sleep spindle amplitude, duration, density and frequency in patients with COS (effect size = 0.61 to 1.96; dependent on metric and EEG derivation). Non-rapid eye movement (NREM) sleep EEG power and coherence in the sigma band (11-16 Hz) corresponding to spindle activity were also markedly diminished in patients with COS as compared to controls. Furthermore, the degree of deficit in power and coherence of spindles was strongly associated with clinician rated hallucinations and positive symptoms over widespread cortical regions. Our finding of diminished spindle activity and its association with hallucinations likely reflect dysfunction of the thalamocortical circuits in children and adolescents with COS. Given the relative ease of sleep EEG recordings in vulnerable populations, this study highlights the potential of such recordings to characterize brain function in schizophrenia.

Gender differences in adolescent sleep neurophysiology: a high-density sleep EEG study.

During adolescence, differences between males and females in physiology, behavior and risk for psychopathology are accentuated. The goal of the current study was to examine gender differences in sleep neurophysiology using high-density sleep EEG in early adolescence. We examined gender differences in sleep EEG power and coherence across frequency bands for both NREM and REM sleep in a sample of 61 adolescents (31 girls and 30 boys; mean age = 12.48; SD = 1.34). In addition, sleep spindles were individually detected and characterized. Compared to boys, girls had significantly greater spindle activity, as reflected in higher NREM sigma power, spindle amplitude, spindle frequency and spindle density over widespread regions. Furthermore, power in higher frequency bands (16.2-44 Hz) was larger in girls than boys in a state independent manner. Oscillatory activity across frequency bands and sleep states was generally more coherent in females as compared to males, suggesting greater connectivity in females. An exception to this finding was the alpha band during NREM and REM sleep, where coherence was higher (NREM) or not different (REM) in boys compared to girls. Sleep spindles are generated through thalamocortical circuits, and thus, the greater spindle activity across regions in females may represent a stronger thalamocortical circuit in adolescent females as compared to males. Moreover, greater global connectivity in females may reflect functional brain differences with implications for cognition and mental health. Given the pronounced gender differences, our study highlights the importance of taking gender into account when designing and interpreting studies of sleep neurophysiology.

Environmental Factors Shape Sleep EEG Connectivity During Early Adolescence.

Quantifying the degree to which genetic and environmental factors shape brain network connectivity is critical to furthering our understanding of the developing human brain. Sleep, a state of sensory disengagement, provides a unique opportunity to study brain network activity noninvasively by means of sleep electroencephalography (EEG) coherence. We conducted a high-density sleep EEG study in monozygotic (MZ; n = 38; mean age = 12.46; 20 females) and dizygotic (DZ; n = 24; mean age = 12.50; 12 females) twins to assess the heritability of sleep EEG coherence in early adolescence-a period of significant brain rewiring. Structural equation modeling was used to estimate three latent factors: genes, environmental factors shared between twins and environmental factors unique to each twin. We found a strong contribution of unique environmental factors (66% of the variance) and moderate genetic influence (19% of the variance) on sleep EEG coherence across frequencies and sleep states. An exception to this was sleep spindle activity, an index of the thalamocortical network, which showed on average a genetic contribution of 48% across connections. Furthermore, we observed high intraindividual stability of coherence across two consecutive nights suggesting that despite only a modest genetic contribution, sleep EEG coherence is like a trait. Our findings in adolescent humans are in line with earlier findings in animals that show the primordial cerebral map and its connections are plastic and it is through interaction with the environment that the pattern of brain network connectivity is shaped. Therefore, even in twins living together, small differences in the environment may cascade into meaningful differences in brain connectivity.

Association between depressive symptoms and sleep neurophysiology in early adolescence.

BACKGROUND: Depression is highly prevalent among adolescents, and depressive symptoms rise rapidly during early adolescence. Depression is often accompanied by subjective sleep complaints and alterations in sleep neurophysiology. In this study, we examine whether depressive symptoms, measured on a continuum, are associated with subjective and objective (sleep architecture and neurophysiology) measures of sleep in early adolescence. METHODS: High-density sleep EEG, actigraphy, and self-reported sleep were measured in 52 early adolescents (12.31 years; SD: 1.121; 25 female). Depressive symptoms were measured on a continuum using the Center for Epidemiological Studies Depression Scale (CES-D). The association between depressive symptoms and 2 weeks of actigraphy, self-reported sleep, sleep architecture, and sleep neurophysiology (slow wave activity and sigma power) was determined via multiple linear regression with factors age, sex, and pubertal status. RESULTS: Despite no association between polysomnography measures of sleep quality and depressive symptoms, individuals with more depressive symptoms manifested worse actigraphically measured sleep. Less sleep spindle activity, as reflected in nonrapid eye movement sleep sigma power, was associated with more depressive symptoms over a large cluster encompassing temporal, parietal, and occipital regions. Furthermore, worse subjectively reported sleep quality was also associated with less sigma power over these same areas. Puberty, age, and sex did not impact this association. CONCLUSIONS: Sleep spindles have been hypothesized to protect sleep against environmental disturbances. Thus, diminished spindle power may be a subtle sign of disrupted sleep and its association with depressive symptoms in early adolescence may signal vulnerability for depression.

Nature and Nurture: Brain Region-Specific Inheritance of Sleep Neurophysiology in Adolescence.

Sleep-specific oscillations of spindles and slow waves are generated through thalamocortical and corticocortical loops, respectively, and provide a unique opportunity to measure the integrity of these neuronal systems. Understanding the relative contribution of genetic factors to sleep oscillations is important for determining whether they constitute useful endophenotypes that mark vulnerability to psychiatric illness. Using high-density sleep EEG recordings in human adolescent twin pairs (n = 60; 28 females), we find that over posterior regions 80-90% of the variance in slow oscillations, slow wave, and spindle activity is due to genes. Surprisingly, slow (10-12 Hz) and fast (12-16 Hz) anterior spindle amplitude and σ power are largely driven by environmental factors shared among the twins. To our knowledge this is the first example of a neural phenotype that exhibits a strong influence of nature in one brain region, and nurture in another. Overall, our findings highlight the utility of the sleep EEG as a reliable and easy to measure endophenotype during adolescence. This measure may be used to measure disease risk in development before the onset of a psychiatric disorder; the location within the brain of deficits in sleep neurophysiology may suggest whether the ultimate cause is genetic or environmental.SIGNIFICANCE STATEMENT Two cardinal oscillations of sleep, slow waves and sleep spindles, play an important role in the core functions of sleep including memory consolidation, synaptic plasticity, and the recuperative function of sleep. In this study, we use a behavioral genetics approach to examine the heritability of sleep neurophysiology using high-density EEG in a sample of early adolescent twins. Our findings reveal a strong influence of both environmental and genetic factors in shaping these oscillations, dependent on brain region. Thus, during a developmental period when brain structure and function is in flux, we find that the sleep EEG is among the most heritable of human traits over circumscribed brain regions.

An update on adolescent sleep: New evidence informing the perfect storm model.

The maturation of sleep regulatory systems during adolescence in combination with psychosocial and societal pressures culminate in a "Perfect Storm" of short and ill-timed sleep and the associated consequences for many youngsters. This model, first described by Carskadon in 2011, guides our current thinking of adolescent sleep behavior. Since the original description, the field has moved forward with remarkable pace, and this review aims to summarize recent progress and describe how this new work informs our understanding of sleep regulation and sleep behavior during this developmental time frame.