ArticleLiterature Review

Long-term sleep disturbances in children: A cause of neuronal loss

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Abstract

Short-term sleep loss is known to cause temporary difficulties in cognition, behaviour and health but the effects of persistent sleep deprivation on brain development have received little or no attention. Yet, severe sleep disorders that last for years are common in children especially when they have neurodevelopmental disabilities. There is increasing evidence that chronic sleep loss can lead to neuronal and cognitive loss in children although this is generally unrecognized by the medical profession and the public. Without the restorative functions of sleep due to total sleep deprivation, death is inevitable within a few weeks. Chronic sleep disturbances at any age deprive children of healthy environmental exposure which is a prerequisite for cognitive growth more so during critical developmental periods. Sleep loss adversely effects pineal melatonin production which causes disturbance of circadian physiology of cells, organs, neurochemicals, neuroprotective and other metabolic functions. Through various mechanisms sleep loss causes widespread deterioration of neuronal functions, memory and learning, gene expression, neurogenesis and numerous other changes which cause decline in cognition, behaviour and health. When these changes are long-standing, excessive cellular stress develops which may result in widespread neuronal loss. In this review, for the first time, recent research advances obtained from various fields of sleep medicine are integrated in order to show that untreated chronic sleep disorders may lead to impaired brain development, neuronal damage and permanent loss of developmental potentials. Further research is urgently needed because these findings have major implications for the treatment of sleep disorders.

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... Sleep disorders, including chronic sleep deprivation, are thought to cause declines in neural function; memory and learning; gene expression; neurogenesis; and cognitive, behavioral, and health functions through a variety of mechanisms. If these changes continue for a long period of time, excessive cellular stress may result, leading to widespread neuronal loss [29]. As mentioned above, sleep deprivation has been reported to cause various problems related to human life-sustaining functions [30][31][32]. ...
... A lifestyle in which sleep deprivation during the weekdays is compensated for by sleeping late into the morning on weekends may lead to "social jet lag" [3,39,40]. (5) If sleep deprivation is insufficiently compensated, the accumulation of sleep deprivation may lead to sleep debt, which may lead to various dysfunctions of the entire body, including decreased brain function [29][30][31][32]. ...
... I will leave the treatment to other papers, but I will provide a brief overview here. It is recommended that sleep disorders, especially those in infancy and early childhood, be addressed promptly and without delay [29,[76][77][78]. It is known that addressing and treating sleep disorders in infancy not only promotes the child's physical and mental development, but also contributes to maintaining the physical and mental health of the parents [79][80][81], so it is best not to leave the problem unattended even for a short period of time. ...
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Sleep disorders in children have a negative impact on mental and physical development, and a lack of sleep is one of the most important problems in infancy. At the age when naps are commonly accepted, the judgment of whether the amount of sleep is adequate has been based on the total amount of sleep per day. In other words, the idea is that even if the amount of sleep at night is insufficient, it is not considered insufficient if it is compensated for by taking a long nap or sleeping late on weekend mornings. However, these lifestyle habits disrupt the circadian rhythm and cause social jet lag, which is not appropriate for healthy mental and physical development. Therefore, in this review, I present the average required nighCime basic sleep duration (NBSD) of 10 h for Japanese and 11 h for Caucasian children as a judgment standard. (1) If the child sleeps less than 8 h at night, and (2) if the child sleeps less than 9 h at night or 30 to 60 min less than the required NBSD, immediate treatment is recommended. I also discuss briefly how to address sleep insufficiency in childhood.
... Short-term and long-term sleep disturbances both have physiological effects on people. According to the review article written by Jan and colleagues, short-term sleep loss can lead to disruptive cognition and behavior functioning temporarily, as well as health problems [7]. It can be caused by a few hours' sleep lost. ...
... It can be caused by a few hours' sleep lost. However, long-term sleep disturbance refers to persistent sleep difficulties with insufficient amount of sleep for a couple of years or even lasts for lifetime [7]. Cumulative evidence has shown that long-term sleep loss give rise to neuronal and cognitive loss in youngsters. ...
... Cumulative evidence has shown that long-term sleep loss give rise to neuronal and cognitive loss in youngsters. Specifically, chronic sleep loss can take away the exposure to healthy environment from children during critical developmental periods, which is the precondition for their cognitive growth [7]. Besides, sleep disturbance can negatively affect the functions of cells, organs, neuroprotective in circadian physiology etc. Neuronal functions are deteriorated widely by sleep loss through many different mechanisms, as well as learning, memory, neurogenesis and many other changes [7]. ...
... Despite the documented benefits of healthy and restorative sleep on brain development and healing [6][7][8][9][10][11], little is known about how SWDs impact cognitive recovery during the acute recovery phase after pediatric TBI, especially among children hospitalized in the Pediatric Intensive Care Unit (PICU) for mild, moderate, or severe TBI. ...
... Prior findings also show TBI results in an increase in SWDs compared to healthy cohorts or orthopedic injury controls [12,13]. This is important because healthy sleep is vital for brain maturation and memory consolidation, which impact cognitive processes such as executive functioning important for normal childhood development and academic achievement [6][7][8][9][10][11][12][14][15][16][17][18][19]. Disturbances in executive function are associated with a number of problematic long-term outcomes for pediatric TBI survivors such as poor adaptive skills, personality changes, impaired social relationships, behavioral problems, and worse academic achievement [20][21][22][23][24][25][26]. ...
... The term executive function is commonly used to describe complex neurocognitive processes such as a person's ability to regulate attention and concentration, self-monitor, plan, organize, utilize cognitive flexibility, engage in abstract reasoning, problem-solve, inhibit impulses, initiate tasks, and regulate emotions [60]. Given the importance of the executive function system, it is clear why it is critical for academic achievement and general childhood development [6][7][8][9][10][11][14][15][16][17][18][19]. Unfortunately, the executive function system is vulnerable to dysfunction after a TBI. ...
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Over 50,000 children are hospitalized annually for traumatic brain injury (TBI) and face long-term cognitive morbidity. Over 50% develop sleep/wake disturbances (SWDs) that can affect brain development and healing. We hypothesized SWDs would portend worse executive function outcomes in children aged 3–18 years with TBI 1–3 months after hospital discharge. SWDs were defined using the Sleep Disturbances Scale for Children (t-scores ≥ 60). Outcomes included the Global Executive Composite (GEC, t-score) from the Behavior Rating Inventory of Executive Function, Second and Preschool Editions, and multiple objective executive function assessments combined through Principal Components Analysis into a Neurocognitive Index (NCI, z-score). Multiple linear regression evaluated associations between SWDs and executive function outcomes, controlling for covariates. Among 131 children, 68% had clinically significant SWDs, which were associated with significantly worse median scores on the GEC (56 vs. 45) and NCI (−0.02 vs. 0.42; both p < 0.05). When controlling for baseline characteristics and injury severity in multivariable analyses, SWDs were associated with worse GEC (β-coefficient = 7.8; 95% Confidence Interval = 2.5, 13.1), and worse NCI (β-coefficient = −0.4; 95% Confidence Interval = −0.8, −0.04). SWDs in children with TBI are associated with worse executive function outcomes after hospital discharge, and may serve as modifiable targets to improve outcomes.
... Additionally, children's sleep problems are commonly found and a study reported that chronic sleep deprivation may shift their biological clock and could lead even to neuronal loss [5]. Furthermore, the circadian rhythm's biological clock controls not only the sleep/wake rhythm, but the so-called life support systems (e.g., the autonomic nervous system, hormone secretion, thermoregulation, energy metabolism, the immune system, coordinated movement, and maintenance of brain function balance) [6,7]. ...
... To put it the other way around, the data in this study prove that some children have insufficient sleep time on weekdays or have a habit of waking after 7 a.m. in the morning due to a shift in their living hours. Life rhythm is the basic factor to create biological clock of children and we cannot ignore the number of children whose biological clocks have shifted [4,5]. ...
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We investigated the sleep-wake rhythm of nursery school children with the aim of supporting their health and balanced mental/physical development. We analyzed 4881 children from infant to 6 years of age, using 2-week sleep tables recorded by their guardians. The table contains sleep onset times, wake times, nighttime/daytime sleep duration, and the differences in these between weekdays and weekends. The total sleep decrement of children with age is due to a decrease in daytime sleep only, and nighttime sleep duration remains almost unchanged at about 10 hours, and is therefore called the nighttime basic sleep duration (NBSD). While sleep onset time stabilizes at around 9:30 pm by the age of 2, wake-up times to be before 7 am, resulted in weekdays sleep insufficiency. This lack of sleep is compensated by long naps on weekdays and by catching up sleep on weekends morning, which may be the background to future social-jet-lag. Guardians are encouraged to know their children's exact NBSD and set an ap-propriate bedtime to maintain it on weekdays, which prevent sleep dept and form a daily rhythm of waking up at the same time both on weekdays/weekends. These conditions are believed to maintain balance in mental/physical development and school-social-adaptation.
... NREM sleep may play an important metabolic role in correcting energy and nutritional imbalances after prolonged wakefulness, whereas REM sleep is more important in providing support for endogenous stimulation, neurogenesis, neurological and emotional development, and learning and memory formation (Jan et al., 2010). In the present study, we observed a significant increase in escape latency in the CSD group compared to the CON group, especially on the second and third days; the administration of melatonin agonists and inhibitors to CSD rats resulted in a significant decrease and increase in escape latency respectively ( Figure 1a). ...
... It is widely accepted that sleep deprivation has a detrimental impact on cognitive functions (Jan et al., 2010;Musiek et al., 2013). Early studies on neurological stromal damage due to sleep deprivation were mostly on neurons, but in recent years, more and more studies have verified the role of neuroglia, such as astrocytes, but less on microglia (Frank & Heller, 2019;Garofalo et al., 2020). ...
Article
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Purpose To investigate the mechanism underlying the regulatory effect of melatonin on chronic sleep deprivation‐related cognitive impairment. Methods Chronic sleep deprivation (CSD) model was established using the MMPM method. After the model was established, melatonin receptor agonist and inhibitor were given, respectively. Water maze was conducted to record the escape latency and the duration of crossing the platform of space exploration. The concentration of TNF‐α, IL‐6, MDA, and SOD was measured by ELISA. Immunofluorescence was used to determine the expression level of CD86 and CD206, while the mRNA expression of Bax, Bcl‐2, P65, IκB, and BMAL1 was detected by qPCR. Western blotting assay was utilized to determine the protein expression of Bax, Bcl‐2, P65, p‐P65, IκB, p‐I κB, and BMAL1. Results Compared with the control, the escape latency was greatly increased on the second and third day, accompanied by the increased expression of TNF‐α, IL‐6, MDA, and SOD in serum. Furthermore, dramatically upregulated Bax, Bcl‐2, P65, IκB, and CD86 were observed in the model group, accompanied by the declined expression level of BMAL1 and CD206. Compared with the model group, the escape latency was declined, the concentration of TNF‐α, IL‐6, MDA, and SOD was decreased, the expression level of Bax, Bcl‐2, P65, IκB, and CD86 was declined, and the level of BMAL1 and CD206 was promoted by the treatment of the melatonin agonist, while the opposite results were observed under the treatment of the melatonin inhibitor. Conclusion Melatonin upregulates BMAL1 to attenuate chronic sleep deprivation‐related cognitive impairment by alleviating oxidative stress.
... Zihinsel engelli çocuklarla yapılan bir çalışmada 3 yaş grubu çocukların %14'ünde gece sık uyanma, %12'sinde uykuya dalmada güçlük, 8 yaş grubunda ise %12 uykuya dalmada güçlük, %3 oranında da gece sık uyanma gibi sorunların olduğu bildirilmiştir. Uyurgezerlik %17, uykuda konuşma %5, uykuda horlama %10-12, obstrüktif uyku apne sendromu %2, uykusuzluk %10-30 oranında bildirilmiştir (24). Uyku ile ilgili yapılan başka bir araştırma ise İzmir ilindeki bir Özel Eğitim İlköğretim Okulu'nda eğitim gören zihinsel yetersizliği olan 59 çocuk ile yürütülmüştür. ...
... Çocukların uyku örüntülerini/ düzenlerini karşılaştıran araştırmalar planlanması önerilebilir. Sağlıklı uyku alışkanlıklarının geliştirilmesi için bebeklik döneminden başlayarak ailelere danışmanlık yapılması, uyku saati rutinlerinin oluşturulması, yatma zamanlarının düzenlenmesi, yatağa gitme zamanı yaklaştığında sessiz bir ortam oluşturulması, yatak odalarının rahat-sessiz-loş-uygun ısıda olmasına özen gösterilmesi gibi önlemler alınabilir (24). Çocuğun hem kendi hem de ailesine ilişkin uyku özellikleri, günlük rutin alışkanlıkları, yatmanda önce yapılan rutinler, uyku çevresi, zamanlaması uyku kalitesini olumlu yönde etkilemektedir (32). ...
Article
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Similar to essential air, water, and food, sleep is a basic physiological requirement for all living beings. Sleep is essential for growth and development in children. Sleep problems are considered to be a major challenge in physiological, psychological, and social dimensions, especially for children with intellectual disabilities as well as their mothers. Therefore, understanding and taking appropriate measures is necessary to address sleep problems that negatively affect these children and their mothers. This review aimed to identify sleep problems and provide solutions for children with intellectual disabilities and their mothers.
... In addition to screen use, growing evidence highlights the critical role of sleep as a fundamental mechanism facilitating behavioural attention and sustained attention in the classroom (Paavonen et al., 2009;Gruber et al., 2012;Davidson et al., 2021). Sleep is essential for brain development and functioning in children (Jan et al., 2010;Gruber et al., 2012). Poor sleep is associated with less efficient attentional processing (Hoyniak et al., 2015) and poorer sustained attention in children (Davidson et al., 2021). ...
... Screen activities that are alerting may increase levels of physiological and psychological arousal, leading to difficulties in falling asleep and reduced REM sleep, and ultimately poorer sleep quality (Higuchi et al., 2005). Given the important implications of sleep in brain and cognitive development (Jan et al., 2010;Gruber et al., 2012), greater awareness by parents and health professionals of the detrimental impact of screen use just before bedtime is needed and this adds to the growing importance of the need to remove screen time prior to bedtime for all children of primary age. ...
Article
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There are growing concerns that increased screen device usage may have a detrimental impact on classroom behaviour and attentional focus. The consequences of screen use on child cognitive functioning have been relatively under-studied, and results remain largely inconsistent. Screen usage may displace the time usually spent asleep. The aim of this study was to examine associations between screen use, behavioural inattention and sustained attention control, and the potential modifying role of sleep. The relations between screen use, behavioural inattention, sustained attention and sleep were investigated in 162 6- to 8-year-old children, using parent-reported daily screen use, the SWAN ADHD behaviour rating scale, The sustained attention to response task and the children’s sleep habits questionnaire. Tablet use was associated with better sustained attention performance but was not associated with classroom behavioural inattention. Shorter sleep duration was associated with poorer behavioural inattention and sustained attention. Sleep quality and duration did not act as mediators between screen usage and behavioural inattention nor sustained attention control. These findings suggest that careful management of the amount of time spent on electronic screen devices could have a beneficial cognitive impact on young children. The results also highlight the critical role of sleep in enhancing both behavioural attention and sustained attention, which are essential for supporting cognitive development and learning.
... F. Cognitive problems: Having standard sleep is essential for neurocognitive function. Sleep problems will affect the cognition in all ages, but the effect is more prominent in children who are in the period of brain development [22,65]. It is documented that an association exists between chronic inadequate sleep and an increased risk of impulsivity, risk-taking behaviors, and immature reasoning as well as decision making [27,28]. ...
... Nearly, all systems in the body show changes during sleep disruptions, although the severity of these effects differs by the chronicity of sleep problem [28,51]. It seems that the adverse effects following sleep disturbances are more prominent in the brain in younger population (children and adolescents), while adults and older ages experience more chronic diseases, such as cardiovascular and metabolism problems [26,65]. Considering the rising prevalence of sleep problems among all ages, increasing use of computer and smartphones during the late afternoon, and higher engagement of young adults in shift-works, more attention should be paid to sleep schedule by societies in order to prevent future development of chronic diseases. ...
Chapter
Almost all organisms have sleep time. In humans, about one third of life is spent in sleeping or trying to fall asleep. Obtaining the standard sleep in each of the life periods is of crucial importance. Adequate duration, good quality, appropriate timing and regularity, along with absence of any associated sleep disorders are the main features of a standard sleep. Genes, gender, and age mainly determine the sleep needs. Sleep is essential for the proper functioning of multiple body organs and systems; thus, its problems will adversely affect nearly all body organs. These adverse health consequences depend on the chronicity of the problem, age, and type of the sleep disturbance. It seems that the adverse effects following sleep disturbances are more prominent in the brain in younger population, i.e., children and adolescents, while adults and older ages experience more chronic diseases. In addition to increasing mortality, sleep problems have short- and long-term impact on increasing the risk of several chronic disorders including cardiovascular diseases, metabolic syndrome, obesity, type 2 diabetes, hormonal imbalances, cognitive and mental health problems, cancer, osteoporosis, and stroke. In the present chapter, we will first briefly explain the mechanisms of sleep regulation and the characteristics of a standard sleep. Then, we will summarize the importance and benefits of a life-course healthy sleep, as well as acute and chronic adverse health effects of sleep disturbances.
... Insufficient sleep is associated with impairments in cognitive function, including learning and executive function. 44 Sleep deprivation has been demonstrated to impair cognitive performance and induce alterations in brain excitability and plasticity. 12 There is evidence that sleep deprivation is associated with impaired synaptic plasticity in the hippocampus, 45 which can result in modifications in protein synthesis, metabolism, neuronal loss and elevated glucocorticoid levels. ...
Article
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Purpose There is a lack of national studies examining the relationship between insufficient sleep and depression among Chinese adolescents, and previous research has not comprehensively considered related factors. This study aimed to investigate the prevalence of depressive symptoms in adolescents with insufficient sleep and explore the role of associated factors using a nationally representative sample in China. Patients and Methods A pen-and-paper survey was conducted among 24147 Chinese adolescents from November 2019 to January 2020. Data on depressive symptoms, maltreatment experiences, psychological resilience, demographic information, parent–child relationships, parental marital status, and sleep duration were collected. Results A total of 22231 valid questionnaires were analyzed. Among the respondents, 67.7% reported insufficient sleep, while 32.3% had sufficient sleep. The prevalence of depressive symptoms was 25.3% in adolescents with insufficient sleep, compared to 8.2% in those with sufficient sleep. Insufficient sleep was identified as an independent risk factor for depressive symptoms (OR = 3.058, 95% CI: 2.753–3.396, P < 0.001). In adolescents with sufficient sleep, being female, emotional abuse, physical abuse, sexual abuse, and physical neglect were significant risk factors for depressive symptoms (P < 0.05), while higher resilience scores and a good parent–child relationship were protective factors (P < 0.05). Among adolescents with insufficient sleep, additional risk factors included higher body mass index (BMI), older age, parental divorce, and living with a single parent (P < 0.05). Conclusion Insufficient sleep is significantly associated with depressive symptoms in Chinese adolescents. The adolescents with insufficient sleep, particularly those who are older, have a higher BMI, or come from divorced or single-parent households, require increased attention.
... sleep duration predicted larger hippocampal subfield volumes, but only in the younger cohort (4-6 vs. 6-8 years) (Riggins and Spencer, 2020). The accumulation of findings has enabled scholars to identify putative neurobiological pathways in the association between early life sleep disturbances and compromised cognitive development (Alrousan et al., 2022;Jan et al., 2010;Mason and Spencer, 2022). Changes in sleep-related brain activity (e.g., sleep spindles and slow oscillations) relevant for brain structure and dendritic density are some mechanisms through which sleep disturbances in early life (Lokhandwala and Spencer, 2022;Kurth et al., 2010;Pittner et al., 2023) may lead to impaired emotion processing, cognition, and memory (Kurth et al., 2015;Lopez et al., 2010), which may in turn impact language. ...
Article
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Sleep disturbances are posited to play a key role in the development of poor mental and physical health outcomes related to early life adversity (ELA), in part through effects on brain development. Language development is critically important for health and developmental outcomes across the lifespan, including academic achievement and emotion regulation. Yet, very little research has focused on the dynamic contributions of ELA, sleep, and brain development on language outcomes. In this mini review, we summarize the current pediatric literature independently connecting ELA and sleep to language development, as well as the effects of ELA and sleep on language-relevant aspects of brain structure and function. We then propose a framework suggesting that sleep disturbances and subsequent effects on brain structure and function may act as key mechanisms linking ELA and language development. Future research investigating the associations among ELA, sleep, brain, and language development will refine our proposed framework and identify whether sleep should be included as an intervention target to mitigate the effects of early life adversity on language development.
... due to a shift in their living hours. Life rhythm is the basic factor in children forming their biological clock, and we must not ignore the number of children whose biological clocks have shifted [7,12]. ...
Article
Full-text available
In this study, we investigated the sleep–wake rhythm of nursery school children with the aim of supporting their health and mental/physical development. We analyzed 4881 children from infancy to 6 years of age, using 2 week sleep tables recorded by their guardians. The tables contained night bedtimes, wake times, nighttime/daytime sleep duration, and the differences in these between weekdays and weekends. The total sleep decrement of children with increasing age is attributed to a decrease in daytime sleep, while nighttime sleep duration remains almost unchanged at about 10 h, which is, therefore, referred to as the nighttime basic sleep duration (NBSD). Although bedtime stabilizes at around 9:30 p.m. by the age of 2, wake-up times tend to be before 7 a.m., which results in sleep insufficiency during weekdays. This lack of sleep is compensated for by long naps on weekdays and by catching up on sleep on weekend mornings, which may contribute to future social jet lag. Guardians are encouraged to know their children’s exact NBSD and set an appropriate bedtime to be maintained on weekdays. This helps to prevent sleep debt and fosters a consistent daily rhythm of waking up at the same time both on weekdays and weekends. These conditions are believed to support mental/physical development and school and social adaptation.
... However, whether the onset of ASD is a primary matter and sleep disorder is only a secondary concomitant symptom [20] and, conversely, whether sleep disorder appears first as the main cause of ASD development [17,18] have long been matters of debate. In drawing conclusions, we would like to introduce an important report that emphasized that-under all circumstances-children with sleep disorder require quick treatment, and there is recognition of the fact that sleep disorder has a negative effect on children's growth and development [21][22][23]. ...
Article
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We investigated whether the abnormal rhythms in infants are related to the future development of autism spectrum disorder (ASD), using a questionnaire from September to October 2016. The parents of 160 children with ASD (male, n = 123; female, n = 37) were recruited from two hospitals in K and H cities, and as a control group, 145 children (male, n = 75; female, n = 70) were recruited from four nursery schools in T city. The associations between ASD and bedtime and waking time on weekdays and weekends in infancy (<1 years of age), at 1–3 years, and at 3–5 years of ages were studied using a multivariable logistic regression analysis. In particular, at <3 years of age, the following factors were associated with an increased prevalence of ASD in the future: (1) short sleep periods (<8 h); (2) taking a long time to fall asleep (>60 min); (3) sleep beginning after 22:00; (4) a wake-up time after 08:00; and (5) frequent (>3 times) and long-term awakening periods (>60 min). The misalignment and/or shift of the circadian rhythm in infants may be one of the precursors and/or risk factors for the future development of ASD.
... However, whether the onset of ASD is a primary matter, and sleep disorder is only a secondary concomitant symptom [20] and conversely, whether sleep disorder appears first as a main cause of ASD development [17,18], have long been matters of debate. In drawing conclusions, we would like to introduce an important report that emphasized that-under all circumstances-children with sleep disorder require quick treatment, and there is recognition of the fact that sleep disorder has a negative effect on children's growth and development [21][22][23]. ...
Preprint
Full-text available
We investigated if the abnormal sleep-wake rhythms in infants are related to the future development of autism spectrum disorder (ASD), using questionnaire from September to October 2016. The parents of a total 160 children with ASD (male, n=123; female, n=37) recruited from the two hospitals in K and H cities and as a control group, 145 children (male, n=75; female, n=70) recruited from four nursery schools in T city. Fisher’s exact test was used for the comparison of categorical variables. The associations of bedtime and waking time on weekdays and holidays in infancy, at 1-3≦ (1-3) years of age and at 3-5 ≦ (3-5)years of age with the prevalence of ASD were analyzed using a multivariable logistic regression analysis. Especially by 3 years of age, the following factors were associated with an increased risk of developing ASD in the future: 1) short sleep (<8h), 2) long time to fall asleep (>60min), 3) sleep onset time after 22:00h, 4) wake-up time after 07:00h and/or 08:00h on weekdays and holidays, respectively, 5) frequent (>3 times) and long-term awakening (>60min). Misalignment and/or shift of the sleep-wake circadian rhythm in infant may be one of the precursors and/or risk factor to the future development of ASD.
... Sleep disturbances may result in decreased prefrontal cortex activity and increased amygdala activation, leading to impaired emotional response regulation (Harvey et al., 2011;Jones and Harrison, 2001). Sleep disturbances can also lead to impaired brain development, neuronal damage, and the permanent loss of developmental potential (Jan et al., 2010). Our results showed that various factors influencing impaired brain development may affect an individual's level of resilience (Chatburn et al., 2013). ...
Article
Sleep disturbance has been recognized as an important factor influencing mental health problems in preschool children. However, no longitudinal studies have investigated the association between sleep change patterns and mental health in preschoolers or the mediating role of resilience. Here, data were collected from 1595 preschool children in 26 kindergartens in four counties in Anhui Province, China, who were followed up (T2) 1 year apart based on baseline surveys (T1). The primary caregivers of the children were asked to complete a structured questionnaire through face-to-face interviews or by completing it themselves. Pearson's correlation and linear regression were used to analyze the relationships among sleep patterns, mental health, and resilience in preschoolers. A structural equation model was used for the mediation analysis. Four patterns of sleep change were identified: persistent-low pattern (1.7%), decreasing pattern (9.8%), increasing pattern (7.3%), and persistent-high pattern (81.3%). Compared to the persistent-low pattern, the increasing pattern and persistent-high pattern were associated with emotional behavioral problems (EBPs) and anxiety. Resilience played a fully mediating role in the relationship between increasing pattern, persistent-high pattern, and EBPs. Resilience partially mediated the effects of increasing and persistent-high pattern on anxiety. More attention should be paid to sleep problems in children with increasing and persistent-high sleep patterns. Resilience is important for understanding the mechanism underlying the correlation between sleep patterns, EBPs, and anxiety. Considering the EBPs and anxiety of preschool children, early intervention for resilience should be considered.
... Although the development of the human brain continues until the end of teenage [60], rapid development of the brain occurs around age 5, thus underlining the importance of adequate sleeping patterns in preschoolers. Sleep deprivation in children is strongly associated with a decrease in the volume of the hippocampal region, which is critical for memory consolidation [61]. Infants and preschoolers benefit from napping, which strengthens neural mechanisms for learning, especially for procedural and declarative memory [62]. ...
Article
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Unlabelled: Unexpected changes brought about by the coronavirus disease 2019 (COVID-19) have affected humans worldwide. This review attempts to address major parental concerns about the development of preschool-aged children during the pandemic from the perspectives of neuropsychology, consultation, and motor development for preschoolers aged 2-5 years. Methods: A total of 273 articles including original data, review articles, national and regional perspectives, government websites, and commentaries were considered in this review, of which 117 manuscripts were excluded because they were unrelated to children, adolescents, or COVID -19 pandemic/upper respiratory infections. A total of 156 manuscripts were included after reading the abstract and entire article. Results: Telehealth could be an effective tool for addressing cognitive and emotional challenges that arise during the pandemic. Online consultations are highlighted for nutritional guidelines and to overcome problems that parents face when caring for children in difficult times. Outdoor activities using sanitisers, proper cleanliness, and following standard operating procedures are recommended. Parental preoccupation with media should be avoided. Interpretation: Many preschoolers show delays in reaching their developmental milestones, and the pandemic has increased parents' concerns, as access to practitioners is limited. Therefore, parents should be encouraged to undergo neuropsychological consultations whenever necessary. This study emphasises important strategies to ensure that children's development is minimally affected while staying in the confined environment of their homes. This study serves as a new guide for parents, as they raise young children in the new normal. Parents should undergo basic yearly physical, neuropsychological, nutritional, and speech checkups.
... Fibre tract coherence and integrity as well as myelination continue to increase with age across many projection and association tracts (Bava et al., 2010;Giorgio et al., 2010;Lebel and Beaulieu, 2011). Sleep functions as a promoter of such neurobiological maturation processes (Jan et al., 2010) and insufficient and irregular sleep patterns may have long-term counteractive effects on normative white-matter trajectories in developing tracts (Jamieson et al., 2021;Telzer et al., 2015). ...
Article
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Sleep is an important contributor for neural maturation and emotion regulation during adolescence, with long-term effects on a range of white matter tracts implicated in affective processing in at-risk populations. We investigated the effects of adolescent sleep patterns on longitudinal changes in white matter development and whether this is related to the emergence of emotional (internalizing) problems. Sleep patterns and internalizing problems were assessed using self-report questionnaires in adolescents recruited in the general population followed up from age 14 to 19 years (N=111). White matter structure was measured using diffusion tensor imaging (DTI) and estimated using fractional anisotropy (FA). We found that longitudinal increases in time in bed (TIB) on weekends and increases in TIB-variability between weekdays to weekend, were associated with an increase in FA in various interhemispheric and cortico-striatal tracts. Extracted FA values from left superior longitudinal fasciculus mediated the relationship between increases in TIB on weekends and a decrease in internalizing problems. These results imply that while insufficient sleep might have potentially harmful effects on long-term white matter development and internalizing problems, longer sleep duration on weekends (catch-up sleep) might be a natural counteractive and protective strategy.
... This includes progressive increases in white matter, considered the product of gradual myelination of nerve fibres (Paus et al., 2008), which is thought to influence overall processing efficiency and subsequently adolescent behaviour (Fields, 2008). However, the highly plastic nature of white matter during development renders it vulnerable to a range of environmental and endogenous stimuli (Dow-Edwards et al., 2019), including sleep-related phenomena (Jan et al., 2010). In addition, evidence from animal models suggests that a range of sleep-related behaviours during developmentally sensitive periods may directly influence brain maturation, including myelination (Bellesi et al., 2018). ...
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Background Morning–evening preference is defined as an individual's preference for a morning‐ or evening‐oriented rhythm. Across adolescence, a preference for eveningness becomes more predominant. Although eveningness is cross‐sectionally associated with internalizing and externalizing psychopathology, few studies have examined developmental changes in eveningness and its potential biological substrates. Here, we investigated the longitudinal relationships among the trajectory of eveningness preference, internalizing and externalizing psychopathology and white matter development, across adolescence. Methods Two‐hundred and nine adolescents (49% male) were assessed longitudinally at four separate time points between 12 and 19 years of age. Morning–evening preference and internalizing and externalizing symptoms were assessed at each time point. Diffusion‐weighted images were acquired on a subset of participants at the final two time points to estimate changes in global mean fractional anisotropy (FA). Linear mixed models were performed to estimate the change in eveningness over time. A series of linear regression models assessed the influence of change in eveningness on psychopathology and white matter development at age 19. Results Across the sample, a preference for eveningness became more predominant by 19 years of age. Greater individual‐level change towards eveningness significantly predicted greater severity in externalizing, but not internalizing, symptoms at 19 years of age. In contrast, change in psychopathology from 12 to 19 years of age was not associated with morning–eveningness at age 19. A change towards eveningness predicted an attenuated increase in FA between 17 and 19 years of age. Conclusions This study suggests that developmental changes in morning–evening preference may predict both neurodevelopmental and psychological outcomes in adolescents.
... These neurobehavioral effects of CSD increase the risk of accidents, physical injury, and social misbehavior, leading to problems in the workplace or school [15][16][17][18]. In humans, sleep loss has been linked to neuronal loss, changes in brain plasticity, morphometry, and network structure, and an increased risk of dementia [19][20][21][22][23]. Sleep deprivation is also known to increase the frequency of epileptiform discharges and clinical seizures in patients with epilepsy [24]. ...
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Chronic sleep deficiency (CSD) poses a threat to physical health, mental well-being, and social functioning. The concept of behaviorally induced CSD has not changed much since it was first introduced four decades ago. Behaviorally induced CSD is currently referred to as insufficient sleep syndrome (ISS). In the latest edition of the International Classification of Sleep Disorders (ICSD-3, 2014), ISS is considered a disorder of central hypersomnolence with diagnostic codes ICD-9-CM 307.44 and ICD-10-CM F51.12. In this review, we will describe the biological importance of sleep, the ramifications of CSD on the individual and society, the nosological status and diagnostic features of ISS, and the apparent lack of attention to ISS in contemporary medical practice and public health programs. The last three decades have seen a global rise in voluntary sleep curtailment such that ISS may already be the leading cause of CSD, not only in adults but also in school-aged children and adolescents. Acknowledging ISS as a public health priority is a necessary first step in our response to the global threat of CSD and CSD-related health consequences. It is only by confronting ISS directly that we can hope to develop and implement effective educational and advocacy programs, along with more responsible public health policies and regulations.
... Research suggests that adolescent brains require more than nine hours of sleep nightly, yet many youth fall short of this threshold, which can create serious detriments (Short and Louca, 2015;Short et al., 2018), including long-term damage to the brain (Jan et al., 2010), mood deficits (Short and Louca, 2015), lower performance at school (Pagel and Kwiatkowski, 2010), mental health disorders such as anxiety and catastrophic thinking (Jamieson et al., 2020;Talbot et al. 2010), risktaking or sensation seeking behaviors (Telzer et al., 2013), delinquency and low self-control (Clinkinbeard et al., 2010;Meldrum et al., 2015), and substance abuse (Wong et al., 2010). Many of the outcomes related to sleep deprivation have also been associated with initiation of or susceptibility to initiate ENDS among adolescents. ...
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In a recent study, we demonstrated a relationship between self-reported sleep deprivation and youth susceptibility to initiate electronic nicotine delivery systems (ENDS) use; however, we were hampered by cross-sectional data. This study builds on our previous work by performing secondary analysis using the nationally representative Population Assessment of Tobacco and Health study datasets from wave 4.5 (2017-2018) and wave 5 (2018-2019) among respondents aged 12-17. Using a longitudinal cohort design, we assessed the extent self-reported sleep troubles at wave 4.5 related to transition from never-to-ever ENDS use by wave 5. We assessed youth who reported never having used any type of tobacco previously and who reported not using alcohol or other illicit substances the previous year. We ran four Poisson regression models on the dependent variable never-to-ever ENDS users at wave 5 and self-reported sleep troubles in the past year at wave 4.5. We controlled for demographic and sociographic factors and, in our final model, tobacco availability in home, exposure to ENDS advertising on social media, past year anxiety, depression, body mass index, physical activity, close friends that use ENDS, perceived harm of ENDS, school performance, sensation seeking, and the susceptibility of youth to initiate ENDS. Even when controlling for these factors, sleep troubles at wave 4.5 significantly and positively related to ENDS initiation by wave 5 (Past year sleep trouble: RR = 1.48 95% CI = [1.14-1.93]). This key and novel finding has important implications for preventing youth ENDS use via protective self-care and social-environmental approaches.
... Additionally, prior behaviour may influence later mental health as well; longitudinal evidence indicates that engaging in more physical activity earlier in life is associated with reduced risk of later depression (Mammen & Faulkner, 2013) and dementia (Blondell, Hammersley-Mather, & Veerman, 2014). It is certainly plausible that neurobiological factors such as the potential neurotrophic and neurodevelopmental effects of physical activity and sleep (Jan et al., 2010) may contribute to better mental health under similar circumstances; it may also be that sport and physical activity provide opportunities for skill development that help youth face unprecedented challenges (Madsen, Hicks, & Thompson, 2011). While the modelling approach used in the present analysis did not directly address prior behaviour as a predictor (i.e., with a lag term), the between-persons terms as a person-mean across years inherently capture some of this prior behaviour in so much that accruing more sleep and MVPA at baseline will increase the person mean, especially when the effects of year-on-year change are held constant in the model. ...
Article
Background The impact of COVID-19 on adolescent mental health is a global concern. Increased screen time and reduced physical activity due to the lockdown measures have been linked to detrimental mental health outcomes; however, the literature remains limited by cross-sectional and retrospective designs, and consideration of behaviours in isolation. Prospective evidence is necessary to examine whether moderate-to-vigorous physical activity (MVPA), sleep and screen time influenced changes in mental health. Method Analyses used data from a prospective cohort study of secondary school students in Canada with baseline data from the 2018–2019 school year and linked follow-up data from online surveys completed during the initial COVID-19 outbreak (May–July 2020). Multilevel linear regression models were used to evaluate the within- and between-person isotemporal substitution effects of sleep, MVPA and screen time behaviours on depression, anxiety, subjective well-being, and trait emotional dysregulation. Results Linked longitudinal data from 2645 students attending 44 schools were available. Between-person effects indicated that individuals who engaged in more MVPA and sleep while minimizing screen time had lower depression scores, less severe emotional dysregulation, and better subjective well-being. While controlling for between-person effects, within-person year-on-year change suggests those who increased screen time while decreasing either MVPA or sleep experienced mental health decline on all outcomes. Conclusion MVPA and sleep were associated with youth mental health during the early COVID-19 lockdown. Increasing MVPA and sleep (or at least mitigating the increase of screen time) compared to the prior year was associated with better mental health during the early pandemic. A limitation to consider is that the screen time measure represents a combination of screen behaviours, and effects of replacing screen time may have varied if distinctions were made.
... Poor sleep during infancy and childhood are associated with impaired brain development [14][15][16] , delayed social-emotional development [17][18][19] , diminished executive functioning [20][21][22] , delayed language development 23 , lower cognitive performance on neurodevelopmental test 24 and increased rates of anxiety and depression 25 . Long-term sleep disturbances in childhood can lead to widespread loss of neurons in several brain regions including the hippocampus 26 . As children from disadvantaged neighbourhoods and lower socioeconomic families are at higher risk of sleep problems 8 , it is important to identify and evaluate the various factors that contribute to impaired sleep. ...
Article
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Healthy sleep supports robust development of the brain and behavior. Modern society presents a host of challenges that can impair and disrupt critical circadian rhythms that reinforce optimal physiological functioning, including the proper timing and consolidation of sleep. While the acute effects of inadequate sleep and disrupted circadian rhythms are being defined, the adverse developmental consequences of disrupted sleep and circadian rhythms are understudied. Here, we exposed mice to disrupting light–dark cycles from birth until weaning and demonstrate that such exposure has adverse impacts on brain and behavior as adults. Mice that experience early-life circadian disruption exhibit more anxiety-like behavior in the elevated plus maze, poorer spatial memory in the Morris Water Maze, and impaired working memory in a delayed match-to-sample task. Additionally, neuron morphology in the amygdala, hippocampus and prefrontal cortex is adversely impacted. Pyramidal cells in these areas had smaller dendritic fields, and pyramidal cells in the prefrontal cortex and hippocampus also exhibited diminished branching orders. Disrupted mice were also hyperactive as adults, but otherwise exhibited no alteration in adult circadian locomotor rhythms. These results highlight that circadian disruption early in life may have long lasting and far-reaching consequences for the development of behavior and the brain.
... Disrupting this restorative process via either sleep fragmentation or hypoxemia may affect frontal cortex functioning and lead to aspects of the behavioural phenotype seen with childhood obstructive sleep apnoea (OSA). [3][4][5] Poor sleep affects the mental status of the child leading to problems in attention and behaviour. [6][7][8][9] Even mild sleep disturbances can be associated with several health problems both somatic as well as psychiatric. ...
Article
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Background: Behaviour problems, poor academic performance and failure to thrive are some of the potential sequelae of sleep problems in children. Hence, there is a need to evaluate the prevalence of sleep problems and significant associations in children with skeletal class II malocclusion with mandibular retrognathism. Aims: This study aimed to determine associations if any between sleep practices and problems and craniofacial characteristics in children with skeletal class II malocclusion with mandibular deficiency. Settings and design: A cross-sectional study was conducted among a group of children with skeletal class II malocclusion with mandibular retrognathism. Materials and methods: Fifty children aged 8-14 years with skeletal class II with mandibular retrognathism and who required myofunctional therapy were selected. A validated sleep questionnaire assessed the sleep practices and problems. A detailed clinical examination including tonsils and evaluation for mouth breathing was performed. A lateral cephalogram recorded specific linear, angular variables as well as upper and lower pharyngeal airway space. Statistical analysis: Descriptive statistics, frequency, and percentages were calculated, and the Chi-square test was used. Results: All children reported at least one sleep problem, with snoring reported by 76% of the children. Forty-two percent of the children showed a decreased upper airway, whereas 80% showed a decreased lower airway. Significant associations were seen between SN-MP and noisy breathing, upper airway, and snoring with a P value of 0.017. We also found significant associations between upper and lower airway and sleep positions with a P value of 0.021 and 0.005, respectively. Conclusion: All the children exhibited at least one sleep problem. There was a strong association of certain sleep practices and sleep problems with cephalometric variables.
... Poor sleep during infancy and childhood are associated with impaired brain development [14][15][16] , delayed socialemotional development [17][18][19] , diminished executive functioning [20][21][22] , delayed language development 23 , lower cognitive performance on neurodevelopmental test 24 and increased rates of anxiety and depression 25 . Long-term sleep disturbances in childhood can lead to widespread loss of neurons in several brain regions including the hippocampus 26 . As children from disadvantaged neighbourhoods and lower socioeconomic families are at higher risk of sleep problems 8 , it is important to identify and evaluate the various factors that contribute to impaired sleep. ...
Preprint
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Healthy sleep supports robust development of the brain and behavior. Modern society presents a host of challenges that can impair and disrupt critical circadian rhythms that reinforce optimal physiological functioning, including the proper timing and consolidation of sleep. While the acute effects of inadequate sleep and disrupted circadian rhythms are being defined, the adverse developmental consequences of disrupted sleep and circadian rhythms are understudied. Here, we exposed mice to disrupting light-dark cycles from birth until weaning and demonstrate that such exposure has adverse impacts on brain and behavior as adults. Mice that experience early-life circadian disruption exhibit more anxiety-like behavior in the elevated plus maze, poorer spatial memory in the Morris Water Maze, and impaired working memory in a delayed match-to-sample task. Additionally, neuron morphology in the amygdala, hippocampus and prefrontal cortex is adversely impacted. Pyramidal cells in these areas had smaller dendritic fields, and pyramidal cells in the prefrontal cortex and hippocampus also exhibited diminished branching orders. Disrupted mice were also hyperactive as adults, but otherwise exhibited no alteration in adult circadian locomotor rhythms. These results highlight that circadian disruption early in life may have long lasting and far-reaching consequences for the development of behavior and the brain.
... In this line, loneliness could modify some students' behaviours and it is related to more frequent use of medical services among youth as well as sleep problems [19]. Given the importance of good sleep for life quality and academic achievement [22], these sleep problems should be taken into account. Sleep provides restorative effects for ensuring good health; however, less efficient sleep could affect brain development, including memory development, executive functioning, and cognitive performance [23,24]. ...
Article
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Loneliness is a distressing feeling that can be a barrier to a student’s development and affect their mental health. This research aimed to analyse the effects of loneliness on psychological and behavioral factors among students aged 12–19 years in Spain. Loneliness, experiential avoidance, psychological inflexibility, physical activity, mobile phone use, and smoke habits were analysed in a sample of 110 men and 122 women assigned into two groups depending on their loneliness levels: higher loneliness group (HLG) and lower loneliness group (LLG). Results showed that experimental avoidance and psychological inflexibility were related with loneliness (r = 0.471; p = 0.000). Experiential avoidance and psychological inflexibility were higher in HLG than LLG. Regarding the use of mobile phones and smoking habits, LLG presented significantly higher values than HLG. Higher age correlated with lower loneliness values (r = −0.155; p = 0.017). The present research found how students with higher loneliness presented higher experiential avoidance and psychological inflexibility and lower age, use of mobile phone, and smoking habits. These findings reveal the importance of considering multiple social behaviours when examining adolescent mental health factors.
... Despite evidence suggesting far-reaching cognitive, behavioral and health consequences of sleep disturbances in childhood, relatively little research has focused on the relationship of childhood sleep to developing brain structure and function (Spruyt, 2019(Spruyt, , 2020. A growing literature suggests that sleep plays a crucial role in neurodevelopment across childhood and adolescence (Dutil et al., 2018;Jan et al., 2010;Maski and Kothare, 2013), and it is likely that sleep plays a similarly crucial role in neurodevelopment in early childhood. Given that early childhood is a time of rapid brain development (Brown and Jernigan, 2012), with the vast majority of recent-large scale studies showing a normative decline in gray matter volume starting by age 5 (Mills et al., 2016;Walhovd et al., 2017), it is plausible that sleep disturbances that occur during this developmental period may have lasting neurodevelopmental consequences. ...
Article
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There is a close relationship between sleep and depression, and certain maladaptive outcomes of sleep problems may only be apparent in individuals with heightened levels of depression. In a sample enriched for preschool depression, we examined how sleep and depression in early childhood interact to predict later trajectories of gray matter volume. Participants (N=161) were recruited and assessed during preschool (ages 3-6 years) and were later assessed with five waves of structural brain imaging, spanning from late childhood to adolescence. Sleep and depression were assessed using a semi-structured parent interview when the children were preschool-aged, and total gray matter volume was calculated at each scan wave. Although sleep disturbances alone did not predict gray matter volume/trajectories, preschool sleep and depression symptoms interacted to predict later total gray matter volume and the trajectory of decline in total gray matter volume. Sleep disturbances in the form of longer sleep onset latencies, increased irregularity in the child’s sleep schedule, and higher levels of daytime sleepiness in early childhood were all found to interact with early childhood depression severity to predict later trajectories of cortical gray matter volume. Findings provide evidence of the interactive effects of preschool sleep and depression symptoms on later neurodevelopment.
... Childhood insomnia is associated with negative outcomes that include emotional, behavioural and cognitive problems. [1][2][3] Prevalence estimates and a description of the course of insomnia may aid preventative and treatment efforts. However, most previous research on this topic in children has examined insomnia symptoms 4-11 that may not have the severity, duration, intensity or associated impairment that warrants a clinical diagnosis. ...
Article
Background Insomnia is prevalent among children and adolescents and is associated with a wide range of negative outcomes. Knowledge about its determinants is therefore important, but due to the lack of longitudinal studies, such knowledge is limited. The aim of the present inquiry is to identify child and family predictors of future pediatric insomnia within a psycho-bio-behavioral framework. Methods A representative community sample (n=1,037) was followed biennially from 4 to 14 years of age (2007−2017). Insomnia was defined based on the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria and was diagnosed by a semistructured clinical interview of children (from age 8 years of age) and parents (all ages). Predictors included parent ratings of child emotional reactivity, family functioning, and marital conflict; self-reports of personality; and teacher-rated emotion regulation skills. Results Random intercept cross-lagged analyses revealed that within-person increases (i.e., relative to the child’s typical levels across childhood) in emotional reactivity and decreases in emotion regulation skills predicted insomnia diagnosis two years later from ages 4 to 14 after adjusting for previous insomnia and all unmeasured time-invariant factors. Previous insomnia was the strongest predictor of later insomnia, whereas family functioning and marital conflict did not predict insomnia. Conclusions Increases in emotional reactivity and decreases in emotion regulation skills predicted insomnia above and beyond all unmeasured time-invariant factors and could be targets for interventions. Previous insomnia predicted later insomnia, thereby underscoring the importance of detecting, preventing, and treating insomnia at an early age.
... Sleep is an essential biological function and, in children, it is critical for brain maturation and development. Early childhood sleep correlates with gray and white matter volumes particularly in the dorsolateral, prefrontal, and hippocampal cortex (Jan et al., 2010;Kocevska et al., 2017). Sleep disturbances during crucial periods of brain development may impact synaptic plasticity, neuronal migration, myelination, and memory consolidation leading to effects on cognition (Astill et al., 2012;Spruyt, 2019). ...
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In the midst of concerns for potential neurodevelopmental effects after surgical anesthesia, there is a growing awareness that children who require sedation during critical illness are susceptible to neurologic dysfunctions collectively termed pediatric post-intensive care syndrome, or PICS-p. In contrast to healthy children undergoing elective surgery, critically ill children are subject to inordinate neurologic stress or injury and need to be considered separately. Despite recognition of PICS-p, inconsistency in techniques and timing of post-discharge assessments continues to be a significant barrier to understanding the specific role of sedation in later cognitive dysfunction. Nonetheless, available pediatric studies that account for analgesia and sedation consistently identify sedative and opioid analgesic exposures as risk factors for both in-hospital delirium and post-discharge neurologic sequelae. Clinical observations are supported by animal models showing neuroinflammation, increased neuronal death, dysmyelination, and altered synaptic plasticity and neurotransmission. Additionally, intensive care sedation also contributes to sleep disruption, an important and overlooked variable during acute illness and post-discharge recovery. Because analgesia and sedation are potentially modifiable, understanding the underlying mechanisms could transform sedation strategies to improve outcomes. To move the needle on this, prospective clinical studies would benefit from cohesion with regard to datasets and core outcome assessments, including sleep quality. Analyses should also account for the wide range of diagnoses, heterogeneity of this population, and the dynamic nature of neurodevelopment in age cohorts. Much of the related preclinical evidence has been studied in comparatively brief anesthetic exposures in healthy animals during infancy and is not generalizable to critically ill children. Thus, complementary animal models that more accurately “reverse translate” critical illness paradigms and the effect of analgesia and sedation on neuropathology and functional outcomes are needed. This review explores the interactive role of sedatives and the neurologic vulnerability of critically ill children as it pertains to survivorship and functional outcomes, which is the next frontier in pediatric intensive care.
... Peak ages for SDB are 2-8 years often due to adenotonsillar hypertrophy relative to airway size (Marcus et al., 2012), with the prevalence of 1% for OSA and 20% for parent report of habitual snoring (Bonuck et al., 2011a(Bonuck et al., , 2011b. Despite differing etiologies, short sleep duration, BSPs, and SDB have comparable adverse effects on the developing child (Jan et al., 2010;Spruyt, 2018). ...
Article
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Background & Aims Poor sleep in young children imperils language learning and use. Both sleep and language problems are prevalent in early childhood. Speech-language pathologists are in a unique position to expand surveillance of sleep problems, which in turn may contribute to communication difficulties. We conducted a feasibility study of speech-language pathologist screening for behavioral sleep problems and sleep-disordered breathing symptoms at a multidisciplinary evaluation and treatment center. Methods Speech-language pathologists administered screeners to parents of 2–6-year-olds: the Short Form-Children's Sleep Habits Questionnaire (for behavioral sleep problems) which includes an item asking if the child has a sleep problem (yes/no), and the pediatric sleep questionnaire (for sleep-disordered breathing). Speech-language pathologists participated in pre- and post-screening focus groups. Pre-screening topics included professional preparation and clinical experience regarding pediatric sleep issues. Post-screening, speech-language pathologists provided feedback about the screening experience and feasibility of incorporating such screening into practice. Results Among 51 children, 31% (16/51) screened positive for sleep-disordered breathing, 78% for behavioral sleep problems (40/51), and 43% (12/28) per parent report. Parent-reported problems were associated with sleep-disordered breathing ( p = 0.00) but not behavioral sleep problems ( p = 0.24). During focus groups, speech-language pathologists reported no formal pediatric sleep training, high parent concern about sleep, and agreed that screening fit their professional mandate. Speech-language pathologists affirmed that the ≤15 min screenings integrated seamlessly into practice but that additional training, particularly for sleep-disordered breathing, was needed. Conclusions The prevalence of sleep problems in 2–6-year-olds presenting to speech-language pathologists was higher than in community samples, but consistent with data from young children with developmental disabilities. Speech-language pathologists endorsed the utility and feasibility of sleep problem screening and education in their clinical practice. Implications Integrating sleep problem screening and education into speech-language pathologist practice is feasible and could widen surveillance of both sleep problems and risk factors for developmental language disorders. Further research should include larger samples and other settings, e.g. home or school.
... Impaired REM sleep can thus be considered as a marker of abnormal brain functioning. Contextually, persistent sleep disturbance was associated with neuronal damage and impaired brain development (Jan et al. 2010;MacDuffie et al. 2020). A correlation between altered subcortical brain volumes and sleep onset problems in first two years of life may predispose infants to ASD; this further implies the neurodevelopmental connection of sleep abnormality in children with ASD (MacDuffie et al. 2020). ...
Article
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Circadian rhythms in most living organisms are regulated by light and synchronized to an endogenous biological clock. The circadian clock machinery is also critically involved in regulating and fine-tuning neurodevelopmental processes. Circadian disruption during embryonic development can impair crucial phases of neurodevelopment. This can contribute to neurodevelopmental disorders like autism spectrum disorder (ASD) in the offspring. Increasing evidence from studies showing abnormalities in sleep and melatonin as well as genetic and epigenetic changes in the core elements of the circadian pathway indicate a pivotal role of circadian disruption in ASD. However, the underlying mechanistic basis through which the circadian pathways influence the risk and progression of ASD are yet to be fully discerned. Well-recognized mechanistic pathways in ASD include altered immune-inflammatory, nitro oxidative stress, neurotransmission and synaptic plasticity, and metabolic pathways. Notably, all these pathways are under the control of the circadian clock. It is thus likely that a disrupted circadian clock will affect the functioning of these pathways. Herein, we highlight the possible mechanisms through which aberrations in the circadian clock might affect immune-inflammatory, nitro-oxidative, metabolic pathways, and neurotransmission, thereby driving the neurobiological sequelae leading to ASD.
... Despite clinical heterogeneity among and even within NDDs, sleep disturbances are highly prevalent (3,4). Clinical evidence points toward a link between sleep dysfunction and other behavioral symptoms in NDDs (5,6,65). Whether sleep disturbances are a by-product of other NDD-related deficits or directly result from developmental disruptions remains a point of debate (3,(7)(8)(9). ...
Article
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Sleep disruptions are among the most commonly reported symptoms across neurodevelopmental disorders (NDDs), but mechanisms linking brain development to normal sleep are largely unknown. From a Drosophila screen of human NDD-associated risk genes, we identified the chromatin remodeler Imitation SWItch/SNF ( ISWI ) to be required for adult fly sleep. Loss of ISWI also results in disrupted circadian rhythms, memory, and social behavior, but ISWI acts in different cells and during distinct developmental times to affect each of these adult behaviors. Specifically, ISWI expression in type I neuroblasts is required for both adult sleep and formation of a learning-associated brain region. Expression in flies of the human ISWI homologs SMARCA1 and SMARCA5 differentially rescues adult phenotypes, while de novo SMARCA5 patient variants fail to rescue sleep. We propose that sleep deficits are a primary phenotype of early developmental origin in NDDs and point toward chromatin remodeling machinery as critical for sleep circuit formation.
... Given that important changes occur to neurological structure and function during this developmental stage, adolescents are also a high-risk cohort for exhibiting long-term post-traumatic deficits (Barlow et al., 2015(Barlow et al., , 2010. Since sleep loss during adolescence has been shown to severely impact behavioral and physiological outcomes under normal conditions (Beebe, 2011;Jan et al., 2010) and following TBI (Salberg et al., 2018), it is likely that the glymphatic system plays a key role in the adolescent TBI outcomes given its proposed heightened functionality during sleep. Furthermore, considering sex differences are common during adolescence, given differences in maturation timelines, but also during other developmental stages, it is important to investigate the functionality of the glymphatic system under normal and abnormal conditions in both sexes. ...
Article
Until recently, both the purpose of the biological need for sleep and the mechanism by which the central nervous system eliminated metabolic waste products were unknown. The glymphatic system is the recently discovered macroscopic waste clearance system for the CNS, which predominantly functions during sleep states. Important implications for the glymphatic system exist for a significant proportion of neurological disorders, including traumatic brain injury, epilepsy, stroke, migraine, and Alzheimer’s disease. Within the limited amount of research pertaining to this novel system there exists controversy regarding several of the key structural and functional aspects of the glymphatic system. In this review we address evidence from both standpoints regarding the prominent debates surrounding the glymphatic system, including the functional differences in wakefulness vs. sleep, the role of glial aquaporin-4 water channels, and whether it reflects a convective flow or a passive diffusion process. The answers that underlie these questions will have crucial and distinct outcomes for the future of the glymphatic system and the disorders it has been implicated in. However, this review also summarizes the potential role of the glymphatic system in the development and progression of the aforementioned neurological disorders. Furthermore, the possible contribution of the orexinergic system to this relationship between the glymphatic system, sleep, and these neurological disorders is also explored. Overall, in order to develop and utilize therapeutic interventions centred around the glymphatic system we must first dedicate further investigation to elucidating these discrepancies and unanswered questions.
Article
Sleep problems positively predict loneliness to a large extent, which would harm adolescent health. However, little is known about the underlying mechanism. This research investigates the potential mediating roles of rumination and resilience in the relation among adolescents and further examines the changing relationships. In Study 1, 1056 adolescents from two schools completed self‐reported measures of sleep problems, loneliness, rumination, and resilience. We found that sleep problems were positively associated with loneliness, and that rumination and resilience mediated this relationship, both individually and sequentially. To examine the varying relationship between rumination, resilience, and loneliness, Study 2 adopted the cross‐lagged design in a long‐term longitudinal study of 131 students and found that rumination and resilience at T1 significantly predict loneliness at T2. To further directly explore the changing relationship between sleep problems and loneliness, we performed a short‐term longitudinal study across 7 weeks of 242 adolescents in Study 3. The results replicated the findings of Study 2 and found sleep problems at T1 positively predicted loneliness at T2. These results underscore the significance of sleep problems in contributing to loneliness through mediating mechanisms and unveil the possible causal relationships, offering robust insights to alleviate adolescent loneliness.
Article
Children who survive septic shock are at high risk of new morbidity. The objective of this study is to evaluate the occurrence and risk factors associated with new or worsening sleep disturbance, comparing baseline to 3 months following admission among children surviving septic shock. A secondary analysis of the Life After Pediatric Sepsis Evaluation prospective cohort study was performed. This study included children <18 years admitted to 12 U.S. Pediatric Intensive Care Units with community-acquired septic shock requiring vasoactive–inotropic support and invasive or noninvasive ventilation who survived discharge. The primary outcome of sleep deterioration was characterized as any increased trouble in sleeping measured by a question from the Pediatric Quality of Life Inventory (PedsQL) at baseline compared with the response at the 3-month follow-up. Child and parent variables were evaluated for association with sleep deterioration using univariable and multivariable analyses. Of the original 389 patients, 229 survived for 3 months and completed the PedsQL. The final cohort included 111 children who had available follow-up data at month 3 and did not report baseline sleep challenges. Overall, 25% (28/111) of children reported declines in sleep at 3 months. There were no patient or illness characteristics associated with sleep decline at 3 months in univariable analysis. In multivariable models controlling for age, sex, insurance type, baseline complex conditions, and immunocompromise, no measures of illness severity were associated with deterioration in sleep at 3 months. Sleep deterioration is common in survivors of community-acquired septic shock but detection may be difficult to identify without routine screening.
Article
Objectives Short sleep is becoming more common in modern society. This study aimed to explore the relationship between accelerometer-measured sleep duration and cognitive performance among young adults as well as the underlying hemodynamic mechanisms. Methods A total of 58 participants were included in this study. Participants were asked to wear an ActiGraph GT3X+ accelerometer to identify their sleep duration for 7 consecutive days. Cognitive function was assessed by the Stroop test. Two conditions, including the congruent and incongruent Stroop, were set. In addition, stratified analyses were used to examine sensitivity. 24-channel functional near-infrared spectroscopy (fNIRS) equipment was applied to measure hemodynamic changes of the prefrontal cortex (PFC) during cognitive tasks. Results Results showed that sleep duration was positively associated with accuracy of the incongruent Stroop test (0.001 (0.000, 0.002), p = 0.042). Compared with the regular sleep (≥7 h) group, lower accuracy of the incongruent Stroop test (−0.012 (−0.023, −0.002), p = 0.024) was observed in the severe short sleep (<6 h). Moreover, a stratified analysis was conducted to examining gender, age, BMI, birthplace, and education’s impact on sleep duration and the incongruent Stroop test accuracy, confirming a consistent correlation across all demographics. In the severe short sleep group, the activation of left middle frontal gyri and right dorsolateral superior frontal gyri were negatively associated with the cognitive performance. Conclusions This study emphasized the importance of maintaining enough sleep schedules in young college students from a fNIRS perspective. The findings of this study could potentially be used to guide sleep time in young adults and help them make sleep schemes.
Chapter
The pathogenesis underlying autism spectrum disorder (ASD) and the causes of rapid increase of ASD patients remain unclear. However, recent reports suggest that chronodisruption, including circadian rhythm sleep-wake disorders of ASD patients, may not only be an associated symptom but may also be deeply related to the pathogenesis of ASD. In fact, the chronodisruption theory is appropriate and convenient to understand and/or explain various clinical symptoms of ASD. Furthermore, it is clinically well known that proper treatment of sleep disorders stabilizes mental and physical development of children with ASD and significantly improves the quality of their life and that of their family members. It has been reported that the circadian rhythm begins to be formed in the fetal period, gradually matures in the neonatal period, and is completed in the suprachiasmatic nuclei (SCN) by about one and a half years old. Early diagnosis and response to ASD patients are desirable to correct their circadian rhythm early in infancy before an inappropriate circadian rhythm is established in the SCN. This chapter provides sleep hygiene guidance and pharmacotherapy for circadian rhythm sleep-wake disorders of infants and toddlers based on our assumption that the guidance and therapy may prevent future development of ASD.
Chapter
Human faces are not growing as wide as they used to. The maxillary component of the craniofacial complex is often narrower than ideal leading to crowding, dental compensations lending to periodontal issues, reduced tongue space, reduced airflow through the nose, and reduced esthetics due to large buccal corridors. It is not possible to accurately assess the skeletal discrepancy clinically, with models, or with traditional pan/ceph images. CBCT imaging allows for far greater accuracy in diagnosis and treatment planning. Treating the transverse discrepancy early allows for a greater component of skeletal correction. In the late mixed or early permanent dentition, it may be preferable to use a bone borne expander to affect a skeletal change, improve nasal airflow, and reduce the negative side effects of tooth borne expanders. This chapter focuses on the importance of the transverse dimension in orthodontic diagnosis and treatment planning. Human faces are growing narrower than they used to, and this can have negative health impacts, not only for the teeth and periodontal structures, but for the whole body. The use of CBCT imaging is necessary to accurately diagnose and treat the transverse dimension. Treatment of the transverse dimension before adulthood is easier due to the patency of the midpalatal suture. Early orthodontic intervention, combined with accurate diagnosis and treatment planning to address deficiencies allows us to avoid extraction of permanent teeth and improve health outcomes.KeywordsOrthodontic expansionAirway healthEarly mixed dentitionMixed dentitionAdolescent treatmentTransverse dimensionDiagnosis and treatment planningCBCT imagingBone borne expansionMSETransverse deficiency
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In this registered report, we evaluated how sleep is related to school functioning. Using data from the Future of Families and Child Wellbeing Study ( N = 3002), we evaluated a series of structural equation models evaluating whether sleep at age 5 has a direct or indirect effect on academic achievement, executive function and classroom behaviour at age 9, and whether this relation is moderated by race or ethnicity, poverty, maternal education or disability. We found that sleep duration (but not other aspects of sleep health) had a direct, linear relation to attention problems, acting‐out behaviours and executive functions, as well as an indirect effect on academic achievement through executive functions. We also found that this model was moderated by disability, poverty, maternal education and race or ethnicity. Our results suggest that experiencing insufficient amounts of sleep may have a disproportionately negative effect on children with disabilities or children whose mothers received less education. Initiatives to promote healthy sleep habits, including increasing sleep duration among these groups, may thus also indirectly raise measures of achievement.
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Children with a history of trauma or adverse childhood experiences may be at higher risk for poor psychological and physical responses to medical experiences aimed at enhancing their well-being. Health care institutions are aware of the need for integration of trauma-informed care (TIC) practices yet struggle to find frameworks that promote resiliency to medical stress. An approach called neuroprotective care buffers the effects of toxic stress negatively affecting child health and well-being. Although often used in neonatal and cardiac intensive care units, the development and broad implementation of universal neuroprotective care measures across age groups and hospital settings has not been previously explored. An expanded neuroprotective care protocol takes a prevention approach to TIC. It fits a TIC framework, accounts for children’s ecological, biological, and developmental needs, protects them against medical traumatic stress and retraumatization, and provides a tailored, measurable approach that systematically preserves child well-being within hospital settings.
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Study objectives: Sleep disturbances impact over half of older children and teens with acquired brain injury (ABI) following critical care hospitalization, but are under-evaluated in infants and young children. Given the importance of sleep in brain development and healing after injury, we hypothesized sleep disturbances would be associated with worse neurodevelopmental outcomes in infants with ABI. Methods: We performed a retrospective cohort study of 68 children aged 2-32 months following critical care hospitalization for ABI. The Brief Infant Sleep Questionnaire (BISQ) assessed sleep disturbances. Bayley Scales of Infant and Toddler Development, 3rd Edition (Bayley-III) and Adaptive Behavior Assessment System, 3rd Edition (ABAS-3) assessed developmental and adaptive functioning outcomes, respectively. T-tests compared sleep characteristics in infants with ABI to historical healthy controls. Spearman's correlation (rs) evaluated relationships among sleep and outcomes. Multiple linear regression investigated relationships controlling for demographic and ABI characteristics. Results: Compared to healthy controls, children with ABI had shorter nighttime sleep duration (p=.01), longer daytime sleep duration (p<.001), and longer duration of nighttime awakenings (p<.001). Duration of night awakenings negatively correlated with Bayley Cognitive scores (rs=-.40). Night awakenings negatively correlated with worse ABAS-3 General Adaptive Composite (GAC) scores (rs=-.42). When controlling for demographic and ABI characteristics, ≥3 awakenings was significantly associated with worse ABAS-3 GAC (β=-11.3; 95% confidence interval=-19.2, -3.5). Conclusions: Sleep disturbances are associated with poorer outcomes in infants and toddlers after ABI. Sleep is vital to recovery and a potentially modifiable target to improve outcomes.
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Background The objectives of this study were to: 1) characterize the sleep behaviors and symptoms of individuals with Christianson Syndrome (CS) by means of validated questionnaires; and 2) determine their associations with daytime emotional and behavioral symptoms in this population. Methods Participants included 16 boys genetically diagnosed with CS, between 2.5 and 40 years of age (M=14.5 ± 8.08). Parents completed questionnaires regarding the sleep, daytime behavior, and health of their child. Results Of the participants, 31% did not obtain the recommended amount of sleep for their age, 43% experienced a prolonged sleep latency, and 88% had a clinical or sub-clinical score for at least one subscale of the Sleep Disturbance Scale for Children (SDSC). Specific problems detected included insomnia, sleep-wake transition disorders, periodic limb movements in sleep, and sleep related breathing disorders. About half of the participants manifested emotional and behavioral problems at clinical levels. Higher levels of sleep disturbances were associated with higher levels of behavioral and emotional daytime symptoms. Conclusions Sleep problems are common in individuals with CS and are associated with daytime behavioral and emotional symptoms.
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Sleep is critical for cognitive health, especially during complex developmental periods such as adolescence. However, its effects on maturating brain networks that support cognitive function are only partially understood. We investigated the impact of shorter duration and reduced quality sleep, common stressors during development, on functional network properties in early adolescence—a period of significant neural maturation, using resting-state fMRI from 5566 children (median age = 120.0 months; 52.1% females) in the Adolescent Brain Cognitive Development (ABCD) cohort. Decreased sleep duration, increased sleep latency, frequent waking up at night, and sleep-disordered breathing symptoms were associated with lower topological efficiency, flexibility, and robustness of visual, sensorimotor, attention, fronto-parietal control, default-mode and/or limbic networks, and with aberrant changes in the thalamus, basal ganglia, hippocampus and cerebellum (p < 0.05). These widespread effects, many of which were BMI-independent, suggest that unhealthy sleep in early adolescence may impair neural information processing and integration across incompletely developed networks, potentially leading to deficits in their cognitive correlates, including attention, reward, emotion processing and regulation, memory, and executive control. Shorter sleep duration, frequent snoring, difficulty waking up and daytime sleepiness had additional detrimental network effects in non-white participants, indicating racial disparities in the influence of sleep metrics.
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Background Behavioural difficulties are common in children with sleep disorders. However, up to now no study has investigated the association between sleep-related movement disorders (SRMD) and behavior in children with craniofacial cleft. The aim of this study was to assess the frequency and impact of SRMD and growing pains in daytime/bedtime behavior in young children with cleft palate. Methods Cross-sectional survey study of sleep and behavior in 2.0 to 6.9 year old children with cleft palate. Parents completed the Pediatric Sleep Questionnaire, which queries reports of periodic limb movements (PLMS), restless leg syndrome (RLS), growing pains, daytime sleepiness, sleep latency/duration, and the Conners’ Early Childhood Questionnaire which asks about behavioral difficulties. Results Among 71 children with cleft palate (52.1% boys) 14.1% screened positive for PLMS, 8.5% reported RLS and 9.9% growing pains. Children who screened positive for PLMS and RLS were more likely to report sleepiness (PLMS 40% vs. 4.9%, p=0.001; RLS 33.3% vs. 7.7%, p=0.04) and long sleep latency (PLMS 80% vs. 32.8%, p=0.005; RLS 100% vs. 33.8%, p=0.002) compared to those who did not endorse the respective sleep problems. Children who reported PLMS had a higher T-score for emotional (58.2±7.6 vs. 50.7±8.4, p=0.01) and somatic symptoms (66.2±15.2 vs. 49.9±9.5, p=0.0001). Sleepiness was associated to an increased frequency of externalizing, psychiatric and somatic problems. While children with long sleep latency reported more emotional and somatic symptoms, and those with reduced sleep duration more internalizing difficulties. Conclusions Parents of young children with cleft palate reported frequently PLMS, RLS and growing pains. Daytime/bedtime behavior varies depending on the presence of SRMD. Sleepiness and sleep variables might play a role on behavioural problems in children with cleft and SRMD symptoms.
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Sleep is closely related to physical and mental health problems as well as problem behaviors among adolescents and young adults. Thus, to better understand sleep seems paramount, including how to best measure it. The Pittsburgh Sleep Quality Index (PSQI) is one of the most widely used sleep measures. Some recent psychometric evidence (i.e., inconsistent dimensionality across studies) has called into question the application of this clinically developed measure. The current study sought to rigorously test the dimensionality of the measure, by comparing a psychometric application of it to a clinical application. It also tested correlates of sleep quality measured by the PSQI, including academic achievement, mental health, and substance use (alcohol and drug use) . Data were collected from 820 college students using an online computer-assisted protocol. Results from factor analyses supported a 2-factor solution for the PSQI. Findings from path analyses using scale scores based on the extracted factor structure as the independent variable provided evidence that the psychometric approach worked equally well as the clinical application using the global sleep quality risk score , providing some support for the use of a psychometric approach of the PSQI. Sleep quality scores (both scale and global sleep quality risk scores) were consistently associated with academic achievement, mental health, and substance use problems, thus providing further support on the importance of good sleep for young adults. (PsycInfo Database Record (c) 2021 APA, all rights reserved).
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Background Neonatal intensive care saves lives, but the environment in which this occurs is complex and has been shown to negatively disrupt some aspects of an infant's early development. Identifying these negative effects has relied on measuring physiological and behavioural responses. Little research has sought to understand and learn from what an individual infant can communicate about their lived experience. Aim To examine what is known of the lived experiences of infants hospitalised in neonatal intensive care. Study design A scoping review using the revised Arksey and O'Malley framework was undertaken. Relevant studies, exploring an infant's experience of hospitalisation were identified through a comprehensive, systematic literature search. Results 4955 articles were retrieved, 88 full texts reviewed, and 23 studies included. We identified no studies that assessed the experience from the infant's perspective. The infant experience was explored using quantitative methodology, characterising, and describing the experience in measurable physiological, behavioural, and neurodevelopmental terms or through the lens of medical outcomes. The environment is described as too loud and too bright and infants are exposed to high levels of medical handling, impacting on physiology, behaviour, sleep, feeding, and both short- and longer-term outcomes. Conclusion The studies captured in this review focused on quantitative, measurable outcomes as a proxy for the experience as it might be felt, interpreted, and processed by an infant. Medical focus has been crucial to advance the field of neonatology, but the review highlights an important gap; the need to explore and better understand the infant's experience through their eyes.
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Purpose of review: Sleep is important in the evaluation of patients with disorders of consciousness (DOC). However, it remains unclear whether reconstitution of sleep could enable consciousness or vice versa. Here we synthesize recent evidence on natural recovery of sleep in DOC, and sleep-promoting therapeutic interventions for recovery of consciousness. Recent findings: In subacute DOC, physiological sleep--wake cycles and complex sleep patterns are related to better outcomes. Moreover, structured rapid-eye-movement (REM), non-REM (NREM) stages, and presence of sleep spindles correlate with full or partial recovery. In chronic DOC, sleep organization may reflect both integrity of consciousness-supporting brain networks and engagement of those networks during wakefulness. Therapeutic strategies have integrated improvement of sleep and sleep--wake cycles in DOC patients; use of bright light stimulation or drugs enhancing sleep and/or vigilance, treatment of sleep apneas, and neuromodulatory stimulations are promising tools to promote healthy sleep architecture and wakeful recovery. Summary: Sleep features and sleep--wake cycles are important prognostic markers in subacute DOC and can provide insight into covert recovery in chronic DOC. Although large-scale studies are needed, preliminary studies in limited patients suggest that therapeutic options restoring sleep and/or sleep--wake cycles may improve cognitive function and outcomes in DOC.
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Study Objectives Various aspects of human performance were assessed in children after sleep loss. Participants Sixteen children (7 males, 9 females) between the ages of 10 and 14 years Design and Interventions Children were randomly assigned to either a control (CTRL) group, with 11 hours in bed, or an experimental sleep restriction (SR) group, with 5 hours in bed, on a single night in the sleep laboratory. Measurements Both groups were evaluated the following day with a battery of performance and sleepiness measures. Psychomotor and cognitive performance tests were given during four 1-hour testing sessions at 2-hour intervals. Results A multiple sleep latency test (MSLT) documented shorter latencies for SR children than controls. Significant treatment differences were discovered in three of four variables of verbal creativity, including fluency, flexibility, and average indices. There were also group differences found on the Wisconsin Card Sorting Test (WCST), which may be indicative of difficulty learning new abstract concepts. Measures of rote performance and less-complex cognitive functions, including measures of memory and learning and figural creativity, did not show differences between groups, perhaps because motivation could overcome sleepiness-related impairment for these tasks. Conclusions Higher cognitive functions in children, such as verbal creativity and abstract thinking, are impaired after a single night of restricted sleep, even when routine performance is relatively maintained.
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The biological clock, the suprachiasmatic nucleus (SCN), is essential for our daily well-being. It prepares us for the upcoming period of activity by an anticipatory rise in heart rate, glucose and cortisol. At the same time the 'hormone of the darkness', melatonin, decreases. Thus, the time-of-day message penetrates into all tissues, interestingly not only by means of hormones but also by a direct neuronal influence of the SCN on the organs of the body. The axis between the SCN and the paraventricular nucleus of the hypothalamus (PVN) is crucial for the organization/ synchronization of the neuroendocrine and autonomic nervous system with the time of day. This SCN– neuroendocrine PVN axis takes care of a timely hormonal secretion. At the same time, the SCN–autonomic PVN axis fine-tunes the organs by means of the autonomic nervous system for the reception of these hormones. Finally, the similar organization of the projections of the human SCN as compared with that in the rodent brain suggests that these basic principles of neuroendocrine autonomic interaction may also be true in the human. The physiological data collected in humans thus far seem to support this hypothesis, while pathological changes in the SCN of humans suffering from depression or hypertension indicate a role for the SCN in the etiology of these diseases.
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Chronic sleep difficulties commonly coexist with neurodevelopmental and psychiatric problems. Children with special needs may have a variety of sleep disturbances and of these circadian rhythm sleep disorders appear to be the most common. Melatonin supplementation for some circadian rhythm sleep disorders is often an effective treatment because it corrects the associated abnormal melatonin secretion. Melatonin has a benign safety profile and significant potential health benefits. Melatonin has many functions including sleep promoting and chronobiotic properties. Melatonin therapy is only beneficial when persistent sleep difficulties are associated with low melatonin secretion and additional supplementation beyond the therapeutic dose does not result in further sleep promotion. Abnormal neurological modulation of pineal melatonin secretion is commonly present in neurodevelopmental and psychiatric disorders. Melatonin deficiency not only leads to sleep disturbance, but also to multiple health problems. Chronic sleep difficulties of special needs children must not be ignored because they may exacerbate the deficits in development which are already present. In this review, misconceptions about sleep and melatonin therapy, functions of this indoleamine, causes and diagnoses of circadian rhythm sleep disorders, physiological principles underlying treatment, selection of candidates, dose, safety and health benefits are discussed.
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Regulation of adult hippocampal neurogenesis is influenced by circadian rhythm, affected by the manipulation of sleep, and is disturbed in animal models of affective disorders. These observations and the link between dysregulation of the circadian production of melatonin and neuropsychiatric disorders prompted us to investigate the potential role of melatonin in controlling adult hippocampal neurogenesis. In vitro, melatonin increased the number of new neurons derived from adult hippocampal neural precursor cells in vitro by promoting cell survival. This effect was partially dependent on the activation of melatonin receptors as it could be blocked by the application of receptor antagonist luzindole. There was no effect of melatonin on cell proliferation. Similarly, in the dentate gyrus of adult C57BL/6 mice in vivo, exogenous melatonin (8 mg/kg) also increased the survival of neuronal progenitor cells and post-mitotic immature neurons. Melatonin did not affect precursor cell proliferation in vivo and also did not influence neuronal and glial cell maturation. Moreover, melatonin showed antidepressant-like effects in the Porsolt forced swim test. These results indicate that melatonin through its receptor can modulate the survival of newborn neurons in the adult hippocampus, making it the first known exogenously applicable substance with such specificity.
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Sleep is universal, strictly regulated, and necessary for cognition. Why this is so remains a mystery, although recent work suggests that sleep, memory, and plasticity are linked. However, little is known about how wakefulness and sleep affect synapses. Using Western blots and confocal microscopy in Drosophila, we found that protein levels of key components of central synapses were high after waking and low after sleep. These changes were related to behavioral state rather than time of day and occurred in all major areas of the Drosophila brain. The decrease of synaptic markers during sleep was progressive, and sleep was necessary for their decline. Thus, sleep may be involved in maintaining synaptic homeostasis altered by waking activities.
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Here we report preliminary findings from a small-sample functional magnetic resonance imaging (fMRI) study of healthy adolescents who completed a working memory task in the context of a chronic sleep restriction experiment. Findings were consistent with those previously obtained on acutely sleep-deprived adults. Our data suggest that, when asked to maintain attention and burdened by chronic sleep restriction, the adolescent brain responds via compensatory mechanisms that accentuate the typical activation patterns of attention-relevant brain regions. Specifically, it appeared that regions that are normally active during an attention-demanding working memory task in the well-rested brain became even more active to maintain performance after chronic sleep restriction. In contrast, regions in which activity is normally suppressed during such a task in the well-rested brain showed even greater suppression to maintain performance after chronic sleep restriction. Although limited by the small sample, study results provide important evidence of feasibility, as well as guidance for future research into the functional neurological effects of chronic sleep restriction in general, the effects of sleep restriction in children and adolescents, and the neuroscience of attention and its disorders in children.
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Good sleep is necessary for physical and mental health. For example, sleep loss impairs immune function, and sleep is altered during infection. Immune signalling molecules are present in the healthy brain, where they interact with neurochemical systems to contribute to the regulation of normal sleep. Animal studies have shown that interactions between immune signalling molecules (such as the cytokine interleukin 1) and brain neurochemical systems (such as the serotonin system) are amplified during infection, indicating that these interactions might underlie the changes in sleep that occur during infection. Why should the immune system cause us to sleep differently when we are sick? We propose that the alterations in sleep architecture during infection are exquisitely tailored to support the generation of fever, which in turn imparts survival value.
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Memories evolve. After learning something new, the brain initiates a complex set of post-learning processing that facilitates recall (i.e., consolidation). Evidence points to sleep as one of the determinants of that change. But whenever a behavioral study of episodic memory shows a benefit of sleep, critics assert that sleep only leads to a temporary shelter from the damaging effects of interference that would otherwise accrue during wakefulness. To evaluate the potentially active role of sleep for verbal memory, we compared memory recall after sleep, with and without interference before testing. We demonstrated that recall performance for verbal memory was greater after sleep than after wakefulness. And when using interference testing, that difference was even more pronounced. By introducing interference after sleep, this study confirms an experimental paradigm that demonstrates the active role of sleep in consolidating memory, and unmasks the large magnitude of that benefit.
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The pineal gland plays an essential role in vertebrate chronobiology by converting time into a hormonal signal, melatonin, which is always elevated at night. Here we have analyzed the rodent pineal transcriptome using Affymetrix GeneChip(R) technology to obtain a more complete description of pineal cell biology. The effort revealed that 604 genes (1,268 probe sets) with Entrez Gene identifiers are differentially expressed greater than 2-fold between midnight and mid-day (false discovery rate <0.20). Expression is greater at night in approximately 70%. These findings were supported by the results of radiochemical in situ hybridization histology and quantitative real time-PCR studies. We also found that the regulatory mechanism controlling the night/day changes in the expression of most genes involves norepinephrine-cyclic AMP signaling. Comparison of the pineal gene expression profile with that in other tissues identified 334 genes (496 probe sets) that are expressed greater than 8-fold higher in the pineal gland relative to other tissues. Of these genes, 17% are expressed at similar levels in the retina, consistent with a common evolutionary origin of these tissues. Functional categorization of the highly expressed and/or night/day differentially expressed genes identified clusters that are markers of specialized functions, including the immune/inflammation response, melatonin synthesis, photodetection, thyroid hormone signaling, and diverse aspects of cellular signaling and cell biology. These studies produce a paradigm shift in our understanding of the 24-h dynamics of the pineal gland from one focused on melatonin synthesis to one including many cellular processes.
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High-frequency oscillations in cortical networks have been linked to a variety of cognitive and perceptual processes. They have also been recorded in small cortical slices in vitro, indicating that neuronal synchronization at these frequencies is generated in the local cortical circuit. However, in vitro experiments have hitherto necessitated exogenous pharmacological or electrical stimulation to generate robust synchronized activity in the beta/gamma range. Here, we demonstrate that the isolated cortical microcircuitry generates beta and gamma oscillations spontaneously in the absence of externally applied neuromodulators or synaptic agonists. We show this in a spontaneously active slice preparation that engages in slow oscillatory activity similar to activity during slow-wave sleep. beta and gamma synchronization appeared during the up states of the slow oscillation. Simultaneous intracellular and extracellular recordings revealed synchronization between the timing of incoming synaptic events and population activity. This rhythm was mechanistically similar to pharmacologically induced gamma rhythms, as it also included sparse, irregular firing of neurons within the population oscillation, predominant involvement of inhibitory neurons, and a decrease of oscillation frequency after barbiturate application. Finally, we show in a computer model how a synaptic loop between excitatory and inhibitory neurons can explain the emergence of both the slow (<1 Hz) and the beta-range oscillations in the neocortical network. We therefore conclude that oscillations in the beta/gamma range that share mechanisms with activity reported in vivo or in pharmacologically activated in vitro preparations can be generated during slow oscillatory activity in the local cortical circuit, even without exogenous pharmacological or electrical stimulation.
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Brain development in the first 2 years after birth is extremely dynamic and likely plays an important role in neurodevelopmental disorders, including autism and schizophrenia. Knowledge regarding this period is currently quite limited. We studied structural brain development in healthy subjects from birth to 2. Ninety-eight children received structural MRI scans on a Siemens head-only 3T scanner with magnetization prepared rapid gradient echo T1-weighted, and turbo spin echo, dual-echo (proton density and T2 weighted) sequences: 84 children at 2-4 weeks, 35 at 1 year and 26 at 2 years of age. Tissue segmentation was accomplished using a novel automated approach. Lateral ventricle, caudate, and hippocampal volumes were also determined. Total brain volume increased 101% in the first year, with a 15% increase in the second. The majority of hemispheric growth was accounted for by gray matter, which increased 149% in the first year; hemispheric white matter volume increased by only 11%. Cerebellum volume increased 240% in the first year. Lateral ventricle volume increased 280% in the first year, with a small decrease in the second. The caudate increased 19% and the hippocampus 13% from age 1 to age 2. There was robust growth of the human brain in the first two years of life, driven mainly by gray matter growth. In contrast, white matter growth was much slower. Cerebellum volume also increased substantially in the first year of life. These results suggest the structural underpinnings of cognitive and motor development in early childhood, as well as the potential pathogenesis of neurodevelopmental disorders.
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Frequently disrupted and restricted sleep is a common problem for many people in our Western society. In the long run, insufficient sleep may have repercussions for health and may sensitize individuals to psychiatric diseases. In this context, we applied an animal model of chronic sleep restriction to study effects of sleep loss on neurobiological and neuroendocrine systems that have been implied in the pathophysiology of depression, particularly the serotonergic system and the hypothalamic-pituitary-adrenal (HPA) axis. Adult rats were exposed to a schedule of chronic partial sleep deprivation allowing them only 4 h of sleep per day. Sleep restriction was achieved by placing the animals in slowly rotating drums. To examine the regulation and reactivity of the HPA axis, blood samples were collected to measure adrenocorticotropin (ACTH) and corticosterone (CORT) responses. While one day of restricted sleep had no significant effect on HPA axis stress reactivity, sleep restriction for a week caused a blunted pituitary ACTH response in a conditioned fear paradigm. Despite this lower ACTH response, adrenal CORT release was normal. The blunted pituitary response may be related to reduced sensitivity of serotonin-1A receptors and/or receptors for corticotropin-releasing hormone (CRH), since sleep restricted rats showed similar reductions in ACTH release to direct pharmacological stimulation with a serotonin-1A agonist or CRH. Chronic sleep restriction may lead to changes in neurotransmitter receptor systems and neuroendocrine reactivity in a manner similar to that seen in depression. This experimental study thus supports the hypothesis that disrupted and restricted sleep may contribute to the symptomatology of psychiatric disorders.
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Sleep is vital to cognitive performance, productivity, health and well-being. Earlier theories of sleep presumed that it occurred at the level of the whole organism and that it was governed by central control mechanisms. However, evidence now indicates that sleep might be regulated at a more local level in the brain: it seems to be a fundamental property of neuronal networks and is dependent on prior activity in each network. Such local-network sleep might be initiated by metabolically driven changes in the production of sleep-regulatory substances. We discuss a mathematical model which illustrates that the sleep-like states of individual cortical columns can be synchronized through humoral and electrical connections, and that whole-organism sleep occurs as an emergent property of local-network interactions.
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Children with prenatal alcohol exposure (PAE) show deficits in verbal learning and spatial memory, as well as abnormal hippocampal development. The relationship between their memory and neuroanatomic impairments, however, has not been directly explored. Given that the hippocampus is integral for the synthesis and retrieval of learned information and is particularly vulnerable to the teratogenic effects of alcohol, we assessed whether reduced learning and recall abilities in children with fetal alcohol spectrum disorders (FASDs) are associated with abnormal hippocampal volumes. Nineteen children with FASDs and 18 typically developing controls aged 9 to 15 years were assessed for verbal learning and verbal and spatial recall and underwent structural magnetic resonance imaging. Images were analyzed for total intracranial volume and for right and left hippocampal volumes. Results revealed smaller left hippocampi and poorer verbal learning and verbal and spatial recall performance in children with FASDs than controls, as well as positive correlations between selective memory indices and hippocampal volumes only in the FASD group. Additionally, hippocampal volumes increased significantly with age in controls only, suggesting that PAE may be associated with long-term abnormalities in hippocampal development that may contribute to impaired verbal learning and verbal and spatial recall.
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The inhibitory neuromodulator adenosine has been proposed as a homeostatic sleep factor that acts potently in the basal forebrain (BF) to increase sleepiness. Here 300 microM of adenosine was dialyzed in the BF of rats, and the effect on vigilance was determined in the rat Psychomotor Vigilance Task (rPVT). Rats experienced all experimental conditions in a repeated-measures, cross-over design. Twelve young adult male Fischer-Norway rats. Sustained attention performance in the rPVT was evaluated following 2 hours of bilateral microdialysis perfusion of vehicle, adenosine (300 microM), or codialysis of 300 microM of adenosine with the A1 receptor antagonist 8-cyclopentyltheophylline. During rPVT performance, response latencies and performance lapses increased significantly after adenosine dialysis when compared with baseline (no dialysis) or vehicle dialysis sessions. The codialysis of 8-cyclopentyltheophylline with adenosine completely blocked the effects produced by adenosine alone, resulting in performance equivalent to that of the vehicle sessions. Pharmacologic elevation of BF adenosine in rats produced vigilance impairments resembling the effect of sleep deprivation on vigilance performance in both man and rats. This effect of exogenous adenosine was completely blocked by codialysis with an adenosine A1 receptor antagonist. The results are consistent with the hypothesis that sleep loss induces elevations of BF adenosine that, acting via A1 receptors, lead to increased sleepiness and impaired vigilance.
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Research over the last few decades has firmly established that new neurons are generated in selected areas of the adult mammalian brain, particularly the dentate gyrus of the hippocampal formation and the subventricular zone of the lateral ventricles. The function of adult-born neurons is still a matter of debate. In the case of the hippocampus, integration of new cells in to the existing neuronal circuitry may be involved in memory processes and the regulation of emotionality. In recent years, various studies have examined how the production of new cells and their development into neurons is affected by sleep and sleep loss. While disruption of sleep for a period shorter than one day appears to have little effect on the basal rate of cell proliferation, prolonged restriction or disruption of sleep may have cumulative effects leading to a major decrease in hippocampal cell proliferation, cell survival and neurogenesis. Importantly, while short sleep deprivation may not affect the basal rate of cell proliferation, one study in rats shows that even mild sleep restriction may interfere with the increase in neurogenesis that normally occurs with hippocampus-dependent learning. Since sleep deprivation also disturbs memory formation, these data suggest that promoting survival, maturation and integration of new cells may be an unexplored mechanism by which sleep supports learning and memory processes. Most methods of sleep deprivation that have been employed affect both non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. Available data favor the hypothesis that decreases in cell proliferation are related to a reduction in REM sleep, whereas decreases in the number of cells that subsequently develop into adult neurons may be related to reductions in both NREM and REM sleep. The mechanisms by which sleep loss affects different aspects of adult neurogenesis are unknown. It has been proposed that adverse effects of sleep disruption may be mediated by stress and glucocorticoids. However, a number of studies clearly show that prolonged sleep loss can inhibit hippocampal neurogenesis independent of adrenal stress hormones. In conclusion, while modest sleep restriction may interfere with the enhancement of neurogenesis associated with learning processes, prolonged sleep disruption may even affect the basal rates of cell proliferation and neurogenesis. These effects of sleep loss may endanger hippocampal integrity, thereby leading to cognitive dysfunction and contributing to the development of mood disorders.
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The neonatal hippocampus exhibits regularly recurring waves of synchronized neuronal activity in vitro. Because active sleep (AS), characterized by bursts of phasic motor activity in the form of myoclonic twitching, may provide conditions that are conducive to activity-dependent development of hippocampal circuits, we hypothesized that the waves of synchronous neuronal activity that have been observed in vitro would be associated with AS-related twitching. Using unanesthetized 1- to 12-d-old rats, we report here that the majority of neurons in CA1 and the dentate gyrus (DG) are significantly more active during AS than during either quiet sleep or wakefulness. Neuronal activity typically occurs in phasic bursts, during which most neurons are significantly cross-correlated both within and across the CA1 and DG fields. All AS-active neurons increase their firing rates during periods of myoclonic twitching of the limbs, and a subset of these neurons exhibit a burst of activity immediately after limb twitches, suggesting that the twitches themselves provide sensory feedback to the infant hippocampus, as occurs in the infant spinal cord and neocortex. Finally, the synchronous bursts of neuronal activity are coupled to the emergence of the AS-related hippocampal gamma rhythm during the first postnatal week, as well as the emergence of the AS-related theta rhythm during the second postnatal week. We hypothesize that the phasic motor events of active sleep provide the developing hippocampus with discrete sensory stimulation that contributes to the development and refinement of hippocampal circuits as well as the development of synchronized interactions between hippocampus and neocortex.
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The results of a series of studies on total and selective sleep deprivation in the rat are integrated and discussed. These studies showed that total sleep deprivation, paradoxical sleep deprivation, and disruption and/or deprivation of non-rapid eye movement (NREM) sleep produced a reliable syndrome that included death, debilitated appearance, skin lesions, increased food intake, weight loss, increased energy expenditure, decreased body temperature during the late stages of deprivation, increased plasma norepinephrine, and decreased plasma thyroxine. The significance of this syndrome for the function of sleep is not entirely clear, but several changes suggested that sleep may be necessary for effective thermoregulation.
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Sleep is characterized by synchronized events in billions of synaptically coupled neurons in thalamocortical systems. The activation of a series of neuromodulatory transmitter systems during awakening blocks low-frequency oscillations, induces fast rhythms, and allows the brain to recover full responsiveness. Analysis of cortical and thalamic networks at many levels, from molecules to single neurons to large neuronal assemblies, with a variety of techniques, ranging from intracellular recordings in vivo and in vitro to computer simulations, is beginning to yield insights into the mechanisms of the generation, modulation, and function of brain oscillations
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The cerebral cortex and thalamus constitute a unified oscillatory machine displaying different spontaneous rhythms that are dependent on the behavioral state of vigilance. In vivo multi-site recordings from a variety of neocortical areas and related thalamic nuclei in cat, including dual simultaneous intracellular recordings, demonstrate that corticofugal volleys are effective in synchronizing fast (20‐50 Hz) and low-frequency (<15 Hz) oscillations in thalamocortical networks, characterizing activated and deafferented states. (i) Fast spontaneous oscillations depend on the depolarization of thalamic and cortical cells and appear in a sustained manner during waking and REM sleep. Corticothalamic neurons, discharging high-frequency (400 Hz) spike-bursts at 30‐40 Hz, are good candidates to synchronize fast oscillations in reentrant thalamocortical loops. Weakly synchronized, fast spontaneous oscillations may be reset and become robustly coherent after relevant sensory stimuli in waking or internal signals during the dreaming state. (ii) During quiescent sleep, the long-range synchronization of brain electrical activity results from synchronous hyperpolarizations in forebrain neurons. The corticothalamic inputs during the depolarizing component of the slow oscillation (<1 Hz) are effective in grouping the thalamic-generated sleep rhythms (spindles at 7‐14 Hz and delta at 1‐4 Hz) into complex wave-sequences. These inputs also control the shape of spindles, and favor the long-range synchronization and nearly simultaneous appearance of spindles. (iii) The cortical control of thalamic activity is also demonstrated in spike-wave seizures developing from sleep patterns. More than half of thalamocortical neurons are silent during spike-wave seizures, being tonically hyperpolarized, and display IPSPs (closely related to the paroxysmal depolarizing shifts of cortical cells) that are determined by the pattern of activities in thalamic reticular cells. All these data congruently show the power of cortical control upon thalamic oscillators.
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To determine whether a cumulative sleep debt (in a range commonly experienced) would result in cumulative changes in measures of waking neurobehavioral alertness, 16 healthy young adults had their sleep restricted to an average 4.98 hrs per night for 7 consecutive nights. Ss slept in the laboratory, and sleep and waking were monitored. Three times each day, Ss were assessed for subjective sleepiness and mood and were evaluated on a brief performance battery that included psychomotor vigilance (PVT), probed memory (PRM), and serial-addition testing. Once each day they completed a series of visual analog scales (VASs) and reported sleepiness and somatic and cognitive/emotional problems. Sleep restriction resulted in statistically robust cumulative effects on waking functions. Subjective sleepiness ratings, subscale scores for fatigue, confusion, tension, and total mood disturbance from the mood and VAS ratings of mental exhaustion and stress were elevated across days of restricted sleep. PVT performance parameters were also significantly increased by restriction. Significant time-of-day effects were evident in subjective sleepiness and PVT data. Findings suggest that cumulative nocturnal sleep debt had a dynamic and escalating analog in cumulative daytime sleepiness and that asymptotic or steady-state sleepiness was not achieved in response to sleep restriction. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
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The comorbidity of 'core characteristics' and sensorimotor abnormalities in autism implies abnormalities in brain development of a general and pervasive nature and atypical organization of sensory cortex. By using magnetoencephalography, we examined the cortical response to passive tactile stimulation of the thumb and index finger of the dominant hand and lip of the individuals with autism spectrum disorder and typically developing persons. The distance between the cortical representations of thumb and the lip was significantly larger in the autism group than in typicals. Moreover, in cortex, the thumb is typically closer to the lip than the index finger. This was not observed in persons with autism. Our findings are arguably the first demonstration of abnormality in sensory organization in the brains of persons with autism.
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Within an interdisciplinary research project, the long-term outcome of children with fetal alcohol syndrome was studied. Methods for the assessment of psychopathology, behavior, and intelligence included psychiatric interviews, behavior checklists for parents and teachers, and intelligence tests. The children were assessed during preschool age, early school age (6 to 12 years), and late school age (≥ 13 years). An excess of psychopathology, (including hyperkinetic disorders, emotional disorders, sleep disorders, and abnormal habits and sterotypies) with a strong persistence over time was found. Cognitive functioning was marked by a large proportion of mentally retarded children and also did not change considerably over time. This long-term outcome study reflects the handicapping effects of fetal alcohol syndrome.
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To examine the effect of melatonin on in vitro fertilization and embryonic development, mouse embryos after insemination in vitro were cultured in a physiological medium with or without melatonin. Melatonin increased the fertilization rate significantly at a concentration between 10−6 and 10−4 M (27.6 vs. 43.9 or 40.4%, P<0.01). Furthermore, a significant increase in the rate of embryos reaching the four-cell stage (16.0 vs. 26.7%, P<0.01), the eight-cell stage (12.1 vs. 25.8 or 23.5%, P<0.01), and blastulation (8.9 vs. 23.5 or 17.5%, P<0.01) was observed when the embryos were cultured in a medium containing 10−8 or 10−6 M melatonin. These results demonstrate that melatonin supports fertilization and early embryo development after in vitro fertilization.
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Abstract The term ‘sleep debt’ is widely used to describe the effects of sleep loss. The construct of sleep debt, however, is poorly defined in the scientific literature. Cumulative build-up of sleep pressure appears to be a key feature of sleep debt. The concepts of ‘core sleep’ and ‘basal sleep need’ have been proposed to provide a theoretical framework, albeit without strong empirical basis. It has been hypothesized that adaptation to sleep debt may be possible over time, but experimental evidence for this hypothesis is ambiguous. Recent experiments using chronic sleep restriction have revealed significant effects of sleep debt on daytime sleep latency and behavioral alertness. In a series of strictly controlled laboratory studies, we found that sleep debt can lead to fundamentally different daytime responses, depending on whether homeostatic sleep pressure (as measured in the waking electroencephalogram (EEG)) or behavioral alertness (as measured with psychomotor vigilance lapses) is considered. This suggests the existence of an as yet unidentified regulatory mechanism of waking neurobehavioral function. To study the nature of this regulatory process under chronic sleep restriction, advantage can be taken of the natural variability in sleep need frequently cited in the literature. We also obtained evidence for interindividual differences in vulnerability to sleep loss regardless of sleep need. Statistical modeling of the effects of chronic sleep restriction on behavioral alertness, taking into account these interindividual differences, provided a reference for defining sleep debt. The results suggested that sleep debt may be defined as the cumulative hours of sleep loss with respect to a subject-specific daily need for sleep.