scholarly journals Bedtime to the brain: How infants sleep habits intertwine with sleep neurophysiology

2021 ◽  
Author(s):  
Sarah Fiona Schoch ◽  
Valeria Jaramillo ◽  
Andjela Markovic ◽  
Reto Huber ◽  
Malcolm Kohler ◽  
...  

Adequate sleep is critical for development and facilitates the maturation of the neurophysiological circuitries at the basis of cognitive and behavioral function. Observational research has associated sleep problems in early life with worse later cognitive, psychosocial, and somatic health outcomes. Yet, the extent to which day-to-day sleep habits in early life relate to neurophysiology - acutely and long-term - remains to be explored. Here, we report that sleep habits in 32 healthy 6-month-olds assessed with actimetry are linked to fundamental aspects of their neurophysiology measured with high-density electroencephalography (hdEEG). Our study reveals four key findings: First, daytime sleep habits are linked to EEG slow wave activity (SWA). Second, habits of nighttime movement and awakenings from sleep are connected with spindle density. Third, habitual sleep timing is linked to neurophysiological connectivity quantified as Delta-coherence. And lastly, Delta-coherence at age 6 months predicts nighttime sleep duration at age 12 months. These novel findings widen our understanding that infants' sleep habits are closely intertwined with three particular levels of neurophysiology: sleep pressure (determined by SWA), the maturation of the thalamocortical system (spindles), and the maturation of cortical connectivity (coherence). Our companion paper complements this insight in the perspective of later developmental outcomes: early thalamocortical connectivity (spindle density) at age 6 months predicts later behavioural status at 12 and 24 months. The crucial next step is to extend this concept to clinical groups to objectively characterize infants' sleep habits "at risk" that foster later neurodevelopmental problems.

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A11-A12
Author(s):  
Carolyn Jones ◽  
Randall Olson ◽  
Alex Chau ◽  
Peyton Wickham ◽  
Ryan Leriche ◽  
...  

Abstract Introduction Glutamate concentrations in the cortex fluctuate with the sleep wake cycle in both rodents and humans. Altered glutamatergic signaling, as well as the early life onset of sleep disturbances have been implicated in neurodevelopmental disorders such as autism spectrum disorder. In order to study how sleep modulates glutamate activity in brain regions relevant to social behavior and development, we disrupted sleep in the socially monogamous prairie vole (Microtus ochrogaster) rodent species and quantified markers of glutamate neurotransmission within the prefrontal cortex, an area of the brain responsible for advanced cognition and complex social behaviors. Methods Male and female prairie voles were sleep disrupted using an orbital shaker to deliver automated gentle cage agitation at continuous intervals. Sleep was measured using EEG/EMG signals and paired with real time glutamate concentrations in the prefrontal cortex using an amperometric glutamate biosensor. This same method of sleep disruption was applied early in development (postnatal days 14–21) and the long term effects on brain development were quantified by examining glutamatergic synapses in adulthood. Results Consistent with previous research in rats, glutamate concentration in the prefrontal cortex increased during periods of wake in the prairie vole. Sleep disruption using the orbital shaker method resulted in brief cortical arousals and reduced time in REM sleep. When applied during development, early life sleep disruption resulted in long-term changes in both pre- and post-synaptic components of glutamatergic synapses in the prairie vole prefrontal cortex including increased density of immature spines. Conclusion In the prairie vole rodent model, sleep disruption on an orbital shaker produces a sleep, behavioral, and neurological phenotype that mirrors aspects of autism spectrum disorder including altered features of excitatory neurotransmission within the prefrontal cortex. Studies using this method of sleep disruption combined with real time biosensors for excitatory neurotransmitters will enhance our understanding of modifiable risk factors, such as sleep, that contribute to the altered development of glutamatergic synapses in the brain and their relationship to social behavior. Support (if any) NSF #1926818, VA CDA #IK2 BX002712, Portland VA Research Foundation, NIH NHLBI 5T32HL083808-10, VA Merit Review #I01BX001643


2013 ◽  
Vol 43 (1) ◽  
pp. 79
Author(s):  
R. Ghalamghash ◽  
H.Z. Mammedov ◽  
H. Ashayeri ◽  
A. Hosseini

2021 ◽  
Vol 12 ◽  
Author(s):  
Kaila N. Parker ◽  
Michael H. Donovan ◽  
Kylee Smith ◽  
Linda J. Noble-Haeusslein

Despite the high incidence of brain injuries in children, we have yet to fully understand the unique vulnerability of a young brain to an injury and key determinants of long-term recovery. Here we consider how early life stress may influence recovery after an early age brain injury. Studies of early life stress alone reveal persistent structural and functional impairments at adulthood. We consider the interacting pathologies imposed by early life stress and subsequent brain injuries during early brain development as well as at adulthood. This review outlines how early life stress primes the immune cells of the brain and periphery to elicit a heightened response to injury. While the focus of this review is on early age traumatic brain injuries, there is also a consideration of preclinical models of neonatal hypoxia and stroke, as each further speaks to the vulnerability of the brain and reinforces those characteristics that are common across each of these injuries. Lastly, we identify a common mechanistic trend; namely, early life stress worsens outcomes independent of its temporal proximity to a brain injury.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A245-A246
Author(s):  
Yu-Ting Wu ◽  
Ya-Chuan Huang ◽  
Yung-Sen Chang ◽  
Chien-Ming Yang

Abstract Introduction ‘Co-sleep’ is defined as the sleep arrangements in which parents and their child sharing a sleeping surface (bed-sharing or room-sharing). Similar to the other Asian countries, Taiwan has a high reported rates of bed-sharing. Previous researches had shown shorter sleep duration and poorer sleep quality in children with co-sleep. However, the association between co-sleep and the children’s emotional and behavioral problems has not been well studied. This study aims to explore the association between sleeping arrangements and children’s sleep, as well as their daytime emotional and behavioral problems. Methods 9,582 caregivers of preschoolers (age= 4.70±0.806; Male: Female=52%:48%) completed a questionnaire regarding their children’s sleep schedule, the Children’s Sleep Habits Questionnaire (CSHQ) and Strength and Difficulties Questions (SDQ). The reported frequency on the items of the CHSQ question regarding co-sleep, asking whether the child falls asleep in parent’s or sibling’ s bed or sleep alone, were used to divide the children into three groups: usually co-sleep group, sometimes co-sleep group and sleep-alone group. Results Among 2,967 preschoolers, 6,272 children (65.5%) reported usually co-sleep, 816 children (8.5%) reported sometimes co-sleep, and 2,494 children (26%) reported sleeping alone. One-way ANOVAs showed significant differences among three groups in: 1) sleep patterns, including weekday nighttime sleep duration (F=24.43, p<.01), weekend nighttime sleep duration (F=3.13, p<.05), weekday nap duration (F=4.24, p<.05), and weekend nap time (F=4.39, p<.05); 2) sleep problems on the CHSQ, including bed time resistance (F=7027.25, p<.01), sleep onset delay (F=33.06, p<.01), sleep duration (F=65.51, p<.01), sleep anxiety (F=788.48, p<.01), night waking (F=37.90, p<.01), parasomnias (F=47.43, p<.01), sleep disorder breathing (F=7.58, p<.01), and sleepiness (F=13.44, p<.01); 3) behavioral problems and development on the SDQ, including hyperactivity (F=21.16, p<.01), emotional symptom (F=23.08, p<.01), conduct problem (F=8.65, p<.01), peer problems (F=20.59, p<.01), and prosocial (F=17.67, p<.01). Conclusion Our results indicate that children with more frequent co-sleep may have shorter sleep duration, more sleep problems as well as more external and internal behavioral problems, while sleep-alone children showed more prosocial behaviors, longer sleep duration, and less sleep problems. The potential developmental problems related to co-sleep may be underestimated in Asian culture and need more attentions. Support (if any):


SLEEP ◽  
2020 ◽  
Vol 43 (8) ◽  
Author(s):  
Pablo E Brockmann ◽  
Helena Poggi ◽  
Alejandro Martinez ◽  
Ivonne D’Apremont ◽  
Rosario Moore ◽  
...  

Abstract Study Objectives Prematurity has been associated with an increased risk for sleep apnea. However, sleep disturbances in children born preterm have not been extensively investigated. Considering that determinants of sleep may originate early in life, the potential impact of prematurity on sleep disturbances later in life could be important. To establish the role of prematurity on sleep disturbances in a cohort of schoolchildren that were born preterm and compare them with healthy controls. Methods A cohort of 147 schoolchildren, 45 born at term (≥37 weeks) and 102 very preterm (<32 weeks), was recruited and evaluated at school age (5–9 years). The Pediatric Sleep Questionnaire (PSQ) and the Sleep Disturbance Scale for Children (SDSC) were used to assess sleep disturbances in different domains. Results PSQ score was significantly higher in former preterm children (0.26 ± 0.18 vs. 0.18 ± 0.14 in controls; p = 0.004), and SDSC total score was also significantly different among groups (21.7 ± 11.6 vs. 14.1 ± 12.6; p < 0.001). Regression models showed significant mean differences in PSQ score, total SDSC score, and two SDSC subscale scores (i.e. sleep-wake transition disorders, sleep-breathing disorders, and sleep hyperhidrosis) even after adjustment for confounders. Maternal age and type of delivery were not significantly associated with total PSQ scores. Conclusions Sleep disturbances may originate early in life since children born preterm exhibit an increased risk for developing long-term sleep problems. These findings may have important implications for management of preterm children and for implementation of early interventions focused on optimizing sleep habits.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A71-A72
Author(s):  
Gianna Rea-Sandin ◽  
Reagan Breitenstein ◽  
Leah Doane ◽  
Emily Vakulskas ◽  
Carlos Valiente ◽  
...  

Abstract Introduction Elementary-aged children in low socioeconomic environments are more likely to experience poor sleep, which can negatively impact academic performance. However, it is unknown whether early-life socioeconomic status (SES) influences associations between sleep and academic achievement later in childhood. Using a demographically diverse sample of children followed longitudinally from 1 to 8 years, we tested linear and nonlinear associations between actigraphy-based sleep duration, midpoint time, sleep duration variability, and parent-reported sleep problems with academic achievement. In addition, we examined whether these associations varied by early SES. Methods The sample comprised 707 twins (52% female; Mage=8.44 years; 28.7% Hispanic/Latinx; 29.7% at or below the poverty line). SES was ascertained at 1 and 8 years, and children wore actigraph watches to assess sleep for 7 nights (Mnights=6.79) and completed the Applied Math, Picture Vocabulary, and Passage Comprehension subtests of the Woodcock-Johnson IV Tests of Achievement. Primary caregivers also reported on their children’s sleep and academic performance (Children’s Sleep Habits Questionnaire and Health and Behavior Questionnaire, respectively). Results Sleep was not linearly related to academic achievement, but there was a significant quadratic association between sleep midpoint with Picture Vocabulary (b=0.28, p<.01) and Passage Comprehension (b=0.17, p<.05). More parent-reported sleep problems were negatively related to Applied Problems performance for lower (b=-1.16, p<.001) and positively associated for higher early SES (b = 1.00, p < .01). More parent-reported sleep problems predicted lower Passage Comprehension for lower (b = -0.59, p < .05), but not higher early SES. Longer sleep duration predicted higher parent-reported academic achievement for lower early SES (b=0.14, p<.01) and lower achievement for higher early SES (b=-0.23, p<.001). Conclusion Our findings illustrate the complex, sometimes nonlinear associations between children’s sleep and academic performance. Many associations varied by early-life SES, suggesting that early childhood environments have long-lasting implications for child functioning, over and above the effect of concurrent SES. Increasing the quantity and quality of children’s sleep could improve academic outcomes, particularly for children who have experienced socioeconomic disadvantage. Support (if any) This research was supported by grants from NICHD (R01HD079520 and R01HD086085) and ASU T. Denny Sanford School of Social and Family Dynamics.


2010 ◽  
Vol 24 (4) ◽  
pp. 249-252 ◽  
Author(s):  
Márk Molnár ◽  
Roland Boha ◽  
Balázs Czigler ◽  
Zsófia Anna Gaál

This review surveys relevant and recent data of the pertinent literature regarding the acute effect of alcohol on various kinds of memory processes with special emphasis on working memory. The characteristics of different types of long-term memory (LTM) and short-term memory (STM) processes are summarized with an attempt to relate these to various structures in the brain. LTM is typically impaired by chronic alcohol intake but according to some data a single dose of ethanol may have long lasting effects if administered at a critically important age. The most commonly seen deleterious acute effect of alcohol to STM appears following large doses of ethanol in conditions of “binge drinking” causing the “blackout” phenomenon. However, with the application of various techniques and well-structured behavioral paradigms it is possible to detect, albeit occasionally, subtle changes of cognitive processes even as a result of a low dose of alcohol. These data may be important for the consideration of legal consequences of low-dose ethanol intake in conditions such as driving, etc.


Author(s):  
Peter R. Breggin

BACKGROUND: The vaccine/autism controversy has caused vast scientific and public confusion, and it has set back research and education into genuine vaccine-induced neurological disorders. The great strawman of autism has been so emphasized by the vaccine industry that it, and it alone, often appears in authoritative discussions of adverse effects of the MMR and other vaccines. By dismissing the chimerical vaccine/autism controversy, vaccine defenders often dismiss all genuinely neurological aftereffects of the MMR (measles, mumps, and rubella) and other vaccines, including well-documented events, such as relatively rare cases of encephalopathy and encephalitis. OBJECTIVE: This report explains that autism is not a physical or neurological disorder. It is not caused by injury or disease of the brain. It is a developmental disorder that has no physical origins and no physical symptoms. It is extremely unlikely that vaccines are causing autism; but it is extremely likely that they are causing more neurological damage than currently appreciated, some of it resulting in psychosocial disabilities that can be confused with autism and other psychosocial disorders. This confusion between a developmental, psychosocial disorder and a physical neurological disease has played into the hands of interest groups who want to deny that vaccines have any neurological and associated neuropsychiatric effects. METHODS: A review of the scientific literature, textbooks, and related media commentary is integrated with basic clinical knowledge. RESULTS: This report shows how scientific sources have used the vaccine/autism controversy to avoid dealing with genuine neurological risks associated with vaccines and summarizes evidence that vaccines, including the MMR, can cause serious neurological disorders. Manufacturers have been allowed by the US Food and Drug Administration (FDA) to gain vaccine approval without placebo-controlled clinical trials. CONCLUSIONS: The misleading vaccine autism controversy must be set aside in favor of examining actual neurological harms associated with vaccines, including building on existing research that has been ignored. Manufacturers of vaccines must be required to conduct placebo-controlled clinical studies for existing vaccines and for government approval of new vaccines. Many probable or confirmed neurological adverse events occur within a few days or weeks after immunization and could be detected if the trials were sufficiently large. Contrary to current opinion, large, long-term placebo-controlled trials of existing and new vaccines would be relatively easy and safe to conduct.


2004 ◽  
pp. 406-412
Author(s):  
Paul Okunieff ◽  
Michael C. Schell ◽  
Russell Ruo ◽  
E. Ronald Hale ◽  
Walter G. O'Dell ◽  
...  

✓ The role of radiosurgery in the treatment of patients with advanced-stage metastatic disease is currently under debate. Previous randomized studies have not consistently supported the use of radiosurgery to treat patients with numbers of brain metastases. In negative-results studies, however, intracranial tumor control was high but extracranial disease progressed; thus, patient survival was not greatly affected, although neurocognitive function was generally maintained until death. Because the future promises improved systemic (extracranial) therapy, the successful control of brain disease is that much more crucial. Thus, for selected patients with multiple metastases to the brain who remain in good neurological condition, aggressive lesion-targeting radiosurgery should be very useful. Although a major limitation to success of this therapy is the lack of control of extracranial disease in most patients, it is clear that well-designed, aggressive treatment substantially decreases the progression of brain metastases and also improves neurocognitive survival. The authors present the management and a methodology for rational treatment of a patient with breast cancer who has harbored 24 brain metastases during a 3-year period.


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