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Neurosci Biobehav Rev. Author manuscript; available in PMC 2017 November 01.
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Published in final edited form as:

Neurosci Biobehav Rev. 2016 November ; 70: 182–188. doi:10.1016/j.neubiorev.2016.08.008.

Sleep in adolescence: physiology, cognition and mental health

Leila Tarokh1,2,3, Jared M. Saletin3,4, and Mary A. Carskadon3,4,5

1UniversityHospital of Child and Adolescent Psychiatry and Psychotherapy, University of Bern,

Bern, Switzerland 2Institute of Pharmacology and Toxicology, University of Zurich, Zurich,
Switzerland 3Department of Psychiatry and Human Behavior, The Alpert Medical School of
Brown University, Providence, USA 4Sleep for Science Research Lab of Brown University, EP
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Bradley Hospital, Providence, USA 5Centre for Sleep Research, School of Psychology, Social
Work and Social Policy, University of South Australia, Adelaide, Australia

Abstract
Sleep is a core behavior of adolescents, consuming up to a third or more of each day. As part of
this special issue on the adolescent brain, we review changes to sleep behaviors and sleep
physiology during adolescence with a particular focus on the sleeping brain. We posit that brain
activity during sleep may provide a unique window onto adolescent cortical maturation and
compliment waking measures. In addition, we review how sleep actively supports waking
cognitive functioning in adolescence. Though this review is focused on sleep in healthy
adolescents, the striking comorbidity of sleep disruption with nearly all psychiatric and
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developmental disorders (for reviews see 1,2) further highlights the importance of understanding
the determinants and consequences of adolescent sleep for the developing brain. Figure 1
illustrates the overarching themes of our review, linking brain development, sleep development,
and behavioral outcomes.

Adolescent Sleep Behavior

Adolescence is a time of increased independence and emergence of new social roles, all of
which affect behavior: sleep is no exception. Driven in part by this newly acquired
autonomy, combined with delays in the circadian timing system (reviewed in T. Lee chapter)
and changes to the homeostatic sleep regulating system that provide greater tolerance for
sleep pressure 3, bedtimes become later with each passing year during adolescence. Rise
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times, by contrast, are more often determined by school start times and thus remain
unchanged or move earlier 4. Whether using self-report 4 or objectively recorded sleep 5,

Corresponding author: Mary A. Carskadon, Professor, Psychiatry & Human Behavior, The Alpert Medical School of Brown
University, Director, Chronobiology & Sleep Research, EP Bradley Hospital, 300 Duncan Drive, Providence, RI 02906, USA,
Professor of Psychology, Director, Centre for Sleep Research, School of Psychology, Social Work and Social Policy, University of
South Australia, GPO Box 2471, Adelaide, South Australia 5001. Australia. Tel.: 401-421-9440; Fax 401-453-3578
mary_carskadon@brown.edu.
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 Tarokh et al. Page 2

studies show that US teens lose about 90 minutes of sleep each school night from grade 6
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(about 11-12 years old) to grade 12 (about 17-18 years old). With both approaches, the
average school-night total sleep time for the youngest adolescents was about 8.4 h and about
6.9 h in the high school seniors. A more recent report from the Center for Disease Control
using data from the Youth Behavior Risk Surveillance Data from 2007, 2009, 2011, and
2014 (N = 50,370 US students) found that two thirds of students in grades 9 to 12 reported 7
h or less sleep on school nights 6. Trends are similar in other countries and circumstances
appear worst for adolescents living in Southeast Asia. Yang et al. in 2005 7, for example,
showed that teens’ reported school-night bedtimes progressively later than in the US from
grades 5/6 (10:42 pm ± 78 m) to grades 11/12 (12:54 am ± 84 m) and that nightly total sleep
time for school nights was nearly 3 h less in the older versus younger adolescents: 8 h 18 m
vs. 5 h 24 min, much shorter in year 12 than in the US.

Despite the dwindling time spent asleep, studies suggest that sleep “need”,per se does not
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undergo dramatic changes during adolescence. An early longitudinal study, following

adolescents yearly from 10-12 till 15-18 years of age found that when given ten hours of
sleep-opportunity, adolescents slept an average of approximately 9.25 hours irrespective of
age or maturational stage. Further evidence for the stability of sleep need comes from
Ohayon and colleagues 8, indicating a decline in sleep duration on school days, but no
change on non-school days, leading the authors to conclude that the school day decline is
driven by environmental rather than biological factors. Given the pervasive discrepancy
between sleep need and sleep obtained for most teens, understanding the consequences of
chronic insufficient sleep is paramount. For example, a laboratory study in which 10th
graders slept on a self-selected school night schedule, found that during a morning nap
opportunity (08:30, roughly equivalent to the first or second class-period of American high
schools), participants fell asleep in approximately 5 minutes, nearly half the time the same
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participants took to fall asleep later in the day. About 50% of the sample fell asleep in less
than 2 minutes and directly into REM sleep. This study indicates that these 10th graders may
in fact suffer from pathological sleepiness during the start of the school day, perhaps a result
of a simultaneous delay in their circadian rhythms and the abridgement of their sleep
opportunity by earlier school-start times 9. Thus, starting the school day sleepy and
unprepared for the cognitive and social challenges of adolescence is quotidian for many
teens.

Measurement and Key Principles of Adolescent Sleep

Sleep can be measured in a variety of ways, including self-reports, actigraphy, and
polysomnography (PSG). Self-reports are useful for assessing perceived sleep difficulties
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and daytime functioning and are, for example, part of the diagnostic criteria for certain
psychiatric illnesses 10. Several specific self-report sleep scales have been developed,
including one focused on assessing the chronic sleep reduction of adolescence 11.
Actigraphy usually involves wearing a small wrist-worn watch-like device that can delineate
sleep and waking based on motion; such devices can provide measures of sleep in broad
strokes (e.g., sleep duration, nocturnal arousals) and can be used to assess sleep over long
periods of time (e.g., several weeks or months). Research-grade activity monitors have
validated and open-sourced algorithms to estimate sleep, whereas newer commercially

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available activity monitors often provide summary measures of sleep and daytime physical
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activity using proprietary software inaccessible to the user. Validation studies of such
devices are limited and have provided mixed results for specificity and sensitivity
(e.g., 12,13). Although actigraphy and self-reports are important tools, the gold standard for
quantifying sleep, is polysomnography (PSG), which requires continuous measurement of
electroencephalogram (EEG), electrooculogram (EOG), and electromyogram (EMG). The
combination of these physiological signals is used to divide sleep into two states: non rapid
eye movement (NREM) sleep (which is further subdivided into 3 or 4 stages) and REM
sleep.

The EEG signal also provides access to several cortical oscillations observed only in the
sleeping brain. Two such oscillations that occur in NREM sleep are the subject of much
study: slow waves and sleep spindles. Slow waves are low frequency (0.4 to 4.6 Hz), high
amplitude oscillations generated primarily in the cortex, although the thalamus has been
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suggested to play a role in modulating these oscillations 14. These slow waves are plentiful
at the beginning of the night and show an exponential decline over the course of sleep
(reviewed in 15). Furthermore, slow waves show an increase in incidence and amplitude
following sleep deprivation 15. The preferential occurrence of slow waves at the beginning of
sleep and the increase when sleep deprived highlight the proposed role of these oscillations
as markers of the sleep homeostatic system 16. Unlike slow waves, which dominate sleep
EEG activity for several hours in the healthy adolescent brain, sleep spindles are transient
(1-2 seconds) oscillations with a frequency between 11 and 16 Hz. Sleep spindles are
generated through thalamocortical loops (see 17) and functional roles in sleep consolidation
and declarative memory systems have been attributed to this activity (reviewed in 18).

The magnitude of these and other EEG oscillations can be calculated from EEG signals
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using the Fourier transform, which computes the strength of the EEG’s constituent
frequencies. Therefore, EEG slow wave activity (SWA) is often defined as total power (μV2)
in the 0.4 - 4.6 Hz frequency range. Spindles are similarly summarized by total EEG power
in the 11 to 16 Hz range. Because the spectral frequency of spindles varies from person to
person and across development, the frequency of the peak power in this band is sometimes
used as a measure of spindle activity sensitivity to inter-individual variation.

Sleep Physiology in Adolescence

In addition to the developmental shifts that occur in circadian rhythms and sleep
homeostasis during development, clear maturational changes are observed in the oscillatory
physiology outlined above. These trajectories are likely driven by maturational modifications
to brain anatomy during this time. The most striking change to the sleep EEG is a marked
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reduction in the EEG amplitude and power of the sleep EEG signal, which occurs earlier for
girls than boys and is in part tied to pubertal maturation 19. This reduction in EEG power of
up to 40% from pre- to post-puberty is seen across EEG frequencies, within both waking
and sleep states19-22. This reduction is likely driven by significant declines in cortical grey
matter which take place during adolescence. Direct support for this association comes from
one study that measured both grey matter (i.e., structural MRI) and sleep EEG power in
participants ages 8 to 19 years and found correlations between these measures over a wide

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range of cortical regions 23. Furthermore, both measures manifested an age-dependent

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decline, further supporting the hypothesis that the decline in sleep EEG power is driven by
reductions in grey matter volume. A separate study that used high-density EEG to measure
cortical activity at a large number of cortical regions found a developmental progression of
maximal sleep slow wave activity (spectral sleep EEG power between 0.6 to 4.6 Hz; SWA)
from posterior to anterior cortical regions 24. This progression is similar to observations
from longitudinal MRI studies regarding regional maximal cortical grey matter volume 25.

Another developmental change manifest in the adolescent brain is an increase in white

matter volume. Although direct evidence for an association between white matter volume
and measures of the sleep EEG is lacking, one EEG measure of connectivity—sleeping EEG
coherence— showed a linear increase in a study of adolescents similar to adolescent changes
in white matter volume 26. As with the decline in sleep EEG power, this increase in
coherence is found across frequencies and sleep states, indicating an anatomical substrate.
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Furthermore, the peak spectral frequency of sleep spindles also shows a linear increase
across adolescence 20,21,27,28. Again, although direct evidence is lacking, we have
hypothesized that this sleep spindle frequency increase reflects a measure of cortical
myelination 29. Interestingly, the rate of change in sleep EEG power and coherence are not
correlated, suggesting separate processes 30.

Sleep: An Active Role in Brain Development?

Sleep is not only an opportunity to measure otherwise unperturbed brain activity, but recent
studies also suggest that sleep itself may play an active role in sculpting the adolescent brain.
Using two-photon microscopy in adolescent mice, for example, Maret and colleagues found
that synaptic spine elimination was higher during sleep than during waking in adolescent but
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not adult mice, suggesting a distinctive role for sleep in the adolescent brain 31. Correlational
studies in humans have also found associations between sleep behavior and brain
development. One such study examined structural MRI scans in 290 children and
adolescents between the ages of 5 and 18 years and found that self-reported sleep duration
was positively correlated with bilateral hippocampal grey matter volume 32. Another study
found an association in adolescents between variability in sleep duration across fourteen
days and white mater integrity as measured with diffusion tensor MRI 33. Although this line
of research is in its nascent stage, evidence for a role of sleep in brain development is
emerging.

Sleep Traits and Associations with Cognition

Several studies have examined the association between sleep neurophysiology and stable
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metrics of cognitive aptitude. The sleep EEG is an attractive target to identify such
associations because the spectrum is stable across consecutive nights of recording, while at
the same time unique to an individual 34. Furthermore, we have shown that the morphology
of the sleep EEG spectrum is largely preserved in adolescents across several years, despite
maturational changes in sleep EEG power and cortical restructuring 29. Thus, the sleep EEG
spectrum is trait-like over several years, and recent data indicate high heritability of the sleep
EEG spectrum, including in adolescence 35. Several studies have examined the association

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between the trait-like oscillations in the sleep EEG and stable metrics of cognitive ability,
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such as intelligence quotient (IQ). These studies describe positive correlations between IQ
and sleep spindles magnitude (e.g., power, amplitude, and density) in children 36-38 and
adolescents 39. Furthermore, a two-year longitudinal study that measured sleep EEG
coherence and waking performance on cognitive tasks of executive function and response
inhibition in early adolescents found associations between spindles and cognitive
performance 30. In this study, adolescents who showed the greatest increases in intra-
hemispheric spindle coherence also manifested the most improvements on these tasks.
Because sleep spindles are generated through long-range thalamocortical loops, this activity
may carry important information about cortical functioning and circuit integrity that support
cognitive function.

Sleep and Learning and Memory

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While the above evidence focuses on the association between sleep physiology and
intelligence as one marker of how sleep may index the stable and healthy development of
cognitive systems across adolescence, a separate yet germane line of studies—mostly in
adults—indicates that even short manipulation of sleep can modulate cognition function.
Both the restorative benefit of sleep and the detrimental impact of sleep loss have been
documented in adults using experimental protocols targeting a number of cognitive domains:
attention40, executive function41, reward sensitivity42, emotional regulation 43, and learning
and memory44. These studies typically use short perturbations in sleep (e.g., a daytime nap,
a night of total sleep deprivation, or sleep restriction over several days); thus, they do not
directly measure the long-term consequences of truncated sleep on cognition. They do,
however, provide an excellent opportunity for experimental probing of the impact of sleep
loss during sensitive developmental windows such as adolescence.
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Healthy development of cognitive systems during this phase of life is paramount to

intellectual pursuits. Despite the ecological importance of cognitive function during
adolescence, a majority of studies investigating sleep-dependent cognition in experimental
settings have focused on adults, with a recent emergence of such work in young children. A
paucity of such studies exists in adolescents. Thus, whether the adolescent brain is as
sensitive to sleep and sleep loss as the adult brain or more sensitive remains poorly
understood.

Of the domains of cognition for which sleep is critically involved, perhaps the largest body
of research has focused on learning and memory—both for declarative, episodic memories,
and non-declarative procedural skills (see 44-46 for reviews). Such studies typically examine
either memory consolidation, i.e., retrieval of items learned prior to either sleep or
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wakefulness, or memory encoding, i.e., the impact of prior sleep on the formation of new
memory traces. With respect to memory consolidation, preliminary data from adolescent
samples (e.g., 9-16 years) suggests that at least for declarative memories, post-sleep
improvement is present as in adults 47-49. While these preliminary results are encouraging, a
number of limitations warrant pause. The lack of a direct adult comparison group limits
these studies from directly addressing whether the benefit of sleep for memory is
systematically different in adolescents and adults. Moreover, the absence of developmental

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measures (e.g., puberty, hormonal measures, and prospective longitudinal designs) limit
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these studies from revealing potentially interesting developmental trajectories by which

sleep-dependent memory consolidation emerges early in life. Finally, relatively small (e.g.,
20 participants) sample sizes combined with the modest effect sizes restrict conclusions
about the role of sleep in learning premature. Nevertheless, an exciting new line of research
indicates that during adolescent development healthy sleep may aid learning.

In contrast to a beneficial role of sleep in consolidating memories, sleep deprivation— both

partial50 and total51,52—impairs the both the initial formation and subsequent consolidation
of memories in adults44. Even when multiple nights of partial sleep deprivation are
employed, however, adolescent verbal memory appears relatively unaffected53-55, in both
younger (e.g., 11-13 years55) and older (e.g., 14-16 years54) cohorts. These studies have
proposed the presence of a neural compensation in this young age group. One recent fMRI56
study compared performance on an N-back working memory task in adolescents (mean age
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= 15 years) who were either sleep restricted (6.5 hours per night) or not (10 hour time-in-bed
per night) for one week. Like adults in other similar paradigms57, performance of the sleep-
restricted adolescents did not suffer and demonstrated hyperactivity in frontal cortical
regions56, which was hypothesized to compensate for the effects of sleep loss, and thus
conserve performance on such simple cognitive tasks. Another explanation is that the
conserved sleep is sufficient to support cognitive performance. Indeed, in one of the studies
noted above, verbal memory performance following sleep restriction was positively
correlated with the amount of NREM sleep in the shortened night54. Moreover, preliminary
evidence from adults has demonstrated that heightened slow wave activity following sleep
deprivation positively indexes a restoration of declarative memory to pre sleep-deprived
levels58. It is intriguing, therefore, to consider whether the greater sleep EEG slow wave
activity in adolescents as compared to adults may beneficially rescue the ability to learn
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following small doses of sleep restriction. Ultimately, more studies examining the interplay
between sleep loss and cognitive function in adolescents are needed to examine this
possibility.

Sleep-dependent Emotion Regulation

Beyond learning and memory, one area receiving much recent attention in the adult sleep
literature is sleep-dependent emotional regulation43. Sleep loss is associated both with
increased negative mood and heightened emotional reactivity to visual scenes and faces 43,
as well as altered emotional memory processing59,60. Thus, sleep loss has been proposed to
exert a modulatory influence on the onset of such psychiatric conditions as anxiety and
major depression61. Preliminary evidence suggests that sleep loss also negatively affects
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mood and emotional regulation in adolescents, both following chronic62, and acute63 doses
of sleep restriction.

Importantly, the studies outlined above each used experimental manipulation of sleep over a
night or two, rather than ecologically valid conditions in childhood and adolescence where
sleep loss occurs over a long interval. Studies in adolescent obstructive sleep apnea, for
example, a condition that disrupts sleep, reveal impaired learning and memory 64 together
with affective and reward processing 65. Moreover, placing the totality of this work in an

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ecological context, chronic sleep problems early in childhood are associated with heightened
risk-taking later in adolescence66. This latter study 66 employed a longitudinal design to
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identify that heightened risk taking emerges in later adolescence by way of a sleep-mediated
deficit in working memory. Thus, while the majority of studies in this review describe
children who sleep normally, these examples suggest that such relationships may have real-
life consequence for the more pernicious forms of sleep fragmentation and sleep reduction
observed chronically in some conditions.

Understanding whether adolescents demonstrate partial resilience of cognitive and affective

processes to sleep loss in experimental conditions, therefore, remains an important
mechanistic question at both the basic science level and clinical level. At a practical level,
the chronic pervasive insufficient sleep seen in teens, and outlined in above sections6747, has
a yet unknown impact on the critical cognitive- and emotion-regulating functions outlined
here. Moreover, beyond healthy children, it is worth noting the high comorbidity of sleep
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problems within adolescent psychopathology. For example, PSG recordings in 106

psychiatric inpatients ages of 7 to 16 years, showed that 95% have moderate to severe sleep
problems 68. Similar sleep disruption is are seen in a number specific patient populations,
including: depression69, ADHD70, impulse control disorders 71, anxiety 72, and bipolar
disorder 73, indicating a key role of sleep in adolescent mental health. While beyond the
scope of this review, the mechanisms by which psychiatric conditions may moderate (or be
moderated by) the developmental trajectories of sleep, brain development, and cognition
outlined above, remain poorly understood and topics of active investigation.

Insufficient Sleep and Behavioral Problems in Teens

When so many adolescents obtain so little sleep 6747, the impact of insufficient sleep on
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behavior must be catalogued. Many studies show that insufficient sleep is associated with
poor emotional functioning in teens without diagnosed psychiatric disorders. For example,
in non-clinical samples, less sleep is associated with more depressive symptoms 74, feelings
of hopelessness 74 and greater anxiety 75. The risks of short/insufficient sleep in adolescents
have also become evident in a number of large epidemiologic studies: Meldrum and
Restivo 76 identified increased relative risk for the following behaviors in high school teens
(n=15,364) reporting 7, 6, 5, or less than 5 hours a night on school nights: drunk driving,
weapon carrying, fighting, contemplated suicide, attempted suicide, smoking, alcohol use,
binge drinking, marijuana use, sexual risk taking, and texting while driving. They also
reported increased relative risk for obesity with shorter sleep. Wheaton and colleagues 67
summarizing data from over 50,000 US teenagers found that reports of five injury-related
risk behaviors were associated with reported school-night sleep length of 7 hours of less.
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These behaviors were infrequent bicycle helmet use; infrequent seatbelt use; riding with a
drinking driver; drinking and driving; and texting while driving.

Other studies have noted that early morning school schedules carry a significant role in the
low sleep times of adolescents. When school start times are delayed, sleep is increased,
enrollment rates and attendance improve, students sleep less in class, and symptoms of
depressed mood are reduced 77, and automobile crash rates in teen drivers are
lower 78798081.

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Recent studies are attempting to identify neural mechanisms that underlie findings from
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experimental study in which adolescents show increased depression, anxiety, vigor and
fatigue following sleep deprivation82. That is, how does short or poor sleep affect such
emotional processes in adolescents? One longitudinal study, for example, examined
insomnia symptoms in early adolescent girls at ages 9 to 13 years and then measured neural
reward processing with fMRI several years later 83. This study found that self-reported non-
restorative sleep (i.e., reporting feeling unrested upon awaking) at ages 9-13 years was
positively associated with the dorsal medial prefrontal cortex (dmPFC) response to reward
anticipation and to depressive symptoms several years later. Because of the important role of
the dmPFC in affective control, these findings suggest that poor sleep may contribute to
depressive affect by disrupting functioning of the dmPFC. Future studies are needed to
examine the mechanisms by which adequate sleep may support emotional functioning in
adolescents and whether unique processes are at work at this time of life.
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Summary: Sleep Matters

To summarize, research overwhelmingly supports an important role for sleep in many areas
of adolescent brain function and behavior. What remains largely unknown, is whether sleep
supports unique functions in adolescence as compared to children and adults. This gap in our
knowledge is due to the limited number of concurrent studies examining given phenomena
in children, adolescents and adults. Furthermore, adolescence presents a unique
neurodevelopmental milieu and though brain activity during sleep reflects this, it is unknown
the degree to which the neuronal benefits of sleep overlap in adolescents and adults. Finally,
teens have unique social, cognitive and behavioral demands; does a greater need for sleep
during adolescence as compared to adulthood reflect this? For example, a major theory
about sleep’s function, the synaptic homeostasis hypothesis, posits that one function of slow
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wave activity during sleep is the rescaling of synapses after the waking day 84. Therefore,
might the greater sleep need and more slow wave activity observed in youth result from
greater number of synapses in the teen brain21? Many such questions remain unanswered.

Nonetheless, ensuring well-timed, adequate, and restorative sleep is important for optimal
maturation. Fortunately, sleep is a modifiable behavior for many teens and effective
interventions exist. At a basic level, practice of good ‘sleep hygiene’ protects sleep 85.
Carskadon 86 has suggested the tips listed in Table 1 to help healthy adolescents improve
their sleep. In addition, parental limit setting can help: teens whose parents set a bedtime of
10:00 pm or earlier, for example, had fewer depressive symptoms and less suicidal ideation
as compared to teens whose parents set a bedtime of midnight or later 87. For youngsters
who have more significant sleep problems, recent studies show that sleep-based
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interventions, such as cognitive behavioral therapy for insomnia (CBT-I), are effective 88,89.
In summary, sleep is a potentially important therapeutic target in adolescence with
emotional, cognitive, or behavioral problems.

Conclusion
Recent and emerging data indicate a key role for sleep in supporting cognitive function and
mental well-being in adolescence. Furthermore, sleep and brain development are

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bidirectionally related – brain maturation is reflected in the sleep EEG and sleep may play a
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role in shaping the brain. Hence, the chronic insufficient and poorly timed sleep that is
endemic amongst adolescents is of concern. Public health interventions targeting sleep can
promote sleep during this important developmental period. For example, delaying school
start times results in longer weeknight sleep and produces cascading positive effects, such as
improved school attendance, less tardiness and better grades (reviewed in 67). Indeed, the
American Academy of Pediatrics has endorsed a policy that middle schools and high schools
not begin the day until 8:30 am or later 90.

Acknowledgments
This work was supported by the National Institute on Alcohol Abuse and Alcoholism (AA13252 to MAC) and the
National Institute of l Health (T32MH019927 to JMS; PI: Spirito)
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Highlights
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• During adolescence, sleep behavior and physiology undergo significant

maturation

• Changes to the biological systems regulating sleep result in later

bedtimes, while rise times, driven by school start times, remain
unchanged or move earlier. This results in a pattern of chronic
insufficient sleep for many teens.

• Sleep in adolescence supports learning, memory, attention, cognition,

and emotion processing

• Maturational changes to brain structure and function are reflected in the

sleep EEG
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• Sleep may offer a unique opportunity to probe the developing brain

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 Tarokh et al. Page 15
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Figure 1. Determinants and Consequences of Adolescent Sleep

This diagram outlines the central theme of the review: a complex milieu of determinants and
consequences of sleep interact during the sensitive window of adolescence. Center:
Developmental shifts in sleep behavior (e.g., sleep need and timing) and physiology (e.g.,
slow waves and sleep spindles) index maturational changes in sleep and circadian regulatory
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systems emerging along with developmental trajectories of grey and white matter within the
brain. Top: Several moderating and mediating extrinsic pressures can alter sleep behavior
and physiology beyond intrinsic developmental forces, including school schedules, extra-
curricular activities, and technology use. Bottom: Healthy development of sleep during
adolescence underlies a variety of functional outcomes. Together this framework highlights
sleep during adolescence as a “perfect storm” (Carskadon, 2011): a sensitive time-period
where developmental changes, together with (mal)-adaptive environmental forces, may yield
powerful consequences for behavior and cognition.
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Table 1

Tips for Teens to Improve Sleep (from 86)

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• Make a plan for sleep: set a bedtime for yourself that will allow enough time to sleep – and keep as close to it as you can
• Get bright light every morning when you wake up to help move your internal clock to an earlier time that can help you
fall asleep earlier
• Avoid light at night before bedtime to keep your internal clock from moving later
• Avoid ‘arousing’ activities in the evening and give yourself a wind-down time to relax for about 30 min before bedtime
• Don’t sleep with your cell phone on, nor the computer, TV, or any other technology (including lights) in your bedroom
• Stick as closely as you can to your sleep schedule on weekends
• Avoid caffeine after school
• Do not nap after 4 p.m.
• Have some fun every day and enjoy your life!
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