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Title
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Insomnia and Sleep Disorders
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Author
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Mason, Elizabeth C.
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Harvey, Allison G.
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Research Area
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Psychopathology
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Topic
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Sleep Disorders
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Abstract
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Sleep is common to all animals and yet there are so many mysteries surrounding its function. Insomnia, the most common sleep disorder, is prevalent and debilitating and has been shown to play a role in the onset and maintenance of other mental health disorders, such as depression, anxiety, and bipolar disorder. This chapter outlines a basic overview of sleep, followed by a summary of cutting‐edge research investigating insomnia as well as its relationship to other psychiatric disorders. It is suggested that a bidirectional relationship exists between sleep and emotion and research supporting this framework is addressed briefly. We describe the treatment of choice for insomnia, cognitive behavioral therapy, as well as outline other exciting developments in the treatment of insomnia, including bright light therapy, intensive sleep retraining therapy, and Internet‐based treatments. Finally, we end on a discussion of areas that are ripe for future investigation, including biological mechanisms, sleep medications, and other sleep disorders such as hypersomnia.
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Identifier
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etrds0184
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extracted text
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Insomnia and Sleep Disorders
ELIZABETH C. MASON and ALLISON G. HARVEY
Abstract
Sleep is common to all animals and yet there are so many mysteries surrounding
its function. Insomnia, the most common sleep disorder, is prevalent and debilitating and has been shown to play a role in the onset and maintenance of other mental
health disorders, such as depression, anxiety, and bipolar disorder. This chapter outlines a basic overview of sleep, followed by a summary of cutting-edge research
investigating insomnia as well as its relationship to other psychiatric disorders. It
is suggested that a bidirectional relationship exists between sleep and emotion and
research supporting this framework is addressed briefly. We describe the treatment
of choice for insomnia, cognitive behavioral therapy, as well as outline other exciting
developments in the treatment of insomnia, including bright light therapy, intensive
sleep retraining therapy, and Internet-based treatments. Finally, we end on a discussion of areas that are ripe for future investigation, including biological mechanisms,
sleep medications, and other sleep disorders such as hypersomnia.
INTRODUCTION
All animals need to sleep, from ants to dolphins to humans. As the knowledge base builds, scientific consensus on why we need sleep is growing. What
is very clear is that if we do not get enough sleep there are serious consequences to both our physical and emotional health. Insomnia, which involves
difficulty falling asleep, staying asleep, or waking earlier than desired in the
morning, is one of the most common health problems. On its own, it is associated with considerable functional impairment but beyond that, insomnia
is very frequently comorbid with, and predicts the development of, several
psychological and medical conditions.
Over the past decade, as an understanding of the adverse consequences of
insufficient sleep has emerged, research on insomnia and other sleep disorders has exploded. The study of insomnia is incredibly interesting from a
scientific point of view as it provides insights into emotion processing and
regulation as well as learning and memory, which are key fields studied in
psychology. Furthermore, it is fascinating from a clinical perspective as it
Emerging Trends in the Social and Behavioral Sciences. Edited by Robert Scott and Stephen Kosslyn.
© 2015 John Wiley & Sons, Inc. ISBN 978-1-118-90077-2.
1
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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
seems likely that effective interventions for insomnia may assist in the prevention of other mental health disorders and physical disorders, too. There
appear to be bidirectional relationships between sleep disturbance and emotional dysregulation in that both impact on one another. Research into these
relationships is providing important clues about mechanisms involved in
insomnia and are detailed later. Other sleep disorders include hypersomnia,
delayed sleep phase disorder (DSPD), sleep apnea, narcolepsy, night terrors,
parasomnias, and restless leg syndrome. This chapter focuses primarily on
insomnia, and touches upon hypersomnia and DSPD.
FOUNDATIONAL RESEARCH
CIRCADIAN RHYTHMS AND SLEEP
Many biological processes, including sleep, occur in a daily rhythm, roughly
around a 24-h clock. Our internal body clock is influenced by several factors in the environment, termed zeitgebers. The most powerful zeitgeber is
light/dark. Other cues that help us entrain our rhythms include temperature,
exercise, and meal times. The internal pacemaker lies in the suprachiasmatic
nucleus (SCN) of the brain, which receives light signals directly from the
retina of the eye.
SLEEP STAGES
Human sleep is divided into REM (rapid eye movement) and non-REM
sleep, which is further divided in to four stages (stages 1, 2, 3, and 4). Stages
1 and 2 are “light” stages of sleep and stages 3 and 4 are “deep,” more
restorative stages of sleep in which slow-wave sleep occurs. Non-REM
sleep appears to be important for conservation of energy and restoration
(Kryger, Roth, & Dement, 2005) as well as the consolidation of certain types
of memories (Diekelmann & Born, 2010). REM sleep is also important in
learning and memory and is particularly critical in emotion processing and
regulation (Karni, Tanne, Rubenstien, Askenasy, & Sagi, 1994; Walker &
Stickgold, 2006; Yoo, Gujar, Hu, Jolesz, & Walker, 2007).
TWO-PROCESS MODEL OF SLEEP
The two-process model is the prevailing theory of sleep regulation, which
proposes that sleep and wakefulness are dependent on two processes, a circadian process and a homeostatic process (Borbely, 1982). The circadian rhythm
is an internal biological clock that runs approximately on a 24-h basis. Variations in melatonin, temperature, and levels of arousal operate according to
Insomnia and Sleep Disorders
3
our circadian rhythms (Lack & Bootzin, 2003). Through the homeostatic process, “sleep pressure” (or the need to sleep) increases with time spent awake.
When a person is sleep deprived, the tendency to sleep increases. Conversely,
when one has a long nap, the tendency to sleep is decreased. These two processes operate in tandem in that the propensity to sleep is more likely when
levels of alertness (the circadian process) are relatively low and sleep pressure
(the homeostatic process) is high. As a corollary, following an afternoon nap,
one may find it difficult to fall asleep at one’s regular “circadian bedtime”
because homeostatic sleep pressure is low. Similarly, circadian arousal may
prevent sleep onset from occurring if one tries to go to sleep early following
a poor night of sleep, even though sleep pressure is high.
CUTTING-EDGE RESEARCH
Exciting developments, outlined later, are being made in the treatment of
insomnia and in the understanding of the mechanisms underpinning the
relationship between insufficient sleep and psychiatric disorders.
SLEEP AND PSYCHIATRIC DISORDERS
Evidence for the importance of sleep in psychiatric disorders has grown enormously in recent years. Certainly, we have all had the experience of poor
sleep affecting our mood and the research is beginning to catch up by explaining this interaction at the behavioral, cognitive, and biological levels. This
research is extremely important in helping to identify possible therapeutic
targets for both insomnia and other psychiatric disorders.
Given that insomnia frequently predates and predicts psychiatric disorders, sleep disturbance is no longer considered an epiphenomenon in
psychiatric disorders; rather, it is now viewed as an important and underrecognized mechanism in the cause and maintenance of psychiatric disorders.
This change has recently been reflected in the latest edition of the Diagnostic
and Statistical Manual (DSM-5), in which the diagnosis of primary insomnia
has been renamed insomnia, to eliminate the distinction between primary
and secondary insomnia.
A BIDIRECTIONAL MODEL BETWEEN SLEEP AND EMOTION
Recently, we and others have proposed that the relationship between sleep
disturbance and processes of emotional dysregulation in psychiatric disorders is likely to be bidirectional (Baglioni, Spiegelhalder, Lombardo, & Riemann, 2010; Harvey, Murray, Chandler, & Soehner, 2011). This simple model
proposes that mood, anxiety, and other emotional symptoms interfere with
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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
sleep, and that, conversely, the effects of sleep deprivation contribute to mood
dysregulation and emotional disturbance. It is clear anecdotally and through
experimental manipulations that worry and rumination, key features of anxiety and depressive disorders, affect our sleep. Equally, exciting research from
Dr. Matthew Walker’s group at the University of California, Berkeley has
shown that just a single night of sleep deprivation causes significant increases
in emotional reactivity to negative stimuli and corresponding increases in
activity in the amygdala, an area of the brain that plays a key role in emotion
(Yoo et al., 2007). Not only has increased emotional activity to negative stimuli been observed but it has also been shown that sleep deprivation leads to
amplified neural reactivity in reward networks in response to pleasant stimuli (Gujar, Yoo, Hu, & Walker, 2011). Indeed, in an article entitled “Overnight
therapy? The role of sleep in emotional brain processing,” Walker and his
colleague emphasize the role of REM sleep in processing emotional memories and note that there has been a “renaissance” of research with a focus
on sleep and neurocognitive processes involved in emotion regulation. Certainly, this is a fascinating area which is sure to grow in the future. We suggest
that this bidirectional model between sleep and emotion is valuable as an
initial organizing structure for the existing and future research. The study of
sleep across psychiatric disorders is an exciting domain for interdisciplinary
research across behavioral, social, cognitive, and neurobiological levels of
explanation.
COGNITIVE BEHAVIORAL THERAPY FOR INSOMNIA (CBT-I)
Cognitive Behavioral Therapy for Insomnia (CBT-I) is the most effective
psychological treatment for insomnia. Unlike pharmacological treatments,
its effects persist after a course of treatment has been terminated (Morin,
2006). The aim of CBT-I is to foster sleep-conducive behaviors and to change
unhelpful and unrealistic expectations about sleep and daytime functioning.
CBT-I has been shown to increase total sleep time and improve sleep quality,
while reducing the time it takes to fall asleep and the number of awakenings
in the night time. It is a multicomponent therapy which involves cognitive
therapy, stimulus control, sleep restriction, behavioral experiments, and
psychoeducation about good sleep habits. One of the more paradoxical
components of CBT-I is sleep restriction. The aim of this is to match time in
bed as closely as possible with time asleep by limiting the amount of time
the patient sleeps in the initial stages of therapy. This helps the patient to
consolidate sleep, associate the bed with sleep, and to shorten sleep onset
times as she/he accumulates a sleep debt through mild sleep deprivation.
Stimulus control, which aims to create a positive association between the
bed/bedroom and sleep by encouraging the patient to get out of bed when
Insomnia and Sleep Disorders
5
not tired and only use the bed for sleep and sex, while restricting other
activities in bed (e.g., watching television, checking e-mails), has also been
shown to be an important contributor to treatment gains. CBT-I is generally
conducted over six to eight sessions, and similar to CBT treatments for
other disorders, it involves in-session activities as well as homework to be
completed between sessions.
TREATMENT DEVELOPMENT
Progress toward establishing treatments has been good. However, given
that effect sizes are small to moderate and many patients derive no benefit,
there is certainly room for improvement (Harvey & Tang, 2003). Advances
in treatment of insomnia are likely to have valuable widespread ramifications because it seems probable that treating insomnia will translate into
reductions in other mental health disorders such as anxiety and depression,
as insomnia is known to be predictive of the onset of these disorders. This
section outlines a few key areas of treatment development currently under
research.
The role of light and dark in sleep is well understood and there is growing
evidence that light and dark therapy is likely to be important in the treatment
of mood disorders (Harvey, 2011). The use of bright light is another key development in the treatment of sleep disorders. Morning bright light will bring
forward (phase advance) the circadian rhythm and is therefore an effective
therapeutic intervention for “owls,” whose preference for staying up late and
sleeping in late interferes with their daily duties. On the other hand, evening
bright light delays the circadian rhythm and is therefore effective for “larks,”
those who wake up earlier that they would like to because of an abnormally
advanced sleep phase (Lack & Wright, 2007). Although the use of light boxes
have been shown to be useful in the treatment of DSPD, adherence is not
optimal and therefore, the use of “informal” light exposure (e.g., sunlight
in the morning, reduced light from electronic devices in the evening) is an
important part of treatment.
Light therapy may also be combined with sleep phase chronotherapy, which
involves moving sleep time 3 h later each night, around the clock, until the
desired sleep time is established. More commonly, however, light therapy is
combined with shifting sleep and wake times more gradually (say, 30 min per
week) forward or backward depending on the desired sleep/wake schedule.
For example, a patient who wishes to move their bedtime from 12 a.m. to
10 p.m. would set a regular wake time and endeavor to get morning light as
soon as possible after waking. Simultaneously, they would shift their bedtime
backwards half an hour each week until a regular pattern is established.
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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
Intensive Sleep Retraining Therapy. Intensive sleep retraining therapy, which
involves a one-off 25-h treatment period of sleep deprivation in which
patients are only allowed to sleep for a few minutes at a time, has shown
promising results for the treatment of insomnia, with reductions observed in
time taken to fall asleep and total sleep time (Harris, Lack, Kemp, Wright, &
Bootzin, 2012). During this treatment, participants are allowed a series of
50 half-hourly sleep opportunities. If they do not sleep within 20 min, the
patient is asked to move out of the bed on to a chair to read or watch DVDs
until the next trial begins. If sleep is initiated, participants are only allowed
to sleep for 3 min before being woken. On each trial where the participant
does sleep, they are asked about their perception of whether or not they
slept and provided with accurate feedback regarding whether sleep onset
occurred or not. Even the most extreme insomnia patients are able to sleep
in this protocol. Intensive sleep retraining therapy is thought to work in
several ways, including (i) by helping people to experience what it is like to
fall asleep quickly and to learn that they are capable of falling asleep fast;
(ii) by providing exposure to sleep deprivation (which is often feared by
patients with insomnia); and (iii) by helping to correct sleep misperception
(sleep/wake discrimination). It has very rapid results, although an even
larger treatment effect size has been observed when this treatment was
combined with five sessions of stimulus control therapy.
Internet-Based Treatments. In recent years, Internet-based treatments for a
number of mental disorders have grown enormously. Indeed, there are a
few different groups of researchers working on Internet-based treatments
for insomnia. For example, Colin Espie and colleagues in Scotland have
developed “Sleepio,” a CBT Internet program developed as a self-help
treatment for insomnia. “SHUTi,” developed in the United States, is another
example of an online self-help program for insomnia and randomized
controlled trials of these programs are currently under way. Internet-based
treatments are particularly helpful in the dissemination of evidence-based
treatments for insomnia because they are easily accessible and lessen the
burden on the health system as specialist clinician time is reduced.
TARGETING SLEEP IN ADOLESCENCE
Adolescence has emerged as a crucial time point to intervene with sleep. This
is due to two key factors—(i) Many mental health disorders such as anxiety
and depression have their onset in adolescence and insomnia is a risk factor
for the emergence of these disorders; and (ii) the natural biological delay in
the circadian cycle that occurs in adolescence along with increased use of
Insomnia and Sleep Disorders
7
technology and other changes in social pressures are now competing more
than ever with the need to sleep.
Clinically, when one’s sleep schedule is heavily delayed and this interferes
with one’s ability to conform to a required schedule (e.g., school or work
start times), one may meet criteria for a diagnosis of DSPD. An obvious
corollary of DSPD in adolescents, who are required to wake early to be at
school, is chronic sleep deprivation. This can put such a teenager at risk
for the development of psychiatric and physical disorders as well as have
deleterious effects in the academic and social domains. Several complex
interactions between biology, psychology, and social context make adolescence a particularly important phase for mechanistic and early intervention
research. Indeed, our group is currently investigating whether a brief
intervention to target DSPD in teenagers will help reduce risk across social,
academic, physical, and psychological domains.
KEY ISSUES FOR FUTURE RESEARCH
One of the great things about working on sleep is that there is so much more
to learn. Despite the fact that sleep takes up about one-third of our life, very
little is known about its function. Certainly, it is clear that insomnia is common and debilitating and there are a number of exciting areas for future
research in this disorder and other sleep disorders.
HYPERSOMNIA
More recently, an understanding of the importance of hypersomnia has
developed (Kaplan & Harvey, 2009). It is still unclear whether hypersomnia
is a disorder of excessive sleep or excessive time in bed. That is, do people
with this disorder actually sleep for excessively long periods or simply
spend large amounts of time in bed? As has been pointed out by our group
previously, the use of objective measures of such as actigraphy (which
assesses an individual’s movement as a fairly accurate proxy of actual sleep)
will help shed light on this quandary (Kaplan & Harvey, 2009). It may also
be the case that psychological factors such as avolition and daytime fatigue
emerge as being more important to this disorder than objective sleep. What
is clear, however, is that as with insomnia, hypersomnia is prevalent and
persistent across mood disorders and there is certainly a need for greater
research into this disorder and its treatment.
TRANSDIAGNOSTIC TREATMENT
Given the high rates of co-occurrence between insomnia and psychiatric disorders as well as evidence suggesting that insomnia contributes to the onset,
8
EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
maintenance, and relapse of a range of psychiatric disorders, we have suggested that insomnia may be a transdiagnostic process across psychiatric
disorders (Harvey, 2008). Therefore, the development of a single treatment
that can be applied to individuals with comorbid insomnia across disorders
has the potential to provide great benefits to public health. However, research
is needed to determine whether it is possible to develop one treatment protocol that will be effective across psychiatric disorders. Secondly, given the
research showing that insomnia predicts the onset and maintenance of other
psychiatric disorders, it appears to be a logical consequence that the treatment of insomnia will improve the functioning and symptomatology of individuals with psychiatric disorders and indeed even prevent the onset of some
cases, yet this is still to be determined empirically.
SLEEP VERSUS CIRCADIAN RHYTHM DISTURBANCE?
Sleep disturbances and circadian rhythm abnormalities, although overlapping, are not identical processes. That is, although the circadian rhythm contributes to sleep disturbance, other factors such as stress also play a role.
Similarly, the circadian rhythm not only controls sleep but also other biological processes. Both sleep and the circadian rhythm have been implicated in
psychiatric disorders, although at this stage their individual contribution to
psychiatric disorders is unknown. Therefore, future research on the involvement of sleep versus circadian influences in psychiatric disorders is needed.
BIOLOGICAL MECHANISMS
Work is already beginning to show that the sleep/circadian systems are
closely linked to serotonergic and dopaminergic function, which points to
one common mechanism potentially underlying sleep and mood/anxiety
disorders (see Harvey et al., 2011 for review). The manipulation of specific
stages of sleep may be a valuable approach to answer important questions
about the contribution of REM and non-REM sleep to psychiatric disorders,
and indeed it may be possible to selectively manipulate different stages
of sleep for therapeutic benefit. For example, it is known that individuals
with depression typically have shortened REM latency and higher REM
density (Coble, Foster, & Kupfer, 1976). Although widely documented,
the underlying mechanisms and reasons for this excess of REM sleep in
depression are poorly understood. Interestingly, antidepressant medications
suppress REM sleep (Mayers & Baldwin, 2005). Similarly, it has been
suggested that individuals with posttraumatic stress disorder (PTSD) fail to
show a suppression of brain adrenergic activity during REM sleep (Shad,
Suris, & North, 2011; Taylor et al., 2008) and this suppression has been
Insomnia and Sleep Disorders
9
proposed to be central to the emotional processing of negative memories
(Walker & van Der Helm, 2009). Consistent with this, an adrenergic antagonist (Prazosin), which reduces adrenergic activity during REM sleep (Shad
et al., 2011; van der Helm et al., 2011) has been shown to reduce symptoms
of PTSD. Understanding the mechanisms underpinning insomnia and the
relationship between sleep processes and psychiatric disorders is invaluable
in developing better treatments for these disorders.
SLEEP MEDICATIONS
Finally, it is worth noting that further research into sleep medications is warranted. Hypnotic medications such as Zolpidem (Ambien) and Temazepam
(Restoril) are some of the most widely used medications in Western societies
(Kripke, Langer, & Kline, 2012). Yet, it seems to be that the type of sleep
one obtains when under the influence of medications such as Zolpidem
is quite different to naturally occurring sleep. That is, naturally occurring
sleep is known to be essential to learning and memory consolidation.
In contrast, pharmacologically induced sleep appears to actually impair
critical sleep-dependent brain processes. For example, in a study involving
developing kittens, Seibt et al. (2008) found that Zolpidem reduced cortical
plasticity by 50%. This suggests that these agents may be of concern to
developing human children and adolescents, potentially as well as adults,
who continue to need sleep for growth, repair, learning, plasticity, and
optimal emotional functioning.
REFERENCES
Baglioni, C., Spiegelhalder, K., Lombardo, C., & Riemann, D. (2010). Sleep and
emotions: A focus on insomnia. Sleep Medicine Reviews, 14, 227–238. doi:10.1016/
j.smrv.2009.10.007
Borbely, A. (1982). A two process model of sleep regulation. Human Neurobiology, 1,
195–204.
Coble, P., Foster, F. G., & Kupfer, D. J. (1976). Electroencephalographic sleep diagnosis of primary depression. Archives of General Psychiatry, 33, 1124.
Diekelmann, S., & Born, J. (2010). The memory function of sleep. Nature Reviews Neuroscience, 11, 114–126.
Gujar, N., Yoo, S.-S., Hu, P., & Walker, M. P. (2011). Sleep deprivation amplifies
reactivity of brain reward networks, biasing the appraisal of positive emotional
experiences. The Journal of Neuroscience, 31, 4466–4474.
Harris, J., Lack, L., Kemp, K., Wright, H., & Bootzin, R. (2012). A randomized controlled trial of intensive sleep retraining (ISR): A brief conditioning treatment for
chronic insomnia. Sleep, 35, 49–60.
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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
Harvey, A. G. (2008). Insomnia, psychiatric disorders, and the transdiagnostic perspective. Current Directions in Psychological Science, 17, 299–303.
Harvey, A. G. (2011). Sleep and circadian functioning: Critical mechanisms in the
mood disorders? Annual Review of Clinical Psychology, 7, 297–319.
Harvey, A. G., Murray, G., Chandler, R. A., & Soehner, A. (2011). Sleep disturbance as
transdiagnostic: Consideration of neurobiological mechanisms. Clinical Psychology
Review, 31, 225–235.
Harvey, A. G., & Tang, N. K. Y. (2003). Cognitive behaviour therapy for primary
insomnia: Can we rest yet? Sleep Medicine Reviews, 7, 237–262.
Kaplan, K. A., & Harvey, A. G. (2009). Hypersomnia across mood disorders: A review
and synthesis. Sleep Medicine Reviews, 13, 275–285.
Karni, A., Tanne, D., Rubenstien, B. S., Askenasy, J. J., & Sagi, D. (1994). Dependence on REM sleep of overnight improvement of a perceptual skill. Science, 265,
679–682.
Kripke, D. F., Langer, R. D., & Kline, L. E. (2012). Hypnotics’ association with mortality or cancer: A matched cohort study. BMJ Open, 2. doi:10.1136/bmjopen2012-000850
Kryger, M. H., Roth, T., & Dement, W. C. (2005). Principles and practice of sleep medicine
(4th ed.). Philadelphia, PA: WB Saunders Co..
Lack, L. C., & Bootzin, R. B. (2003). Circadian rhythm factors in insomnia and their
treatment. In M. Perlis & K. Lichstein (Eds.), Treatment of sleep disorders: Principles
and practice of behavioral sleep medicine. New York, NY: John Wiley and Sons, Inc.
Lack, L. C., & Wright, H. R. (2007). Treating chronobiological components of chronic
insomnia. Sleep Medicine, 8, 637–644.
Mayers, A. G., & Baldwin, D. S. (2005). Antidepressants and their effect on sleep.
Human Psychopharmacology: Clinical and Experimental, 20, 533–559. doi:10.1002/
hup.726
Morin, C. M. (2006). Cognitive-behavioral therapy of insomnia. Sleep Medicine Clinics,
1, 375–386.
Seibt, J., Aton, S. J., Jha, S. K., Coleman, T., Dumoulin, M. C., & Frank, M. G.
(2008). The non-benzodiazepine hypnotic zolpidem impairs sleep-dependent cortical plasticity. Sleep, 31, 1381–1391.
Shad, M. U., Suris, A. M., & North, C. S. (2011). Novel combination strategy to optimize treatment for PTSD. Human Psychopharmacology: Clinical and Experimental, 26,
4–11.
Taylor, F. B., Martin, P., Thompson, C., Williams, J., Mellman, T. A., Gross, C., …
Raskind, M. A. (2008). Prazosin effects on objective sleep measures and clinical
symptoms in civilian trauma posttraumatic stress disorder: A placebo-controlled
study. Biological Psychiatry, 63, 629–632.
van der Helm, E., Yao, J., Dutt, S., Rao, V., Saletin, J. M., & Walker, M. P. (2011). REM
sleep depotentiates amygdala activity to previous emotional experiences. Current
Biology, 21(23), 2029–2032.
Walker, M. P., & Stickgold, R. (2006). Sleep, memory, and plasticity. In Annual review
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Insomnia and Sleep Disorders
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Walker, M. P., & van Der Helm, E. (2009). Overnight therapy? The role of sleep in
emotional brain processing. Psychological Bulletin, 135, 731.
Yoo, S.-S., Gujar, N., Hu, P., Jolesz, F. A., & Walker, M. P. (2007). The human emotional brain without sleep—a prefrontal amygdala disconnect. Current Biology, 17,
R877–R878.
FURTHER READING
Harvey, A. G. (2011). Sleep and circadian functioning: Critical mechanisms in the
mood disorders? Annual Review of Clinical Psychology, 7, 297–319.
Harvey, A. G., Murray, G., Chandler, R. A., & Soehner, A. (2011). Sleep disturbance as
transdiagnostic: Consideration of neurobiological mechanisms. Clinical Psychology
Review, 31, 225–235.
Morin, C. M. (2006). Cognitive-behavioral therapy of insomnia. Sleep Medicine Clinics,
1, 375–386.
Walker, M. P., & van Der Helm, E. (2009). Overnight therapy? The role of sleep in
emotional brain processing. Psychological Bulletin, 135, 731.
ELIZABETH C. MASON SHORT BIOGRAPHY
Elizabeth C. Mason is a visiting postdoctoral fellow at the University of
California, Berkeley. She was awarded an American-Australian Association
Fellowship to pursue research in the field of sleep in the laboratory of Dr.
Allison Harvey. Dr. Mason also holds an academic appointment at the University of New South Wales. On completion of her fellowship, she will return
to her role as a Clinical and Research Psychologist at the Clinical Research
Unit for Anxiety and Depression (CRUfAD), St Vincent’s Hospital, in Sydney, Australia. Dr. Mason is particularly interested in research related to the
mechanisms underlying sleep, anxiety and other mental health disorders in
order to improve treatments for these conditions.
ALLISON G. HARVEY SHORT BIOGRAPHY
Allison G. Harvey is a Professor of Clinical Psychology and Director of the
Golden Bear Sleep Research Clinic at the University of California, Berkeley.
Dr. Harvey is also an Adjunct Professor at the University of Bergen, Norway.
Her training was completed in Sydney, Australia. Dr. Harvey then moved
to the University of Oxford as a postdoctoral fellow in the Department of
Psychiatry then a faculty member in the Department of Experimental Psychology, University. She was also a Fellow of St. Anne’s College. In 2004, she
moved to UC Berkeley. Dr. Harvey’s team aims to develop more effective
treatments for psychiatric and health problems by (i) applying a multisystems and mechanisms-focused framework in which basic science findings
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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
on cognitive, affective, biological, behavioral and developmental contributors are used as sources for deriving novel interventions and (ii) intervention
research is used to develop hypotheses about and/or confirm mechanisms.
Dr. Harvey’s research is funded by NIMH and NICHD. She has published
over 130 research articles and book chapters and authored two books. Her
research has been acknowledged with various awards including an Honorary Doctorate from the University of Orebro, Sweden. Dr. Harvey serves
on numerous editorial boards and is an Associate Editor for SLEEP.
RELATED ESSAYS
Depression (Psychology), Ian H. Gotlib and Daniella J. Furman
Mental Imagery in Psychological Disorders (Psychology), Emily A. Holmes
et al.
Dissociation and Dissociative Identity Disorder (DID) (Psychology), Rafaële
J. C. Huntjens and Martin J. Dorahy
Computer Technology and Children’s Mental Health (Psychology), Philip C.
Kendall et al.
Evolutionary Perspectives on Animal and Human Personality (Anthropology), Joseph H. Manson and Lynn A. Fairbanks
Disorders of Consciousness (Psychology), Martin M. Monti
Clarifying the Nature and Structure of Personality Disorder (Psychology),
Takakuni Suzuki and Douglas B. Samuel
Rumination (Psychology), Edward R. Watkins
-
Insomnia and Sleep Disorders
ELIZABETH C. MASON and ALLISON G. HARVEY
Abstract
Sleep is common to all animals and yet there are so many mysteries surrounding
its function. Insomnia, the most common sleep disorder, is prevalent and debilitating and has been shown to play a role in the onset and maintenance of other mental
health disorders, such as depression, anxiety, and bipolar disorder. This chapter outlines a basic overview of sleep, followed by a summary of cutting-edge research
investigating insomnia as well as its relationship to other psychiatric disorders. It
is suggested that a bidirectional relationship exists between sleep and emotion and
research supporting this framework is addressed briefly. We describe the treatment
of choice for insomnia, cognitive behavioral therapy, as well as outline other exciting
developments in the treatment of insomnia, including bright light therapy, intensive
sleep retraining therapy, and Internet-based treatments. Finally, we end on a discussion of areas that are ripe for future investigation, including biological mechanisms,
sleep medications, and other sleep disorders such as hypersomnia.
INTRODUCTION
All animals need to sleep, from ants to dolphins to humans. As the knowledge base builds, scientific consensus on why we need sleep is growing. What
is very clear is that if we do not get enough sleep there are serious consequences to both our physical and emotional health. Insomnia, which involves
difficulty falling asleep, staying asleep, or waking earlier than desired in the
morning, is one of the most common health problems. On its own, it is associated with considerable functional impairment but beyond that, insomnia
is very frequently comorbid with, and predicts the development of, several
psychological and medical conditions.
Over the past decade, as an understanding of the adverse consequences of
insufficient sleep has emerged, research on insomnia and other sleep disorders has exploded. The study of insomnia is incredibly interesting from a
scientific point of view as it provides insights into emotion processing and
regulation as well as learning and memory, which are key fields studied in
psychology. Furthermore, it is fascinating from a clinical perspective as it
Emerging Trends in the Social and Behavioral Sciences. Edited by Robert Scott and Stephen Kosslyn.
© 2015 John Wiley & Sons, Inc. ISBN 978-1-118-90077-2.
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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
seems likely that effective interventions for insomnia may assist in the prevention of other mental health disorders and physical disorders, too. There
appear to be bidirectional relationships between sleep disturbance and emotional dysregulation in that both impact on one another. Research into these
relationships is providing important clues about mechanisms involved in
insomnia and are detailed later. Other sleep disorders include hypersomnia,
delayed sleep phase disorder (DSPD), sleep apnea, narcolepsy, night terrors,
parasomnias, and restless leg syndrome. This chapter focuses primarily on
insomnia, and touches upon hypersomnia and DSPD.
FOUNDATIONAL RESEARCH
CIRCADIAN RHYTHMS AND SLEEP
Many biological processes, including sleep, occur in a daily rhythm, roughly
around a 24-h clock. Our internal body clock is influenced by several factors in the environment, termed zeitgebers. The most powerful zeitgeber is
light/dark. Other cues that help us entrain our rhythms include temperature,
exercise, and meal times. The internal pacemaker lies in the suprachiasmatic
nucleus (SCN) of the brain, which receives light signals directly from the
retina of the eye.
SLEEP STAGES
Human sleep is divided into REM (rapid eye movement) and non-REM
sleep, which is further divided in to four stages (stages 1, 2, 3, and 4). Stages
1 and 2 are “light” stages of sleep and stages 3 and 4 are “deep,” more
restorative stages of sleep in which slow-wave sleep occurs. Non-REM
sleep appears to be important for conservation of energy and restoration
(Kryger, Roth, & Dement, 2005) as well as the consolidation of certain types
of memories (Diekelmann & Born, 2010). REM sleep is also important in
learning and memory and is particularly critical in emotion processing and
regulation (Karni, Tanne, Rubenstien, Askenasy, & Sagi, 1994; Walker &
Stickgold, 2006; Yoo, Gujar, Hu, Jolesz, & Walker, 2007).
TWO-PROCESS MODEL OF SLEEP
The two-process model is the prevailing theory of sleep regulation, which
proposes that sleep and wakefulness are dependent on two processes, a circadian process and a homeostatic process (Borbely, 1982). The circadian rhythm
is an internal biological clock that runs approximately on a 24-h basis. Variations in melatonin, temperature, and levels of arousal operate according to
Insomnia and Sleep Disorders
3
our circadian rhythms (Lack & Bootzin, 2003). Through the homeostatic process, “sleep pressure” (or the need to sleep) increases with time spent awake.
When a person is sleep deprived, the tendency to sleep increases. Conversely,
when one has a long nap, the tendency to sleep is decreased. These two processes operate in tandem in that the propensity to sleep is more likely when
levels of alertness (the circadian process) are relatively low and sleep pressure
(the homeostatic process) is high. As a corollary, following an afternoon nap,
one may find it difficult to fall asleep at one’s regular “circadian bedtime”
because homeostatic sleep pressure is low. Similarly, circadian arousal may
prevent sleep onset from occurring if one tries to go to sleep early following
a poor night of sleep, even though sleep pressure is high.
CUTTING-EDGE RESEARCH
Exciting developments, outlined later, are being made in the treatment of
insomnia and in the understanding of the mechanisms underpinning the
relationship between insufficient sleep and psychiatric disorders.
SLEEP AND PSYCHIATRIC DISORDERS
Evidence for the importance of sleep in psychiatric disorders has grown enormously in recent years. Certainly, we have all had the experience of poor
sleep affecting our mood and the research is beginning to catch up by explaining this interaction at the behavioral, cognitive, and biological levels. This
research is extremely important in helping to identify possible therapeutic
targets for both insomnia and other psychiatric disorders.
Given that insomnia frequently predates and predicts psychiatric disorders, sleep disturbance is no longer considered an epiphenomenon in
psychiatric disorders; rather, it is now viewed as an important and underrecognized mechanism in the cause and maintenance of psychiatric disorders.
This change has recently been reflected in the latest edition of the Diagnostic
and Statistical Manual (DSM-5), in which the diagnosis of primary insomnia
has been renamed insomnia, to eliminate the distinction between primary
and secondary insomnia.
A BIDIRECTIONAL MODEL BETWEEN SLEEP AND EMOTION
Recently, we and others have proposed that the relationship between sleep
disturbance and processes of emotional dysregulation in psychiatric disorders is likely to be bidirectional (Baglioni, Spiegelhalder, Lombardo, & Riemann, 2010; Harvey, Murray, Chandler, & Soehner, 2011). This simple model
proposes that mood, anxiety, and other emotional symptoms interfere with
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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
sleep, and that, conversely, the effects of sleep deprivation contribute to mood
dysregulation and emotional disturbance. It is clear anecdotally and through
experimental manipulations that worry and rumination, key features of anxiety and depressive disorders, affect our sleep. Equally, exciting research from
Dr. Matthew Walker’s group at the University of California, Berkeley has
shown that just a single night of sleep deprivation causes significant increases
in emotional reactivity to negative stimuli and corresponding increases in
activity in the amygdala, an area of the brain that plays a key role in emotion
(Yoo et al., 2007). Not only has increased emotional activity to negative stimuli been observed but it has also been shown that sleep deprivation leads to
amplified neural reactivity in reward networks in response to pleasant stimuli (Gujar, Yoo, Hu, & Walker, 2011). Indeed, in an article entitled “Overnight
therapy? The role of sleep in emotional brain processing,” Walker and his
colleague emphasize the role of REM sleep in processing emotional memories and note that there has been a “renaissance” of research with a focus
on sleep and neurocognitive processes involved in emotion regulation. Certainly, this is a fascinating area which is sure to grow in the future. We suggest
that this bidirectional model between sleep and emotion is valuable as an
initial organizing structure for the existing and future research. The study of
sleep across psychiatric disorders is an exciting domain for interdisciplinary
research across behavioral, social, cognitive, and neurobiological levels of
explanation.
COGNITIVE BEHAVIORAL THERAPY FOR INSOMNIA (CBT-I)
Cognitive Behavioral Therapy for Insomnia (CBT-I) is the most effective
psychological treatment for insomnia. Unlike pharmacological treatments,
its effects persist after a course of treatment has been terminated (Morin,
2006). The aim of CBT-I is to foster sleep-conducive behaviors and to change
unhelpful and unrealistic expectations about sleep and daytime functioning.
CBT-I has been shown to increase total sleep time and improve sleep quality,
while reducing the time it takes to fall asleep and the number of awakenings
in the night time. It is a multicomponent therapy which involves cognitive
therapy, stimulus control, sleep restriction, behavioral experiments, and
psychoeducation about good sleep habits. One of the more paradoxical
components of CBT-I is sleep restriction. The aim of this is to match time in
bed as closely as possible with time asleep by limiting the amount of time
the patient sleeps in the initial stages of therapy. This helps the patient to
consolidate sleep, associate the bed with sleep, and to shorten sleep onset
times as she/he accumulates a sleep debt through mild sleep deprivation.
Stimulus control, which aims to create a positive association between the
bed/bedroom and sleep by encouraging the patient to get out of bed when
Insomnia and Sleep Disorders
5
not tired and only use the bed for sleep and sex, while restricting other
activities in bed (e.g., watching television, checking e-mails), has also been
shown to be an important contributor to treatment gains. CBT-I is generally
conducted over six to eight sessions, and similar to CBT treatments for
other disorders, it involves in-session activities as well as homework to be
completed between sessions.
TREATMENT DEVELOPMENT
Progress toward establishing treatments has been good. However, given
that effect sizes are small to moderate and many patients derive no benefit,
there is certainly room for improvement (Harvey & Tang, 2003). Advances
in treatment of insomnia are likely to have valuable widespread ramifications because it seems probable that treating insomnia will translate into
reductions in other mental health disorders such as anxiety and depression,
as insomnia is known to be predictive of the onset of these disorders. This
section outlines a few key areas of treatment development currently under
research.
The role of light and dark in sleep is well understood and there is growing
evidence that light and dark therapy is likely to be important in the treatment
of mood disorders (Harvey, 2011). The use of bright light is another key development in the treatment of sleep disorders. Morning bright light will bring
forward (phase advance) the circadian rhythm and is therefore an effective
therapeutic intervention for “owls,” whose preference for staying up late and
sleeping in late interferes with their daily duties. On the other hand, evening
bright light delays the circadian rhythm and is therefore effective for “larks,”
those who wake up earlier that they would like to because of an abnormally
advanced sleep phase (Lack & Wright, 2007). Although the use of light boxes
have been shown to be useful in the treatment of DSPD, adherence is not
optimal and therefore, the use of “informal” light exposure (e.g., sunlight
in the morning, reduced light from electronic devices in the evening) is an
important part of treatment.
Light therapy may also be combined with sleep phase chronotherapy, which
involves moving sleep time 3 h later each night, around the clock, until the
desired sleep time is established. More commonly, however, light therapy is
combined with shifting sleep and wake times more gradually (say, 30 min per
week) forward or backward depending on the desired sleep/wake schedule.
For example, a patient who wishes to move their bedtime from 12 a.m. to
10 p.m. would set a regular wake time and endeavor to get morning light as
soon as possible after waking. Simultaneously, they would shift their bedtime
backwards half an hour each week until a regular pattern is established.
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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
Intensive Sleep Retraining Therapy. Intensive sleep retraining therapy, which
involves a one-off 25-h treatment period of sleep deprivation in which
patients are only allowed to sleep for a few minutes at a time, has shown
promising results for the treatment of insomnia, with reductions observed in
time taken to fall asleep and total sleep time (Harris, Lack, Kemp, Wright, &
Bootzin, 2012). During this treatment, participants are allowed a series of
50 half-hourly sleep opportunities. If they do not sleep within 20 min, the
patient is asked to move out of the bed on to a chair to read or watch DVDs
until the next trial begins. If sleep is initiated, participants are only allowed
to sleep for 3 min before being woken. On each trial where the participant
does sleep, they are asked about their perception of whether or not they
slept and provided with accurate feedback regarding whether sleep onset
occurred or not. Even the most extreme insomnia patients are able to sleep
in this protocol. Intensive sleep retraining therapy is thought to work in
several ways, including (i) by helping people to experience what it is like to
fall asleep quickly and to learn that they are capable of falling asleep fast;
(ii) by providing exposure to sleep deprivation (which is often feared by
patients with insomnia); and (iii) by helping to correct sleep misperception
(sleep/wake discrimination). It has very rapid results, although an even
larger treatment effect size has been observed when this treatment was
combined with five sessions of stimulus control therapy.
Internet-Based Treatments. In recent years, Internet-based treatments for a
number of mental disorders have grown enormously. Indeed, there are a
few different groups of researchers working on Internet-based treatments
for insomnia. For example, Colin Espie and colleagues in Scotland have
developed “Sleepio,” a CBT Internet program developed as a self-help
treatment for insomnia. “SHUTi,” developed in the United States, is another
example of an online self-help program for insomnia and randomized
controlled trials of these programs are currently under way. Internet-based
treatments are particularly helpful in the dissemination of evidence-based
treatments for insomnia because they are easily accessible and lessen the
burden on the health system as specialist clinician time is reduced.
TARGETING SLEEP IN ADOLESCENCE
Adolescence has emerged as a crucial time point to intervene with sleep. This
is due to two key factors—(i) Many mental health disorders such as anxiety
and depression have their onset in adolescence and insomnia is a risk factor
for the emergence of these disorders; and (ii) the natural biological delay in
the circadian cycle that occurs in adolescence along with increased use of
Insomnia and Sleep Disorders
7
technology and other changes in social pressures are now competing more
than ever with the need to sleep.
Clinically, when one’s sleep schedule is heavily delayed and this interferes
with one’s ability to conform to a required schedule (e.g., school or work
start times), one may meet criteria for a diagnosis of DSPD. An obvious
corollary of DSPD in adolescents, who are required to wake early to be at
school, is chronic sleep deprivation. This can put such a teenager at risk
for the development of psychiatric and physical disorders as well as have
deleterious effects in the academic and social domains. Several complex
interactions between biology, psychology, and social context make adolescence a particularly important phase for mechanistic and early intervention
research. Indeed, our group is currently investigating whether a brief
intervention to target DSPD in teenagers will help reduce risk across social,
academic, physical, and psychological domains.
KEY ISSUES FOR FUTURE RESEARCH
One of the great things about working on sleep is that there is so much more
to learn. Despite the fact that sleep takes up about one-third of our life, very
little is known about its function. Certainly, it is clear that insomnia is common and debilitating and there are a number of exciting areas for future
research in this disorder and other sleep disorders.
HYPERSOMNIA
More recently, an understanding of the importance of hypersomnia has
developed (Kaplan & Harvey, 2009). It is still unclear whether hypersomnia
is a disorder of excessive sleep or excessive time in bed. That is, do people
with this disorder actually sleep for excessively long periods or simply
spend large amounts of time in bed? As has been pointed out by our group
previously, the use of objective measures of such as actigraphy (which
assesses an individual’s movement as a fairly accurate proxy of actual sleep)
will help shed light on this quandary (Kaplan & Harvey, 2009). It may also
be the case that psychological factors such as avolition and daytime fatigue
emerge as being more important to this disorder than objective sleep. What
is clear, however, is that as with insomnia, hypersomnia is prevalent and
persistent across mood disorders and there is certainly a need for greater
research into this disorder and its treatment.
TRANSDIAGNOSTIC TREATMENT
Given the high rates of co-occurrence between insomnia and psychiatric disorders as well as evidence suggesting that insomnia contributes to the onset,
8
EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
maintenance, and relapse of a range of psychiatric disorders, we have suggested that insomnia may be a transdiagnostic process across psychiatric
disorders (Harvey, 2008). Therefore, the development of a single treatment
that can be applied to individuals with comorbid insomnia across disorders
has the potential to provide great benefits to public health. However, research
is needed to determine whether it is possible to develop one treatment protocol that will be effective across psychiatric disorders. Secondly, given the
research showing that insomnia predicts the onset and maintenance of other
psychiatric disorders, it appears to be a logical consequence that the treatment of insomnia will improve the functioning and symptomatology of individuals with psychiatric disorders and indeed even prevent the onset of some
cases, yet this is still to be determined empirically.
SLEEP VERSUS CIRCADIAN RHYTHM DISTURBANCE?
Sleep disturbances and circadian rhythm abnormalities, although overlapping, are not identical processes. That is, although the circadian rhythm contributes to sleep disturbance, other factors such as stress also play a role.
Similarly, the circadian rhythm not only controls sleep but also other biological processes. Both sleep and the circadian rhythm have been implicated in
psychiatric disorders, although at this stage their individual contribution to
psychiatric disorders is unknown. Therefore, future research on the involvement of sleep versus circadian influences in psychiatric disorders is needed.
BIOLOGICAL MECHANISMS
Work is already beginning to show that the sleep/circadian systems are
closely linked to serotonergic and dopaminergic function, which points to
one common mechanism potentially underlying sleep and mood/anxiety
disorders (see Harvey et al., 2011 for review). The manipulation of specific
stages of sleep may be a valuable approach to answer important questions
about the contribution of REM and non-REM sleep to psychiatric disorders,
and indeed it may be possible to selectively manipulate different stages
of sleep for therapeutic benefit. For example, it is known that individuals
with depression typically have shortened REM latency and higher REM
density (Coble, Foster, & Kupfer, 1976). Although widely documented,
the underlying mechanisms and reasons for this excess of REM sleep in
depression are poorly understood. Interestingly, antidepressant medications
suppress REM sleep (Mayers & Baldwin, 2005). Similarly, it has been
suggested that individuals with posttraumatic stress disorder (PTSD) fail to
show a suppression of brain adrenergic activity during REM sleep (Shad,
Suris, & North, 2011; Taylor et al., 2008) and this suppression has been
Insomnia and Sleep Disorders
9
proposed to be central to the emotional processing of negative memories
(Walker & van Der Helm, 2009). Consistent with this, an adrenergic antagonist (Prazosin), which reduces adrenergic activity during REM sleep (Shad
et al., 2011; van der Helm et al., 2011) has been shown to reduce symptoms
of PTSD. Understanding the mechanisms underpinning insomnia and the
relationship between sleep processes and psychiatric disorders is invaluable
in developing better treatments for these disorders.
SLEEP MEDICATIONS
Finally, it is worth noting that further research into sleep medications is warranted. Hypnotic medications such as Zolpidem (Ambien) and Temazepam
(Restoril) are some of the most widely used medications in Western societies
(Kripke, Langer, & Kline, 2012). Yet, it seems to be that the type of sleep
one obtains when under the influence of medications such as Zolpidem
is quite different to naturally occurring sleep. That is, naturally occurring
sleep is known to be essential to learning and memory consolidation.
In contrast, pharmacologically induced sleep appears to actually impair
critical sleep-dependent brain processes. For example, in a study involving
developing kittens, Seibt et al. (2008) found that Zolpidem reduced cortical
plasticity by 50%. This suggests that these agents may be of concern to
developing human children and adolescents, potentially as well as adults,
who continue to need sleep for growth, repair, learning, plasticity, and
optimal emotional functioning.
REFERENCES
Baglioni, C., Spiegelhalder, K., Lombardo, C., & Riemann, D. (2010). Sleep and
emotions: A focus on insomnia. Sleep Medicine Reviews, 14, 227–238. doi:10.1016/
j.smrv.2009.10.007
Borbely, A. (1982). A two process model of sleep regulation. Human Neurobiology, 1,
195–204.
Coble, P., Foster, F. G., & Kupfer, D. J. (1976). Electroencephalographic sleep diagnosis of primary depression. Archives of General Psychiatry, 33, 1124.
Diekelmann, S., & Born, J. (2010). The memory function of sleep. Nature Reviews Neuroscience, 11, 114–126.
Gujar, N., Yoo, S.-S., Hu, P., & Walker, M. P. (2011). Sleep deprivation amplifies
reactivity of brain reward networks, biasing the appraisal of positive emotional
experiences. The Journal of Neuroscience, 31, 4466–4474.
Harris, J., Lack, L., Kemp, K., Wright, H., & Bootzin, R. (2012). A randomized controlled trial of intensive sleep retraining (ISR): A brief conditioning treatment for
chronic insomnia. Sleep, 35, 49–60.
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Harvey, A. G. (2008). Insomnia, psychiatric disorders, and the transdiagnostic perspective. Current Directions in Psychological Science, 17, 299–303.
Harvey, A. G. (2011). Sleep and circadian functioning: Critical mechanisms in the
mood disorders? Annual Review of Clinical Psychology, 7, 297–319.
Harvey, A. G., Murray, G., Chandler, R. A., & Soehner, A. (2011). Sleep disturbance as
transdiagnostic: Consideration of neurobiological mechanisms. Clinical Psychology
Review, 31, 225–235.
Harvey, A. G., & Tang, N. K. Y. (2003). Cognitive behaviour therapy for primary
insomnia: Can we rest yet? Sleep Medicine Reviews, 7, 237–262.
Kaplan, K. A., & Harvey, A. G. (2009). Hypersomnia across mood disorders: A review
and synthesis. Sleep Medicine Reviews, 13, 275–285.
Karni, A., Tanne, D., Rubenstien, B. S., Askenasy, J. J., & Sagi, D. (1994). Dependence on REM sleep of overnight improvement of a perceptual skill. Science, 265,
679–682.
Kripke, D. F., Langer, R. D., & Kline, L. E. (2012). Hypnotics’ association with mortality or cancer: A matched cohort study. BMJ Open, 2. doi:10.1136/bmjopen2012-000850
Kryger, M. H., Roth, T., & Dement, W. C. (2005). Principles and practice of sleep medicine
(4th ed.). Philadelphia, PA: WB Saunders Co..
Lack, L. C., & Bootzin, R. B. (2003). Circadian rhythm factors in insomnia and their
treatment. In M. Perlis & K. Lichstein (Eds.), Treatment of sleep disorders: Principles
and practice of behavioral sleep medicine. New York, NY: John Wiley and Sons, Inc.
Lack, L. C., & Wright, H. R. (2007). Treating chronobiological components of chronic
insomnia. Sleep Medicine, 8, 637–644.
Mayers, A. G., & Baldwin, D. S. (2005). Antidepressants and their effect on sleep.
Human Psychopharmacology: Clinical and Experimental, 20, 533–559. doi:10.1002/
hup.726
Morin, C. M. (2006). Cognitive-behavioral therapy of insomnia. Sleep Medicine Clinics,
1, 375–386.
Seibt, J., Aton, S. J., Jha, S. K., Coleman, T., Dumoulin, M. C., & Frank, M. G.
(2008). The non-benzodiazepine hypnotic zolpidem impairs sleep-dependent cortical plasticity. Sleep, 31, 1381–1391.
Shad, M. U., Suris, A. M., & North, C. S. (2011). Novel combination strategy to optimize treatment for PTSD. Human Psychopharmacology: Clinical and Experimental, 26,
4–11.
Taylor, F. B., Martin, P., Thompson, C., Williams, J., Mellman, T. A., Gross, C., …
Raskind, M. A. (2008). Prazosin effects on objective sleep measures and clinical
symptoms in civilian trauma posttraumatic stress disorder: A placebo-controlled
study. Biological Psychiatry, 63, 629–632.
van der Helm, E., Yao, J., Dutt, S., Rao, V., Saletin, J. M., & Walker, M. P. (2011). REM
sleep depotentiates amygdala activity to previous emotional experiences. Current
Biology, 21(23), 2029–2032.
Walker, M. P., & Stickgold, R. (2006). Sleep, memory, and plasticity. In Annual review
of psychology (Vol. 57, pp. 139–166). Palo Alto, CA: Annual Reviews.
Insomnia and Sleep Disorders
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Walker, M. P., & van Der Helm, E. (2009). Overnight therapy? The role of sleep in
emotional brain processing. Psychological Bulletin, 135, 731.
Yoo, S.-S., Gujar, N., Hu, P., Jolesz, F. A., & Walker, M. P. (2007). The human emotional brain without sleep—a prefrontal amygdala disconnect. Current Biology, 17,
R877–R878.
FURTHER READING
Harvey, A. G. (2011). Sleep and circadian functioning: Critical mechanisms in the
mood disorders? Annual Review of Clinical Psychology, 7, 297–319.
Harvey, A. G., Murray, G., Chandler, R. A., & Soehner, A. (2011). Sleep disturbance as
transdiagnostic: Consideration of neurobiological mechanisms. Clinical Psychology
Review, 31, 225–235.
Morin, C. M. (2006). Cognitive-behavioral therapy of insomnia. Sleep Medicine Clinics,
1, 375–386.
Walker, M. P., & van Der Helm, E. (2009). Overnight therapy? The role of sleep in
emotional brain processing. Psychological Bulletin, 135, 731.
ELIZABETH C. MASON SHORT BIOGRAPHY
Elizabeth C. Mason is a visiting postdoctoral fellow at the University of
California, Berkeley. She was awarded an American-Australian Association
Fellowship to pursue research in the field of sleep in the laboratory of Dr.
Allison Harvey. Dr. Mason also holds an academic appointment at the University of New South Wales. On completion of her fellowship, she will return
to her role as a Clinical and Research Psychologist at the Clinical Research
Unit for Anxiety and Depression (CRUfAD), St Vincent’s Hospital, in Sydney, Australia. Dr. Mason is particularly interested in research related to the
mechanisms underlying sleep, anxiety and other mental health disorders in
order to improve treatments for these conditions.
ALLISON G. HARVEY SHORT BIOGRAPHY
Allison G. Harvey is a Professor of Clinical Psychology and Director of the
Golden Bear Sleep Research Clinic at the University of California, Berkeley.
Dr. Harvey is also an Adjunct Professor at the University of Bergen, Norway.
Her training was completed in Sydney, Australia. Dr. Harvey then moved
to the University of Oxford as a postdoctoral fellow in the Department of
Psychiatry then a faculty member in the Department of Experimental Psychology, University. She was also a Fellow of St. Anne’s College. In 2004, she
moved to UC Berkeley. Dr. Harvey’s team aims to develop more effective
treatments for psychiatric and health problems by (i) applying a multisystems and mechanisms-focused framework in which basic science findings
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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
on cognitive, affective, biological, behavioral and developmental contributors are used as sources for deriving novel interventions and (ii) intervention
research is used to develop hypotheses about and/or confirm mechanisms.
Dr. Harvey’s research is funded by NIMH and NICHD. She has published
over 130 research articles and book chapters and authored two books. Her
research has been acknowledged with various awards including an Honorary Doctorate from the University of Orebro, Sweden. Dr. Harvey serves
on numerous editorial boards and is an Associate Editor for SLEEP.
RELATED ESSAYS
Depression (Psychology), Ian H. Gotlib and Daniella J. Furman
Mental Imagery in Psychological Disorders (Psychology), Emily A. Holmes
et al.
Dissociation and Dissociative Identity Disorder (DID) (Psychology), Rafaële
J. C. Huntjens and Martin J. Dorahy
Computer Technology and Children’s Mental Health (Psychology), Philip C.
Kendall et al.
Evolutionary Perspectives on Animal and Human Personality (Anthropology), Joseph H. Manson and Lynn A. Fairbanks
Disorders of Consciousness (Psychology), Martin M. Monti
Clarifying the Nature and Structure of Personality Disorder (Psychology),
Takakuni Suzuki and Douglas B. Samuel
Rumination (Psychology), Edward R. Watkins
Insomnia and Sleep Disorders
ELIZABETH C. MASON and ALLISON G. HARVEY
Abstract
Sleep is common to all animals and yet there are so many mysteries surrounding
its function. Insomnia, the most common sleep disorder, is prevalent and debilitating and has been shown to play a role in the onset and maintenance of other mental
health disorders, such as depression, anxiety, and bipolar disorder. This chapter outlines a basic overview of sleep, followed by a summary of cutting-edge research
investigating insomnia as well as its relationship to other psychiatric disorders. It
is suggested that a bidirectional relationship exists between sleep and emotion and
research supporting this framework is addressed briefly. We describe the treatment
of choice for insomnia, cognitive behavioral therapy, as well as outline other exciting
developments in the treatment of insomnia, including bright light therapy, intensive
sleep retraining therapy, and Internet-based treatments. Finally, we end on a discussion of areas that are ripe for future investigation, including biological mechanisms,
sleep medications, and other sleep disorders such as hypersomnia.
INTRODUCTION
All animals need to sleep, from ants to dolphins to humans. As the knowledge base builds, scientific consensus on why we need sleep is growing. What
is very clear is that if we do not get enough sleep there are serious consequences to both our physical and emotional health. Insomnia, which involves
difficulty falling asleep, staying asleep, or waking earlier than desired in the
morning, is one of the most common health problems. On its own, it is associated with considerable functional impairment but beyond that, insomnia
is very frequently comorbid with, and predicts the development of, several
psychological and medical conditions.
Over the past decade, as an understanding of the adverse consequences of
insufficient sleep has emerged, research on insomnia and other sleep disorders has exploded. The study of insomnia is incredibly interesting from a
scientific point of view as it provides insights into emotion processing and
regulation as well as learning and memory, which are key fields studied in
psychology. Furthermore, it is fascinating from a clinical perspective as it
Emerging Trends in the Social and Behavioral Sciences. Edited by Robert Scott and Stephen Kosslyn.
© 2015 John Wiley & Sons, Inc. ISBN 978-1-118-90077-2.
1
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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
seems likely that effective interventions for insomnia may assist in the prevention of other mental health disorders and physical disorders, too. There
appear to be bidirectional relationships between sleep disturbance and emotional dysregulation in that both impact on one another. Research into these
relationships is providing important clues about mechanisms involved in
insomnia and are detailed later. Other sleep disorders include hypersomnia,
delayed sleep phase disorder (DSPD), sleep apnea, narcolepsy, night terrors,
parasomnias, and restless leg syndrome. This chapter focuses primarily on
insomnia, and touches upon hypersomnia and DSPD.
FOUNDATIONAL RESEARCH
CIRCADIAN RHYTHMS AND SLEEP
Many biological processes, including sleep, occur in a daily rhythm, roughly
around a 24-h clock. Our internal body clock is influenced by several factors in the environment, termed zeitgebers. The most powerful zeitgeber is
light/dark. Other cues that help us entrain our rhythms include temperature,
exercise, and meal times. The internal pacemaker lies in the suprachiasmatic
nucleus (SCN) of the brain, which receives light signals directly from the
retina of the eye.
SLEEP STAGES
Human sleep is divided into REM (rapid eye movement) and non-REM
sleep, which is further divided in to four stages (stages 1, 2, 3, and 4). Stages
1 and 2 are “light” stages of sleep and stages 3 and 4 are “deep,” more
restorative stages of sleep in which slow-wave sleep occurs. Non-REM
sleep appears to be important for conservation of energy and restoration
(Kryger, Roth, & Dement, 2005) as well as the consolidation of certain types
of memories (Diekelmann & Born, 2010). REM sleep is also important in
learning and memory and is particularly critical in emotion processing and
regulation (Karni, Tanne, Rubenstien, Askenasy, & Sagi, 1994; Walker &
Stickgold, 2006; Yoo, Gujar, Hu, Jolesz, & Walker, 2007).
TWO-PROCESS MODEL OF SLEEP
The two-process model is the prevailing theory of sleep regulation, which
proposes that sleep and wakefulness are dependent on two processes, a circadian process and a homeostatic process (Borbely, 1982). The circadian rhythm
is an internal biological clock that runs approximately on a 24-h basis. Variations in melatonin, temperature, and levels of arousal operate according to
Insomnia and Sleep Disorders
3
our circadian rhythms (Lack & Bootzin, 2003). Through the homeostatic process, “sleep pressure” (or the need to sleep) increases with time spent awake.
When a person is sleep deprived, the tendency to sleep increases. Conversely,
when one has a long nap, the tendency to sleep is decreased. These two processes operate in tandem in that the propensity to sleep is more likely when
levels of alertness (the circadian process) are relatively low and sleep pressure
(the homeostatic process) is high. As a corollary, following an afternoon nap,
one may find it difficult to fall asleep at one’s regular “circadian bedtime”
because homeostatic sleep pressure is low. Similarly, circadian arousal may
prevent sleep onset from occurring if one tries to go to sleep early following
a poor night of sleep, even though sleep pressure is high.
CUTTING-EDGE RESEARCH
Exciting developments, outlined later, are being made in the treatment of
insomnia and in the understanding of the mechanisms underpinning the
relationship between insufficient sleep and psychiatric disorders.
SLEEP AND PSYCHIATRIC DISORDERS
Evidence for the importance of sleep in psychiatric disorders has grown enormously in recent years. Certainly, we have all had the experience of poor
sleep affecting our mood and the research is beginning to catch up by explaining this interaction at the behavioral, cognitive, and biological levels. This
research is extremely important in helping to identify possible therapeutic
targets for both insomnia and other psychiatric disorders.
Given that insomnia frequently predates and predicts psychiatric disorders, sleep disturbance is no longer considered an epiphenomenon in
psychiatric disorders; rather, it is now viewed as an important and underrecognized mechanism in the cause and maintenance of psychiatric disorders.
This change has recently been reflected in the latest edition of the Diagnostic
and Statistical Manual (DSM-5), in which the diagnosis of primary insomnia
has been renamed insomnia, to eliminate the distinction between primary
and secondary insomnia.
A BIDIRECTIONAL MODEL BETWEEN SLEEP AND EMOTION
Recently, we and others have proposed that the relationship between sleep
disturbance and processes of emotional dysregulation in psychiatric disorders is likely to be bidirectional (Baglioni, Spiegelhalder, Lombardo, & Riemann, 2010; Harvey, Murray, Chandler, & Soehner, 2011). This simple model
proposes that mood, anxiety, and other emotional symptoms interfere with
4
EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
sleep, and that, conversely, the effects of sleep deprivation contribute to mood
dysregulation and emotional disturbance. It is clear anecdotally and through
experimental manipulations that worry and rumination, key features of anxiety and depressive disorders, affect our sleep. Equally, exciting research from
Dr. Matthew Walker’s group at the University of California, Berkeley has
shown that just a single night of sleep deprivation causes significant increases
in emotional reactivity to negative stimuli and corresponding increases in
activity in the amygdala, an area of the brain that plays a key role in emotion
(Yoo et al., 2007). Not only has increased emotional activity to negative stimuli been observed but it has also been shown that sleep deprivation leads to
amplified neural reactivity in reward networks in response to pleasant stimuli (Gujar, Yoo, Hu, & Walker, 2011). Indeed, in an article entitled “Overnight
therapy? The role of sleep in emotional brain processing,” Walker and his
colleague emphasize the role of REM sleep in processing emotional memories and note that there has been a “renaissance” of research with a focus
on sleep and neurocognitive processes involved in emotion regulation. Certainly, this is a fascinating area which is sure to grow in the future. We suggest
that this bidirectional model between sleep and emotion is valuable as an
initial organizing structure for the existing and future research. The study of
sleep across psychiatric disorders is an exciting domain for interdisciplinary
research across behavioral, social, cognitive, and neurobiological levels of
explanation.
COGNITIVE BEHAVIORAL THERAPY FOR INSOMNIA (CBT-I)
Cognitive Behavioral Therapy for Insomnia (CBT-I) is the most effective
psychological treatment for insomnia. Unlike pharmacological treatments,
its effects persist after a course of treatment has been terminated (Morin,
2006). The aim of CBT-I is to foster sleep-conducive behaviors and to change
unhelpful and unrealistic expectations about sleep and daytime functioning.
CBT-I has been shown to increase total sleep time and improve sleep quality,
while reducing the time it takes to fall asleep and the number of awakenings
in the night time. It is a multicomponent therapy which involves cognitive
therapy, stimulus control, sleep restriction, behavioral experiments, and
psychoeducation about good sleep habits. One of the more paradoxical
components of CBT-I is sleep restriction. The aim of this is to match time in
bed as closely as possible with time asleep by limiting the amount of time
the patient sleeps in the initial stages of therapy. This helps the patient to
consolidate sleep, associate the bed with sleep, and to shorten sleep onset
times as she/he accumulates a sleep debt through mild sleep deprivation.
Stimulus control, which aims to create a positive association between the
bed/bedroom and sleep by encouraging the patient to get out of bed when
Insomnia and Sleep Disorders
5
not tired and only use the bed for sleep and sex, while restricting other
activities in bed (e.g., watching television, checking e-mails), has also been
shown to be an important contributor to treatment gains. CBT-I is generally
conducted over six to eight sessions, and similar to CBT treatments for
other disorders, it involves in-session activities as well as homework to be
completed between sessions.
TREATMENT DEVELOPMENT
Progress toward establishing treatments has been good. However, given
that effect sizes are small to moderate and many patients derive no benefit,
there is certainly room for improvement (Harvey & Tang, 2003). Advances
in treatment of insomnia are likely to have valuable widespread ramifications because it seems probable that treating insomnia will translate into
reductions in other mental health disorders such as anxiety and depression,
as insomnia is known to be predictive of the onset of these disorders. This
section outlines a few key areas of treatment development currently under
research.
The role of light and dark in sleep is well understood and there is growing
evidence that light and dark therapy is likely to be important in the treatment
of mood disorders (Harvey, 2011). The use of bright light is another key development in the treatment of sleep disorders. Morning bright light will bring
forward (phase advance) the circadian rhythm and is therefore an effective
therapeutic intervention for “owls,” whose preference for staying up late and
sleeping in late interferes with their daily duties. On the other hand, evening
bright light delays the circadian rhythm and is therefore effective for “larks,”
those who wake up earlier that they would like to because of an abnormally
advanced sleep phase (Lack & Wright, 2007). Although the use of light boxes
have been shown to be useful in the treatment of DSPD, adherence is not
optimal and therefore, the use of “informal” light exposure (e.g., sunlight
in the morning, reduced light from electronic devices in the evening) is an
important part of treatment.
Light therapy may also be combined with sleep phase chronotherapy, which
involves moving sleep time 3 h later each night, around the clock, until the
desired sleep time is established. More commonly, however, light therapy is
combined with shifting sleep and wake times more gradually (say, 30 min per
week) forward or backward depending on the desired sleep/wake schedule.
For example, a patient who wishes to move their bedtime from 12 a.m. to
10 p.m. would set a regular wake time and endeavor to get morning light as
soon as possible after waking. Simultaneously, they would shift their bedtime
backwards half an hour each week until a regular pattern is established.
6
EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
Intensive Sleep Retraining Therapy. Intensive sleep retraining therapy, which
involves a one-off 25-h treatment period of sleep deprivation in which
patients are only allowed to sleep for a few minutes at a time, has shown
promising results for the treatment of insomnia, with reductions observed in
time taken to fall asleep and total sleep time (Harris, Lack, Kemp, Wright, &
Bootzin, 2012). During this treatment, participants are allowed a series of
50 half-hourly sleep opportunities. If they do not sleep within 20 min, the
patient is asked to move out of the bed on to a chair to read or watch DVDs
until the next trial begins. If sleep is initiated, participants are only allowed
to sleep for 3 min before being woken. On each trial where the participant
does sleep, they are asked about their perception of whether or not they
slept and provided with accurate feedback regarding whether sleep onset
occurred or not. Even the most extreme insomnia patients are able to sleep
in this protocol. Intensive sleep retraining therapy is thought to work in
several ways, including (i) by helping people to experience what it is like to
fall asleep quickly and to learn that they are capable of falling asleep fast;
(ii) by providing exposure to sleep deprivation (which is often feared by
patients with insomnia); and (iii) by helping to correct sleep misperception
(sleep/wake discrimination). It has very rapid results, although an even
larger treatment effect size has been observed when this treatment was
combined with five sessions of stimulus control therapy.
Internet-Based Treatments. In recent years, Internet-based treatments for a
number of mental disorders have grown enormously. Indeed, there are a
few different groups of researchers working on Internet-based treatments
for insomnia. For example, Colin Espie and colleagues in Scotland have
developed “Sleepio,” a CBT Internet program developed as a self-help
treatment for insomnia. “SHUTi,” developed in the United States, is another
example of an online self-help program for insomnia and randomized
controlled trials of these programs are currently under way. Internet-based
treatments are particularly helpful in the dissemination of evidence-based
treatments for insomnia because they are easily accessible and lessen the
burden on the health system as specialist clinician time is reduced.
TARGETING SLEEP IN ADOLESCENCE
Adolescence has emerged as a crucial time point to intervene with sleep. This
is due to two key factors—(i) Many mental health disorders such as anxiety
and depression have their onset in adolescence and insomnia is a risk factor
for the emergence of these disorders; and (ii) the natural biological delay in
the circadian cycle that occurs in adolescence along with increased use of
Insomnia and Sleep Disorders
7
technology and other changes in social pressures are now competing more
than ever with the need to sleep.
Clinically, when one’s sleep schedule is heavily delayed and this interferes
with one’s ability to conform to a required schedule (e.g., school or work
start times), one may meet criteria for a diagnosis of DSPD. An obvious
corollary of DSPD in adolescents, who are required to wake early to be at
school, is chronic sleep deprivation. This can put such a teenager at risk
for the development of psychiatric and physical disorders as well as have
deleterious effects in the academic and social domains. Several complex
interactions between biology, psychology, and social context make adolescence a particularly important phase for mechanistic and early intervention
research. Indeed, our group is currently investigating whether a brief
intervention to target DSPD in teenagers will help reduce risk across social,
academic, physical, and psychological domains.
KEY ISSUES FOR FUTURE RESEARCH
One of the great things about working on sleep is that there is so much more
to learn. Despite the fact that sleep takes up about one-third of our life, very
little is known about its function. Certainly, it is clear that insomnia is common and debilitating and there are a number of exciting areas for future
research in this disorder and other sleep disorders.
HYPERSOMNIA
More recently, an understanding of the importance of hypersomnia has
developed (Kaplan & Harvey, 2009). It is still unclear whether hypersomnia
is a disorder of excessive sleep or excessive time in bed. That is, do people
with this disorder actually sleep for excessively long periods or simply
spend large amounts of time in bed? As has been pointed out by our group
previously, the use of objective measures of such as actigraphy (which
assesses an individual’s movement as a fairly accurate proxy of actual sleep)
will help shed light on this quandary (Kaplan & Harvey, 2009). It may also
be the case that psychological factors such as avolition and daytime fatigue
emerge as being more important to this disorder than objective sleep. What
is clear, however, is that as with insomnia, hypersomnia is prevalent and
persistent across mood disorders and there is certainly a need for greater
research into this disorder and its treatment.
TRANSDIAGNOSTIC TREATMENT
Given the high rates of co-occurrence between insomnia and psychiatric disorders as well as evidence suggesting that insomnia contributes to the onset,
8
EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
maintenance, and relapse of a range of psychiatric disorders, we have suggested that insomnia may be a transdiagnostic process across psychiatric
disorders (Harvey, 2008). Therefore, the development of a single treatment
that can be applied to individuals with comorbid insomnia across disorders
has the potential to provide great benefits to public health. However, research
is needed to determine whether it is possible to develop one treatment protocol that will be effective across psychiatric disorders. Secondly, given the
research showing that insomnia predicts the onset and maintenance of other
psychiatric disorders, it appears to be a logical consequence that the treatment of insomnia will improve the functioning and symptomatology of individuals with psychiatric disorders and indeed even prevent the onset of some
cases, yet this is still to be determined empirically.
SLEEP VERSUS CIRCADIAN RHYTHM DISTURBANCE?
Sleep disturbances and circadian rhythm abnormalities, although overlapping, are not identical processes. That is, although the circadian rhythm contributes to sleep disturbance, other factors such as stress also play a role.
Similarly, the circadian rhythm not only controls sleep but also other biological processes. Both sleep and the circadian rhythm have been implicated in
psychiatric disorders, although at this stage their individual contribution to
psychiatric disorders is unknown. Therefore, future research on the involvement of sleep versus circadian influences in psychiatric disorders is needed.
BIOLOGICAL MECHANISMS
Work is already beginning to show that the sleep/circadian systems are
closely linked to serotonergic and dopaminergic function, which points to
one common mechanism potentially underlying sleep and mood/anxiety
disorders (see Harvey et al., 2011 for review). The manipulation of specific
stages of sleep may be a valuable approach to answer important questions
about the contribution of REM and non-REM sleep to psychiatric disorders,
and indeed it may be possible to selectively manipulate different stages
of sleep for therapeutic benefit. For example, it is known that individuals
with depression typically have shortened REM latency and higher REM
density (Coble, Foster, & Kupfer, 1976). Although widely documented,
the underlying mechanisms and reasons for this excess of REM sleep in
depression are poorly understood. Interestingly, antidepressant medications
suppress REM sleep (Mayers & Baldwin, 2005). Similarly, it has been
suggested that individuals with posttraumatic stress disorder (PTSD) fail to
show a suppression of brain adrenergic activity during REM sleep (Shad,
Suris, & North, 2011; Taylor et al., 2008) and this suppression has been
Insomnia and Sleep Disorders
9
proposed to be central to the emotional processing of negative memories
(Walker & van Der Helm, 2009). Consistent with this, an adrenergic antagonist (Prazosin), which reduces adrenergic activity during REM sleep (Shad
et al., 2011; van der Helm et al., 2011) has been shown to reduce symptoms
of PTSD. Understanding the mechanisms underpinning insomnia and the
relationship between sleep processes and psychiatric disorders is invaluable
in developing better treatments for these disorders.
SLEEP MEDICATIONS
Finally, it is worth noting that further research into sleep medications is warranted. Hypnotic medications such as Zolpidem (Ambien) and Temazepam
(Restoril) are some of the most widely used medications in Western societies
(Kripke, Langer, & Kline, 2012). Yet, it seems to be that the type of sleep
one obtains when under the influence of medications such as Zolpidem
is quite different to naturally occurring sleep. That is, naturally occurring
sleep is known to be essential to learning and memory consolidation.
In contrast, pharmacologically induced sleep appears to actually impair
critical sleep-dependent brain processes. For example, in a study involving
developing kittens, Seibt et al. (2008) found that Zolpidem reduced cortical
plasticity by 50%. This suggests that these agents may be of concern to
developing human children and adolescents, potentially as well as adults,
who continue to need sleep for growth, repair, learning, plasticity, and
optimal emotional functioning.
REFERENCES
Baglioni, C., Spiegelhalder, K., Lombardo, C., & Riemann, D. (2010). Sleep and
emotions: A focus on insomnia. Sleep Medicine Reviews, 14, 227–238. doi:10.1016/
j.smrv.2009.10.007
Borbely, A. (1982). A two process model of sleep regulation. Human Neurobiology, 1,
195–204.
Coble, P., Foster, F. G., & Kupfer, D. J. (1976). Electroencephalographic sleep diagnosis of primary depression. Archives of General Psychiatry, 33, 1124.
Diekelmann, S., & Born, J. (2010). The memory function of sleep. Nature Reviews Neuroscience, 11, 114–126.
Gujar, N., Yoo, S.-S., Hu, P., & Walker, M. P. (2011). Sleep deprivation amplifies
reactivity of brain reward networks, biasing the appraisal of positive emotional
experiences. The Journal of Neuroscience, 31, 4466–4474.
Harris, J., Lack, L., Kemp, K., Wright, H., & Bootzin, R. (2012). A randomized controlled trial of intensive sleep retraining (ISR): A brief conditioning treatment for
chronic insomnia. Sleep, 35, 49–60.
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EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
Harvey, A. G. (2008). Insomnia, psychiatric disorders, and the transdiagnostic perspective. Current Directions in Psychological Science, 17, 299–303.
Harvey, A. G. (2011). Sleep and circadian functioning: Critical mechanisms in the
mood disorders? Annual Review of Clinical Psychology, 7, 297–319.
Harvey, A. G., Murray, G., Chandler, R. A., & Soehner, A. (2011). Sleep disturbance as
transdiagnostic: Consideration of neurobiological mechanisms. Clinical Psychology
Review, 31, 225–235.
Harvey, A. G., & Tang, N. K. Y. (2003). Cognitive behaviour therapy for primary
insomnia: Can we rest yet? Sleep Medicine Reviews, 7, 237–262.
Kaplan, K. A., & Harvey, A. G. (2009). Hypersomnia across mood disorders: A review
and synthesis. Sleep Medicine Reviews, 13, 275–285.
Karni, A., Tanne, D., Rubenstien, B. S., Askenasy, J. J., & Sagi, D. (1994). Dependence on REM sleep of overnight improvement of a perceptual skill. Science, 265,
679–682.
Kripke, D. F., Langer, R. D., & Kline, L. E. (2012). Hypnotics’ association with mortality or cancer: A matched cohort study. BMJ Open, 2. doi:10.1136/bmjopen2012-000850
Kryger, M. H., Roth, T., & Dement, W. C. (2005). Principles and practice of sleep medicine
(4th ed.). Philadelphia, PA: WB Saunders Co..
Lack, L. C., & Bootzin, R. B. (2003). Circadian rhythm factors in insomnia and their
treatment. In M. Perlis & K. Lichstein (Eds.), Treatment of sleep disorders: Principles
and practice of behavioral sleep medicine. New York, NY: John Wiley and Sons, Inc.
Lack, L. C., & Wright, H. R. (2007). Treating chronobiological components of chronic
insomnia. Sleep Medicine, 8, 637–644.
Mayers, A. G., & Baldwin, D. S. (2005). Antidepressants and their effect on sleep.
Human Psychopharmacology: Clinical and Experimental, 20, 533–559. doi:10.1002/
hup.726
Morin, C. M. (2006). Cognitive-behavioral therapy of insomnia. Sleep Medicine Clinics,
1, 375–386.
Seibt, J., Aton, S. J., Jha, S. K., Coleman, T., Dumoulin, M. C., & Frank, M. G.
(2008). The non-benzodiazepine hypnotic zolpidem impairs sleep-dependent cortical plasticity. Sleep, 31, 1381–1391.
Shad, M. U., Suris, A. M., & North, C. S. (2011). Novel combination strategy to optimize treatment for PTSD. Human Psychopharmacology: Clinical and Experimental, 26,
4–11.
Taylor, F. B., Martin, P., Thompson, C., Williams, J., Mellman, T. A., Gross, C., …
Raskind, M. A. (2008). Prazosin effects on objective sleep measures and clinical
symptoms in civilian trauma posttraumatic stress disorder: A placebo-controlled
study. Biological Psychiatry, 63, 629–632.
van der Helm, E., Yao, J., Dutt, S., Rao, V., Saletin, J. M., & Walker, M. P. (2011). REM
sleep depotentiates amygdala activity to previous emotional experiences. Current
Biology, 21(23), 2029–2032.
Walker, M. P., & Stickgold, R. (2006). Sleep, memory, and plasticity. In Annual review
of psychology (Vol. 57, pp. 139–166). Palo Alto, CA: Annual Reviews.
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Walker, M. P., & van Der Helm, E. (2009). Overnight therapy? The role of sleep in
emotional brain processing. Psychological Bulletin, 135, 731.
Yoo, S.-S., Gujar, N., Hu, P., Jolesz, F. A., & Walker, M. P. (2007). The human emotional brain without sleep—a prefrontal amygdala disconnect. Current Biology, 17,
R877–R878.
FURTHER READING
Harvey, A. G. (2011). Sleep and circadian functioning: Critical mechanisms in the
mood disorders? Annual Review of Clinical Psychology, 7, 297–319.
Harvey, A. G., Murray, G., Chandler, R. A., & Soehner, A. (2011). Sleep disturbance as
transdiagnostic: Consideration of neurobiological mechanisms. Clinical Psychology
Review, 31, 225–235.
Morin, C. M. (2006). Cognitive-behavioral therapy of insomnia. Sleep Medicine Clinics,
1, 375–386.
Walker, M. P., & van Der Helm, E. (2009). Overnight therapy? The role of sleep in
emotional brain processing. Psychological Bulletin, 135, 731.
ELIZABETH C. MASON SHORT BIOGRAPHY
Elizabeth C. Mason is a visiting postdoctoral fellow at the University of
California, Berkeley. She was awarded an American-Australian Association
Fellowship to pursue research in the field of sleep in the laboratory of Dr.
Allison Harvey. Dr. Mason also holds an academic appointment at the University of New South Wales. On completion of her fellowship, she will return
to her role as a Clinical and Research Psychologist at the Clinical Research
Unit for Anxiety and Depression (CRUfAD), St Vincent’s Hospital, in Sydney, Australia. Dr. Mason is particularly interested in research related to the
mechanisms underlying sleep, anxiety and other mental health disorders in
order to improve treatments for these conditions.
ALLISON G. HARVEY SHORT BIOGRAPHY
Allison G. Harvey is a Professor of Clinical Psychology and Director of the
Golden Bear Sleep Research Clinic at the University of California, Berkeley.
Dr. Harvey is also an Adjunct Professor at the University of Bergen, Norway.
Her training was completed in Sydney, Australia. Dr. Harvey then moved
to the University of Oxford as a postdoctoral fellow in the Department of
Psychiatry then a faculty member in the Department of Experimental Psychology, University. She was also a Fellow of St. Anne’s College. In 2004, she
moved to UC Berkeley. Dr. Harvey’s team aims to develop more effective
treatments for psychiatric and health problems by (i) applying a multisystems and mechanisms-focused framework in which basic science findings
12
EMERGING TRENDS IN THE SOCIAL AND BEHAVIORAL SCIENCES
on cognitive, affective, biological, behavioral and developmental contributors are used as sources for deriving novel interventions and (ii) intervention
research is used to develop hypotheses about and/or confirm mechanisms.
Dr. Harvey’s research is funded by NIMH and NICHD. She has published
over 130 research articles and book chapters and authored two books. Her
research has been acknowledged with various awards including an Honorary Doctorate from the University of Orebro, Sweden. Dr. Harvey serves
on numerous editorial boards and is an Associate Editor for SLEEP.
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