Download Insomnia

Chapter 18:
Sleep Disorders
Jennifer C. Kanady
Allison G. Harvey
Sleep Basics
 Human sleep can be broadly classified into nonrapid
eye movement (NREM) sleep, which can be
subdivided into four stages (Stages 1, 2, 3, and 4), and
rapid eye movement (REM) sleep.
 NREM and REM sleep alternate throughout the night, and the
ratio of NREM to REM sleep changes throughout the night,
such that NREM dominates early in the night whereas REM
sleep dominates later in the night.
 Each NREM-REM cycle spans 70 to 120 minutes.
 NREM sleep is thought to be important for energy
conservation and restoration.
 REM sleep is thought to play a role in learning, memory
consolidation, emotional processing, and mood/emotion
regulation.
Sleep Basics (cont.)
 The two-process model of sleep regulation (Borbely,
1982) proposes that sleep and wake are dependent on
a homeostatic process and a circadian process.
 Sleep homeostasis results in increased sleep pressure the
longer one is awake and decreased sleep pressure as one
sleeps.
 The circadian rhythm is an internal biological clock that is
responsible for 24-hour oscillations of melatonin, cortisol,
temperature, and biological functions.
 Sleep disturbance is a characteristic of psychiatric
disorders and can play a critical role in the
maintenance of psychiatric disorders (Harvey, 2001).
 Insomnia is the most common sleep disorder, reported
by 10% of the population (Ancoli-Israel & Roth, 1999).
DSM-5 Diagnostic Criteria for
Insomnia Disorder
 “Predominant” subjective complaint of dissatisfaction with sleep
quantity or quality associated with one (or more) of the following:
 Difficulty falling asleep.
 Difficulty maintaining sleep, characterized by frequent awakenings or
problems returning to sleep after awakenings
 Early-morning awakening with inability to return to sleep.
 Sleep disturbance must be associated with daytime distress or
impairment in functioning.
 Occurs at least 3 nights per week, for at least 3 months, and
occurs despite adequate opportunity for sleep.
 Sleep disturbance cannot be better explained by another sleepwake disorder, physiological effects of a substance, or coexisting
mental disorders and medical conditions.
 But insomnia can be comorbid with other psychiatric disorders
and medical problems.
Models of Insomnia
 Spielman, Caruso, and Glovinsky (1987) three-factor model
 A diathesis-stress model in which acute insomnia occurs as a result
of predisposing factors (e.g., traits such as a tendency to worry) and
precipitating factors (e.g., life stressors), and can develop into chronic
insomnia as a result of perpetuating factors (e.g., poor coping
strategies).
 Bootzin (1972) stimulus control model
 A behavioral model in which insomnia occurs when the bed or
bedroom ceases to be paired specifically with sleep, but has become
paired with many possible responses.
 Harvey (2002) cognitive model
 Insomnia is maintained by cognitive processes that occur at night
and during the day, including worry and rumination, selective
attention and monitoring, misperception of sleep and daytime deficits,
dysfunctional beliefs about sleep, and counterproductive safety
behaviors that serve to maintain beliefs.
Models of Insomnia (cont.)
 Monroe (1967) hyperarousal model
 Increased physiological activation results in decreased sleep
efficiency and increased daytime fatigue.
 Perlis et al. (1997) neurocognitive model
 Somatic, cognitive, and cortical arousal may act as a perpetuating
factor in sleep disturbance.
• Somatic arousal refers to metabolic rate.
• Cognitive arousal refers to worry and rumination.
• Cortical arousal refers to abnormal levels of sensory and information
processing and long-term memory around sleep onset and during NREM sleep.
 Lack of consensus on homeostatic and circadian influences
 Individuals with insomnia may have impaired sleep homeostasis and
environmentally induced circadian phase shifts may cause acute
insomnia.
Hybrid Models of Insomnia
 Morin (1993)
 Cognitive (e.g., worry), temporal (e.g., bedtime routines), and
environmental (e.g., bedroom) variables are both precipitating
and perpetuating factors of hyperarousal and insomnia.
 Lundh (1998)
 Cognitive and physiological arousal, stressful life events, and
sleep interpreting processes (cognitions and perceptions about
poor sleep) play a role in maintaining insomnia.
 Espie (2002)
 Psychobiological inhibition model suggests that selectively
attending to sleep, explicitly intending to sleep, and introducing
effort into the sleep engagement process interferes with the
automaticity of the homeostatic and circadian processes.
Assessment
 Subjective Assessment
 Insomnia is defined subjectively through clinical interview, selfreport questionnaires, and sleep diaries.
 Clinical history includes estimates of sleep onset latency,
number of awakening after sleep onset, total amount of time
awake after sleep onset, total sleep time, and subjective sleep
quality, as well as daytime consequences of insomnia.
 Validated self-report questionnaires include Pittsburgh Sleep
Quality Index (Buysse et al., 1989), Insomnia Severity Index
(Bastien et al., 2001), and Stanford Sleepiness Scale (Hoddes
et al., 1973).
 Sleep diaries are prospective self-report records of sleep
parameters, including “what time did you get into bed?,” “how
long did it take you to fall asleep,” “what time was your final
awakening?,” “how would you rate the quality of your sleep?”
Assessment (cont)
 Objective Estimates
 Objective estimates of sleep are not required for the
assessment or diagnosis of insomnia.
 Polysomnography (PSG) is the gold standard of objective
sleep measures, records changes that occur during
sleep, including electrical currents in the brain, eye
movements, muscle activity, and heart rhythm.
 Actigraphy uses a small wristwatch-like device that
contains an acceleration sensor to detect and store
information about physical motion, which can be used to
obtain objective estimates of sleep.
Cognitive Behavior Therapy for
Insomnia (CBT-I)
 CBT-I is a multicomponent, psychological treatment of
insomnia designed to:
 Address the cognitive and behavioral maintaining mechanisms
involved in perpetuating sleep disturbance.
 Teach coping techniques that patients can use in instances of
residual sleep difficulty.
 CBT-I is made up of one or more components:
 4 to 10 weekly sessions to implement chosen components.
 RCTs have compared one or more components of CBT-I to each
other and/or to placebo in individual therapy, group therapy, or selfhelp formats.
 CBT-I can be implemented and is effective in treating
insomnia that is comorbid with another psychiatric or
medical disorder, even if that other disorder is not under
control.
Components of CBT-I
 Stimulus Control (Bootzin, Epstein, & Wood, 1991)
 Behavioral treatment in which patients must: set a regular sleep
schedule with consistent wake time and no daytime naps, go to bed
and stay in bed only when sleepy, and eliminate from the bedroom all
sleep-incompatible activities (e.g., watching TV).
 Well-supported empirically based treatment on its own.
 Sleep Restriction (Spielman, Saskin, & Thorpy, 1987)
 Behavioral treatment that limits time in bed to the equivalent of the
time the patient estimates he or she spends sleeping in order to
heighten homeostatic sleep drive and increase sleep efficiency.
 Well-supported empirically based treatment on its own.
 Sleep Hygiene (Morin & Espie, 2003)
 Psychoeducation and behavioral treatment targeting sleepincompatible routines including alcohol, tobacco caffeine, diet,
exercise, and the bedroom environment.
 Not effective as a solo treatment for insomnia.
Components of CBT-I (cont.)
 Paradoxical Intention
 Aims to reduce performance anxiety related to sleep and
replace the tendency to actively try to get to sleep, and instead
instructs patients to stay awake for as long as possible.
 Well-supported empirically based treatment on its own.
 Relaxation Therapy
 Patients are taught in therapy exercises focusing on imagery,
breathing exercises, and the release of muscle tension in order
to set a context in which sleep is more likely to occur.
 Cognitive Restructuring
 Formal cognitive therapy component of CBT-I involving altering
faulty beliefs about sleep with psychoeducation about sleep
requirements, the biological clock, and the effects of sleepwake functions.
Pharmacological Interventions
 Several different classes of medications may be used to treat
insomnia, including hypnotics, antihistamines, and
antidepressants.
 There is no official indication for the use of nonhypnotics as an insomnia
treatment.
 There is little data to support the use of antidepressants in
nondepressed patients with insomnia, and the mechanism by which
antidepressants affect sleep is unknown.
 Hypnotics are medications whose primary purpose is to induce
sleep.
 Hypnotics, including benzodiazepine receptor agonists (e.g.,
clonazepam, zolpidem), have been shown to be effective and safe for
the treatment of insomnia.
 Short-term effects of CBT-I and BzRA treatments for insomnia
are comparable (Morin et al., 1999).
 Individuals who received CBT-I alone or in combination with a BzRA
sustained treatment gains up to 2 years later.
Other Sleep Disorders
 The presence of these disorders is an exclusionary criteria for diagnosis
of insomnia:
 Sleep Apnea: Transient closure of the upper airway during sleep, with symptoms
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during sleep including snoring, pauses in breathing during sleep, and choking
during sleep.
Restless Legs Syndrome: A sensation of an urge to move the limbs and feeling of
restlessness because of sensations in the limbs associated with a circadian
pattern.
Periodic Limb Movement Disorder: Repetitive episodes of limb movements
during sleep associated with partial or full awakening.
Circadian Rhythm Disorders: Advance sleep phase (falling asleep early and
waking up early) or delayed sleep phase (falling asleep late and waking up late)
Narcolepsy: Excessive sleepiness, short uncontrollable naps during the day.
Hypersomnia: Prolonged nighttime sleep episodes, excessive daytime
sleepiness, and frequent napping.
• Associated with emotional disturbance, interpersonal problems, substance abuse, and major
depressive episodes.
Future Directions
 Bidirectional relationship between sleep and emotion
regulation (Harvey, 2008), and the role of emotion in
insomnia:
 Emotion regulation difficulties make it difficult to get to sleep,
and impaired sleep impacts emotion and mood the next day.
 The impact of environmental factors (e.g.,
interpersonal context, technology, busy schedules) on
insomnia.
 Evaluate efficacy of CBT-I in adolescence:
 There are significant psychological, cognitive, social, and
emotional changes over the course of adolescence, in addition
to changes in circadian rhythms and sleep-wake timing
(Carskadon, 2002).
Future Directions (cont)
 Improving treatment targets and outcomes:
 A minority of patients treated for insomnia become good
sleepers, and daytime impairment may be independent of
sleep and may instead be associated with subjective
perceptions of sleep quality.
 Comorbid conditions:
 Treating sleep disturbance may improve symptoms of
PTSD (Germain et al., 2007), chronic pain (Currie et al.,
2000), and depression (Manber et al., 2008), and may
prevent mood episodes in bipolar disorder (Harvey,
2011).