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 sleep- wake 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, self- report 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 self- help 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 sleep- incompatible 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 sleep- wake 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 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).