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Chapter 22. Sleep Disorders

Daniel J. Buysse, M.D.; Patrick J. Strollo, M.D.; Jed E. Black, M.D.; Phyllis G. Zee, M.D., Ph.D.; John W. Winkelman, M.D., Ph.D.
DOI: 10.1176/appi.books.9781585623402.311529

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Excerpt

Sleep and wakefulness are fundamental behavioral-neurobiological states present in all animals, including human beings. Although the function of sleep and sleep–wake rhythms has long been debated, it is unlikely that such a fundamental process will ever be equated with a single function. Theories of the function of sleep focus on several possibilities:

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FIGURE 22–1. Polysomnography in different sleep stages.The six panels show activity in the electroencephalogram (EEG), electrooculogram (EOG), and electromyogram (EMG) during wakefulness and the different sleep stages. Each tracing shows 30 seconds. A, Wakefulness is characterized by low-voltage, fast-frequency EEG, voluntary eye movements, and tonic muscle tone. The EEG segments marked "A" show alpha rhythm, which is characteristic of relaxed wakefulness with eyes closed. The arrows marked "REMs" show rapid eye movements. The channels are labeled on the left side: C3, C4, O1, and O2 are EEG leads, which are measured relative to a common, or referential (REF), lead. LOC and ROC are leads at the left and right outer canthus of the eye. B, Stage 1 non–REM (NREM) sleep is characterized by a slight increase in EEG amplitude and slowing of EEG frequencies (A), slow rolling eye movements (indicated by reciprocal "hills and valleys" in the EOG channels, [B]) and lower muscle tone (C). C, Stage 2 NREM sleep is characterized by further slowing of the EEG, together with an increase in amplitude. Phasic events include "K complexes," isolated large-amplitude slow EEG waves (K) and "sleep spindles," episodic bursts of fast EEG activity lasting approximately 0.5 seconds (S). EOG shows underlying brain electrical activity, and therefore resembles the EEG. Muscle tone is further reduced. D, Stage 3 sleep is characterized by large-amplitude, slow (0.5–4.0 Hz) EEG activity, also known as "delta" or "slow-wave sleep" activity, that constitutes 20%–50% of the 30-second epoch. EOG mirrors EEG activity, and muscle tone is low. E, Stage 4 sleep is identical to Stage 3, except that delta activity occupies greater than 50% of the epoch. F, REM sleep is characterized by the return of faster-frequency, mixed-voltage EEG, similar to Stage 1 NREM sleep. The hallmark of REM is the appearance of phasic rapid eye movements, which present as large-amplitude "spiky" waveforms that clearly differ from the slower eye movements of Stage 1 NREM. Muscle tone is essentially absent, except for the intermittent occurrence of phasic muscle twitches, which often accompany eye movements.Source. Reprinted from Buysse DJ (ed): Sleep Disorders and Psychiatry (Review of Psychiatry Series, Volume 24, Number 2; Oldham JM and Riba MB, series editors). Washington, DC, American Psychiatric Publishing, 2005, pp. 7–9. Copyright 2005, American Psychiatric Publishing. Used with permission.

FIGURE 22–2. Hypnograms of sleep stages in healthy subjects.Each 20- to 30-second epoch of sleep for an entire night is assigned a sleep stage by a human "scorer." These epoch scores can then be displayed graphically in a "hypnogram," to display the progression of sleep stages across the night. A, Hypnogram for an entire night of sleep in a healthy young adult. Sleep stages are indicated by increasing "depth" on the vertical axis, with REM sleep represented by heavy horizontal lines. Time is indicated on the horizontal axis. Note that most Stage 3–4 NREM sleep occurs in the early part of the night, and REM periods get longer toward the end of the night. B, Hypnogram for an older adult. Note the absence of Stage 3–4 NREM sleep and the greater amount of wakefulness during the sleep period.Source. Reprinted from Buysse DJ (ed): Sleep Disorders and Psychiatry (Review of Psychiatry Series, Volume 24, Number 2; Oldham JM and Riba MB, series editors). Washington, DC, American Psychiatric Publishing, 2005, p. 10. Copyright 2005, American Psychiatric Publishing. Used with permission.

FIGURE 22–3. The two-process model.Alertness level is determined by the interaction between two processes. The sleep homeostatic drive (Process S) promotes sleep and builds up during wake, reaching a maximum in the late evening (near the usual sleep time). The circadian rhythm system (Process C) promotes wakefulness during the day. It is biphasic and tends to dip in the midafternoon. Process C also reaches its peak in the evening to counterbalance the accumulation of homeostatic drive that has built up throughout the day and it begins to fall just before the usual bedtime. This system promotes wakefulness during the day and consolidates sleep at night.Source. Reprinted from Buysse DJ (ed): Sleep Disorders and Psychiatry (Review of Psychiatry Series, Vol 24, No 2; Oldham JM and Riba MB, series editors). Washington, DC, American Psychiatric Publishing, 2005, p. 191. Copyright 2005, American Psychiatric Publishing. Used with permission.

FIGURE 22–4. Sleep–wake diaries.A, In a graphic sleep diary, the subject "blocks out" the times he or she was actually asleep. In this example, the subject had very irregular sleep timing with some very long sleep episodes. B, In a text sleep diary, the subject writes in the times of going to bed, waking up, napping, and so on.Source. Reprinted from Buysse DJ (ed): Sleep Disorders and Psychiatry (Review of Psychiatry Series, Volume 24, Number 2; Oldham JM and Riba MB, series editors). Washington, DC, American Psychiatric Publishing, 2005, p. 16. Copyright 2005, American Psychiatric Publishing. Used with permission.

FIGURE 22–5. A 30-second epoch of a typical clinical polysomnogram (PSG).In addition to an electroencephalogram (EEG [C4-A1A2, C3-A1A2, O2-A1A2]), electrooculogram (EOG [EOG1-A1A2, EOG2-A1A2]), and electromyogram (EMG [EMG1]), a clinical PSG includes additional channels for monitoring leg movements (anterior tibialis leads [TIBS EMG]), breathing patterns (nasal pressure [RESPRS], oral–nasal thermistors [RESP]), chest and abdominal wall movements (THOR EFF, ABDO EFF), oximetry (OXIM), and electrocardiogram (ECG [ECG1]).Source. Reprinted from Buysse DJ (ed): Sleep Disorders and Psychiatry (Review of Psychiatry Series, Volume 24, Number 2; Oldham JM and Riba MB, series editors). Washington, DC, American Psychiatric Publishing, 2005, p. 18. Copyright 2005, American Psychiatric Publishing. Used with permission.

FIGURE 22–6. Heuristic model of the development of insomnia.This behavioral model of insomnia proposes that individuals have varying predisposition for insomnia and that specific precipitating factors will lead vulnerable individuals to cross the insomnia "threshold." Behavioral factors lead to perpetuation of the insomnia after the original precipitants have receded. The y axis indicates sleep disturbance (higher numbers = worse), and the x axis represents successive stages of insomnia.Source. Adapted from Spielman AJ: "Assessment of Insomnia." Clinical Psychology Review 6:11–25, 1986.

FIGURE 22–7. Obstructive apnea and obstructive hypopnea.A, Diagrammatic representation of obstructive apnea. Increasing ventilatory effort is seen in the rib cage, the abdomen, and the level of esophageal pressure (measured with an esophageal balloon), despite lack of oronasal airflow. Arousal on the electroencephalogram (EEG) is associated with increasing ventilatory effort, as indicated by the esophageal pressure. Oxyhemoglobin desaturation follows the termination of apnea. Note that during apnea, the movements of the rib cage and the abdomen (Effort) are in opposite directions (arrows) as a result of attempts to breathe against a closed airway. Once the airway opens in response to arousal, rib-cage and abdominal movements become synchronous. B, Diagrammatic representation of obstructive hypopnea. Decreased airflow is associated with increasing ventilatory effort (reflected by the esophageal pressure) and subsequent arousal on the EEG. Rib-cage and abdominal movements are in opposite directions during hypopnea (arrows), reflecting increasingly difficult breathing against a partially closed airway. Rib-cage and abdominal movements become synchronous after arousal produces airway opening. Oxyhemoglobin desaturation follows the termination of hypopnea.Source. Adapted from Strollo PJ, Rogers RM: "Obstructive Sleep Apnea." New England Journal of Medicine 334:99–104, 1996.

FIGURE 22–8. Potential sites of airway instability.Cross-sectional view of the upper airway depicting the potential sites of airway instability (arrows).Source. Reprinted from Buysse DJ (ed): Sleep Disorders and Psychiatry (Review of Psychiatry Series, Volume 24, Number 2; Oldham JM and Riba MB, series editors). Washington, DC, American Psychiatric Publishing, 2005, p. 82. Copyright 2005, American Psychiatric Publishing. Used with permission.

FIGURE 22–9. Upper airway in obstructive sleep apnea, without treatment and with CPAP treatment.Cross-sectional view of the upper airway, illustrating closure at the level of the palate and base of tongue typically seen in obstructive sleep apnea (A) and when the airway is pneumatically splinted open with continuous positive airway pressure (CPAP) (B).Source. Reprinted from Buysse DJ (ed): Sleep Disorders and Psychiatry (Review of Psychiatry Series, Vol 24, No 2; Oldham JM and Riba MB, series editors). Washington, DC, American Psychiatric Publishing, 2005, p. 93. Copyright 2005, American Psychiatric Publishing. Used with permission.

FIGURE 22–10. Surgical treatment for adult obstructive sleep apnea.A, Appearance of the oropharynx prior to uvulopalatopharyngoplasty (UPP), with dotted line identifying site of incision. B, Postoperatively, with sutures in place. C, Phase I, UPP and genioglossal advancement. D, Phase II, maxillomandibular advancement.Source. Reprinted from Buysse DJ (ed): Sleep Disorders and Psychiatry (Review of Psychiatry Series, Volume 24, Number 2; Oldham JM and Riba MB, series editors). Washington, DC, American Psychiatric Publishing, 2005, pp. 98–99. Copyright 2005, American Psychiatric Publishing. Used with permission.

FIGURE 22–11. Schematic representations of normal sleep and circadian rhythm sleep disorders.Data are shown for 7 days and nights for each condition. Black bars: Sleep; Open rectangles: Wakefulness. For each hypothetical condition, sleep–wake data are "double plotted" (i.e., each day's data are shown both to the right of and below the previous day) to facilitate viewing the pattern across days. Each horizontal line shows 2 days; the heavy vertical line separates successive days. The dashed vertical line indicates midnight. For comparative purposes, each condition is shown with a total sleep time of approximately 8 hours. A, Normal sleep. Sleep hours across successive days fall at about midnight to 7:00 a.m.B, Delayed sleep phase disorder (DSPD). Sleep hours are consistently delayed, with average sleep times of approximately 4:00 a.m. to noon. C, Advanced sleep phase disorder (ASPD). Sleep hours are consistently advanced, with average sleep times of approximately 8:00 p.m. to 4:00 a.m.D, Nonentrained type. Sleep hours are progressively later each day, following an underlying circadian rhythm period closer to 25 hours than 24. E, Irregular sleep–wake type. Sleep–wake hours occur irregularly over the 24-hour day, with no discernible circadian pattern.

FIGURE 22–12. Polysomnographic recording of periodic limb movements of sleep.EEG = electroencephalogram; EMG = electromyogram; R.A.T. = right anterior tibialis; L.A.T. = left anterior tibialis.Source. Reprinted from Czeisler CA, Winkelman JW, Richardson GS: "Sleep Disorders," in Harrison's Principles of Internal Medicine, 16th Edition. Edited by Kasper DL, Braunwald E, Fauci A, et al. New York, McGraw-Hill Professional, 2004, pp. 153–162. Copyright 2004, The McGraw-Hill Co. Used with permission.
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TABLE 22–1. Physiological characteristics of sleep–wake states
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TABLE 22–2. Medical and psychiatric disorders and conditions associated with insomnia
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TABLE 22–3. Medications and substances associated with insomnia
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TABLE 22–4. ICSD-2 sleep disorder classifications
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TABLE 22–5. Cognitive-behavioral interventions for insomnia
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TABLE 22–6. Benzodiazepine receptor agonists: pharmacokinetics
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TABLE 22–7. Summary of other drugs used to treat insomniaa
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TABLE 22–8. Comorbidities and consequences associated with obstructive sleep apnea syndrome
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TABLE 22–9. Common alerting agents for the treatment of excessive daytime sleepiness
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TABLE 22–10. Overview of parasomnias
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Human sleep is regulated physiologically by the interaction of homeostatic sleep drive and the circadian timing system. Dysregulation of these factors can contribute to insomnia, hypersomnia, and circadian rhythm sleep disorders. Behavioral treatments of sleep disorders work in part by reinforcing the activity of these regulatory processes.

Insomnia is a complaint of poor sleep and impaired daytime function in an individual with adequate sleep opportunity. Efficacy has been well demonstrated for behavioral treatments and BzRAs.

OSA should be suspected in overweight patients with daytime sleepiness, loud snoring, and neurocognitive symptoms including depression. Continuous positive pressure applied via nasal mask is an efficacious first-line treatment.

Narcolepsy, a disorder characterized by extreme sleepiness, cataplexy, and sleep-related hallucinations and paralysis, is caused by dysfunction of hypocretin-containing neurons in the hypothalamus. Treatment includes stimulants for improving daytime sleepiness and agents such as antidepressants or sodium oxybate to control cataplexy.

CRSDs result from misalignment of the individual's circadian timing system with the light–dark cycle of the work, social, or physical environment. Behavioral interventions, appropriately timed exposure to light and darkness, and exogenous melatonin may all improve circadian alignment.

RLS is characterized by unpleasant feelings in the legs and an urge to move, which are temporarily relieved by movement. Efficacious treatments include dopamine receptor agonists, BzRAs, antiepileptic drugs, and opiate analgesics.

Parasomnias are abnormal behavioral or affective events that occur in association with sleep or arousals from sleep. Distinctive clinical features characterize those occurring in association with NREM sleep and those occurring in association with REM sleep.

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Circadian rhythms are generated and controlled within the central nervous system (CNS). The major pacemakers of the circadian system are located in. . .
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Which of the following are physiological characteristics of rapid eye movement (REM) sleep?
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According to the International Classification of Sleep Disorders, 2nd Edition (ICSD-2; American Academy of Sleep Medicine 2005), bruxism is an example of what type of sleep disorder?
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