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The study of human sleep is a remarkably young field. Until the 1930s, sleep was viewed as a passive state during which the brain was “turned off.” As such, there was little interest in further characterization of normal sleep or exploration of sleep disorders. In 1937, A. L. Loomis first described the characteristic electroencephalographic patterns of the stages of NREM sleep, challenging the notion of sleep as a homogeneous and passive state.1 This was followed in 1951 by the discovery of REM sleep and its correlation with dreaming.2 A schema of sleep architecture consisting of repeated cycles of NREM and REM sleep was formulated shortly thereafter, a concept that has persisted largely unchanged into the modern era of sleep medicine.

Discovery of the electroencephalographic substrate of sleep prompted increasing curiosity about sleep physiology. Overnight polysomnography—a technique of simultaneous recording of sleep EEG, respiratory parameters, and muscle activity—was developed and employed to describe normal and abnormal sleep patterns (Fig. 18-1). During the second half of the twentieth century, polysomnographic characterization of obstructive sleep apnea (OSA), insomnia, periodic leg movements of sleep (PLMS), REM behavior disorder (RBD), and narcolepsy facilitated improved understanding of the pathophysiology of these disorders and expanded treatment options.

Figure 18-1

Polysomnography. A 30-second epoch of sleep recorded by polysomnography. Eye movements, muscle tone in the chin and legs, 6 EEG channels, EKG, nasal airflow, and respiratory effort are depicted here.

In addition to its utility in primary sleep disorders, polysomnography was also applied to the study of a variety of neurological and psychiatric conditions. In patients with depression, consistent abnormalities of sleep architecture were identified.3 These included shortened REM latency (time from sleep onset to the first episode of REM), prolongation of the first REM period, and increased density of eye movements during REM. These observations led to the hypothesis that “disinhibition” of REM sleep may play a role in the pathophysiology of depression. Furthermore, REM abnormalities may constitute a biomarker that predicts the onset of new depression and increased vulnerability to relapse in remitted patients.4 Thus, the abnormalities in sleep seen in depressed patients may not be merely incidental but may be closely tied to the precipitation and perpetuation of the illness.

In light of these significant sleep abnormalities in depressed patients, primary sleep disorders may also be expected to affect mood. Indeed, a markedly increased risk for depression has been identified in a variety of sleep disorders, including insomnia, OSA, and restless legs syndrome (RLS), among others. Recognition of these epidemiologic links has spawned further research into the pathophysiologic and prognostic implications of sleep disorders in depressed patients, investigations that have improved understanding of both conditions. In this chapter, we discuss the bidirectional and complex relationships between sleep disorders and depression. Although much is known about the depression–sleep ...

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