Chapter 15: Neuropsychiatry of Sleep and Sleep Disorders

INTRODUCTION

Sleep comprises roughly one-third of an adult’s life. It is an active physiological process with wide effects on health. Poor/insufficient sleep has the potential to aggravate any disease and many diseases impact sleep. Therefore, an understanding of sleep and sleep disorders is essential for the practice of neuropsychiatry. Sleep disorders epitomize neuropsychiatry, capturing the overlap between altered brain networks, behavior, and cognition. Sleep deprivation impairs almost all cognitive functions, and evidence has rapidly accumulated implicating amount and quality of sleep in disturbances of memory processing and consolidation. Furthermore, sleep disorders contribute to the morbidity of both psychiatric and neurological disease. The likelihood of having sleep problems increases with the number of psychiatric diagnoses,¹ and parasomnias are more common in psychiatric populations.² Sleep disturbance is now a well-recognized common consequence of traumatic brain injury (TBI) across all levels of TBI severity,³ and sleep disruption is also prevalent in neurodegenerative disorders.⁴ Sleep disorders (e.g., obstructive sleep apnea [OSA], REM behavior disorder [RBD], other parasomnias) should be carefully considered in patients with a variety of cognitive and behavioral presenting complaints. This chapter will review the basics of sleep physiology, our present understanding of the purpose of sleep, and briefly review sleep disorders.

BASICS OF HUMAN SLEEP PHYSIOLOGY

In humans, sleep typically occurs during the biological night—a phase regulated by the circadian cycle. Sleep is characterized by relative physical inactivity and unawareness of the surrounding environment, higher melatonin levels, lower cortisol levels, lower urine volume, and lower body temperature.

The most frequently used technique for studying sleep in humans is polysomnography (PSG), which records simultaneously electroencephalography (EEG), eye movements (EOG), and muscular activity (EMG). PSG data help distinguish non-rapid eye movement (NREM) sleep from rapid eye movement (REM) sleep. Physiologically, normal NREM sleep starts with a gradual change in consciousness, loss of memory for the immediately preceding interval, and overall slower activity, with a decreased heart rate (40–90 BPM), regular, slower respirations, and a mild decrease in oxygen saturation (about 2%), reflecting a lower brain metabolic activity and decreased demand. Electrographically, NREM sleep is associated with synchronous neuronal activity, represented on the EEG by high-amplitude, low-frequency rhythms. NREM sleep can be further subdivided into three distinct stages. Stage N1 represents the transition from wakefulness to sleep and is usually of short duration. It is characterized by slow roving eye movements, disappearance of the alpha activity on EEG, and appearance of slower theta rhythms. Stage N2 is the stage occupying the most time during the night, and is characterized by K complexes (biphasic negative-positive waveforms of high amplitude, 0.5 seconds in duration) and sleep spindles (brief sigma frequency activity of 15 Hz for less than a second). Progressively, the appearance of slow delta waves will delineate the transition of stage N2 to stage N3. After about 90 minutes of sleep, the first REM period is seen, characterized by eye movements, often ...