Sleep and Sleep Disturbance

Approximately 30% of our life is spent asleep (up to 50% in infants). The interaction between sleep and disease, however, remains a neglected area of study. Although we now have a much clearer understanding of the normal structure of sleep, despite 40 years of study there remain unresolved questions regarding the consequences of sleep disturbance and sleep deprivation. Sleep is not a heterogeneous state. Normal sleep is comprised of two distinct states, rapid eye movement (REM) and non-rapid eye movement (NREM), each being associated with distinct EEG and behavioral characteristics (1). Each sleep state can be further subdivided. NREM is comprised of four distinct patterns, ranging from stage 1 (light sleep) to stage 4 (deep sleep), while REM can be subdivided into tonic and phasic periods. During a normal night, an adult has four or five sleep cycles, each approximately 90 minutes in length, characterized by alternating periods of NREM and REM sleep. During the initial sleep cycles, slow wave (stage 3 and 4) NREM sleep is the predominant pattern, with increasing amounts of REM and stage 1 and 2 NREM sleep as the night progresses. Although any physician can attest to the consequences of insufficient sleep, the precise role of sleep and the specific function of each sleep state remain matters for debate. NREM sleep is associated with a reduction in motor tone and respiratory and cortical activity, as well as a slowing of metabolic rate, compatible with a quiescent or reparative function. REM sleep is characterized by both increased cortical activity (2), and increased CNS glucose metabolism (3). It is believed that REM sleep has a role in integration of CNS activity, either in consolidating new information (explaining the predominance of REM sleep in infancy) or in integration of new information into long-term memory (4). It is fairly easy to document the behavioral consequences of sleep deprivation in adults, “being sleepy” being primarily due to overall loss of slow wave sleep, resulting in measurable decrements both in alertness and intellectual performance (5). Initial studies simply looked at the effect of overall sleep deprivation on daytime functioning. As discussed by Stores et al., subsequent studies have suggested that not only overall sleep quantity, but also sleep quality and the consequences of sleep fragmentation may have significant impact on subsequent daytime functioning (5,6). Moreover, sleep has roles other than just maintaining alertness. Recent work has shown a complex interrelationship between sleep and neuroendocrine, immune function, and thermal regulation (7), sleep disturbance having an adverse impact on these systems. What remains unclear is how sleep disturbance affects these systems, and precisely how much sleep disturbance, as well as which sleep state and over how long a period, is required to have a significant impact. The impact of sleep disturbance in children is even less well established. First, children spend significantly more time in REM sleep than do adults (up to 50% of overall sleep compared to as little as 6% in adults) (8). As noted, the biologic necessity for REM remains unclear, but its predominance during childhood would suggest a role in intellectual maturation or organization. Since muscle hypotonia is a primary feature of REM sleep, obstructive sleep apnea in children tends to occur primarily during this sleep stage, frequently resulting in selective REM sleep fragmentation. This REM sleep fragmentation has the potential for subtle but long-term impact on intellectual performance. It is, however, difficult to document the consequences of sleep fragmentation in children, since their symptoms differ significantly from adults. Rather than producing hypersomnolence, sleep deprivation in children produces symptoms of ir-