Neurobehavioral consequences of arousals

The neurobehavioral deficits of obstructive sleep apnea syndrome (OSAS) are often attributed to the rate of respiratory disturbance or rate of arousals during sleep. However, sleep disordered breathing is also associated with other changes in sleep infrastructure that may account for cumulative waking deficits. This was illustrated in polysomnographic data from 1,521 patients with OSAS where increasing arousal indices were associated with increased duration of stage 1 sleep and concomitant reduction in total sleep time. Similar results have been found in paradigms in which sleep was experimentally fragmented in healthy individuals. It appears that chronic fragmentation of sleep, whether by apneas or acoustic stimuli, leads to cumulative homeostatic pressure for sleep, which may explain a number of phenomenon characteristic of both untreated OSAS patients and experimentally fragmented sleepers: (1) increased arousal threshold, (2) rapid return to sleep after arousal, (3) fewer awakenings over time, (4) increased sleep inertia on awakenings, (5) increased amnesia for arousals, and (6) daytime sleepiness. Elevated homeostatic drive for sleep appears to be a function of both the frequency of arousals within a night and the chronicity of sleep fragmentation across nights, neither of which have been adequately modeled in experimental studies of healthy subjects.