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 polysomnograp
hic data from 1,521 patients with OSAS where increasing arousal indice
s were associated with increased duration of stage 1 sleep and concomi
tant reduction in total sleep time. Similar results have been found in
paradigms in which sleep was experimentally fragmented in healthy ind
ividuals. It appears that chronic fragmentation of sleep, whether by a
pneas or acoustic stimuli, leads to cumulative homeostatic pressure fo
r sleep. which may explain a number of phenomenan characteristic of bo
th 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 awaken
ings, (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 f
ragmentation across nights, neither of which have been adequately mode
led in experimental studies of healthy subjects.