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A
conceptual model for homeostatic sleep has largely been developed and confirmed
over the past two decades, however the brain mechanisms underlying this
model remain unknown. In this model, a sleep process (Process S)
builds throughout the waking period and is discharged, or restored, during
sleep. Extensive research has shown that EEG power in the delta frequency
spectrum (delta power) is highly correlated with Process S and accordingly,
that sleep deprivation (an increase in Process S) significantly alters
delta power during recovery sleep. Thus, sleep deprivation (or, for
that matter, recovery sleep) can be used as a tool to modulate delta power
in a predictable fashion. Recent functional neuroimaging and EEG
topography studies indicate that sleep homeostasis may have some localization
within the brain. In order to clarify whether there is regional localization,
this pilot study will analyze the effects of both 38 hours of sleep deprivation
and recovery sleep on waking A.M. regional cerebral metabolism and NREM
sleep regional cerebral metabolism. To our knowledge, this will
be the first functional neuroimaging study to compare baseline NREM sleep
to recovery NREM sleep. It will also be the first FDG PET study
to compare post-sleep deprivation waking to post-recovery sleep waking.
Results from this pilot study will be used to generate effect sizes to
be used in developing a confirmatory study. We hypothesize that:
1) delta EEG power during NREM sleep will increase from baseline NREM sleep
to recovery NREM sleep; 2) relative cerebral metabolism in the prefrontal
cortex will decrease from baseline NREM sleep to recovery NREM sleep; 3)
waking A.M. prefrontal cortex glucose metabolism will decline from baseline
to post-sleep deprivation and normalize after recovery sleep; and 4) the
degree of this respective decline and increase will be directly proportional
to performance on neuropsychological tests that have been shown to be sensitive
to sleep loss.
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