The most prominent symptom of obstructive sleep apnea syndrome (OSAS) is excessive daytime sleepiness (EDS). There is significant morbidity associated with EDS. EDS is the symptom which brings the patient to medical attention and the symptom which must be clinically monitored during treatment. Much evidence suggests that the major cause of the EDS of OSAS is sleep fragmentation. But little is yet known regarding the recovery process of sleep and alertness after treatment, particularly the acute versus chronic impact of sleep fragmentation on the recovery process. In monitoring EDS, recognition of exacerbating factors is important and one such factor, not studied, but typically mentioned by patients, is alcohol. Since studies in other populations have shown an interaction of alcohol and basal sleepiness on daytime function, the morbidity of EDS in OSAS must be assessed in patients consuming alcohol. Finally, the impact of EDS on neuropsychological function also contributes to the behavioral morbidity of OSAS. Both hypoxemia and sleepiness contribute to these neuropsychological deficits, but the aspects of neuropsychological function mediated by EDS have not been identified. This proposal outlines a series of studies to further understand the causes, exacerbating factors, and other consequences of EDS. A 32-hour protocol previously shown to maximize recovery sleep will be used to define the nature of recovery sleep in acute versus chronic sleep fragmentation. To evaluate alcohol as a risk factor in EDS related impairment, both impairing and non-impairing doses of alcohol will be studied in OSAS patients. Finally, the EDS mediated neuropsychological deficits will be identified by studying OSAS patients with and without hypoxemia, by comparing patients with sleepiness and no hypoxemia (i.e., narcolepsy) and patients with hypoxemia and no sleepiness (i.e., COPD) and also by studying OSAS patients after varying amounts of recovery sleep.
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