OBJECTIVES: This study evaluated slow wave activity homeostatic response to a mild sleep challenge in alcohol-dependent adults compared to healthy controls. DESIGN: Participants maintained a 23:00-06:00 schedule for 5 days verified by actigraphy and diary, followed by 3 nights in the lab: adaptation, baseline, and a sleep delay night with an 02:00-09:00 schedule. SETTING: Sleep ' Chronophysiology laboratory. PARTICIPANTS: 48 alcohol-dependent adults (39 men, 9 women) who were abstinent for at least 3 weeks and 16 healthy control adults (13 men, 3 women), 21-55 years of age participated in study. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Slow wave EEG activity (SWA) in consecutive NREM periods was compared between baseline and sleep delay nights and between AD and HC groups, using age and sex as statistical covariates. The AD group showed a blunted SWA response to sleep delay with significantly lower SWA power than the HC group. Exponential regression analyses confirmed lower asymptotic SWA with a slower decay rate over NREM sleep time in the AD group. Results were similar for raw SWA and %SWA on the delay night expressed relative to baseline SWA. CONCLUSIONS: Alcohol dependence is associated with impaired SWA regulation and a blunted response to a mild homeostatic sleep challenge.
OBJECTIVES: This study evaluated slow wave activity homeostatic response to a mild sleep challenge in alcohol-dependent adults compared to healthy controls. DESIGN:Participants maintained a 23:00-06:00 schedule for 5 days verified by actigraphy and diary, followed by 3 nights in the lab: adaptation, baseline, and a sleep delay night with an 02:00-09:00 schedule. SETTING: Sleep ' Chronophysiology laboratory. PARTICIPANTS: 48 alcohol-dependent adults (39 men, 9 women) who were abstinent for at least 3 weeks and 16 healthy control adults (13 men, 3 women), 21-55 years of age participated in study. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Slow wave EEG activity (SWA) in consecutive NREM periods was compared between baseline and sleep delay nights and between AD and HC groups, using age and sex as statistical covariates. The AD group showed a blunted SWA response to sleep delay with significantly lower SWA power than the HC group. Exponential regression analyses confirmed lower asymptotic SWA with a slower decay rate over NREM sleep time in the AD group. Results were similar for raw SWA and %SWA on the delay night expressed relative to baseline SWA. CONCLUSIONS:Alcohol dependence is associated with impaired SWA regulation and a blunted response to a mild homeostatic sleep challenge.
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