Monday, October 12, 2009

Effects of Alcohol and Sleep Restriction on Simulated Driving Performance in Untreated Patients With Obstructive Sleep Apnea

Effects of Alcohol and Sleep Restriction on Simulated Driving Performance in Untreated Patients With Obstructive Sleep Apnea: "

Background: Because of previous sleep disturbance and sleep hypoxia, patients with obstructive sleep apnea (OSA) might be more vulnerable to the effects of alcohol and sleep restriction than healthy persons.

Objective: To compare the effects of sleep restriction and alcohol on driving simulator performance in patients with OSA and age-matched control participants.

Design: Driving simulator assessments in 2 groups under 3 different conditions presented in random order.

Setting: Adelaide Institute for Sleep Health, Sleep Laboratory, Adelaide, Australia.

Participants: 38 untreated patients with OSA and 20 control participants.

Measurements: Steering deviation, crashes, and braking reaction time.

Intervention: Unrestricted sleep, sleep restricted to a maximum of 4 hours, and ingestion of an amount of 40% vodka calculated to achieve a blood alcohol level of 0.05 g/dL.

Results: Patients with OSA demonstrated increased steering deviation compared with control participants (mean, 50.5 cm [95% CI, 46.1 to 54.9 cm] in the OSA group and 38.4 cm [CI, 32.4 to 44.4 cm] in the control group; P < 0.01) and significantly greater steering deterioration over time (group by time interaction, P = 0.02). The increase in steering deviation after sleep restriction and alcohol was approximately 40% greater in patients with OSA than in control participants (group by condition interaction, P = 0.04). Patients with OSA crashed more frequently than control participants (1 vs. 24 participants; odds ratio [OR], 25.4; P = 0.03) and crashed more frequently after sleep restriction (OR, 4.0; P < 0.01) and alcohol consumption (OR, 2.3; P = 0.02) than after normal sleep. In patients with OSA, prolonged eye closure (>2 seconds) and microsleeps (> 2 seconds of theta activity on electroencephalography) were significant crash predictors (OR, 19.2 and 7.2, respectively; P < 0.01). Braking reaction time was slower after sleep restriction than after normal sleep (mean, 1.39 [SD, 0.06] seconds vs. 1.22 [SD, 0.04] seconds; P < 0.01) but not after alcohol consumption. No group differences were found.

Limitation: Simulated driving was assessed rather than on-road driving.

Conclusion: Patients with OSA are more vulnerable than healthy persons to the effects of alcohol consumption and sleep restriction on various driving performance variables.

Primary Funding Source: Australian National Health and Medical Research Council.

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