Alcohol Effects on Driving Performance and Neurocognition in Obstructive Sleep Apnoea.

Introduction: Studies using neurocognitive tasks, event-related potentials (ERP) and driving simulators indicate neurobehavioural deficits in Obstructive Sleep Apnoea (OSA), likely due to hypoxic pre-frontal cortex damage. Low-dose alcohol (0.035 g/dL) has been found to negatively affect driving ability in young healthy subjects. We hypothesise that the apneic brain, exposed to alcohol, may have reduced ability to compensate and maintain neurocognitive performance. Methods: Preliminary data from our study of driving and neurocognitive impairment in OSA was analysed for 5 severely affected patients (mean [SD]: age = 42.8 [9.9] y; BMI = 43.1 [9.6]; RDI = 68.4 [20.5]/ hr), and 4 healthy controls (age = 44.25 [9.0] y; BMI = 23.5 [2.8]; RDI = 11.5 [2.7]/hr). All completed 90 min of simulated mid-afternoon driving following alcohol consumption (BAC 0.05 g/dL). EEG was recorded and analysed for alpha/theta activity, and subjective sleepiness/ performance recorded. Following the drive, neurocognitive testing including ERP was administered. Results: Repeated Measures ANOVA showed that alcohol increased subjective sleepiness with significant group (p = 0.043), condition (p < 0.001) and time (p = 0.005) effects. Similarly, alcohol decreased subjective driving performance, with significant effects for group (p = 0.03), condition (p = 0.015) and time nearing significance (p = 0.056). Steering deviation data showed differences which were approaching significance for group (p = 0.059) and time (p = 0.073). No significant differences were found for neurocognitive or ERP measures. Conclusion: Preliminary data show differences between OSA and control groups under both normal and alcohol conditions, indicating increased sleepiness in OSA, possibly affecting driving ability. Neurocognition in OSA appears unaffected by low-dose alcohol. Individual differences and small sample size may contribute to these early findings.