Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/68949
Type: Thesis
Title: The effects of sleep restriction and alcohol on simulated driving and cortical function in obstructive sleep apnoea.
Author: Vakulin, Andrew
Issue Date: 2011
School/Discipline: School of Medical Sciences
Abstract: Obstructive sleep apnoea (OSA) is a common sleep disorder associated with neurobehavioural daytime abnormalities including poor driving simulator performance and an increased risk of motor-vehicle accidents. Treating OSA with continuous positive airway pressure (CPAP) significantly improves many of the daytime consequences of OSA. Until recently it was believed that CPAP treatment can completely resolve excessive daytime sleepiness and neurobehavioural abnormalities associated with OSA. However, recent evidence suggests that compared to results in well-matched healthy subjects, levels of daytime vigilance and cortical activation and some domains of cognitive function in OSA patients may not return to normal, even after effective OSA treatment with good treatment compliance. Sleep restriction and low-dose alcohol consumption are common “life style” factors that have a negative impact on the central nervous system and driving performance in healthy subjects. However, their impact on driving simulator performance and cortical information processing in patients with OSA has not been examined. The hypotheses tested in the work presented in this thesis were that: a) Sleep restriction and alcohol have a greater deleterious effect on driving simulator performance and cortical information processing in untreated OSA patients than in healthy subjects. b) Treatment of severe OSA with CPAP improves, but does not normalise driving simulator performance and cortical information processing. Consequently, the broad aims were: a) To compare the effects of sleep restriction and alcohol on driving simulator performance and auditory cortical event-related potentials in OSA patients and healthy age and gender-matched controls. b) To compare driving simulator performance and auditory cortical eventrelated potentials in severe OSA patients before and after 3-months of CPAP therapy and to compare these results with those of healthy, untreated subjects also studied 3-months apart. Study 1 (CHAPTER 2) compared performance during a 90-minute simulated drive in 38 patients with OSA and 20 healthy age and gender-matched control subjects under 3 conditions studied in random order: 1) normal sleep, 2) sleep restriction (4 hours in bed on the night prior to study) and 3) low-dose alcohol (blood alcohol concentration 0.05 g/dL). Compared to control subjects, OSA patients exhibited a higher crash rate, increased overall steering deviation and more steering deterioration with time-on-task. Following sleep restriction and alcohol there was a ~40% greater increase in steering deviation in OSA patients than in control subjects. Crashes were more likely to occur in patients with OSA compared with control subjects. OSA patients were more likely to crash under sleep restriction and alcohol conditions compared to the normal sleep condition. Simulator crashes were associated with behavioural and physiological evidence of increased sleepiness. The results of this study showed that compared with healthy subjects, OSA patients have worse driving simulator performance and are more vulnerable to the effects of prior alcohol and sleep restriction on various driving performance parameters. To the extent that these simulator findings may be indicative of real on-road driving performance, it may be advisable for untreated OSA patients to avoid sleep restriction and even legal doses of alcohol prior to extended driving. Study 2 (CHAPTER 3) assessed the effectiveness of ~3 months CPAP treatment in improving driving simulator performance. Eleven severe OSA patients and nine age- and gender-matched controls were studied on two occasions 3 months apart using the same protocol as in Study 1. In the intervening period OSA patients were treated with CPAP during which they showed a high level of compliance with therapy (mean ± SD, 6.0 ± 1.4 hours/night). At baseline, OSA patients demonstrated worse driving simulator performance compared to controls under all conditions, and showed greater steering decrements following sleep restriction and alcohol than control subjects. After CPAP treatment, OSA patients showed significant improvements in steering deviation under all conditions, but steering deviation did not reach the level of control subjects and crash frequency remained significantly elevated. Braking reaction time was not significantly different between groups, conditions, or treatments and there were no significant interaction effects. Taken together, these findings suggest that CPAP treatment is only partially effective in improving driving performance during simulated long and monotonous driving. To the extent that driving simulator findings may be indicative of real onroad driving performance it may be appropriate to advise patients, even after apparent optimal CPAP treatment, to be cautious when undertaking long distance driving, as they could remain at higher than normal accident risk. Given the behavioural finding of residual driving simulator impairment in CPAPtreated, severe OSA patients in studies 1 and 2, the final study (CHAPTER 4) explored whether cortical information processing during a simple attention task demonstrated similar treatment resistant abnormalities. The effects of CPAP treatment on cortical information processing in OSA patients were examined by comparing early and late components of auditory target (odd-ball) event-related potential responses in 9 patients with severe OSA and 9 healthy age- and gendermatched controls. The results showed that compared to controls, early and late auditory event related potentials were abnormal in severe OSA patients at baseline. Specifically, N2 and P3 peaks were smaller and delayed in latency, and P2 amplitude was larger. At follow-up, P3 latency was the only measure to show improvement following CPAP treatment, but remained prolonged in patients compared to control subjects despite high CPAP treatment compliance in OSA patients (mean ± SD, 6.0 ± 1.6 hours/night). None of the abnormalities in earlier components (N2 and P2) observed at baseline changed in CPAP-treated OSA patients. In summary, driving simulator performance is impaired in patients with OSA compared to healthy controls, and patients demonstrate a greater susceptibility to the detrimental effects of sleep restriction and alcohol. Driving simulator performance is only partially improved in CPAP-treated OSA patients. Thus, it may be prudent to advise patients with OSA to be cautious and avoid sleep loss or alcohol prior to long distance driving, even when optimally treated. Residual abnormalities were also evident in auditory cortical evoked responses in optimally treated OSA patients, suggesting the possibility of a permanent reduction in information processing capacity. The mechanisms underlying the observed vulnerability to additional stressors (sleep loss and alcohol) and the residual driving performance and electrophysiological abnormalities observed in CPAP-treated patients warrants further investigation. In addition, examining how these driving simulator and electrophysiological findings relate to on-road motor vehicle accident risk in patients with OSA is another important question worthy of further investigation.
Advisor: McEvoy, Doug
Catcheside, Peter G.
Dissertation Note: Thesis (Ph.D.) -- University of Adelaide, School of Medical Sciences, 2011
Keywords: sleep restriction; alcohol; driving; obstructive sleep apnoea
Provenance: Copyright material removed from digital thesis. See print copy in University of Adelaide Library for full text.
Appears in Collections:Research Theses

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