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It has been shown that many patients with obstructive sleep apnea (OSA) have increased auto accidents and impaired performance on laboratory driving tests (see Article #1, Article #7, and Article #25 at this website). This is obviously an issue of great concern as it might eventually lead to driving restrictions on sleep apneics, and it is important to determine whether effective treatment can alleviate these driving impairments. The authors approached this issue by using their divided attention driving test (DADT) to retest patients with OSA several months after starting CPAP, while also retesting controls subjects who had undergone testing at the previous time.
The DADT consists of a driving simulation machine equipped with a steering wheel and a computer screen on which is displayed either side of a schematic roadway, an icon to show the driver's position, and a "target" which the driver attempts to follow, while his "vehicle" travels at constant speed but is pushed randomly from side to side as if by gusts of wind. The "divided attention" part of the task involves pushing a button on the wheel corresponding to the corner of the screen in which a target number appears from time to time. The main outcome measures on this test include the tracking error (distance from vehicle to target), number of times the vehicle goes out of bounds, and numbers of correct, incorrect, and missed target numbers.
Each such test was administered for 20 minutes prior to each of four daytime Multiple Sleep Latency Tests following a full night's sleep in the laboratory for OSA patients, at home for controls.
Of the 21 patients with OSA who took the initial pre-treatment testing and then started CPAP, 17 were available for retesting 1-12 months after starting CPAP. Of the control subjects initially tested, 18 were available for retesting at the same interval. Note that patients, all male, had originally presented with complaints of snoring and/or daytime sleepiness and had been excluded for use of sedatives or stimulants, diagnoses other than OSA, or Apnea/Hypopnea Index (AHI) less than 15. Age- and sex-matched controls had no complaints of sleepiness and AHI less than 15, without any use of drugs active on the central nervous system. The two groups were similar in age (OSA vs. controls, 49.7 SD=11.2 vs. 45.6 SD=14.6).
At pre-treatment testing, controls averaged a normal AHI of 3.1 (SD=6.1) and OSA patients averaged a much higher AHI of 73.0 (28.9), whereas with retesting on CPAP OSA patients had much lower, essentially normal AHIs (6.5, SD=7.1). Likewise, at pretreatment OSA patients had more awakenings (32.8 SD=16.7) than controls (27.4 SD=9.2) and on CPAP had essentially the same number as controls (26.2 SD=12.2). Sleep stage changes in OSA patients were not initially more frequent than in controls (18.4 SD=6.9 vs. 17.3 SD=15.5) but they were significantly reduced on CPAP (13.7 SD=3.9--note also the reduced variability). Prior to treatment, OSA patients had many more arousals/hour than controls (67.5 SD=28.5 vs. 9.9 SD=7.7) while on CPAP the patients had much reduced and essentially normal frequency of arousals (11.4 SD=5.9). Prior to treatment, sleep stages 1 and 2 did not differ significantly between OSA patients and controls, nor did they change significantly in OSA patients on CPAP, although such changes as existed (more light sleep in OSA prior to treatment) were in the expected directions. On the other hand, both slow wave sleep (stages 3 and 4) and REM sleep were lower in untreated OSA patients (6.9 SD=6.8 and 13.2 SD=6.3) than in controls (18.5 SD=7.2 and 19.0 SD=6.4) and after CPAP these were increased in OSA patients (15.0 SD=5.8 and 22.1 SD=6.1) as expected. Patients claimed to use CPAP at least 6 hours a night, at least 6 nights a week. The fact that their sleep parameters largely normalized supports this.
The key finding, of course, derived from the repeat DADT results. One reason for using controls here was to control for the effect of improvement through learning as a result of prior testing. However, neither patients nor controls showed much evidence of learning effects, either from initial testing to later retesting, or within a series of trials at a given testing. The main effect found was one of marked improvement in all measures in patients treated for OSA. Tracking errors decreased significantly, by about half, from 228 (17.2) to 113 (9.5). Number of correct responses improved significantly though to a lesser degree, from 36.2 (0.5) to 37.8 (0.5). Missed responses decreased significantly, from 3.7 (0.5) to 2.2 (0.5). Out of bounds errors decreased markedly and significantly, from 12.6 (2.1) to 2.6 (1.2). The only measure that failed to improve significantly was response time, which decreased from 3.2 (0.1) to 2.8 (0.1). At treated retesting, OSA patients as a whole, however, did not do quite as well as control subjects on initial or retesting--specifically, correct and missed responses were still significantly different from controls--but DADT outcome measures generally fell in the range of controls, except for one patient whose persistent symptoms seemed to represent sleep fragmentation from previously unrecognized periodic leg movements of sleep.
Note also that sleepiness, as measured by the MSLT, improved in treated OSA patients from 7.2 minutes sleep latency (SD=0.8) to 13.2 (0.8), slightly better than the control averages (12.3 SD=0.9 and 12.9 SD=0.8). However, improvement in this variable correlated strongly with improvement in the DADT variable of tracking errors, but not with other variables of the DADT.
The authors had retested their patients an average of 9.2 (SD=4.2) months after starting CPAP, but they had reexamined two patients after one month and found their tracking errors returned to the control range. They noted other results suggesting that sleepiness improves within a couple of weeks of starting CPAP and suggested that improvement might occur much earlier than the 9 months average they allowed between testing. They mentioned other studies showing performance improvement with CPAP on driving simulation, and one showing improvement after UPPP. However, clinical history reports have been contradictory, some finding a fall in reported accidents with treatment, others a rise, perhaps related to the willingness of subjects to admit to accidents depending on their fears of loss of licensure.
This type of study and its results seem to me vitally important to the vast majority of people with OSA who drive and consider it important if not crucial that they be able to continue doing so. As evidence accumulates for increased risk of accidents and impairment in driving-related skills comparable to intoxicated alcoholics in untreated sleep apnea, it is critical to demonstrate that effective treatment generally reverses these impairments and allows for safe driving.
In rejoicing at such findings, however, we must keep in mind some reservations: first, that this is just a laboratory test presumed related to driving skill and that the most crucial test will depend on actual accident statistics, or possibly in vivo driving tests in real cars; second, that treated patients did not quite attain the levels of accuracy seem with normals and the question may be raised as to just how much devaiation from normalcy raises the accident risk significantly; third, that nine months of treatment is a long time to wait to drive if one is warned against driving, and that from a practical standpoint it will be very important for similar studies to take place at much shorter intervals of 2-4 weeks after starting treatment.
Once studies like this have established a basis to believe in the efficacy of CPAP in reversing driving impairment, it will be even more crucial that other studies be done with other treatments for people who decide to adopt these approaches. In fact, without such studies, competing treatments which may be quite effective and advantageous for some, may find themselves unable to compete. Still more problematic will become the position of those diagnosed with sleep apnea who refuse treatment or use it erratically, who will have to be viewed as essentially untreated and subject to all the increased driving risks demonstrated for people in that category. This could be helpful in pushing people who need a push into getting treatment, but until the boundary of OSA severity is established which makes for unsafe driving, it is possible that people with relatively mild OSA who may not need treatment, or no more treatment than assuming a different sleeping position, will find themselves forced into CPAP in order to retain their driving licenses. Incidentally, licensure may not be all that is at stake; insurability as a driver may be severely compromised by untreated sleep apnea.
Finally, thinking of insurance, those patients with OSA who have difficulty getting benefits for their diagnosis and treatment from their insurers may find this and other articles useful to send to those third parties, as evidence that deprivation of these benefits may result in removal of one's ability to drive, to say nothing of accidental injury and death to oneself, one's family, and other people on the road!
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