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Damaged Brains?

© Kerrin Leon White

Few research findings raise more anxiety among sufferers from Obstructive Sleep Apnea (OSA) than impairment shown on tests of neuropsychological function--attention, memory, speed of thinking. Because such abnormalities often occur in diseases of the brain, they lead people to wonder whether OSA can cause "brain damage."

Especially alarming--though less well established--are suggestions that these impairments may persist long after commencement of treatment with Continuous Positive Airway Pressure (CPAP).

How much basis exists for these fears?

We should distinguish between brain dysfunction that occurs only during periods of excessive sleepiness, and that which occcurs even when the patient feels fully alert. Unfortunately, most studies fail to establish such distinctions.

No one should be surprised to learn that sleepiness, a common result of not only OSA but even more commonly of "voluntary sleep deprivation" (such as students impose upon themselves during "all nighters")can cause poor attention and memory retention. In general, this unquestionable effect of sleep deprivation gets less attention than it deserves from most sectors of our society.

The importance of sleepiness as a cause of impaired brain function stems from the fact that typically, the Excessive Daytime Sleepiness (EDS) of OSA varies from hour to hour during the day, just as alertness varies in all people as a result of biological rhythms. The EDS of OSA may be more severe or prolonged than that of the ordinary person who has lost some sleep--but it is rarely constant or invariable. The person with OSA may suffer impairment at one time and not another: this does not represent what most people would call "brain damage." Rather, it is what I would call a "state-dependent" impairment such as that due to intoxication with alcohol and drugs.

Comparing the effect of sleepiness with that of intoxication seems justified from studies showing equivalent impairment in drunk versus sleepy drivers.

Confusion may arise from the assumption that CPAP treatment, properly prescribed and used, should almost always resolve all symptoms of OSA, including EDS. However, evidence mounts that, like most chronic diseases, OSA often responds incompletely to the best of treatment--even in the absence of demonstrable apneas and hypopneas.

In other words, before we conclude that OSA causes "brain damage" in the usual sense of the word--meaning not a state-dependent, but a continuous impairment of mental function--we must await studies yet to take place.

At the same time, we should pay attention to recent evidence suggesting that a chronic sleep-wake disruption caused by abnormal environmental factors--such as jet lag--may result in abnormalities of the physical structure of the brain demonstratable on brain imaging. Might chronic sleep-wake disruption from any cause, including OSA, have similar effects? Again, we must await further research.