SEATTLE—Many people try to reduce the amount of sleep that they obtain, but increasing evidence suggests that such reductions inevitably lead to partial sleep deprivation. “Sleep restriction does not come without physiologic, cognitive, and functional costs,” said David Dinges, PhD. “There appears to be some cognitive price for every minute of sleep you reduce below what you need to endogenously sustain waking alertness.”

However, he added, “not everybody is affected as profoundly, and we don’t understand why some people suffer neurobehavioral deficits earlier and more severely than do others.” Dr. Dinges is a Professor of Psychology in Psychiatry and Chief of the Division of Sleep and Chronobiology in the Department of Psychiatry at the University of Pennsylvania School of Medicine. He presented the keynote address at the 16th Annual Meeting of the Associated Professional Sleep Societies.

Loss of sleep insidiously affects sustained attention, cognitive speed and accuracy, working memory, reaction time, and overall behavioral capability, often without the sleep-deprived person being aware of the deficits, according to Dr. Dinges. Workers in the fields of transportation, public safety, health care, and the military, as well as night shift workers, are the most critically affected by sleep debt, which refers to chronically sleeping too little each day. One of the more common ways people try to combat sleepiness is to consume caffeine, an adenosine-binding drug that is widely recognized as a “socially acceptable stimulant.” Approximately 80% of Americans (165 million people) are regular or occasional coffee drinkers, and 52% drink it daily. “The widespread consumption of caffeine in larger dosages in recent years is perhaps the most common way that millions of us attempt to promote our alertness and cognitive capability in the face of a sleep debt,” said Dr. Dinges.

In many of the studies, subjects agree to remain isolated from the outside world and be continuously monitored, in a controlled environment with no clocks, outside light, visitors, telephones, or televisions for 10 to 20 days, depending on the experiment. Such an effort requires “a small army of staff and trainees” to systematically monitor and measure 24 hours a day, the reactions of hundreds of subjects each year, he said. All participants are screened to ensure that they are medically, psychologically, and behaviorally healthy before being randomized to one of many conditions of sleep restriction and circadian displacement of sleep. In performing these dose-response experiments on the effects of chronically restricted sleep for seven to 14 days, Dr. Dinges noted that “what was discovered was that many of the published reports on chronic sleep restriction of the last 100 years missed finding the cumulative neurobehavioral deficits we observed when sleep was restricted to daily dosages below eight hours, because these earlier studies failed to adequately control how much sleep was actually obtained by subjects, their caffeine intake, and a host of other confounding variables…. This perpetuated a 30-year-old myth that you don’t need eight hours of sleep each day.” Ironically, the research being performed by Dr. Dinges resulted from the efforts that he and his collaborators were making on behalf of various federal agencies “to find ways to reduce sleep need.”

LURKING SLEEP

Another important development in our understanding of sleepiness was the concept of “microsleeps,” said Dr. Dinges, which refer to the sudden and often very brief initiation of sleep during wakefulness that results in the characteristic “lapses” during performance by sleep-deprived subjects. Dr. Dinges asserts that both elevated sleep latency (falling asleep rapidly when allowed to do so) and microsleeps (falling asleep during waking performance) support the theory that as sleep deprivation progresses, the neurobiologic mechanisms of sleep cannot be held at bay, becoming activated even in the presence of waking neurobiology.

But the expression of sleepiness during waking is even more complicated, according to Dr. Dinges. His research findings require a revision of the “lapse hypothesis,” which has been the predominant explanation for the past 45 years for how sleep loss affects cognition. The lapse hypothesis posits “as you get sleepy, you can function normally until a microsleep occurs, causing a lapse [failure to respond to a salient stimulus in timely manner]…. When the transient microsleep ends, cognitive functions return to normal levels.” However, extensive research by Dr. Dinges and colleagues has shown that although lapses (errors of omission) do commonly occur and debilitate sleep-deprived subjects, errors of commission (responding without a stimulus being present) co-occur with lapses, and together these two phenomena reveal what Dr. Dinges refers to as a progressive “state instability” in sleep-deprived subjects attempting to perform basic cognitive tasks. When sleepiness is severe enough, the shifts between sleep and wake are subtle, frequent, and often outside our conscious awareness.

FUNCTIONING SLEEPY

Deficits in sustained attention performance revealed by the PVT occur early and profoundly in sleep deprivation, but according to Dr. Dinges, lapses of attention measured by the PVT also increase the longer a person performs the task, revealing the limited capacity of sleepy persons to maintain performance, and making time-on-task a critical factor to consider in evaluating impairment from sleepiness.

There is also ample evidence of a speed/accuracy tradeoff on tasks involving cognitive throughput, such as mental arithmetic and digit substitution tasks, said Dr. Dinges. “Sleep-deprived subjects slow down their cognitive operations in order to maintain accuracy,” he said. There are also negative effects of sleep loss on learning, on recall and working memory, and on executive functions.

However, not everyone responds to sleep deprivation in the same degree, and Dr. Dinges offered several reasons why. Although everyone who undergoes sleep deprivation eventually manifests the neurobehavioral hallmarks of cognitive impairment as sleep loss progresses, Dr. Dinges noted that there are large inter-individual differences in the magnitude of these cognitive deficits—differences that are often ignored by investigators. “It has been assumed that these differences reflect sleep need. Some people need six hours, some need eight hours,” he offered.

However, the differences show up among people who habitually sleep seven to eight hours each night, and who feel this is reflective of their basal sleep need. When these subjects were retested weeks or months later for their cognitive sensitivity to sleep deprivation, Dr. Dinges and his colleague, Dr. Hans Van Dongen, found that 79% of the variance in the response to sleep deprivation was stable and predictable. “The same subjects who were markedly impaired by moderate sleep loss the first time were as impaired the second time, and those who were less affected one time were less affected the second time as well.” The fact that people seem to differ in a predictable way in their ability to resist the effects of sleep deprivation may mean that, suggested Dr. Dinges, “we may need to add a third component to our theoretical model of the neurobiologic systems that produce sustained stable wakefulness. In addition to understanding wakefulness as the product of an endogenous circadian wake drive interacting with a sleep homeostatic drive, we should also be thinking about ‘differential vulnerability,’ and the possibility that what underlies individual differences in the magnitude of neurobehavioral impairment from sleep loss is the strength of the waking drive.”

ZONED OUT

“These experiments have consistently demonstrated that neurobehavioral deficits develop in proportion to the dosage of sleep that people were allowed each night. When sleep was less than eight hours night after night, subjects showed systematic accumulation of cognitive impairments,” said Dr. Dinges.

Across 10 days of restricted sleep, participants became progressively worse and eventually entered a zone of impairment comparable to that found after total sleep deprivation, observed Dr. Dinges. “This is a zone of impairment where it would be unsafe to drive or engage in other safety-sensitive tasks. Sleep debt definitely has consequences,” said Dr. Dinges. Ongoing experiments in his laboratory for the space program seek to determine if splitting sleep into two periods each day—one being a nap—could prevent the development of the cumulative effects of sleep debt. “Until we have these studies completed, it appears that there is a delicate balance between sleep duration and waking cognitive functions,” said Dr. Dinges.

MEASURING SLEEPINESS IN THE WORKPLACE

Dr. Dinges reported that the US Department of Transportation has supported research in this area that has led to the development of one promising technique that involves tracking of slow eyelid closures during sustained attention performance. Two double-blind experiments performed by Dr. Dinges and his colleagues to quantify the validity and reliability of this measure and a number of other methods to detect drowsiness revealed that slow eyelid closures during cognitive performance had a much higher degree of validity than did other techniques, including EEG measures. Dr. Dinges concluded that “this suggests that there is a close relationship between the tonic activity of the levator palpebrae muscle and the level of alertness, and therefore there are likely to be as yet undiscovered connections between hypothalamic and/or reticular nuclei involved in sleep and waking, and midbrain oculomotor nuclei involved in control of the eyelid, and the slow rolling of the eyes during sleep onset.”

ON BEING AWAKE

NR

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