Sleep deprivation is associated with considerable social, financial, and health-related costs, in large measure because it produces impaired cognitive performance due to increasing sleep propensity and instability of waking neurobehavioral functions. Cognitive functions particularly affected by sleep loss include psychomotor and cognitive speed, vigilant and executive attention, working memory, and higher cognitive abilities. Chronic sleep-restriction experiments-which model the kind of sleep loss experienced by many individuals with sleep fragmentation and premature sleep curtailment due to disorders and lifestyle-demonstrate that cognitive deficits accumulate to severe levels over time without full awareness by the affected individual. Functional neuroimaging has revealed that frequent and progressively longer cognitive lapses, which are a hallmark of sleep deprivation, involve distributed changes in brain regions including frontal and parietal control areas, secondary sensory processing areas, and thalamic areas. There are robust differences among individuals in the degree of their cognitive vulnerability to sleep loss that may involve differences in prefrontal and parietal cortices, and that may have a basis in genes regulating sleep homeostasis and circadian rhythms. Thus, cognitive deficits believed to be a function of the severity of clinical sleep disturbance may be a product of genetic alleles associated with differential cognitive vulnerability to sleep loss. KeywordsNeurobehavioral performance; sleep restriction; attention and executive function; functional neuroimaging; prefrontal cortex; thalamus; sensory processing areas; genetics SLEEP DEPRIVATION AND ACCIDENT RISKThe overall prevalence of insufficient sleep in adults has been estimated at 20%. 1 The effects of insufficient sleep on cognitive processing are described below; of these, daytime sleepiness has been the most common measure assessed in population-based studies. One study determined the prevalence of daytime sleepiness using interviews conducted over 5.5 years which followed 1,007 randomly selected young adults ages 21 to 30 years in southeast Michigan. 2 That study found the average nocturnal sleep time during weekdays was 6.7 hours and on weekends was 7.4 hours. Sleepiness was inversely proportional to hours slept, and difficulty falling asleep was more prevalent in single adults with a full-time job. 2 Studies in young adults indicate that 8 to 9 hours of extended nocturnal sleep are needed to © 2009 by Thieme Medical Publishers, Inc. Address for correspondence and reprint requests: David F. Dinges, Ph.D., Division of Sleep and Chronobiology, Department of Psychiatry, University of Pennsylvania School of Medicine, 1013 Blockley Hall, 423 Guardian Drive, Philadelphia, PA 19104-6021 (dinges@mail.med.upenn.edu NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript resolve sleepiness caused by decreased sleep time. 3,4 The apparent chronic partial sleep deprivation experienced by the young adults surveyed in 1...

Sleep deprivation is associated with considerable social, financial, and health-related costs, in large measure because it produces impaired cognitive performance due to increasing sleep propensity and instability of waking neurobehavioral functions. Cognitive functions particularly affected by sleep loss include psychomotor and cognitive speed, vigilant and executive attention, working memory, and higher cognitive abilities. Chronic sleep-restriction experiments—which model the kind of sleep loss experienced by many individuals with sleep fragmentation and premature sleep curtailment due to disorders and lifestyle—demonstrate that cognitive deficits accumulate to severe levels over time without full awareness by the affected individual. Functional neuroimaging has revealed that frequent and progressively longer cognitive lapses, which are a hallmark of sleep deprivation, involve distributed changes in brain regions including frontal and parietal control areas, secondary sensory processing areas, and thalamic areas. There are robust differences among individuals in the degree of their cognitive vulnerability to sleep loss that may involve differences in prefrontal and parietal cortices, and that may have a basis in genes regulating sleep homeostasis and circadian rhythms. Thus, cognitive deficits believed to be a function of the severity of clinical sleep disturbance may be a product of genetic alleles associated with differential cognitive vulnerability to sleep loss.

Revised diagnostic criteria for pediatric RLS have been developed, which are intended to improve clinical practice and promote further research.

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