What are the effects of sleep deprivation?

Updated: Nov 05, 2019
  • Author: Pradeep C Bollu, MD; Chief Editor: Selim R Benbadis, MD  more...
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As the full function of sleep has not been fully determined, the absolute number of hours necessary to fulfill its function is still unknown. Some individuals claim full effectiveness with only 3–5 hours of sleep per night, while most admit needing at least 8 hours or more of sleep per night to perform effectively. The inability to meet this biological requirement is what constitutes sleep deprivation and this loss of sleep can be total or partial or selective sleep deprivation or chronic sleep deprivation. Total sleep deprivation results from the elimination of sleep for at least one night to significantly prolong wakefulness. Partial sleep deprivation results from reducing the amount of nighttime sleep preventing the individuals from obtaining their usual sleep time. When this partial sleep deprivation happens over extended periods of time, it results in a state of chronic sleep deprivation. Selective sleep deprivation is achieved by depriving subjects of a specific stage of sleep.

With decreased sleep, higher-order cognitive tasks are affected early and disproportionately. Tests requiring both speed and accuracy demonstrate considerably slowed speed before accuracy begins to fail. Total sleep duration of 7 hours per night over 1 week has resulted in decreased speed in tasks of both simple reaction time and more demanding computer-generated mathematical problem-solving. Total sleep duration of 5 hours per night over 1 week shows both reduction in speed and the beginning of the failure of accuracy. [25]

Total sleep duration of 7 hours per night over a 1-week period leads to impairment of cognitive work requiring a simultaneous focus on several tasks. In driving simulations, for example, accidents increase progressively as total sleep duration is decreased to 7, 5, and 3 hours per night over 1 week. In the same simulations, 3 hours total sleep duration was associated with loss of ability to simultaneously appreciate peripheral and centrally presented visual stimuli, which could be termed as a form of visual simultanagnosia and peripheral visual neglect. [26, 27, 28]

In tasks requiring judgment, increasingly risky behaviors emerge as the total sleep duration is limited to 5 hours per night. The high cost of action seemingly is ignored as the sleep-deprived individual focuses on limited benefit. [26]

One explanation for decreasing performance in sleep deprivation is the occurrence of microsleep. Microsleep is defined as a brief (several seconds) runs of theta or delta activities that break through the otherwise beta or alpha EEG of waking. It has been seen to increase with sleep deprivation. In studies in which polysomnography is recorded simultaneously, microsleep impairs continuity of cognitive function and occurs prior to performance failure. However, the occurrence of microsleep has not been shown in most instances of polysomnographic correlated performance failure. Other explanations for performance impairments include sensory-perceptual impairments such as the development of visual neglect phenomena. [29]

These experimental findings can be explained by FDG glucose-PET studies, which show that individuals deprived of sleep for 24 hours have a decrease in metabolism in the prefrontal and parietal associational areas. The areas most important for judgment, impulse control, attention, and visual association are disproportionately hypometabolic compared to the primary sensory and motor areas necessary for receiving and acting upon the environmental inputs. This finding leads to the hypothesis that the areas of the brain most responsible for higher-order cognition are to some degree less functional during sleep-deprived wakefulness. [16, 30]

Sleep deprivation is a relative concept. Small amounts of sleep loss (eg, 1 hour per night over many nights) have subtle cognitive costs, which appear to go unrecognized by the individual experiencing the sleep loss. More severe restriction of sleep for a week leads to profound cognitive deficits similar to those seen in some stroke patients, which also appear to go unrecognized by the individual. The lack of recognition of the effects of sleep deprivation appears to be a constant feature, one which, it is hoped, will be overcome by further research and education. [26, 31]

Short-term sleep deprivation has been implicated in contributing to obesity as well as glycemic dysregulation contributing to poor control of type II diabetes. [32, 33, 34, 35]  In chronically sleep-deprived individuals, sleep extension to more than 6 hours per night showed improvement in glucose metabolism. [36]  Exposure to bright light during the early night, as seen in many adolescents with the use of electronic device screens, leads to insufficient sleep and irregular sleep pattern. Sleep deprivation and irregular sleep are implicated in metabolic dysfunction, obesity, and excessive caffeine intake among school-age children. [37]  Sleep deprivation is also shown to affect the normal physiological profiles of various hormones including TSH, cortisol, [38]  and growth hormone. [39, 40]

Sleep deprivation is a risk factor for cardiovascular and cerebrovascular disease. Part of the risk is attributed to the wide range of metabolic abnormalities and increased prevalence of obesity, diabetes, dyslipidemia, and hypertension in the sleep-deprived population. [41]  However, sleep loss constitutes an independent risk factor for stroke in the setting of sleep deprivation with alterations in immune response and heightened sympathetic drive possibly contributing to this independent link between sleep deprivation and cerebrovascular disease. [42, 40]

Sleep deprivation also affects many neurological and psychiatric disorders. Sleep deprivation is a well-known trigger for seizure precipitation in patients with epilepsy. [43]  Chronic headaches, including migraines and tension headaches, are more common in sleep-deprived individuals. [44, 45] Shift work that increases sleep deprivation can be a risk factor for multiple sclerosis. [46, 40]

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