Consequences of Sleep Deprivation

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Li Ling Lim

Department of Neurology, Sleep Disorders Unit, Singapore General Hospital, National Neuroscience Institute, Singapore, Republic of Singapore

Nancy Foldvary-Schaefer

Department of Neurology, Sleep Disorders Center, Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A.


With the invention of the light bulb and ready availability of electrical power, sleep loss has become increasingly prevalent in industrialized nations. Air travel across multiple time zones, globalization of commercial markets, shift work, 24/7 services, television, and the Internet have contributed to longer waking hours and reduced sleep. The mean number of hours of nocturnal sleep has fallen steadily in the last century from about 9 to 6.9 hours in 2005, based on the most recent National Sleep Foundation Poll (1). The proportion of Americans sleeping 8 or more hours on weekday nights has fallen steadily from 38% in 2001 to 26% in 2005. Therefore, sleep deprivation (SD) has become one of the most important yet understated public health issues of modern times.

Restless legs syndrome (RLS) can result in marked SD. In one tertiary center that specializes in RLS, the SD seen in RLS on polysomnography was greater than that of any illness except mania and fatal familial insomnia (Allen, personal communication). In this chapter, we will discuss the medical and neuropsychiatric consequences of SD.

How Much Sleep Do We Need?

Sleep needs vary from one individual to another and with age. Most adults require 6 to 10 hours of sleep per night to function optimally. Experts often recommend at least 8 hours of sleep, estimating that 1 hour of sleep is needed for every 2 hours awake (2). A recent dose-response sleep restriction experiment showed that cumulative wakefulness in excess of 16 hours resulted in performance lapses, whereas cognitive performance remained stable with 8 hours of sleep (3). With the exception of ''short sleepers'' who function well with less sleep than expected for their age, most people sleeping fewer than 5 to 6 hours per night are not getting enough sleep (4). In the 2005 National Sleep Foundation Poll, adult Americans reported that a minimum of 6.5 hours of sleep on average was needed for optimal daytime functioning. The median sleep duration was 7 to 7.9 hours and 16% of respondents slept less than 6 hours on weekday nights.

Large epidemiological surveys have consistently demonstrated a U-shaped association between sleep duration and mortality, with a nadir at 7 hours (5,6). Life expectancy is significantly reduced in people sleeping less than 4.5 hours per night and the mortality risk is even greater in subjects sleeping over 7.5 hours per night, even after controlling for comorbidities. These findings strongly suggest that sleep needs should be individualized and that a standard recommendation of 8 hours of sleep per night should not be uniformly made.

Sleep Deprivation vs. Sleep Fragmentation

While Dement has stated ''all wakefulness is sleep deprivation,'' SD usually refers to the ''failure to obtain sufficient nocturnal sleep to support normal alert wakefulness'' (2). Volitional chronic partial SD with its detrimental effects, classified as behaviorally induced insufficient sleep syndrome by the International Classification of Sleep Disorders 2, is the most common form of SD in humans (7).

Sleep loss can be voluntary or produced by a variety of environmental factors, or medical, psychiatric, and sleep disorders which disrupt sleep, including chronic pain, depression, sleep apnea, and RLS. High-frequency sleep fragmentation due to repeated arousals from sleep produces nonrestorative sleep and results in similar neurobehavioral consequences and performance deficits as voluntary SD (8). Sleep fragmentation and SD both result in daytime sleepiness, decreased psychomotor performance, and comparable physiological changes (9). In combination, voluntary sleep restriction and sleep fragmentation due to underlying medical or sleep disorders, both individually common occurrences, are likely to have synergistic and therefore even greater negative impact.

Behaviorally Induced Insufficient Sleep Syndrome

Volitional, but unintentional lack of sleep, is often chronic and a result of the excessive social and occupational demands of modern life and inadequate sleep hygiene. Excessive daytime sleepiness is the chief complaint, associated with a host of secondary symptoms such as fatigue, low energy, poor concentration, inattention, irritability, and dysphoria. The nocturnal habitual sleep period is shorter in duration than expected for age, leading to the common habit of sleeping in on weekends to ''catch up.'' Polysomnography features include a short sleep onset latency, high sleep efficiency, and prolonged total sleep time if allowed to sleep in. A short sleep latency with or without multiple sleep onset rapid eye movement (REM) sleep periods (SOREMPs) is typically observed on multiple sleep latency testing (MSLT).

SD can be acute or chronic, partial or total. While prolonged total sleep loss is rarely encountered in humans outside of a research setting, chronic partial sleep loss is a frequent occurrence, affecting an estimated one-third or more of normal adults, with especially severe sleep loss seen in night-shift workers (10).


Although the optimal duration and function of sleep remain unclear, the detrimental effects of SD have been studied for over a century. Human SD studies are discussed in detail below. Animal studies are also briefly reviewed for comparison. Experiments have addressed the effects of total, partial, and selective SD and recovery sleep.

The effects of total SD and partial SD in humans are qualitatively similar, with differences mainly in the time course of symptom evolution (3). Selective deprivation of specific stages, such as REM or slow wave sleep (SWS), has not consistently been shown to cause major psychological disturbances or performance decrements (11).

Total SD experiments, including one of the first in 1896 (90 hours) and the longest documented (264 hours or 11 days), have consistently produced the following effects (12,13):

1. Sleepiness, especially severe at night (circadian variation), which can be overcome with arousal (e.g., external stimulation and physical activity) and brief sleep episodes (''microsleep''), which are usually imperceptible to the subject.

2. Mild dysphoria and irritability.

3. Impaired performance in tasks requiring close attention such as vigilance testing, but not visually stimulating motor activity such as exciting arcade games. Performance can be transiently improved with motivation and incentives.

4. Neurological disturbances including visual illusions and hallucinations, blurred vision, ptosis, disorientation incoordination, slurred speech, memory lapses, delusions, slowed mentation, and difficulty in thinking.

5. Mild decrease in body temperature, but no major physical or metabolic abnormalities.

6. Relatively short recovery sleep over 1 to 3 nights with apparent return to baseline alertness and function, comprising approximately 25% of total sleep lost: two-thirds of lost SWS, one-third of lost REM sleep, and less than 10% of lost light non-REM (NREM) sleep.

A recent large-scale, dose-response chronic sleep restriction experiment compared the neurobehavioral and physiological effects of partial and total SD (3). Chronic partial SD of 4 to 6 hours per night over 14 days resulted in significant cumulative, dose-dependent deficits in cognitive performance and an increase in self-reported daytime sleepiness. The cognitive effects of chronic partial SD of 6 hours or less per night was equivalent to that produced by 2 nights of total SD. The rate of deterioration was inversely related to the duration of sleep time, with total SD producing more rapid decrements. Relatively moderate sleep restriction seriously impaired waking neurobehavioral functions in healthy adults. The subjects were largely unaware of these.

Effect of Sleep Deprivation on Alertness, Mood, and Performance


Sleepiness is the most evident consequence of SD. Carskadon and Dement performed the earliest studies using the MSLT to measure the effects of total SD on young adults. A marked and persistent decline in mean sleep latency (MSL) approaching zero and returning to baseline after the second recovery night was observed. Performance and mood similarly declined following two nights of total SD (14). The same authors reported similar relative reductions in MSL with partial SD, when the normal sleep period was shortened by only 30 to 60 minutes (15). When partial SD was prolonged, the MSL was further reduced.

These early observations of the cumulative effect of partial sleep restriction on waking functions have since been confirmed in other studies and have led to the concept that SD results in the accumulation of a ''sleep debt'' that must be repaid in order to restore normal alertness (16).


A meta-analysis of 19 studies reported over the last several decades concluded that mood is more vulnerable to SD than either cognitive or motor performance (17).

Mood ratings of sleep-deprived subjects were found to be more than three standard deviations worse than non-sleep-deprived individuals.

One study of partial SD for seven consecutive nights in healthy young adults reported increased mood disturbances and negative mood states, which the authors postulated may be exacerbated by the stresses of coping with daytime sleepiness, impaired cognition, and the compensatory effort required to stay awake and motivated during the day (16). In physician trainees who slept an average of only 5.95 hours daily, a higher incidence of depression was found in the internship year than expected for age group, with risk factors being female sex, unmarried status, and a past history of major depression (18). In another study, surgical residents whose sleep was acutely restricted to less than 4 hours per night were found to be more depressed, tense, and angry than in the rested state (19).

Interestingly, in depressed subjects, SD has the reverse effect (i.e., antidepres-sant), which is short-lived and reversible in most cases after a single night of recovery sleep (20). Although the mechanism remains unclear, partial, total, and selective SD have all been used successfully to treat depression (21).


Sleep loss has consistently been shown to significantly impair psychomotor performance. One meta-analysis found that the mean level of functioning of sleep-deprived subjects was comparable to that of only the ninth percentile of non-sleep-deprived subjects (17). Cognitive performance was found to be more affected than motor performance, and mood was much more affected than either cognitive or motor performance.

Performance deficits involving vigilance are evident after only two nights of mild sleep restriction to 5 hours (15,22). With longer duration (60 days) of comparable degrees of sleep loss, progressive decline in vigilance is seen (23). Similar cumulative deficits in alertness and performance have been shown in partial and total SD, with greater and more rapidly accumulating deficits with total SD.

In contrast to vigilance tasks, a controlled study of 11 male subjects showed that up to 60 hours of sleep loss did not significantly impair physical performance testing, including isometric and isokinetic muscular strength and endurance, and cardiovascular and respiratory responses to treadmill running (24). Military studies have also shown that physical performance remains relatively unaffected in spite of severe sleep restriction (0-3 hours of sleep) for up to nine days (25,26).

The impact of SD on performance is particularly relevant in everyday tasks such as driving and in certain occupations where chronic sleep restriction is common. The U.S. Department of Transportation recently identified fatigue as the number one safety problem in transportation operations, costing billions of dollars annually (27). In June 2003, the state of New Jersey was the first in the United States to pass legislation prohibiting driving a motor vehicle while impaired by lack of sleep (28).

Impairment in simulated driving tests after modest sleep loss has been shown to be comparable to that produced by alcohol. In one study, 18.5 and 21 hours of wakefulness produced deficits of the same magnitude as 0.05% and 0.08% blood alcohol concentration, respectively (29). The combined effect of sleep restriction and alcohol is additive, reducing alertness, and impairing simulated automobile driving in healthy young men, even with low alcohol intake and safe alcohol concentrations below 0.08% blood alcohol concentration, the legal intoxication level in most states (30,31). The effects of regular sleep loss on driving are further exacerbated by coexisting disorders like sleep apnea, the treatment of which with positive airway pressure therapy has been shown to reduce the risk of traffic accidents (32).

Certain high-risk occupations such as physician trainees are particularly vulnerable to chronic partial SD. One study showed that interns slept an average of less than 6 hours per night (18). Acutely sleep-deprived house officers exhibited significant deficits in mental tasks involving rote memory, language, numeric skills, and high-level cognitive tasks (33). A study of rested vs. fatigued anesthesia residents showed significant deterioration in tasks requiring vigilance in a simulated monitoring situation (34). Physician trainees were also shown to have a higher incidence of drowsy driving and sleep-related motor vehicle accidents, especially post-call, than a control group of rested physicians (35).

Factors Affecting the Impact of SD on Alertness, Mood, and Performance

The impact of SD on alertness, mood, and performance is influenced by extrinsic factors such as those causing arousal, and intrinsic factors such as sleep homeo-stasis, circadian rhythm effects, and age.

Extrinsic Factors

Because our propensity to sleep is a balance of sleep debt and level of arousal, it stands to reason that extrinsic factors that increase arousal can counteract and even mask the effects of sleep loss. Physical activity or exercise and stimulant drugs, including caffeine, are common examples.

In a study of 12 normal adults, a five-minute walk produced a significant elevation of heart rate, a measure of physiological arousal, and prolongation of mean sleep onset latency on the MSLT (36). The performance benefits of exercise are short-lived. Longer periods of physical activity do not improve overall performance in sleep-deprived individuals (37). Bright light, noise, and ambient temperature are other extrinsic factors that have also been shown to increase arousal (38-42). For example, a driving simulator study using noise (radio) and cold air as a countermeasure to sleepiness in partially sleep-deprived young adults demonstrated improvement in subjective sleepiness scores and a trend toward reduction of ''lane-drifting'' incidents. The increased alertness was, however only marginal and transient, and comparatively less effective than a short nap (<15 minutes) or 150 mg of caffeine (42).

There is an extensive body of literature demonstrating the effects of stimulant drugs on mood, alertness, and performance following SD. Amphetamines reverse the effects of 48 hours SD on sleep latency and behavior in a dose-dependent manner (43). Methylphenidate increased MSL, improved performance on vigilance tasks, as well as depression and fatigue scores in a placebo-controlled study (44). Similar alerting and performance benefits have been demonstrated with modafinil (45,46). Caffeine has also been shown to reverse the effects of SD on alertness and mood. A double-blind study of normal subjects sleep deprived for 49 hours showed that a 600 mg dose of caffeine significantly increased sleep latency and decreased sleepiness, fatigue, and confusion to near resting levels (47).

Performance can also be affected by factors related to the test situation such as level of interest in a given task and by incentives such as financial rewards for good performance (48,49). Immediate feedback produces momentary arousal that can improve performance, while increasing task duration has the opposite effect (50). Increasing the difficulty and complexity of a task also adversely affects performance (51,52). Generally, the most profound deficits are observed on tasks that are long in duration, newly learned, difficult, externally paced, devoid of feedback, and have a memory component (51,53-55).

Sleep Homeostasis, Circadian Rhythm, and Other Intrinsic Factors Wakefulness accumulates sleep debt, which leads to increased sleepiness that, in turn, is discharged during sleep. This homeostatic process is modulated by the circadian pacemaker, which regulates level of alertness, usually lowest during the nocturnal hours and in the mid-afternoon (56) (Chapter 3).

A study of the effects of 72 hours of SD in 12 subjects, in whom levels of alertness, affect, motivation, and cognition were measured, showed that most of these variables were significantly affected by the number of days of sleep loss and all were significantly affected by the hour of the day (57). The peak time for self-reported complaints was in the early morning between 4:00 a.m. and 8:00 a.m., while the fewest symptoms were reported in the late afternoon between 4:00 p.m. and 8:00 p.m.

Sleep homeostasis is affected by daytime napping, which reduces sleep debt. Taking a nap before a period of prolonged wakefulness transiently improves alertness, mood, and performance in a dose-related manner (58). The beneficial effects of three- to four-hour prophylactic naps are comparable to a moderate dose of caffeine (300 mg), and the combined effect of naps and caffeine is additive (59).

Intrinsic factors such as age may have an impact, although relatively minor, on the effects of sleep loss. Tests of performance and alertness in normal older sleep-deprived subjects reveal loss of performance and alertness similar to that seen in younger individuals. However, older individuals may tolerate sleep loss with less decrease in ability compared to baseline than young adults, and may recover function faster than young adults (60).

Neurologic Effects of Sleep Deprivation prolonged SD produces reversible neurologic signs such as slurred speech, hand tremor, ptosis, nystagmus and abnormal corneal, gag, and deep tendon reflexes (61,62). Sleep loss also affects immediate recall and short-term memory, causing memory deficits on testing similar to that seen with alcohol intoxication and aging, postulated to be due to impaired encoding and retrieval of information (55,63). On positron emission tomography studies, 24-hour SD resulted in a global decline in brain activity, most marked in the thalamus and prefrontal and posterior parietal cortices, areas mediating attention, and higher-order cognitive processes (64).

Electroencephalographic (EEG) studies have shown a progressive slowing of the waking alpha rhythm in proportion to the duration of sleep loss, with loss of alpha reactivity after prolonged SD (65). In one study, a correlation between theta and delta activity during wakefulness and impaired performance following SD was observed (66). Microsleep episodes lasting up to 10 seconds are also seen in the EEGs of healthy human subjects sleep deprived for 60 hours (67). Such microsleep episodes are ameliorated with stimulating agents such as modafinil (46).

SD has long been recognized as a precipitating factor for seizure recurrence in people with epilepsy. Patients with epilepsy frequently report SD as a seizure precipitant (68). SD is also often used as an activating procedure during routine EEG and long-term video EEG monitoring (69-71). Early studies in nonepileptic, mostly military populations who were profoundly sleep deprived, found a significantly higher incidence of seizures than in demographically similar populations who were not sleep deprived (72). EEG studies of both normal healthy subjects (65,73) and subjects with suspected epilepsy (74-77) have also demonstrated a clear increase in interictal epileptiform abnormalities following SD.

Other Physiological Changes Associated with SD

Despite the vast body of evidence supporting the multitude of adverse consequences of SD on neurologic function, similarly marked changes in other organ systems have not been found (78). Accelerated metabolism (and premature death) following partial and total SD seen in animals has not been demonstrated in humans. However, sleep-deprived humans do exhibit similar declines in body temperature and increased sympathetic tone (12,79). The range of physiological changes associated with SD in cardiovascular, respiratory, endocrine, and immune function is discussed.

Several epidemiologic studies have found an association between cardiovascular morbidity and chronic sleep restriction (6,80). In the Nurses' Health Study, women sleeping less than 7 hours per night had an increased risk of coronary events compared to those averaging 8 hours. Precisely, how chronic SD affects cardiovascular morbidity remains unknown.

Respiratory testing in healthy adults has shown small but significant decreases in forced vital capacity, hypoxic and hypercapneic ventilatory responses after SD (81,82). SD has also been shown to cause reversible worsening of respiratory events in normal infants and adults with obstructive sleep apnea syndrome (83,84).

With the exception of thyroid hormones, appreciable hormonal alterations have not been observed after total SD, including catecholamine, cortisol, or sex hormone levels (85). With partial SD, impaired glucose tolerance, elevated evening cortisol levels, and thyroid function abnormalities have been reported (79). Sleep loss can alter the pattern of secretion of hormones under circadian influence. For example, selective deprivation of SWS can diminish the secretion of growth hormone (86).

Human studies have demonstrated a variety of changes in immune function following SD. However, firm evidence for increased susceptibility to infections is lacking. Some reported findings include

1. enhanced ability of lymphocytes to produce interferon (87),

2. impaired natural killer cell activity and T-cell cytokine production (88),

3. decreased DNA synthesis of blood lymphocytes (89),

4. altered antigen uptake (90), and

5. decreased antibody responses in humans to viral vaccines (91,92).

Although the studies examining the effect of SD on immune function in humans are difficult to compare due to differences in methodology, it is generally believed that sleep loss does influence the immune system. Short-term SD may enhance immune responses, while chronic sleep loss is probably detrimental.

Selective Sleep Deprivation

The earliest REM SD experiments were conducted in an attempt to determine the function and necessity of REM sleep. Initial interest in this area of research was stimulated by the Freudian belief that subconscious impulses and desires, if unexpressed as dreams during REM sleep, would cause a buildup of ''psychic pressure,'' and eventually lead to neurosis and psychosis. REM SD in rats induces hyperactivity, irritability, aggressiveness, stereotypy, and hypersexuality, which some authors consider a model for mania (93). In selective deprivation experiments in which human volunteers would be awoken at the first sign of REM sleep, REM sleep onset latency decreased and REM sleep duration increased progressively, eventually producing SOREMPs. REM SD caused confusion, bad temperedness, and severe sleepiness, but not psychosis (2). While animal studies have shown an association between REM sleep and memory and learning, firm evidence for this in humans is lacking. REM density has been reported to increase after training in humans, implicating REM sleep in memory processing (94). Yet, antidepressant drugs that suppress REM sleep are used commonly without apparent adverse effect on memory, suggesting that the role of REM sleep in human memory and learning is complex and poorly understood.

In comparison to selective REM deprivation, there are fewer studies addressing selective deprivation of SWS in humans. Selective SWS deprivation studies are difficult to perform and often affected by methodological problems. Selective SWS disruption, without reducing total sleep or sleep efficiency, has been associated with fatigue, decreased pain threshold, and reduced vigor (95). However, daytime performance testing following several nights of either REM or SWS deprivation has not been shown to result in apparent decrements (11).

Changes in Sleep Architecture During and After SD

The effect of SD on sleep architecture was studied in healthy subjects who underwent partial sleep restriction (50% or 4 hours) for four nights followed by three recovery nights of 8 hours (96). During the period of SD, there was decreased light NREM sleep (stages 1, 2) and REM sleep, but SWS was mostly unaffected. On the first recovery night, there was shortening of the sleep onset latency and increased total sleep time, including enhanced SWS and REM sleep. On the second recovery night, SWS duration approached normal while REM sleep rebound continued. Sleep architecture subsequently normalized by the third recovery night.

Recovery from Sleep Deprivation

The effects of SD on alertness and performance reverse after 1 to 3 nights of recovery sleep, regardless of the duration of prior wakefulness (63,97,98). Studies of prolonged total SD have shown that the amount of recovery sleep required to restore baseline performance is only about 25% of the amount of sleep loss incurred (12,13). It is unclear whether this means that accumulated sleep debt need not be repaid in full as originally thought, or if residual deficits may be too small to be measurable or difficult to measure in typical SD paradigms.


Animal models of SD, employing in some cases long periods of sleep loss, have demonstrated more pronounced abnormalities than observed in sleep-deprived humans (99,100). Rats subjected to SD experience weight loss and assume a malnourished appearance in spite of increased food intake. Skin lesions (ulcers and discolored fur), increased energy expenditure due to increased heat loss, decreased body temperature during the late stages of deprivation, biochemical changes including increased plasma norepinephrine and decreased plasma thyroxine are observed. Eventual death ensues after an average of 19 days of near-total SD. Animals subjected to selective REM or SWS deprivation survive longer. The mechanisms leading to death after total SD are unclear and confounded by the effect of stress, which accompanies profound sleep loss. Proposed mechanisms include hypothermia, hypermetabolism, and impaired immunity, but none have been firmly proven. For example, septicemia involving opportunistic microbes, implicating impaired immunity in the hypercatabolic, malnourished, and ultimately life-threatening state associated with prolonged SD was described (101). However, subsequent studies demonstrated that elimination of the bacterial invasion did not prevent hypothermia or early death in rats subjected to total SD (102).

Studies of recovery sleep in surviving rats have shown near-complete reversal of SD-related changes in appearance, metabolism, temperature, biochemistry, and high energy expenditure (103). Recovery sleep is characterized by immediate and prominent REM sleep rebound, which contrasts with the SWS rebound seen in humans.


Human studies have consistently demonstrated significant detrimental effects of SD on alertness, mood, performance, and neurological function. Chronic SD has been associated with increased all-cause and cardiovascular mortality. Physiological effects are relatively minor and include changes in thermoregulation, respiratory, endocrine, and immune function. Chronic partial SD is often unrecognized and likely represents one of the most important public health issues in modern society. Dement considered ''the pervasive lack of awareness about SD a national emergency'' (2). The additive effects of alcohol, drugs, social and occupational demands, and the coexistence of common disorders that disrupt sleep, including chronic pain, depression, sleep apnea, and RLS, exacerbate the problem. The impact of SD on transportation and occupational safety, comparable to the effects of alcohol intoxication, are potentially catastrophic. Measures to address these concerns have included legislation against drowsy driving, later school start times, and restriction of duty hours for physician trainees. These measures underscore the serious health and socioeconomic consequences of sleep loss, but represent just a few of the initiatives required to manage this enormous problem.


1. National Sleep Foundation. 2005 Sleep in America Poll, 2005.

2. Dement WC, Vaughan C. The promise of sleep. The scientific connection between health, happiness, and a good night's sleep. 1999.

3. Van Dongen HP, Maislin G, Mullington JM, Dinges DF. The cumulative cost of additional wakefulness: dose-response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation. Sleep 2003; 26(2):117-126.

4. American Academy of Sleep Medicine. International Classification of Sleep Disorders, revised. Diagnostic and Coding Manual. 2001:87-90.

5. Tamakoshi A, Ohno Y. Self-reported sleep duration as a predictor of all-cause mortality: results from the JACC study, Japan. Sleep 2004; 27(1):51-54.

Kripke DF, Garfinkel L, Wingard DL, Klauber MR, Marler MR. Mortality associated with sleep duration and insomnia. Arch Gen Psychiatry 2002; 59(2):131-136. Sateia MJ. ICSD-2-The International Classification of Sleep Disorders. In: Diagnostic and Coding Manual-2, Westchester. 2nd. Illinois: American Academy of Sleep Medicine, 2005:104-106.

Bonnet MH, Arand DL. Clinical effects of sleep fragmentation versus sleep deprivation. Sleep Med Rev 2003; 7(4):297-310.

Bonnet MH. Effect of sleep disruption on sleep, performance, and mood. Sleep 1985; 8(1):11-19.

Bonnet MH, Arand DL. We are chronically sleep deprived. Sleep 1995; 18(10):908-911. Johnson LC, Naitoh P, Moses JM, Lubin A. Interaction of REM deprivation and stage 4 deprivation with total sleep loss: experiment 2. Psychophysiology 1974; 11(2):147-159. Patrick GT, Gilbert JA. On the effects of loss of sleep. Psychol Rev 1896; 3:469. Gulevich G, Dement W, Johnson L. Psychiatric and EEG observations on a case of prolonged (264 hours) wakefulness. Arch Gen Psychiatry 1966; 15(1):29-35. Carskadon MA, Dement WC. Effects of total sleep loss on sleep tendency. Percept Mot Skills 1979; 48(2):495-506.

Carskadon MA, Dement WC. Cumulative effects of sleep restriction on daytime sleepiness. Psychophysiology 1981; 18(2):107-113.

Dinges DF, Pack F, Williams K, et al. Cumulative sleepiness, mood disturbance, and psychomotor vigilance performance decrements during a week of sleep restricted to 4-5 hours per night. Sleep 1997; 20(4):267.

Pilcher JJ, Huffcutt AI. Effects of sleep deprivation on performance: a meta-analysis. Sleep 1996; 19(4):318-326.

Ford CV, Wentz DK. The internship year: a study of sleep, mood states, and psycho-physiologic parameters. South Med J 1984; 77(11):1435-1442.

Bartle EJ, Sun JH, Thompson L, Light AI, McCool C, Heaton S. The effects of acute sleep deprivation during residency training. Surgery 1988; 104(2):311-316. Wu JC, Bunney WE. The biological basis of an antidepressant response to sleep deprivation and relapse: review and hypothesis. Am J Psychiatry 1990; 147(1):14-21. Giedke H. The usefulness of therapeutic sleep deprivation in depression. J Affect Disord 2004; 78(1):85-86.

Wilkinson RT. Performance following a night of reduced sleep. Psychonom Sci 1966; 5:471.

Webb WB, Agnew HW, Jr. The effects of a chronic limitation of sleep length. Psycho-physiology 1974; 11(3):265-274.

Symons JD, VanHelder T, Myles WS. Physical performance and physiological responses following 60 hours of sleep deprivation. Med Sci Sports Exerc 1988; 20(4):374-380.

Haslam DR. Sleep loss, recovery sleep, and military performance. Ergonomics 1982; 25(2):163-178.

Haslam DR. The military performance of soldiers in sustained operations. Aviat Space Environ Med 1984; 55(3):216-221.

Statistics. U.S. Department of Transportation. 2005; internet communication. Senate and General Assembly of the State of New Jersey. An Act concerning vehicular homicide. Assembly, No. 1347 State of New Jersey 210th Legislature. 2003. Arnedt JT, Wilde GJ, Munt PW, MacLean AW. How do prolonged wakefulness and alcohol compare in the decrements they produce on a simulated driving task?. Accid Anal Prev 2001; 33(3):337-344.

Roehrs T, Beare D, Zorick F, Roth T. Sleepiness and ethanol effects on simulated driving. Alcohol Clin Exp Res 1994; 18(1):154-158.

Horne JA, Reyner LA, Barrett PR. Driving impairment due to sleepiness is exacerbated by low alcohol intake. Occup Environ Med 2003; 60(9):689-692.

Cassel W, Ploch T, Becker C. Risk of traffic accidents in patients with sleep-disordered breathing: reduction with nasal CPAP. Eur Resp J 1996; 9:2606-2611. Hawkins MR, Vichick DA, Silsby HD, Kruzich DJ, Butler R. Sleep and nutritional deprivation and performance of house officers. J Med Educ 1985; 60(7):530-535.

34. Denisco RA, Drummond JN, Gravenstein JS. The effect of fatigue on the performance of a simulated anesthetic monitoring task. J Clin Monit 1987; 3(1):22-24.

35. Marcus CL, Loughlin GM. Effect of sleep deprivation on driving safety in housestaff. Sleep 1996; 19(10):763-766.

36. Bonnet MH, Arand DL. Sleepiness as measured by modified multiple sleep latency testing varies as a function of preceding activity. Sleep 1998; 21(5):477-483.

37. Angus RG, Heslegrave RJ, Myles WS. Effects of prolonged sleep deprivation, with and without chronic physical exercise, on mood and performance. Psychophysiology 1985; 22(3):276-282.

38. Dijk DJ, Cajochen C, Borbely AA. Effect of a single 3-hour exposure to bright light on core body temperature and sleep in humans. Neurosci Lett 1991; 121(1-2):59-62.

39. Komada Y, Tanaka H, Yamamoto Y, Shirakawa S, Yamazaki K. Effects of bright light pre-exposure on sleep onset process. Psychiatry Clin Neurosci 2000; 54(3):365-366.

40. Tassi P, Nicolas A, Seegmuller C, Dewasmes G, Libert JP, Muzet A. Interaction of the alerting effect of noise with partial sleep deprivation and circadian rhythmicity of vigilance. Percept Mot Skills 1993; 77(3 Pt 2):1239-1248.

41. Poulton EC, Edwards RS, Colquhoun WP. The interaction of the loss of a night's sleep with mild heat: task variables. Ergonomics 1974; 17(1):59-73.

42. Reyner LA, Horne JA. Evaluation ''in-car'' countermeasures to sleepiness: cold air and radio. Sleep 1998; 21(1):46-50.

43. Newhouse PA, Belenky G, Thomas M, Thorne D, Sing HC, Fertig J. The effects of d-amphetamine on arousal, cognition, and mood after prolonged total sleep deprivation. Neuropsychopharmacology 1989; 2(2):153-164.

44. Bishop C, Roehrs T, Rosenthal L, Roth T. Alerting effects of methylphenidate under basal and sleep-deprived conditions. Exp Clin Psychopharmacol 1997; 5(4):344-352.

45. Pigeau R, Naitoh P, Buguet A, et al. Modafinil, d-amphetamine and placebo during 64 hours of sustained mental work. I. Effects on mood, fatigue, cognitive performance and body temperature. J Sleep Res 1995; 4(4):212-228.

46. Lagarde D, Batejat D, Van BP, Sarafian D, Pradella S. Interest of modafinil, a new psychostimulant, during a sixty-hour sleep deprivation experiment. Fundam Clin Pharmacol 1995; 9(3):271-279.

47. Penetar D, McCann U, Thorne D, et al. Caffeine reversal of sleep deprivation effects on alertness and mood. Psychopharmacology (Berl) 1993; 112(2-3):359-365.

48. Wilkinson RT. Effects of up to 60 hours' sleep deprivation on different types of work. Ergonomics 1964; 7:175-186.

49. Horne JA, Pettitt AN. High incentive effects on vigilance performance during 72 hours of total sleep deprivation. Acta Psychol (Amst) 1985; 58(2):123-139.

50. Steyvers FJ, Gaillard AW. The effects of sleep deprivation and incentives on human performance. Psychol Res 1993; 55(1):64-70.

51. Williams HL, Lubin A. Speeded addition and sleep loss. J Exp Psychol 1967; 73: 313-317.

52. Babkoff H, Mikulincer M, Caspy T, Kempinski D, Sing H. The topology of performance curves during 72 hours of sleep loss: a memory and search task. Q J Exp Psychol A 1988; 40(4):737-756.

53. Donnell JM. Performance decrement as a function of total sleep loss and task duration. Percept Mot Skills 1969; 29(3):711-714.

54. Light AI, Sun JH, McCool C, Thompson L, Heaton S, Bartle EJ. The effects of acute sleep deprivation on level of resident training. Curr Surg 1989; 46(1):29-30.

55. Nilsson LG, Backman L, Karlsson T. Priming and cued recall in elderly, alcohol intoxicated and sleep-deprived subjects: a case of functionally similar memory deficits. Psychol Med 1989; 19(2):423-433.

56. Richardson GS, Carskadon MA, Orav EJ, Dement WC. Circadian variation of sleep tendency in elderly and young adult subjects. Sleep 1982; 5(suppl 2):S82-S94.

57. Mikulincer M, Babkoff H, Caspy T, Sing H. The effects of 72 hours of sleep loss on psychological variables. Br J Psychol 1989; 80(Pt 2):145-162.

58. Bonnet MH, Gomez S, Wirth O, Arand DL. The use of caffeine versus prophylactic naps in sustained performance. Sleep 1995; 18(2):97-104.

59. Bonnet MH, Arand DL. The use of prophylactic naps and caffeine to maintain performance during a continuous operation. Ergonomics 1994; 37(6):1009-1020.

60. Bonnet MH, Arand DL. Sleep loss in aging. Clin Geriatr Med 1989; 5(2):405-420.

61. Kollar EJ, Namerow N, Pasnau RO, Naitoh P. Neurological findings during prolonged sleep deprivation. Neurology 1968; 18(9):836-840.

62. Ross JJ. Neurological findings after prolonged sleep deprivation. Arch Neurol 1965; 12:399-403.

63. Williams HL, Gieseking CF, Lubin A. Some effects of sleep loss on memory. Percept Mot Skills 1966; 23(3):1287-1293.

64. Thomas M, Sing H, Belenky G, et al. Neural basis of alertness and cognitive performance impairments during sleepiness. I. Effects of 24 h of sleep deprivation on waking human regional brain activity. J Sleep Res 2000; 9(4):335-352.

65. Rodin EA, Luby ED, Gottlieb JS. The electroencephalogram during prolonged experimental sleep deprivation. Electroencephalogr Clin Neurophysiol 1962; 14:544-551.

66. Naitoh P, Pasnau RO, Kollar EJ. Psychophysiological changes after prolonged deprivation of sleep. Biol Psychiatry 1971; 3(4):309-320.

67. Lagarde D, Batejat D. Evaluation of drowsiness during prolonged sleep deprivation. Neurophysiol Clin 1994; 24(1):35-44.

68. Nakken KO, Solaas MH, Kjeldsen MJ, Friis ML, Pellock JM, Corey LA. Which seizure-precipitating factors do patients with epilepsy most frequently report? Epilepsy Behav 2005; 6(1):85-89.

69. Gastaut H, Tassinari C. Triggering mechanisms in epilepsy. The electroclinical point of view. Epilepsia 1966; 7:85-138.

70. Dinner DS. Effect of sleep on epilepsy. J Clin Neurophysiol 2002; 19(6):504-513.

71. Mendez M, Radtke RA. Interactions between sleep and epilepsy. J Clin Neurophysiol 2001; 18(2):106-127.

72. Gunderson CH, Dunne PB, Feyer TL. Sleep deprivation seizures. Neurology 1973; 23(7):678-686.

73. Bennett DR. Sleep deprivation and major motor convulsions. Neurology 1963; 13: 953-958.

74. Bennett DR, Mattson RH, Ziter FA, Calverley JR, Liske EA, Pratt KL. Sleep deprivation: neurological and electroencephalographic effects. Aerosp Med 1964; 35:888-890.

75. Welch LK, Stevens JB. Clinical value of the electroencephalogram following sleep deprivation. Aerosp Med 1971; 42(3):349-351.

76. Mattson RH, Pratt KL, Calverley JR. Electroencephalograms of epileptics following sleep deprivation. Arch Neurol 1965; 13(3):310-315.

77. Pratt KL, Mattson RH, Weikers NJ, Williams R. EEG activation of epileptics following sleep deprivation: a prospective study of 114 cases. Electroencephalogr Clin Neuro-physiol 1968; 24(1):11-15.

78. Horne JA. A review of the biological effects of total sleep deprivation in man. Biol Psychol 1978; 7(1-2):55-102.

79. Spiegel K, Leproult R, Van CE. Impact of sleep debt on metabolic and endocrine function. Lancet 1999; 354(9188):1435-1439.

80. Ayas NT, White DP, Manson JE, et al. A prospective study of sleep duration and coronary heart disease in women. Arch Intern Med 2003; 163(2):205-209.

81. Cooper KR, Phillips BA. Effect of short-term sleep loss on breathing. J Appl Physiol 1982; 53(4):855-858.

82. White DP, Douglas NJ, Pickett CK, Zwillich CW, Weil JV. Sleep deprivation and the control of ventilation. Am Rev Respir Dis 1983; 128(6):984-986.

83. Canet E, Gaultier C, D'Allest AM, Dehan M. Effects of sleep deprivation on respiratory events during sleep in healthy infants. J Appl Physiol 1989; 66(3):1158-1163.

84. Persson HE, Svanborg E. Sleep deprivation worsens obstructive sleep apnea. Comparison between diurnal and nocturnal polysomnography. Chest 1996; 109(3): 645-650.

85. Gary KA, Winokur A, Douglas SD, Kapoor S, Zaugg L, Dinges DF. Total sleep deprivation and the thyroid axis: effects of sleep and waking activity. Aviat Space Environ Med 1996; 67(6):513-519.

86. Beck U, Marquetand D. Effects of selective sleep deprivation on sleep-linked prolactin and growth hormone secretion. Arch Psychiatr Nervenkr 1976; 223(1):35-44.

87. Palmblad J, Cantell K, Strander H. Stressor exposure and immunological response in man: interferon producing capacity and phagocytosis. Psychosom Res 1976; 20: 193-199.

88. Irwin M, McClintick J, Costlow C, Fortner M, White J, Gillin JC. Partial night sleep deprivation reduces natural killer and cellular immune responses in humans. FASEB J 1996; 10(5):643-653.

89. Palmblad J, Petrini B, Wasserman J, Akerstedt T. Lymphocyte and granulocyte reactions during sleep deprivation. Psychosom Med 1979; 41(4):273-278.

90. Casey FB, Eisenberg J, Peterson D, Pieper D. Altered antigen uptake and distribution due to exposure to extreme environmental temperatures or sleep deprivation. J Reticu-loendothel Soc 1974; 15(2):87-95.

91. Lange T, Perras B, Fehm HL, Born J. Sleep enhances the human antibody response to hepatitis A vaccination. Psychosom Med 2003; 65(5):831-835.

92. Spiegel K, Sheridan JF, Van CE. Effect of sleep deprivation on response to immunization. JAMA 2002; 288(12):1471-1472.

93. Gessa GL, Pani L, Fadda P, Fratta W. Sleep deprivation in the rat: an animal model of mania. Eur Neuropsychopharmacol 1995; 5(suppl):89-93.

94. Smith CT, Nixon Mr, Nader RS. Posttraining increases in REM sleep intensity implicate REM sleep in memory processing and provide a biological marker of learning potential. Learn Mem 2004; 11(6):714-719.

95. Lentz MJ, Landis CA, Rothermel J, Shaver JL. Effects of selective slow wave sleep disruption on musculoskeletal pain and fatigue in middle aged women. J Rheumatol 1999; 26(7):1586-1592.

96. Brunner DP, Dijk DJ, Borbely AA. Repeated partial sleep deprivation progressively changes in EEG during sleep and wakefulness. Sleep 1993; 16(2):100-113.

97. Lubin A, Hord DJ, Tracy ML, Johnson LC. Effects of exercise, bedrest and napping on performance decrement during 40 hours. Psychophysiology 1976; 13(4):334-339.

98. Webb WB, Agnew HW, Jr. Effects on performance of high and low energy-expenditure during sleep deprivation. Percept Mot Skills 1973; 37(2):511-514.

99. Rechtschaffen A, Bergmann BM, Everson CA, Kushida CA, Gilliland MA. Sleep deprivation in the rat: I. Conceptual issues. Sleep 1989; 12(1):1-4.

100. Rechtschaffen A, Bergmann BM, Everson CA, Kushida CA, Gilliland MA. Sleep deprivation in the rat: X. Integration and discussion of the findings. Sleep 1989; 12(1):68-87.

101. Everson CA. Sustained sleep deprivation impairs host defense. Am J Physiol 1993; 265(5 Pt 2):R1148-R1154.

102. Bergmann BM, Gilliland MA, Feng PF, et al. Are physiological effects of sleep deprivation in the rat mediated by bacterial invasion? Sleep 1996; 19(7):554-562.

103. Everson CA, Gilliland MA, Kushida CA, et al. Sleep deprivation in the rat: IX. Recovery. Sleep 1989; 12(1):60-67.

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