What is the relationship between sleep deprivation and wakefulness

Sleep deprivation - Scholarpedia

what is the relationship between sleep deprivation and wakefulness

Summary: The effect of repeated partial sleep deprivation on sleep stages and electroencephalogram (EEG) the EEG spectra of REM sleep and wakefulness. Because the time course ments show an inverse relationship to the intensity of. Sleep deprivation is the restriction of sleep below the level of basal sleep period of extended wakefulness), or chronic (the accumulation of sleep relationship with the number of hours a subject has been sleep deprived. Sleep deprivation commonly known as insufficient sleep is the condition of not having enough . The link between sleep deprivation and psychosis was further documented in . For instance, laboratory sleep deprivation studies in young men have demonstrated that one night of wakefulness (typically found in shift.

However, the number of new cases of cardiovascular disease was independent of CPAP treatment compliance. Although observational evidence of this type is not conclusive proof, because it may be subject to confounding by indication and other biases, it still lends weight to the strength of the association.

Most studies finding elevated cardiovascular disease risk have been conducted in adults. Whether or not children with sleep-disordered breathing are at risk for cardiovascular effects is not known. Children with OSAas noted previously, do experience changes in blood pressure profiles, heart rate variability, and ventricular wall changes as measured by echocardiography Marcus et al. The paucity of longitudinal data on OSA in children, in whom levels of OSA may vary during growth and development and in whom responses to therapies such as tonsillectomy may be variable Morton et al.

Nonetheless, evidence that as many as 20 to 25 percent of children may have persistent OSA even after tonsillectomy underscores the potential importance of OSA as an early childhood risk factor for later cardiovascular diseases Amin et al. Those outcomes were more prevalent in those with the highest apnea-hypopnea index. The study also found a relationship between sleep-related hypoxemia and glucose intolerance, which has implications for understanding mechanisms behind the OSA-glucose intolerance link see below.

The Sleep Heart Health Study, as noted earlier, was a large, cross-sectional, community-based study that used polysomnography to identify OSA. The analyses adjusted for obesity BMI and waist circumferenceself-reported sleep duration, and other confounding factors. The findings suggest that OSA contributes to the onset of diabetes through the development of glucose intolerance and insulin resistance, which are established pathophysiological processes in diabetes Martin et al.

The study found that, after 10 years of follow-up, occasional snoring versus nonsnoring was associated with an elevated risk of new onset diabetes in women, and the risk was even greater for regular snoring Al-Delaimy et al. Regular or habitual snoring is an indicator of OSA. CPAP alleviates glucose intolerance in the short term and long term Brooks et al. The mechanisms by which OSA disrupts glucose metabolism are not established.

Drawing on human studies and animal models, the biochemical cascade begins with intermittent hypoxia and recurrent sleep arousals sleep fragmentation. These events stimulate the sympathetic nervous system, hypothalamic-pituitary-adrenal axis, and adipocytes Punjabi and Beamer, Their activation, in turn, leads to release of catecholamines, cortisol, and inflammatory cytokines and other vasoactive intermediates, which may mediate the development of glucose intolerance, insulin resistance, and, ultimately, type 2 diabetes.

Because diabetes is also a risk factor for cardiovascular disease, the interrelationships may partly explain why OSA predisposes to cardiovascular disease Punjabi and Beamer, This finding may reflect the role of obesity as a well-established risk factor for the development of OSA. It may also reflect obesity as a consequence of OSA, although the evidence is not yet conclusive Grunstein, b.

Patients with newly diagnosed OSA, compared with controls matched for BMI and percent body fat, show recent weight gain Phillips et al. Data from the Wisconsin Sleep Cohort also show that individuals with OSA have reduced levels of physical activity; OSA-related sleepiness may contribute to changes in activity and energy expenditure, and thus contribute to weight gain.

OSA-related hormonal changes may also contribute to obesity. In general, patients with OSA have higher levels of leptin, the appetite-suppressing hormone Phillips et al. However, their morning levels are relatively lower than evening levels Patel et al. Furthermore, obesity also affects the severity of OSA.

Significant weight loss in adolescents who underwent gastric bypass surgery mean, 58 kg was associated with a dramatic reduction of OSA severity Kalra et al.

what is the relationship between sleep deprivation and wakefulness

Etiology and Risk Factors In simplest terms, OSA is caused by narrowing or collapse of the airway as a result of anatomical and physiological abnormalities in pharyngeal structures. Apnea episodes cause hypoxemia insufficient oxygen in the blood and hypercapnia high concentration of blood carbon dioxide.

The episodes also increase the output of the sympathetic nervous system Narkiewicz and Somers,the effect of which is to restore pharyngeal muscle tone and reopen the airway. Although increased sympathetic activity is beneficial for restoring normal breathing and oxygen intake over the short term, it has long-term deleterious effects on vascular tone and blood pressure, among other effects Caples et al.

These early events—which are mediated by a variety of chemoreceptors in the carotid body and brainstem—trigger pathophysiological changes that occur not only during the obstructive apneas, but also extend into wakeful states during the day. For example, during daytime wakefulness, people with OSA have higher sympathetic activity Somers, et al. The full pathophysiology of OSA remains somewhat elusive, although research is piecing together the relationships between OSA and a range of the previously described long-term health effects.

The etiology of central sleep apnea, although also not well understood, is hypothesized to result from instability of respiratory control centers White, There are a number of risk factors for OSAincluding: Obesity, male gender, and increasing age Table Young et al.

It is unclear how incidence changes with older age; some data suggest that snoring and OSA may decline after age 65 years Young et al. The pathophysiological roles of these risk factors are not well understood, although evidence suggests that fat deposition in the upper airways, which is more likely in males, contributes to the physical narrow ing that causes OSA Robinson et al.

Menopause also increases the risk of OSA Bixler et al. However, recent studies suggest that there may be a referral bias that results in a lower apparent rate of sleep apnea in females than in males Kapsimalis and Kryger, ; Shepertycky et al.

Epidemiological evidence suggests that hormone replacement therapy lessens the risk of OSA Shahar et al. In children, the main risk factor for OSA is tonsillar hypertrophy, although OSA may also occur in children with congenital and neuromuscular disorders and in children who were born prematurely Rosen et al.

Asthma, a common childhood respiratory illness, is also associated with OSA in children Sulit et al. In adolescents, risk factors may be more similar to those seen in adults and include obesity Redline et al. Being a minority is a risk factor for both increased prevalence and severity of sleep-disordered breathing in both children and adults Rosen et al.

what is the relationship between sleep deprivation and wakefulness

The prevalence of sleep-disordered breathing in the United States is approximately three times higher in middle-aged members of minority groups compared to non-Hispanic whites Kripke et al. African American children are at increased risk, even after adjusting for obesity or respiratory problems Redline et al.

Familial and probably genetic factors strongly contribute to OSA Buxbaum et al. Patients with cardiovascular disease and diabetes are also at higher risk for developing both OSA and central sleep apnea Sin et al. Patients with impaired baroreflexes e. In these patient groups, bradyarrhythmias, hypoxia, hypoperfusion, and sympathetic activation during apnea may predispose to sudden death Somers et al.

Risk Factors for Obstructive Sleep Apnea. Studies of patients at sleep clinics tend to show an association between sleep apnea and mortality He et al. The subgroup experienced twice the risk of mortality Lindberg et al. Other options, although less effective, include a variety of dental appliances Ferguson and Lowe, or surgery e. In children, the first-line treatment for most cases of OSA is adenotonsillectomy, according to clinical practice guidelines developed by the American Academy of Pediatrics Marcus et al.

Children who are not good candidates for this procedure can benefit from CPAP. Central apnea treatment is tailored to the cause of the ventilatory instability. Commonly used treatments include oxygen, CPAP, and acetazolamide, a drug that acts as a respiratory stimulant White, It is a highly prevalent disorder that often goes unrecognized and untreated despite its adverse impact on health and quality of life Benca, a see also Chapter 4.

what is the relationship between sleep deprivation and wakefulness

The diagnostic criteria for primary insomnia include: Difficulty initiating or maintaining sleep or nonrestorative sleep. Causing clinically significant distress or impairment in social, occupational, or other important areas of functioning. Not occurring exclusively during the course of another sleep disorder.

Electroencephalographic changes after one nigth of sleep deprivation

Not due to the direct physiological effects of a substance or a medical condition APA, Insomnia symptoms are remarkably common, affecting at least 10 percent of adults in the United States Ford and Kamerow, ; Ohayon et al. Prevalence is higher among women and older individuals Mellinger et al. Severe insomnia tends to be chronic, with about 85 percent of patients continuing to report the same symptoms and impairment months or years after diagnosis Hohagen et al.

The comorbidity of sleep disorders with psychiatric disorders is covered later in this chapter. Etiology and Risk Factors The precise causes of insomnia are poorly understood but, in general terms, involve a combination of biological, psychological, and social factors. Insomnia is conceptualized as a state of hyperarousal Perlis et al.

Stress is thought to play a leading role in activating the hypothalamic-pituitary axis and setting the stage for chronic insomnia. A key study showed that adults with insomnia, compared with normal sleepers, have higher levels, over a hr period, of cortisol and adrenocorticotropic hormone ACTHwhich are hormones released by the hypothalamic-pituitary-adrenal axis after stress exposure Vgontzas et al.

The hour pattern of cortisol and ACTH secretion is different, however, from that in individuals who are chronically stressed. Cognitive factors, such as worry, rumination, and fear of sleeplessness, perpetuate the problem through behavioral conditioning.

Other perpetuating factors include light exposure and unstable sleep schedules Partinen and Hublin, Insomnia patients often attribute their difficulty sleeping to an overactive brain.

Several lines of evidence, from preclinical to sleep neuroimaging studies in insomnia patients, suggest that there are multiple neural systems arranged hierarchically in the central nervous system that contribute to arousal as well as insomnia complaints.

Disturbances in these systems may differ according to the nature of insomnia. Structures that regulate sleep and wakefulness, for example the brainstem, hypothalamus and basal forebrain, are abnormally overactive during sleep in primary insomnia patients Nofzinger et al.

In addition, limbic and paralimbic structures that regulate basic emotions and instinctual behaviors such as the amygdala, hippocampus, ventromedial prefrontal cortex and anterior cingulate cortex have been shown to be abnormally active during sleep in individuals with primary insomnia and secondary insomnias related to depression Nofzinger et al.

Abnormal activity in neocortical structures that control executive function and are responsible for modulating behavior related to basic arousal and emotions has been observed in individuals with insomnias associated with depression Nofzinger et al. The two main risk factors of insomnia are older age and female gender Edinger and Means, One large, population-based study found that insomnia was nearly twice as common in women than men, although reporting bias cannot be ruled out as a contributing factor Ford and Kamerow, The reason behind the apparent higher prevalence in women is not understood.

Other risk factors for insomnia include family history of insomnia Dauvilliers et al. Although adolescent age is not viewed a risk factor, insomnia has rarely been studied in this age group.

Treatment Insomnia is treatable with a variety of behavioral and pharmacological therapies, which may be used alone or in combination. While the therapies currently available to treat insomnia may provide benefit, the NIH State of the Science Conference on the Manifestations and Management of Chronic Insomnia concluded that more research and randomized clinical trials are needed to further verify their efficacy, particularly for long-term illness management and prevention of complications like depression NIH, Behavioral therapies appear as effective as pharmacological therapies Smith et al.

Behavioral therapies, according to a task force review of 48 clinical trials, benefit about 70 to 80 percent of patients for at least 6 months after completion of treatment Morin et al. The therapies are of several main types Table The major problem with current behavioral therapies is not their efficacy; rather it is lack of clinician awareness of their efficacy and lack of providers sufficiently trained and skilled in their use. Other problems are their cost and patient adherence Benca, a.

The most efficacious pharmacological therapies for insomnia are hypnotic agents of two general types, benzodiazepine or nonbenzodiazepine hypnotics Nowell et al.

what is the relationship between sleep deprivation and wakefulness

Nonbenzodiazepine hypnotics are advantageous because they generally have shorter half-lives, thus producing fewer impairments the next day, but the trade-off is that they may not be as effective at maintaining sleep throughout the night Morin, ; Benca, a. It is still unclear whether hypnotics lead to dependence. It is suggested that they should not be taken for more than 10 days in a row; however, recent studies suggest that hypnotics do not always lead to dependence Hajak et al.

There have been no large-scale trials examining the safety and efficacy of hypnotics in children and adolescents. Other pharmacological classes used for insomnia include sedating antidepressants, antihistamines, and antipsychotics, but their efficacy and safety for treating insomnia have not been thoroughly studied Walsh et al.

The most frequent types of sleep disturbances are insomnia, excessive daytime sleepiness hypersomniaand parasomnia. Sleep disturbances are so commonly seen as symptoms of certain psychiatric disorders that they are listed as diagnostic criteria under DSM-IV APA, For example, insomnia is a symptom used with others to diagnose major depression.

The comorbidity, or coexistence, of a full-blown sleep disorder particularly insomnia and hypersomnia with a psychiatric disorder is also common. The adverse effects of total SD shown in experimental designs have also been confirmed in real-life settings, mainly among health care workers, professional drivers and military personnel Samkoff and Jacques ; Otmani et al ; Philibert ; Russo et al Performance of residents in routine practice and repetitive tasks requiring vigilance becomes more error-prone when wakefulness is prolonged for a review, see Samkoff and Jacques However, in new situations or emergencies, the residents seem to be able to mobilize additional energy sources to compensate for the effects of tiredness.

More recent meta-analysis shows that SD of less than 30 h causes a significant decrease in both the clinical and overall performance of both residents and non-physicians Philibert Motivation What role does motivation play in cognitive performance? Can high motivation reverse the adverse effect of SD? Does poor motivation further deteriorate performance?

According to a commonly held opinion, high motivation compensates for a decrease in performance, but only a few attempts have been made to confirm this theory. Estimating the compensatory effect of motivation in performance during SD is generally difficult, because persons participating in research protocols, especially in SD studies, usually have high initial motivation.

Harrison and Hornesuggest that the deterioration of cognitive performance during SD could be due to boredom and lack of motivation caused by repeated tasks, especially if the tests are simple and monotonous.

They used short, novel, and interesting tasks to abolish this motivational gap, yet still noted that SD impaired performance. In contrast, other researchers suggest that sleep-deprived subjects could maintain performance in short tasks by being able to temporarily increase their attentional effort. When a task is longer, performance deteriorates as a function of time.

A meta-analysis by Pilcher and Huffcutt provides support for that: Based on this, it is probably necessary to make a distinction between mere attentional effort and more general motivation.

Although attentional effort reflects motivational aspects in performance, motivation in a broader sense can be considered a long-term process such as achieving a previously set goal, eg, completing a study protocol.

If one has already invested a great deal of time and effort in the participation, motivation to follow through may be increased. Different aspects of motivation were investigated in a study with 72 h SD, where the subjects evaluated both motivation to perform the tasks and motivation to carry out leisure activities Mikulincer et al Cognitive tasks were repeated every two hours.

Sleep deprivation: Impact on cognitive performance

Performance motivation decreased only during the second night of SD, whereas leisure motivation decreased from the second day until the end of the study on the third day. The authors concluded that the subjects were more motivated to complete experimental testing than to enjoy leisure activities because by performing the tasks, they could advance the completion of the study. Providing the subjects with feedback on their performance or rewarding them for effort or good performance is shown to help maintain performance both in normal, non-deprived conditions Tomporowski and Tinsley and during SD Horne and Pettitt ; Steyvers ; Steyvers and Gaillard As result, no deteriorating effect on cognitive performance was found.

Unfortunately, a non-motivated control group was not included and thus the effect of motivation remained uncertain. In general, since this issue has not been addressed sufficiently, it is difficult to specify the role of motivation in performance.

It seems that motivation affects performance, but it also appears that SD can lead to a loss of motivation. Self-evaluation of cognitive performance It has been suggested that the self-evaluation of cognitive performance is impaired by SD.

During 36 h SD, the subjects became more confident that their answers were correct as the wakefulness continued Harrison and Horne Confidence was even stronger when the answer was actually wrong. In another study, performance was similar between sleep-deprived and control groups in several attentional assessments, but the deprived subjects evaluated their performance as moderately impaired Binks et al The controls considered that their performance was high.

Sleep deprivation

Young people seem to underestimate the effect of SD, whereas older people seem to overestimate it. In a simple reaction time task, both young aged 20—25 years and aging aged 52—63 years subjects considered that their performance had deteriorated after 24 h SD, although performance was actually impaired only in young subjects Philip et al When it comes to the study design and methodology, the way in which the self-evaluation is done may affect the outcome.

The answers possibly reflect presuppositions of the subjects or their desire to please the researcher. The repetition of tasks is also essential. Evaluation ability is poor in studies with one measurement only Binks et al ; Harrison and Horne ; Philip et alwhereas in repeated measures, the subjects are shown to be able to assess their performance quite reliably during 60—64 h SD and recovery Baranski et al ; Baranski and Pigeau Thus, self-evaluation is likely to be more accurate when subjects can compare their performance with baseline.

Chronic partial sleep restriction Although chronic partial sleep restriction is common in everyday life and even more prevalent than total SD, surprisingly few studies have evaluated its effects on cognitive performance. Even fewer studies have compared the effects of acute total sleep deprivation and chronic partial sleep restriction. Belenky and co-workers evaluated the effect of partial sleep restriction in a laboratory setting in groups which were allowed to spend 3, 5 or 7 h in bed daily for seven consecutive days.

The control group spent 9 h in bed. In the 3 h group, both speed and accuracy in the PVT deteriorated almost linearly as the sleep restriction continued.

In this group, performance was clearly the worst. In the 5- and 7 h groups, performance speed deteriorated after the first two restriction nights, but then remained stable though impaired during the rest of the sleep restriction from the third night onwards.

Impairment was greater in the 5- than 7 h group. Accuracy followed the same pattern in the 7 h group, but further declined in the 5 h group as the study went on. Both speed and accuracy were impaired at the beginning of the sleep restriction period followed by a plateau and finally, another drop after the seventh night of deprivation.

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