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Insufficient syndrome By KK Jain MD (Dr. Jain is a consultant in neurology and has no relevant financial relationships to disclose.) Originally released July 9, 1993; last updated July 18, 2017; expires July 18, 2017

Introduction

This article includes discussion of insufficient sleep syndrome, chronic insufficient sleep, sleep deprivation, voluntary sleep curtailment, voluntary sleep reduction, and voluntary sleep restriction. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Sleep deprivation, or insufficient sleep syndrome, is a serious sleep problem of epidemic proportions. Outlined in this article are the causes, consequences, and management of sleep deprivation and ways of recognizing it. In this article, the author elaborates on the clinical manifestations of the condition and the negative consequences of insufficient sleep during pregnancy.

Key points • Insufficient sleep syndrome is the most common cause of daytime sleepiness among the general population. • This condition is due to insufficient duration of sleep nightly, resulting in daytime sleepiness. • Insufficient sleep affects all systems of the body, but cognitive impairment, , and are the most pronounced. • Consequences of insufficient sleep syndrome are often under-recognized by the patient and include sleepiness, tiredness, , and . • Chronic sleep deprivation has been linked to increased risk of automobile and industrial accidents, declining job performance, and disrupted sociability. • Treatment consists of extending nocturnal sleep time every day by 1 to several hours nightly.

Historical note and terminology

Insufficient sleep syndrome, also referred to as “chronic insufficient sleep,” “voluntary sleep curtailment,” “sleep reduction,” “sleep restriction,” “inadequate sleep,” or “sleep deprivation” was first recognized as a clinical syndrome in 1979 with its inclusion in the Diagnostic Classification of Sleep and Arousal Disorders (Association of Sleep Disorders Centers 1979). Sleep deprivation experiments were conducted more than a century ago in an attempt to understand the function of sleep. Since then, several studies have shown that neurologic function and cognition deteriorate during sleep loss, with reaction time, , and judgment from being awake for too long. However, the first series of patients with insufficient sleep syndrome were reported in 1983. Prior to its identification, patients presenting with excessive daytime sleepiness, but having none of the accessory symptoms and signs of , received diagnoses of idiopathic hypersomnolence, NREM narcolepsy, a , or were considered malingerers. In the International Classification of Sleep Disorders (ICSD-3), insufficient sleep syndrome is included in the section “ of central origin” (American Academy of 2014). Diagnostic criteria for idiopathic include lack of improvement of sleepiness after an adequate trial of increased nocturnal time in .

Clinical manifestations

Presentation and course

Insufficient sleep syndrome typically presents in younger to middle-aged adults (25 to 34 years old), with prevalence decreasing with age. It is more common in individuals who work the night shift or more than 40 hours per week. It has a slight female predominance. Patients often report daytime sleepiness that interferes with their activities and functioning. For example, patients with insufficient sleep may inadvertently fall asleep during sedentary activities, such as meetings, reading, watching television or movies, or while driving. Insufficient sleep is associated with an increased risk for motor vehicle accidents (Komada et al 2008).

The sleep history suggests insufficient sleep by the disparity in reported amount of sleep on weekends relative to weekdays, often 2 hours or more. The excessive daytime sleepiness may become more pronounced in the late afternoon and early evening. Sleepiness usually improves during vacations, but patients do not recognize that they have also increased their time in bed. They may have no history of alcohol or illicit drug ; however, some patients consume large amounts of or resort to the use of over-the-counter to combat sleepiness. One half of patients in 1 series had been previously prescribed stimulants.

Symptoms commonly associated with excessive daytime sleepiness of any cause are also seen in insufficient sleep syndrome, including lack of energy, fatigue, muscle weakness, muscle pain, gastrointestinal disturbances, dry mouth, , double vision, difficulties with concentration and attention, reduced motivation, irritability, and dysphoria. Any of these symptoms may become the primary focus of the patient and obscure the excessive daytime sleepiness. Importantly, functional and cognitive impairment due to chronic sleep deprivation is often unrecognized by the sufferer.

Prognosis and complications

Complications of insufficient sleep may involve all systems of the body, and important sequelae are listed in Table 1. Recovery from short-term sleep deprivation may occur by restoration of adequate sleep, but long-term sleep deprivation may result in permanent sequelae.

Table 1. Effects of Insufficient Sleep • Daytime sleepiness • Emotional disturbances • Effects on functions of the brain -- Cognitive impairment -- disorders • Effects on structure of the brain (sleep deprivation studies on rats) -- Reduction of cells in the dentate gyrus of the hippocampus -- Structural changes in the cortical neurons -- Degeneration of locus ceruleus neurons • Effects on body weight -- during insufficient sleep reverses when normal sleep is resumed -- Decrease of appetite-suppressing hormone while levels of , a hunger promoter, increase spurring a greater desire for food • Glucose metabolism -- Glucose tolerance test shows a prediabetic state in otherwise normal persons -- Increased insulin resistance in diabetes • Cardiovascular system -- Hypertension -- Coronary heart disease • Reproductive system -- Impairment of sperm • Genes linked with immune and inflammatory processes: up- or downregulation

The sleepiness associated with insufficient sleep syndrome persists and may get worse without a change in sleep habits. The excessive sleepiness places the subject at increased risk of automobile and industrial accidents, declining job performance, and disrupted social relationships. Sleep deprivation in physicians adversely affects patient care. Impairment of driving abilities due to sleep deprivation is comparable to driving when intoxicated with alcohol and is further exacerbated with concurrent alcohol use. There also are risks associated with excessive caffeine intake or use that often occurs in patients with insufficient sleep syndrome. Other complications of sleep deprivation include , impaired cognitive functions including language tasks, serial subtraction, memory, attention, and decision making.

Many adolescents are sleep deprived and cannot obtain the required 9 hours of nocturnal sleep because of their circadian tendency to have a late and an early start time in school. In adolescents, inadequate sleep impairs attention as well as concentration and has a negative impact on academic performance. One study supports the notion that sleep loss worsens mood states in healthy adolescents, with females having heightened vulnerability (Short and Louca 2015). Findings from the National Sleep Foundation's Sleep in America poll from 2007 revealed that tiredness is an epidemic in adolescents. Twenty-eight percent of high school students admitted to falling asleep at least once a week while in school, and 10% of high school seniors admitted to have nodded off while driving over a 1-year period (National Sleep Foundation 2009). In children, there is also an association between short sleep duration and being overweight (Hart and Jelalian 2008).

Emotional disturbances. A study evaluating the relationship between sleep and the regulation of physical and emotional well-being showed that chronic insufficient sleep (“reduced to at least 50% of habitual time…”) resulted in a more negative mood, with reduced optimism and sociability. Complaints of pain were also observed (Haack and Mullington 2005).

Impairment of brain function. The effects of sleep deprivation on neurocognitive abilities are complex and have been the subject of many studies over the past decade. There is an increasing body of evidence that cognitive complications of sleep deprivation are numerous and are a result of negative effects on the and posterior parietal systems. In addition to prefrontal cortex dysfunction, various brain regions involved in verbal working memory have been evaluated and demonstrated vulnerability in the context of sleep deprivation. Novelty detection, a mechanism that involves the frontal lobes, seems to also be negatively affected in total sleep-deprived patients as it has been shown to be associated with a smaller novel P3 (event-related potential) (Gosselin et al 2005). Furthermore, impairment of orthostatic control of , hypothermia, and decreased postural control have also been observed in experimental models of sleep deprivation in .

Structural changes in hippocampal subfields resulting from sleep deprivation play a role in determining vulnerability to impairment of memory and are also associated with the quality of NREM slow-wave oscillations during recovery sleep; they also play a role in determining the extent of memory restoration (Saletin et al 2016). These findings may serve as a predictive biomarker of susceptibility to memory impairment and recovery from sleep deprivation in professions where memory function is critical and insufficient sleep is prevalent.

Structural and biochemical changes in the brain. Sleep deprivation also has caused structural changes in the central nervous system of rats, including reduction in the proliferation of cells in the dentate gyrus of the hippocampus (Guzman-Marin et al 2003; Roman et al 2005). Sleep-deprived basal forebrain—one of the brain's main wakefulness centers—experiences an increased release of nitric oxide leading to a buildup of adenosine, a nucleoside that can also affect neural function. Sleep deprivation increases heat shock protein expression in mice. In experiments on mice, extended wakefulness results in reduced sirtuin type 3 (SirT3) activity and, ultimately, degeneration of locus ceruleus neurons (Zhang et al 2014). Prolonged wakefulness is a metabolic stressor to locus ceruleus neurons leading to failure of adaptive mitochondrial metabolic responses mediated by SirT3, which coordinates mitochondrial energy production and redox .

Cardiovascular effects. Research in the cardiac effects of sleep deprivation has shown that both acute total and short- term partial sleep deprivation results in elevated high-sensitivity C-reactive protein concentrations, a biomarker of inflammation that has been shown to be predictive of cardiovascular morbidity. A review of clinical trials has shown that sleep deprivation can induce autonomic nervous dysfunction, hypertension, arrhythmia, oxidative stress, endothelial dysfunction, inflammation, and metabolic disorder in coronary heart disease patients (Rong et al 2016).

Effects on the reproductive system. Results of a randomized study on Chinese men showed that sleep deprivation with late bedtime was associated with impaired sperm health in the study cohort, partly through increase of antisperm antibody production in the semen (Liu et al 2017).

Metabolic syndrome. Several epidemiologic studies show an association between sleep duration of less than 6 hours nightly and obesity and diabetes. Sleep restriction decreases glucose tolerance and insulin sensitivity without adequate compensation in beta cell function. Sleep deprivation has also been shown to reduce leptin and increase ghrelin levels, hormones that increase hunger and appetite (Knutson and Van Cauter 2008). Even a relatively brief period of mild sleep deprivation (1.5 hours of sleep loss per night over 3 weeks) can lead to changes in insulin sensitivity and body weight (Robertson et al 2013). Furthermore, sleep deprivation may alter the content of the foods we choose to eat. In a study, 11 subjects increased their consumption of calories from snacks, choosing foods with higher carbohydrate content when sleep deprived to 5.5 hours nightly, as compared to when sleeping 8.5 hours per night (Nedeltcheva et al 2009). A small study looking at cerebral functional MRI showed that subjects who were sleep deprived to 5 hours had a greater increase in brain activity in areas associated with reward when exposed to food stimuli as compared to when they were well rested (St-Onge et al 2012).

Immune system, inflammation, and infection. Systemic infections have been induced in animal models by sleep deprivation. The impact of sleep deprivation on the immune response in humans has been shown to have important consequences. Sleep deprivation has been shown to decrease antibody production following influenza vaccination. In a small study, sleep deprivation dampened the normal circadian T-cell function and regulation, which occurs over a 24- hour period (Bollinger et al 2009). A prospective observational study involving over 50,000 nurses showed that sleeping less than 5 hours per night was associated with a 1.39 relative risk of developing pneumonia (Patel et al 2012).

A study performed on 30 healthy adults who were subjected to partial sleep deprivation (awake from 11 PM to 3 AM) showed alterations in their inflammatory response biomarkers (such as interleukin 6 and tumor necrosis factor alpha), which could lead to , insulin resistance, and osteoporosis (Irwin et al 2006).

Genetic factors in susceptibility to effects of sleep deprivation. Although sleep duration can be influenced by environmental factors and , human familial sleep disorders indicate that there is a strong genetic modulation of sleep. Studies on identical and fraternal twins have shown that resiliency and vulnerability to sleep loss are highly heritable (Kuna et al 2012). There is an ongoing search for genes related to vulnerability phenotype, but none has been identified that can explain the different responses to sleep deprivation. Individual differences in energy balance responses to sleep restriction indicate these responses are phenotypic, with behavioral, physiological, and genetic differences underlying these responses. High-density genome-wide association studies for sleep duration in European populations have identified an intronic variant in the ABCC9 gene that explains approximately 5% of the variation in sleep duration (Allebrandt et al 2013). ABCC9 encodes an ATP-sensitive potassium channel subunit (SUR2), which serves as a sensor of intracellular energy metabolism.

Identification of biomarkers, including genetic polymorphisms related to signaling, are important for predicting an individual's vulnerability to overeating and gaining weight when sleep deprived as they will be an important factor in the management of these problems (Spaeth et al 2015).

Effect of insufficient sleep on circadian rhythms. Sleep homeostasis, circadian rhythmicity, and metabolism are interrelated. In mice, sleep restriction leads to approximately an 80% reduction in circadian transcripts in the brain and severe disruption of the liver transcriptome, whereas in humans, sleep restriction leads to a 1.9% reduction in circadian transcripts in whole blood (Archer and Oster 2015). In spite of significant reduction in the circadian regulation of transcription in peripheral tissues, rhythms within the suprachiasmatic nucleus are not disrupted. Molecular pathways associated with these disruptions point to molecular mechanisms underlying established adverse effects of sleep deprivation.

Clinical vignette

A 27-year-old, right-handed woman presented to the sleep center outpatient clinic for initial evaluation of her longstanding excessive daytime sleepiness. For the past 7 years, the patient had been excessively sleepy during the day, falling asleep in sedentary situations. Specifically, she reported falling asleep when grading her students' papers (she used to fall asleep in class when she was a student herself), in traffic at red lights, when talking to people, and when watching television. She stated that her sleepiness worsened after she began working 2 jobs several years ago. On weekdays, she usually went to bed around 11:30 PM to midnight and got up at 5:30 AM, sleeping a solid 5.5 hours. On weekends, she usually went to bed around 4 AM and slept until noon or 1 PM. When she slept in longer, she felt more refreshed, but was still sleepy and tended to fall asleep, although less frequently, during sedentary situations. She did not take any scheduled . She rarely drank caffeinated beverages. She drank alcohol every other weekend. She denied smoking or using recreational drugs. She denied , gasping for air, spells, or being told she stops breathing when asleep. She denied or hypnagogic . On occasion, however, she endorsed the presence of . She did not have any restless leg symptoms or .

Past medical history. Noncontributory.

Medications. Fexofenadine hydrochloride and fluticasone propionate.

Social history. She was a teacher and a part-time bartender. She was single and lived with her boyfriend. She did not smoke or abuse alcohol or drugs. She only used alcohol in social situations.

Family history. This was significant for excessive daytime sleepiness in an aunt whom she thought may have had obstructive .

Review of systems. Negative for any psychiatric problems.

Neurologic exam. Completely normal.

During all-night , the patient slept for a total of 8.2 hours. Sleep efficiency was normal at 90%. Sleep latency was 5 minutes and REM latency was 63 minutes. No significant sleep-disordered breathing or periodic limb movements of sleep were observed. Urine toxicological screen was normal; a multiple sleep latency test the following day was also normal, with a mean sleep latency of 18.4 minutes.

Soon after the , she went on her summer break and increased her daily sleep significantly. Her symptoms resolved over 10 days.

Biological basis

Etiology and pathogenesis

Insufficient sleep syndrome results when an individual persistently, but unwittingly, fails to obtain a sufficient amount of sleep to maintain normal alertness throughout the day (American Academy of Sleep Medicine 2014). By far, the most common cause of excessive daytime sleepiness in modern society is chronic sleep deprivation. We sleep 25% less than our forebears did a century ago. There is no evidence that they required more sleep than we do or that we require less sleep than they did. In modern societies, sleep deprivation is often driven by socioeconomic factors. Twenty-four hour availability of email, shopping, and stock market information on the Internet, as well as 24-hour news networks and television programming, encourage wakefulness at the expense of sleep. More and more businesses, including fast food restaurants, remain open 24 hours a day and unwittingly contribute to their clients' sleep deprivation. Demands of schools, extracurricular activities, and technology use have increased the incidence of insufficient sleep syndrome among children and adolescents (Calamaro et al 2009).

Sufficient sleep is not measured in absolute hours obtained; rather, it is measured in terms of the amount of sleep an individual needs to maintain alertness relative to the amount of sleep they get. The amount of sleep needed is genetically determined and can vary by individual. Some individuals require 9 hours of sleep per night to maintain normal wakefulness, and if they receive 7 hours they may become hypersomnolent during the day. Average total sleep time for adults is 7.5 to 8 hours, and epidemiological studies indicate that most adults require 7 to 8 hours of sleep to maintain good health. Sleeping less than 6 hours per night is associated with excessive daytime sleepiness (Ohayon 2012). Sleep deprivation is cumulative so that after several nights of moderate sleep restriction, deficits in cognitive performance are equivalent to fewer nights of total sleep deprivation.

The cause of sleepiness in insufficient sleep syndrome is a voluntary restriction of daily sleep time below the individual's specific biological sleep requirements.

Long working hours and shift work increase the risk for insufficient sleep syndrome. Night-shift workers sleep at least 8 hours less each week than do day workers -- an amount equaling the loss of an entire night of sleep every week. A metaanalysis of literature has concluded that health and safety consequences of shift work and insufficient sleep are very similar, and they are likely to share common mechanisms, but further research is required to determine whether insufficient sleep is the cause of adverse health effects associated with shift work (Kecklund and Axelsson 2016). Studies of healthy normal sleepers have shown that a reduction of sleep time by as little as 2 hours per night produces increased daytime sleepiness as measured by the multiple sleep latency test and that the daytime sleepiness accumulates over successive nights of restricted sleep. Most patients with insufficient sleep syndrome are healthy, normal sleepers who chronically deprive themselves of an adequate daily amount of sleep for professional or personal purposes. The extended sleep times these patients report getting on weekends are not sufficient for full recovery (Pejovic et al 2013).

The essential feature of insufficient sleep syndrome is that the patient is biologically normal; thus, the syndrome should be considered a behavioral one. No pathological process disturbs the patient's ability to initiate or maintain sleep and to remain normally alert during the day following a night of adequate amount of sleep for that person.

The resulting sleep deprivation may have an impact on the hypocretin and orexin secreting neurons' responses to noradrenaline (Grivel et al 2005). In this in vitro experiment, it was demonstrated that after a 2-hour sleep deprivation period, the hypocretin and orexin secreting neurons became inhibitory rather than excitatory in response to noradrenaline. This change may be at least in part responsible for the symptom of excessive sleepiness encountered in the insufficient sleep syndrome.

Epidemiology"

Insufficient sleep syndrome is diagnosed in about 2% of patients presenting at United States sleep disorders centers. Insufficient sleep was reported by 23% of a representative survey from Japan (Liu et al 2000), 12% of a representative survey from Sweden (Broman et al 1996), and by 9% of a representative survey from Finland (Hublin et al 1996). In 2008, the Centers for Disease Control and Prevention examined data from over 400,000 subjects throughout the United States and found that 11.1% reported insufficient rest or sleep every day during the preceding 30 days. Females (12.4%) were more likely than males (9.9%), and non-Hispanic blacks (13.3%) were more likely than other racial/ethnic groups, to report insufficient rest or sleep (Centers for Disease Control and Prevention 2009). In a cross- sectional study in Japan, using a web-based questionnaire, health-related quality of life showed that 11% of participants aged 20 to 25 years suffer from insufficient sleep syndrome and that the condition is associated with a social status of student or full-time employee (Morita et al 2015).

Prevention

Education regarding the inevitable consequences of restricted sleep and the cumulative effects of such restriction may reduce the occurrence of insufficient sleep syndrome. Although the relation between sleep time and daytime sleepiness seems obvious to most people, socioeconomic circumstances of individuals can lead to a chronic restriction of sleep time and denial of the obvious cause of the symptoms. Individuals at risk include those working 2 or more jobs, those who report to work extremely early, or those with extensive work and homecare responsibilities. As mentioned above, children and adolescents are becoming more and more at risk for developing insufficient sleep syndrome. It is, therefore, important that health care providers of individuals in this age group inquire about their and counsel patients and families about age-appropriate sleep needs.

Differential diagnosis

Insufficient sleep syndrome is differentiated from narcolepsy based on the absence of the accessory of narcolepsy, from other sleep disorders of excessive sleepiness (ie, sleep apnea syndrome or periodic limb movement disorder based on a polysomnogram showing normal sleep), from insomnia based on absence of difficulty initiating or maintaining sleep, from based on shortened habitual sleep times, and from mood disorders based on the normal psychological screening. The differentiation from idiopathic hypersomnia can be a diagnostic challenge because both entities are associated with high sleep efficiency, difficulty on awaking in the morning, and reduced latency on the multiple sleep latency test. Idiopathic hypersomnia, however, does not respond to trials of increased amount of sleep at night. The diagnosis should not be made when the sleep environment is not conducive to sleep or when the patient's sleep schedule has been acutely restricted due to work or school deadlines, is irregular, or periodically shifts due to changes in the patient's work schedule. In addition, it should not be made when the patient also has an insomnia complaint. In the survey cited above, 54% of those describing themselves as getting insufficient sleep also had insomnia complaints (Broman et al 1996). In other conditions presenting with excessive daytime , such as environmental and posttraumatic hypersomnia, the clinical history is important in establishing the correct diagnosis (American Academy of Sleep Medicine 2014). Diagnostic workup

The person complaining of excessive daytime sleepiness should be asked to increase his or her time of sleep during the week preceding the testing. This is usually documented by having him or her fill out sleep diaries or sleep logs that chart the daily amount of sleep. can also be used to estimate sleep time, but it is not readily available in most sleep centers.

A nocturnal polysomnographic evaluation can be used to establish the patient's sleep. This evaluation, conducted the night before the multiple sleep latency test, will typically show a rapid and maintenance of undisturbed sleep well beyond the patient's reported weekday sleep times. The polysomnogram usually shows a sleep efficiency (sleep time per time in bed) of 90% or greater. A normal progression of sleep stages occurs with unusually low amounts of stage 1 sleep; there is abundant stage 3 and stage 4 sleep and no evidence of a primary sleep disorder, such as and periodic limb movements of sleep. There may also be increased amounts of REM sleep when the sleep restriction has been extreme or of long duration. A multiple sleep latency test that is administered the following day is usually normal with sleep latencies lasting longer than 10 minutes. However, patients with the insufficient sleep syndrome tend to have decreased mean sleep onset latencies. The naps during the multiple sleep latency test have a greater percentage of stage 2 sleep (of more than 80% of the total time) and may include periods of REM sleep that have latencies of 5 minutes or greater. The medical history and physical examination, drug-use history, and psychological screening are all normal.

Management

Management of insufficient sleep syndrome requires a complete evaluation that establishes the presence of excessive daytime sleepiness and rules out the various biological causes of sleepiness. Having reached an accurate diagnosis, the patient can be educated about the reason for excessive sleepiness and instructed to increase nocturnal bedtime or add midday naps, or both, if feasible. Short naps of 10- to 15-minutes duration during the day can improve alertness and performance. With increase of daily sleep time every day of the week, sleepiness should resolve in a matter of weeks. However, patient cooperation is often difficult to attain because the circumstances that led to reduced sleep time may be difficult to alter. If a 2-week or longer trial of extended sleep fails, the diagnosis must be reconsidered.

Stimulants are rarely indicated and are not a substitution for obtaining an adequate amount of sleep. Caffeine is the most commonly used stimulant in the world and may be an effective alternative in managing short-term, limited sleep deprivation. and armodafinil have been shown to improve alertness but are approved by the U.S. Food and Drug Administration only in the context of treating sleepiness from shift work disorder, narcolepsy, or residual excessive daytime sleepiness, despite adequate treatment of obstructive sleep apnea (Darwish et al 2009).

Sleep deprivation as a therapeutic measure for . This article deals with adverse effects of insufficient sleep, and depression is listed among these. However, sleep deprivation has been used for treatment of depression since the 1970s. An fMRI study demonstrated that sleep deprivation reduced functional connectivity between the posterior cingulate cortex and the bilateral anterior cingulate cortex, but enhanced connectivity between the dorsal nexus and the distinct areas in the right dorsolateral prefrontal cortex (Bosch et al 2013). Although the onset of the therapeutic effect of sleep deprivation is rapid, the duration of action is short-lived. A systematic review of clinical studies combining sleep deprivation with repetitive transcranial stimulation indicates some augmentation of antidepressant effect, but more studies are needed to confirm this (Tang et al 2015).

Special considerations

Pregnancy

Up to 15% of women report insufficient sleep during pregnancy (Okun et al 2013). Insufficient sleep and short sleep duration during pregnancy greatly increase the risk for preterm birth, gestational hyperglycemia, and depression symptoms (Micheli et al 2011; Okun et al 2013; Herring et al 2014).

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Former authors

Timothy Roehrs PhD (original author), Hrayr P Attarian MD, Daniela N Minecan MD, Michael Zupancic MD, and Leslie M Swanson PhD

ICD and OMIM codes

ICD codes

ICD-9: Transient disorder of initiating or maintaining sleep: 307.41 Persistent disorder of initiating or maintaining sleep: 307.42

ICD-10: Nonorganic insomnia: F51.0 Other nonorganic sleep disorder: F51.8

Profile

Age range of presentation

13-18 years 19-44 years 45-64 years 65+ years

Sex preponderance male=female

Family history none

Heredity none

Population groups selectively affected none selectively affected

Occupation groups selectively affected none selectively affected

Differential diagnosis list narcolepsy other sleep disorders of excessive sleepiness sleep apnea syndrome periodic limb movement disorder idiopathic hypersomnia mood disorder insomnia complaints

Other topics to consider Advanced sleep-wake phase disorder Delayed sleep phase syndrome Drug-induced sleep disorders Environmental and behavioral sleep disorders Hypersomnolence Irregular sleep-wake rhythm disorder disorder Non-24-hour sleep-wake rhythm disorder Shift-work sleep disorder Sleep and cerebral degenerative disorders Sleep and Sleep disorders

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