Insufficient sleep syndrome

Sleep Disorders

Updated 06.14.2024
Released 07.09.1993
Expires For CME 06.14.2027

Insufficient sleep syndrome

Authors: Lourdes M DelRosso MD PhD, Farnaz Abbasimoradi MD

See Contributor Disclosures

Editor: Antonio Culebras MD FAAN FAHA FAASM

Insufficient sleep syndrome

In This Article

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Introduction

Overview

Insufficient sleep syndrome is a serious sleep problem of epidemic proportions. Outlined in this article are the causes, consequences, and management of insufficient sleep syndrome and ways of recognizing it. This article describes the clinical manifestations of the condition and the negative consequences of insufficient sleep on various body functions and neurologic disorders.

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 and other symptoms.
	• Insufficient sleep affects all systems of the body.
	• Consequences of insufficient sleep syndrome are often under-recognized by the patient and include sleepiness, tiredness, fatigue, and irritability, among others.
	• 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 one 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 (06). Sleep deprivation experiments were conducted more than a century ago to understand the function of sleep. Since then, several studies have shown that neurologic function and cognition deteriorate during sleep loss, with reaction time, mood, and judgment suffering 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 narcolepsy, received diagnoses of idiopathic hypersomnolence, NREM narcolepsy, a mood disorder, or were considered malingerers. In the International Classification of Sleep Disorders (ICSD-3-TR), insufficient sleep syndrome is included in the section “Central Disorders of Hypersomnolence” (03). The current established diagnostic criteria state that the symptoms of daytime sleepiness must be secondary to a curtailed sleep pattern present on most days for at least 3 months, as evidenced by sleep logs and actigraphy, demonstrating shorter sleep for age. A key in the diagnosis is that symptoms resolve once sleep extension is instituted.

Clinical manifestations

Presentation and course

	• Persons affected by insufficient sleep syndrome report daytime sleepiness or behavioral abnormalities attributed to the sleepiness. These interfere with their activities and functioning.
	• Other symptoms commonly associated with insufficient sleep include lack of energy, muscle weakness, muscle pain, gastrointestinal disturbances, headache, and difficulties with concentration and attention.
	• Various functions of the body are affected.

Insufficient sleep syndrome affects all ages and both sexes.

Patients with sleep insufficiency 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 by affecting visual search patterns and response times to hazards (46).

The sleep history suggests insufficient sleep by the disparity in reported amount of sleep, often 2 hours or more, when the patient is given the opportunity to sleep ad lib (ie, on a holiday). The excessive daytime sleepiness may become more pronounced in the late afternoon and early evening. Sleepiness usually improves during vacations or holidays. Other symptoms include lack of energy, fatigue, muscle weakness, muscle pain, gastrointestinal disturbances, dry mouth, headache, blurred 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. Consequences of Insufficient Sleep

	• Daytime sleepiness • Anxiety and depression • Neurocognitive
		-- Cognitive impairment -- Memory disorders
	• Neurologic consequences
		-- Reduction of cells in the dentate gyrus of the hippocampus -- Structural changes in the cortical neurons -- Degeneration of locus ceruleus neurons
		-- Activation of interictal EEG and precipitation of seizures in epileptic subjects (40)
		--Increased accumulation of beta amyloid proteins, even in 1 day of sleep deprivation
	• Metabolic consequences
		-- Weight gain during insufficient sleep reverses when normal sleep is resumed -- Decrease of appetite-suppressing hormone leptin whereas levels of ghrelin, a hunger promoter, increase spurring a greater desire for food
		-- Glucose tolerance test shows a prediabetic state in otherwise normal persons -- Increased insulin resistance in diabetes
	• Cardiovascular
		-- Atherosclerosis -- Coronary heart disease -- Increased risk of hypertension
	• Immunological
		-- Response to vaccine
		-- Reaction to infection
	• Reproductive system
		-- Impairment of sperm health
	• Genes linked with immune and inflammatory processes: up- or downregulation • Effects related to disruption of circadian rhythms and insufficient sleep --Increased risk of cancer
	• Disturbance of thermal homeostasis -- Susceptibility to cold- and heat-related illnesses

Sleepiness associated with insufficient sleep syndrome persists and may get worse without a change in sleep habits. 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 stimulant use that often occurs in patients with insufficient sleep syndrome. Other complications of sleep deprivation include headaches, impaired cognitive functions including language tasks, serial subtraction, memory, attention, and decision making.

In children and adolescents, inadequate sleep impairs attention and concentration and negatively impacts academic performance (11).

A new field of research on bedtime procrastination illuminates a multifaceted phenomenon deeply entrenched in the fabric of modern society. It is defined as the volitional delay of going to bed, without any cause for the delay, resulting in insufficient sleep (20) and has been found to be associated with a myriad of variables, ranging from work obligations to the rigors of parenthood. Studies have demonstrated deficits in self-control and attentional impulsivity. Notably, the insidious allure of smartphone addiction emerges as a potent modulator, exerting its sway over procrastinatory tendencies (16).

Furthermore, psychological stress contributed to further smartphone addiction during the COVID-19 pandemic. In a study by Ma and colleagues, bedtime procrastination predicted the severity of poor sleep quality in children (30).

Anxiety and depression. Chronic insufficient sleep usually results in a more negative mood, with reduced optimism and sociability. Sleep is a potential biomarker for suicidal behavior. A systematic review of literature has revealed a significant association between sleep disturbances and risk of suicide with significant contribution from sleep deprivation-induced neurocognitive deficits, emotional dysregulation, and negative feelings, among other factors (43).

Chronic sleep deprivation is associated with elevated cortisol and decreased testosterone levels. Testosterone is known to enhance the function of the gamma-aminobutyric acid and serotonin systems in the brain. This reduced function provides one possible causal link between two of the most commonly associated psychiatric disorders, depression, and anxiety.

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 prefrontal cortex 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.

Structural changes in human 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 (41). 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. A double-blind, placebo-controlled randomized study to determine the impact of sleep restriction (reduction of 1 hour of habitual sleep duration) on cognitive performance showed impairment of a test of working memory but no effect on tests of sustained attention or decision making (42). Sleep deprivation causes impairment of cognitive flexibility, ie, feedback is less effective in driving behavior modification under changing circumstances (22).

Sleep deprivation may affect the performance in professions requiring intact cognitive function. There has been considerable concern about the performance of overworked and sleep-deprived residents in university hospitals. A study has shown that sleep-deprived surgeons' technical skills are between 11.9% and 32% negatively impacted in a standardized simulated environment, which is likely to have clinical implications for patient safety (50).

Structural and biochemical changes in the brain. Several experimental studies in rats have shown that sleep deprivation causes structural changes in the central nervous system. 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 (51). 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 homeostasis.

Animal studies have indicated that sleep is essential for maintenance of integrity of cell membranes and myelin in the brain, which are susceptible to sleep deprivation. A diffusion tensor imaging study of normal human volunteers showed that sleep deprivation was associated with widespread decreases in fractional anisotropy that indicate reductions in axial diffusivity, mainly including bilateral frontotemporal and parieto-occipital white matter, the corpus callosum, the thalamus, and the brain stem (14). The findings of this study are consistent with the view that microstructural changes occur in the white matter of the adult human brain over hours to days of sleep deprivation. Permeability of the blood-brain barrier is increased in rats subjected to sleep loss of long duration and is restored following sleep recovery. An ultrastructural study in rats has shown that chronic sleep loss disrupts interendothelial junctions that leads to blood-brain barrier hyperpermeability in the hippocampus (23). The authors of the study suggest that this is because expression of claudin-5, which regulates blood-brain barrier permeability by modifying brain microvascular endothelial cells, is decreased after chronic sleep loss as compared to intact animals.

Diffusion tensor imaging has been applied to the study of diseases characterized by cognitive instability, which is amplified by sleep deprivation and measured by number of lapses on the psychomotor vigilance test (52). There was a considerable inter-individual variation of cognitive instability in response to sleep deprivation, which was associated with differences in white matter integrity.

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 patients with coronary heart disease (39). Furthermore, sleep insufficiency positively associates with systolic blood pressure or diastolic blood pressure fluctuations (01).

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 (29).

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 (26). Even a relatively brief period of mild sleep deprivation (one and half hours of sleep loss per night over 3 weeks) can lead to changes in insulin sensitivity and body weight (38). 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 (33). 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 (45).

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 (08). 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 (35).

Genetic factors in susceptibility to effects of sleep deprivation. Although sleep duration can be influenced by environmental factors and chronotype, 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 (27). 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 (02). 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 orexin 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 (44).

Sleep deprivation and the epigenome. Although neuronal effects of sleep deprivation start at the DNA and RNA level resulting in dysregulation of cognitive functions, the epigenome plays an important role in regulating gene expression in this context (15). One example is that sleep deprivation disrupts the cyclic adenosine 3′,5′-monophosphate (cAMP) pathway and CREB (cAMP response element-binding) protein, which mediates histone deacetylase inhibitors, a common epigenetic mechanism.

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 (05). Despite 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.

Increased risk of cancer due to disruption of circadian rhythms and insufficient sleep. Epidemiologic studies suggest increased risk for breast cancer in night- and rotating-shift female workers, which may be due to several interconnected mechanisms resulting from shift work, such as suppression of melatonin by exposure to light at night, impairment of the immune system due to sleep-deprivation, and metabolic changes with generation of proinflammatory reactive oxygen species (18). This topic, however, is controversial. A large prospective study in Sweden found no association between insufficient sleep and risk of prostate cancer (31).

Disturbance of thermal homeostasis. Short-term, ie, less than or equal to four nights, sleep deprivation can disturb thermal homeostasis, which affects autonomic and behavioral thermoeffectors during acute exposure to low and high ambient temperatures (25). This may be a predisposing factor for the development of thermal injuries.

Sleep deprivation and neurologic disorders. The MedLink article on insomnia describes sleep disorders that occur in various neurologic disorders. The impact of sleep deprivation in several neurologic disorders has been reviewed (07). Important findings are summarized in a Table 2.

Table 2. Effect of Sleep Deprivation on Neurologic Disorders Disease

Neurologic disorders disease	Role of sleep deprivation (SD)
Alzheimer disease (AD)	Sleep deprivation increases neuronal firing, upregulates BACE1 proteins, and aggravates neuroinflammation and oxidative stress in Alzheimer disease. Sleep deprivation-induced impairment of clearance of toxins through glymphatic pathway leads to the accumulation of amyloid beta and tau proteins. Sleep deprivation has a negative impact on the cholinergic neurons with cognitive dysfunction and impaired memory.
Parkinson disease (PD)	Sleep deprivation causes downregulation of D2/D3 receptors through decreased wakefulness and other altered behavioral effects, which are mediated through the dopaminergic system and result in Parkinson disease-like symptoms. Sleep deprivation-induced impairment of clearance of toxins through glymphatic pathway leads to the accumulation of alpha-synuclein.
Huntington disease	Sleep deprivation disturbs balanced discharge and firing of basal ganglia, which require appropriate REM sleep and wakefulness. Sleep deprivation adversely affects the cerebellar and basal ganglia loops, which may in turn lead to pathogenesis of Huntington disease.
Multiple sclerosis	Disruption of circadian rhythm by sleep deprivation leads to the release of cellular and molecular inflammatory mediators, which cause neuroimmune dysregulation. Sleep deprivation affects the expression of genes involved in the synthesis and maintenance of the myelin proteins.
Stroke	Sleep deprivation aggravates pathophysiology of stroke by increasing the expression of growth-inhibiting genes, neuroinflammation, and oxidative stress. Sleep deprivation following cerebral ischemia increases the levels of growth-inhibiting gene Neurocan, which forms a barrier and inhibits neuronal reconnection and recovery by neuroplasticity.
Epilepsy	Sleep deprivation initiates epileptic seizures and facilitates epileptiform discharges.
Autism spectrum disorders (ASD)	Sleep deprivation is associated with an increase in the severity of autism scores and affects the daily functioning of autism spectrum disorder patients.
Neuropathic pain	In animal experimental studies, sleep deprivation following chronic constriction injury increases microglial activation in the cuneate nucleus and aggravates neuropathic pain induced by nerve injury.

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 two 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 naps. She rarely drank caffeinated beverages. She drank alcohol every other weekend. She denied smoking or using recreational drugs. She denied snoring, gasping for air, choking spells, or being told she stops breathing when asleep. She denied cataplexy or hypnagogic hallucinations. On occasion, however, she endorsed the presence of sleep paralysis. She did not have any restless leg symptoms or insomnia.

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 sleep apnea.

Review of systems. Negative for any psychiatric problems.

Neurologic examination. Completely normal.

Actigraphy confirmed the patient’s clinical history, showing an average sleep time of 5.5 hours at night during weekdays and 8 to 9 hours during the weekends.

After actigraphy was done, she went on her summer break and increased her daily sleep significantly. Her symptoms resolved over 10 days. No further evaluation was needed.

Biological basis

Etiology and pathogenesis

	• Chronic sleep deprivation is the most common cause of excessive daytime sleepiness.
	• 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.
	• Several metabolomic biomarkers have been identified in experimental insufficient sleep in human volunteers, of which the most important ones involved ATP binding cassette transporters.
	• Sleep deprivation may have an impact on the hypocretin and orexin secreting neurons, which may explain the resulting excessive sleepiness.

Insufficient sleep syndrome results when an individual fails to obtain sufficient to maintain normal alertness throughout the day (03). By far, the most common cause of excessive daytime sleepiness in modern society is chronic sleep deprivation. Twenty-four-hour availability of smartphones, 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 (47).

Sufficient sleep is not measured in absolute hours obtained; rather, it is measured in terms of the amount of sleep that individuals need 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 sleepy during the day. Average total sleep time for adults is seven and a half 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 (21). 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 are like insufficient sleep syndrome, 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 (24).

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 (36).

A study found that cognitive impairment caused by sleep loss varies considerably among individuals and resembles the effect of alcohol intoxication; molecular brain imaging showed that ethanol induces an upregulation of cerebral A1 adenosine receptors with increase up to 26% like in sleep deprivation (13). Therefore, targeting the brain’s adenosine system might enable discovery of countermeasures against cognitive impairment induced by both sleep deprivation and alcohol intoxication.

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.

Sleep deprivation modulates the gain control and synaptic gating in orexin neurons, which tune them to strong wake-promoting excitatory signals, while dampening weak synaptic inputs to allow transition to sleep in the absence of such strong signals (10).

Biomarkers of insufficient sleep. Biomarkers may be indicators of various disturbances in the human body that may be either causes or effects of insufficient sleep. They may offer insight into pathomechanisms and form the basis of diagnostic tests and help in monitoring the effect of management.

A machine-learning approach using panels of 6 to72 mRNA biomarkers showed that accuracy of classifying acute sleep loss was 92%, but only 57% for classifying chronic sleep insufficiency, and there was little overlap with biomarkers for circadian phase (28).

A crossover laboratory study on humans undergoing experimental insufficient sleep identified 65 metabolomic biomarkers, of which the most important ones involved ATP binding cassette transporters in lipid homeostasis, phospholipid metabolic process, plasma lipoprotein remodeling, and sphingolipid metabolism (12). These biomarkers require further development and validation to advance our understanding of the ill effects of insufficient sleep, improve diagnosis of sleep disorders, and identify targets for interventions to counteract the negative health consequences of insufficient sleep.

Differential diagnosis

Confusing conditions

Insufficient sleep syndrome is differentiated from narcolepsy based on the absence of the accessory signs and symptoms 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 idiopathic hypersomnia 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 waking 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 other conditions presenting with excessive daytime somnolence, such as environmental sleep disorder and posttraumatic hypersomnia, the clinical history is important in establishing the correct diagnosis (03).

A neuropsychological study has shown that the effect of insufficient sleep at baseline can make a non-injured athlete look like a concussed athlete with sufficient sleep because of cognitive underperformance, which would skew post-concussion comparisons (37). Therefore, there may need to be consideration of prior night's sleep when determining whether a baseline can be used as a valid comparison.

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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Authors

Lourdes M DelRosso MD PhD

Dr. DelRosso University of Washington School of Medicine has no relevant financial relationships to disclose.
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Farnaz Abbasimoradi MD

Dr. Abbasimoradi of the University of California San Francisco has no relevant financial relationships to disclose.
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Editor

Antonio Culebras MD FAAN FAHA FAASM

Dr. Culebras of SUNY Upstate Medical University at Syracuse has no relevant financial relationships to disclose.
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Former Authors

Timothy Roehrs PhD
Hrayr P Attarian MD
Daniela N Minecan MD
Michael J Zupancic MD
Leslie M Swanson PhD
K K Jain MD†

Patient Profile

Age range of presentation: 13 to 65+ years
Sex preponderance: male=female
Heredity: none
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

ICD & OMIM codes

ICD-10: Nonorganic insomnia: F51.0

Other nonorganic sleep disorder: F51.8
ICD-11: Insufficient sleep syndrome: 7A26

Insomnia disorders, unspecified: 7A0Z

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Insufficient sleep syndrome

Differential Diagnosis

narcolepsy
other sleep disorders of excessive sleepiness
sleep apnea syndrome
periodic limb movement disorder
idiopathic hypersomnia
- mood disorder
- insomnia complaints
- 24. Other topics to consider
- Advanced sleep-wake phase disorder
- Delayed sleep phase syndrome
- Drug-induced insomnia and excessive daytime sleepiness
- Drug-induced parasomnias, sleep apnea, and restless legs syndrome
- Environmental and behavioral sleep disorders
- Hypersomnolence
- Insomnia
- Irregular sleep-wake rhythm disorder
- Jet lag disorder
- Non-24-hour sleep-wake disorder
- Shift work disorder
- Sleep and cerebral degenerative disorders
- Sleep and dementia
- Sleep disorders

Clinical Categories

Sleep Disorders

Patient Handouts

Web References

Clinical Trials

NIH: Sleep Disorders

Insufficient sleep syndrome

Insufficient sleep syndrome

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Table 1. Consequences of Insufficient Sleep

Table 2. Effect of Sleep Deprivation on Neurologic Disorders Disease

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Special considerations

Pregnancy

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

Telehealth and cognitive behavioral therapy for insomnia (CBT-I)

NonREM parasomnias

Neurologic disorders associated with obesity

Hypersomnolence

Sleep disorders in women

Sleep, stroke, and vascular dementia

Parasomnia overlap disorder and status dissociatus

Stimulant-dependent sleep disorder

	• Clinical history and physical exam
	• Sleep diaries charting the daily amount of sleep
	• Actigraphy

	• Education of the patient about the reason for excessive sleepiness
	• Sleep extension

Insufficient sleep syndrome

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Table 1. Consequences of Insufficient Sleep

Table 2. Effect of Sleep Deprivation on Neurologic Disorders Disease

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Special considerations

Pregnancy

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Telehealth and cognitive behavioral therapy for insomnia (CBT-I)

NonREM parasomnias

Neurologic disorders associated with obesity

Hypersomnolence

Sleep disorders in women

Sleep, stroke, and vascular dementia

Parasomnia overlap disorder and status dissociatus

Stimulant-dependent sleep disorder

This is an article preview.
Start a Free Account
to access the full version.