Environmental and behavioral sleep disorders …

Sleep Disorders

Updated 01.27.2024
Released 01.18.1994
Expires For CME 01.27.2027

Environmental and behavioral sleep disorders

Authors: Roneil Gopal Malkani MD MS, Mariam Mirza MD

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Editor: Bradley V Vaughn MD

Environmental and behavioral sleep disorders

In This Article

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Introduction

Overview

Environmental and behavioral sleep disorders encompass all disorders that cause sleep disruption or excessive daytime sleepiness, resulting from exogenous factors, ie, the causes originate from outside the body. Removal of these external factors leads to resolution of the sleep disorder. In this article, the authors review environmental and behavioral sleep disorders. This clinical article update reflects the organization system found in the International Classification of Sleep Disorders, 3rd edition (ICSD-3).

Key points

	• Behavioral and environmental sleep disorders may appear at any age.
	• Multiple environmental sleep disorders may occur simultaneously in the same patient, which may pose challenges to treatment.
	• Behavioral and environmental sleep disorders can also be related to drug or substance abuse.
	• Removal of the inciting environmental factor can ultimately lead to resolution of the subsequent sleep disorder.

Historical note and terminology

The first International Classification of Sleep Disorders (ICSD) listed 13 extrinsic sleep disorders (06). Extrinsic sleep disorders are those that result in sleep disruption or excessive daytime sleepiness from causes that arise outside the body. This contrasts with intrinsic sleep disorders, which lead to sleep disruption or excessive daytime sleepiness due to factors that are based within various body systems. The International Classification of Sleep Disorders, 2nd edition (ICSD-2), did not use the term “extrinsic sleep disorders.” Instead, diagnoses previously listed in this category fell into various categories: insomnia; hypersomnias of central origin not due to a circadian rhythm sleep disorder, sleep-related breathing disorder, or other cause of disturbed nocturnal sleep; circadian sleep disorders; and other sleep disorders (02). For some of the original extrinsic sleep disorders, this designation was continued in the International Classification of Sleep Disorders, 3rd edition (ICSD-3), see Table 1. However, the ICSD-3 eliminated the specific diagnostic criteria for many of the extrinsic sleep disorders (03).

Inadequate sleep hygiene, behavioral insomnia of childhood (both limit-setting and sleep-onset type), and insomnia due to drug or substance use are now part of a single diagnosis of chronic insomnia. The American Academy of Sleep Medicine eliminated these diagnostic subtypes due to the large amount of overlap between them, the difficulty in clinically identifying a single factor as the cause of many patients’ insomnia, and common treatment modalities for these subtypes (04). In the case of behavioral insomnia of childhood, the factors related to this subtype can often be seen in many age groups and its defining features are ultimately the same as those for global insomnia. Although there are no longer specific diagnostic criteria for the above-mentioned extrinsic sleep disorders, these subtypes may still be of use in clinical practice when assessing and treating a patient with sleep disorders (47). Additionally, adjustment insomnia is now named short-term insomnia disorder. Environmental sleep disorder is a component of “other sleep disorder” in the ICSD-3TR as it is rarely diagnosed in clinical practice and there is controversy regarding it as a true clinical diagnosis (04). The clinical manifestations, etiology, pathophysiology, diagnostic evaluation, and management of each diagnosis will be discussed in this clinical article as they are found in the ICSD-3TR.

Table 1. Extrinsic Sleep Disorders

Sleep Disorders from ICSD-1 Criteria	ICSD-3 Category
Inadequate sleep hygiene	Insomnia
Environmental sleep disorder	Other sleep disorder and normal variant
Adjustment insomnia	Insomnia
Behaviorally induced insufficient sleep syndrome	Central disorder of hypersomnolence
Behavioral insomnia of childhood, limit-setting type	Insomnia
Behavioral insomnia of childhood, sleep-onset type	Insomnia
Insomnia due to drug or substance	Insomnia
Hypersomnia due to drug or substance	Central disorder of hypersomnolence
Other circadian rhythm sleep disorder due to drug or substance	Circadian rhythm sleep-wake disorder

Clinical manifestations

Presentation and course

	• Common complaints with extrinsic sleep disorders include sleep-onset and/or sleep-maintenance insomnia, poor sleep quality, frequent nocturnal awakenings, and daytime sleepiness.
	• Sleep disruption from these disorders can lead to excessive daytime sleepiness; emotional disturbances; difficulties with attention span, concentration, memory, and executive function; and impaired occupational and academic performance.
	• Short sleep duration is associated with obesity and metabolic disorder.
	• Contributors to extrinsic sleep disorders include poor sleep hygiene, stress, noise, inappropriate light exposure, and medications or other substances.

Sleep problems are common in the general population and have been identified as an important contributor to poor health and well-being (51). The American Academy of Sleep Medicine and Sleep Research Society recommend seven to nine hours of sleep for optimum health in an adult (62). Similarly, The American Academy of Sleep Medicine has made recommendations for sleep associated with better health outcomes in pediatric populations by age (Table 2) (49). Environmental and behavioral sleep disorders can often contribute to poor sleep and should be evaluated in patients who are not obtaining the recommended amount of sleep for their age group.

Extrinsic sleep disorders can cause nighttime and daytime symptoms. Sleep-onset and/or sleep-maintenance insomnia, poor sleep quality, and frequent nocturnal awakenings are common complaints in patients with extrinsic sleep disorders. Individuals may report difficulty with their daytime level of functioning, which is often attributed to excessive daytime sleepiness. Insomnia and excessive daytime sleepiness may occur concordantly and can further impair a patient’s overall quality of life.

Patients may report various degrees of cognitive dysfunction, and these symptoms must be investigated further by the clinician. Studies have shown that attention span, working memory, and executive function are impaired in patients with insomnia (46). In children with insomnia, daytime behavioral problems, cognitive impairment, and mood disturbances (largely depression) have been reported (47). Insomnia has also been shown to increase the risk of cardiovascular disease and type II diabetes (51). Short sleep duration has been associated with obesity and metabolic disorder and can ultimately increase mortality (41; 51). Sleep plays an essential role in the healthy growth and development of children; however, sleep disorders are often underdiagnosed by primary medical providers and pediatricians (25). In both the pediatric and adult population, insomnia is associated with an increased risk of accidents (motor vehicle accidents, workplace accidents, self-harm) and may even be associated with an increased risk of child abuse for children with insomnia (41; 47; 51). Uncontrolled asthma has been associated with insomnia symptoms, whereas controlled or partially controlled asthma was not (58). Therefore, patients presenting with these seemingly unrelated medical problems should also have a screening for insomnia or poor sleep to determine if there is an intrinsic or extrinsic factor causing sleep disturbance.

Table 2. Age-Appropriate Recommendations for Adequate Sleep

	Hours of sleep per 24 hours
Infants 4 to 12 months	12 to 16
Children 1 to 2 years	11 to 14
Children 3 to 5 years	10 to 13
Children 6 to 12 years	9 to 12
Teenagers 13 to 18 years	8 to 10

Chronic insomnia related to extrinsic factors. Chronic insomnia is characterized by difficulty with falling asleep or maintaining sleep. The ICSD-3 gives six diagnostic criteria for chronic insomnia that incorporate the previous definitions of inadequate sleep hygiene and behavioral insomnia of childhood.

Table 3. ICSD-3 Criteria for Chronic Insomnia

• The patient reports, or the patient’s parent or caregiver observes, one or more of the following:
	1. Difficulty initiating sleep 2. Difficulty maintaining sleep 3. Waking up earlier than desired 4. Resistance to going to bed on appropriate schedule 5. Difficulty sleeping without parent or caregiver intervention
• The patient reports, or the patient’s parent or caregiver observes, one or more of the following related to the nighttime sleep difficulty:
	1. Fatigue or malaise 2. Attention, concentration, or memory impairment 3. Impaired social, family, occupational or academic performance 4. Mood disturbance or irritability 5. Daytime sleepiness 6. Behavioral problems (eg, hyperactivity, impulsivity, aggression) 7. Reduced motivation or energy or initiative 8. Proneness for errors or accidents 9. Concerns about or dissatisfaction with sleep
• The reported sleep-wake complaints cannot be explained purely by inadequate opportunity (ie, enough time is allotted for sleep) or inadequate circumstances (ie, the environment is safe, dark, quiet, and comfortable) for sleep.
• The sleep disturbance and associated daytime symptoms occur at least three times per week.
• The sleep disturbance and associated daytime symptoms have been present for at least three months.
• The sleep-wake difficulty is not better explained by another sleep disorder.

Sleep hygiene is an important factor in chronic insomnia and includes various activities and behaviors that, in certain individuals, cause sleep disruption. These behaviors may seem innocuous, but alone or in combination, they cause difficulties with sleep onset or sleep maintenance. Activities that contribute to inadequate sleep hygiene may be due to dietary factors (eg, use of caffeine or alcohol close to bedtime) or behavioral tendencies (eg, unusual late-evening exercise, nighttime social engagements, smoking, watching television, or other inappropriate light exposures such as with use of computers or other devices with screens such as phones and tablets). In children 5 to 17 years of age, screen time such as computer use, video game, mobile devices, and television is associated with later bedtime and shorter sleep duration (Hale and Guan 2015). Use of mobile phones after lights out is a common behavior in adolescence and has been reported to have a negative impact on sleep quality (52). A suboptimal sleeping environment, such as one shared with pets or one that is not comfortable, or lack of a regular sleep-wake schedule can also cause sleep disruption. Participation in stressful activities, such as working or studying in the bedroom or close to bedtime, can also worsen sleep hygiene. Poor sleep quality is associated with poor academic performance in high school children (13). Some individuals may exhibit inadequate sleep hygiene persistently, whereas others may only do so on occasion.

Chronic insomnia in children may also be due to what was previously characterized as behavioral insomnia of childhood. This may be due to a child’s refusal or resistance to bedtime, known as “limit-setting type.” The child intentionally remains awake and often makes several requests or employs various stalling techniques to delay going to sleep. Behaviors may include requests for drinks, bathroom trips, television, or books; they may also involve a refusal to stay in the bed or even in the bedroom. These behaviors often result from parental difficulties with setting firm, consistent limits in response to these actions, eg, allowing the child to stay up late on weekends. Children may report fear at bedtime. In some children, this may be due to separation anxiety; in others, there is no related anxiety but, rather, a realization that reports of fear may successfully delay bedtime. When co-sleeping occurs, parental problems with limit-setting may also influence parents’ responses to nocturnal awakenings. Children may leave the bed or call for their parents three to five times per night, resulting in a total loss of one to two hours of sleep (45). Difficulties with limit setting may not be seen until a child has transitioned from a crib to a bed or when a child can climb out of a crib (03). The etiology of bedtime resistance and night waking in childhood is multifactorial due to biological, circadian, and neurodevelopmental factors that interact with environmental and behavioral variables. Furthermore, parents or caregivers may not set or enforce regular bedtimes and wake-up times. If a child is allowed to “sleep in” on weekend days, then the child will likely have difficulty with sleep onset those following nights. This may also be seen in cognitively impaired older adults who are allowed to sleep throughout the day and stay awake at night instead of setting daytime limits for napping (03). Behavioral interventions for children (such as unmodified extinction, graduated extinction, positive routines/faded bedtime, and scheduled awakenings) have shown to significantly improve sleep-onset latency, night waking frequency, and night waking duration (34).

In the prior sleep-onset association form of behavioral insomnia of childhood, a child “associates” behaviors or environments with the act of sleeping (47). These include falling asleep while feeding, rocking, driving in a car, or with bottle or pacifier. The environment the child falls asleep in must be recreated through the entirety of the night. Normally, children awaken approximately six to eight times nightly. If the child does not see the same environment as that in which he fell asleep during these normal awakenings, the child will cry out, and parents typically need to recreate the initial environment for sleep to continue. In the absence of these conditions, sleep onset is delayed and nocturnal awakenings may also occur; sleep occurs quickly when these conditions are restored. This disorder most often results in children waking up two to three times a night for five to 10 minutes at least five days a week (45). The ICSD-3 recognizes that sleep onset associations are not limited to children as many adults require television, white noise, or certain light conditions to fall asleep and remain asleep throughout the night (03).

Chronic insomnia may also be due to drug or substance use. It may result from use of prescription and nonprescription medications, illicit drugs, or other substances, such as alcohol. A comprehensive review of sleep effects from substance use showed that chronic use of alcohol, cocaine, cannabis, and opiates all cause decreased sleep time, increased sleep latency and wake time after sleep onset, and deficiency in a slow-wave sleep (07). A systematic review and meta-analysis identified smoking as a significant risk factor for insomnia (32). Many categories of medications can also cause sleep disruption, including serotonin reuptake inhibitors, tricyclic antidepressants, dopamine agonists, acetylcholinesterase inhibitors, and corticosteroids (22). Chronic insomnia occurs not only with administration of drugs or substances but also with discontinuation of certain substances. For example, both alcohol and marijuana withdrawal after chronic use has been implicated as a cause of insomnia (17).

Short-term insomnia disorder (adjustment insomnia). The clinical picture and diagnostic criteria for short-term insomnia disorder are like those for chronic insomnia (Table 4) with the exception that this disorder, by definition, lasts no longer than three months (03). These symptoms occur despite having adequate time and opportunity to sleep. In some patients, this sleep disorder can occur intermittently with temporal relation to daytime stressors. Patients may find that they alternate between difficulty initiating sleep and difficulty maintaining sleep on alternate nights. This disorder often occurs with the appearance of a stressor and dissipates as the stress resolves or as the patient develops coping mechanisms for a chronic stressor (03). The psychological stress is acute and may be related to excitement, conflict, grief, worry, or environmental change. Ruminating thoughts, anxiety, sadness, or depression may also be associated symptoms. The familial aggregation that is found in chronic insomnia disorders is expected to also occur in transient forms of insomnia. The extent of familial aggregation not only represents genetic predisposition but also shared environment and learned behavior.

Other sleep disorder due to sleep-disruptive environmental circumstances. External environmental factors may cause sleep disruption and negatively impact sleep quality. Symptoms of difficulty initiating sleep, difficulty maintaining sleep, and daytime symptoms of fatigue, cognitive impairment, and emotional disturbance can occur directly related to environmental factors. This condition can be transient, intermittent, or chronic. One important factor is inappropriate light exposure. Light pollution is the alteration of natural night lighting levels caused by inappropriate use of artificial light. High intensity outdoor artificial light at night is associated with obesity, delayed sleep pattern, short sleep duration, insomnia, and habitual snoring (35). Other factors include excessive noise and extreme temperature in the sleep environment. These can affect sleep onset, maintenance, or both. Road traffic noise has been associated with difficulties falling asleep, awakening during the night, and waking up too early (33). A study looking at sleep difficulty in Hispanic populations showed that those who lived in noisy neighborhoods were more likely to have insomnia than those in quiet neighborhoods (55). Similarly, noise in the sleeping space has detrimental effects. Bed partners of heavy snorers are exposed to noise at or above thresholds for a healthy sleep environment, increasing their risk for chronic sleep disturbance and adverse health effects (56). Sudden changes in the sleep setting, such as a move to a new residence, may also contribute to poor sleep due to environmental factors. In elderly patients who are more susceptible to sleep fragmentation and nocturnal awakenings, certain sleep environment factors were significantly associated with insomnia symptoms, particularly uncomfortable pillows and noisy bedrooms (19). Perception of personal safety has been shown in multiple studies to affect sleep as well (55). External factors may be particularly important in group settings, such as dormitories or hospitals. Environmental noise may be an important cause of sleep disruption in the hospital setting. Social features of the sleep environment such as being in a disadvantaged neighborhood also adversely affect sleep (11). Sleepwalking is a parasomnia emerging out of non-REM sleep consisting of ambulation, altered consciousness, or an impaired judgment during ambulation (16). Although the cause of sleepwalking is unknown, stress and stressful events can trigger severe or more frequents episodes. Sleepwalking is more frequent in children than in adults and improves during the teenage years in 80% of cases (08).

The COVID-19 pandemic has exposed people to stress, such as the social restrictions and changes in daily routine, which have impacted sleep patterns and sleep quality. The colloquial terms “coronasomnia” or “COVID-somnia” have been used to comprise the symptoms related to sleep disruptions, including insomnia, disrupted sleep continuity, changes in sleep-wake cycle, feelings of nonrestorative sleep, and decreased sleep quality due to stresses related to fear of the virus itself or the psychosocial impact on daily living. Many studies report an increase in prevalence of these sleep disorders from prepandemic to during the pandemic. Several contributing factors include anxiety, depression, PTSD, psychological distress, and stress. Risk factors were reported to be presence of chronic/psychiatric illnesses, female gender, younger age group (less than 40 years of age), unemployment, and constant exposure to social media/news concerning COVID-19. The optimum treatment strategy is unclear at this time; however, prior strategies, including CBT, have been suggested given their known efficacy, especially in those with psychological stressors (10). In addition, SARS-CoV-2 can enter the brain, directly altering the brain blood barrier integrity and producing the COVID-19-related sleep disorders. Post-COVID sleep disturbances are common, occurring in about 29% and is more common in those with severe COVID (39). Research into sleep dysfunction in patients diagnosed with COVID-19 in both the acute and chronic phases of the illness is still ongoing.

A summary of the relationship of environmental exposures to sleep outcomes can be seen in the figure.

Neighborhood-level environmental exposures in sleep

Neighborhood-level environmental exposures in sleep)(Contributed by Dr. Bissonnette)

Behaviorally induced insufficient sleep syndrome (BIISS). This syndrome is caused by self-induced sleep deprivation and occurs when an individual fails to receive an amount of sleep that is necessary to maintain normal alertness throughout the day (02; 03). BIISS is characterized by excessive daytime sleepiness, short habitual sleep duration, and sleeping considerably longer during weekends or vacation than usual during weekdays (63). The most common cause of short sleep duration in adolescents is self-induced wake extension or sleep restriction, which leads to chronic sleep deprivation due to decreased time asleep (Table 4). People with BIISS will sleep longer at times when they do not implement measures employed to wake up early (such as alarm clocks). Recurrent short sleep is associated with adverse cortisol release pattern throughout the day (01). Individuals have different sleep requirements, largely due to genetic factors. Thus, sufficient sleep is not defined by an absolute number, but by the quantity of sleep needed for the patient to feel refreshed on awakening. For example, people who need 10 hours of sleep per night but receive only eight hours may become severely sleep deprived and subsequently develop excessive daytime sleepiness. Schoolwork and extracurricular activities increase the incidence of insufficient sleep syndrome among children and adolescents. In fact, behaviorally induced insufficient sleep syndrome is the most common sleep disorder in adolescents (37). In the Spit for Science study, 10% of college students had behaviorally induced insufficient sleep syndrome and these students had higher levels of depression than normal sleepers (63). It has been shown to cause emotional problems, such as depression and impulsiveness. In one study, adolescents who had behaviorally induced insufficient sleep syndrome were also found to perform poorer academically than their peers without behaviorally induced insufficient sleep syndrome (37). Furthermore, chronic sleep deprivation is an influential predictor of academic success among college students (15). Chronic partial sleep deprivation from behaviorally induced insufficient sleep syndrome may also lead to inattention and may impair performance on daytime tasks of vigilance (37). Young athletes with insufficient sleep are at a high risk of musculoskeletal injury (24). One study found that sleep deprivation impacted driving behavior similar to substances such as alcohol and alprazolam (59).

Table 4. ICSD-3 Criteria for Insufficient Sleep Syndrome

	• The patient has periods of irrepressible need to sleep or daytime lapses into sleep, or, in cases of prepubertal children, there is a complaint of behavioral abnormalities attributable to sleepiness.
	• The patient’s sleep time, established by personal or collateral history, sleep logs, or actigraphy is usually shorter than expected for age.
	• The curtailed sleep pattern is present for most days in at least three months.
	• The patient curtails sleep time by such measures as an alarm clock or being awakened by another person and generally sleeps longer when such measures are not used, such as on weekends or vacations.
	• Extension of total sleep time results in resolution of the symptoms of sleepiness.
	• The symptoms are not better explained by another untreated sleep disorder, the effects of medications or drugs, or other medical, neurologic, or mental disorder.

Hypersomnia due to drug or substance. This condition describes excessive daytime sleepiness that is attributable to the use of a drug or other substance. As described above, it may occur after use of prescription medications, illicit drugs, or other substances such as alcohol. It also may occur with withdrawal of medication or substances.

Other circadian rhythm sleep disorder due to drug or substance. All disorders meet three criteria for circadian rhythm sleep-wake disorders as outlined in the ICSD-3 (Table 5). The use of prescription medication, illicit drugs, and alcohol can disrupt the sleep-wake cycle and induce a circadian rhythm sleep-wake disorder mimicking other circadian rhythm disorder patterns such as delayed sleep-phase disorder, advanced sleep-phase disorder, irregular sleep-wake rhythm, or free-running (non-entrained) type. However, these specific disorders require that it not be due to drug or substance.

Table 5. ICSD-3 Criteria for Circadian Rhythm Sleep-Wake Disorders

	• A chronic or recurrent pattern of sleep-wake rhythm disruption primarily due to alteration of the endogenous circadian timing system or misalignment between the endogenous circadian rhythm and the sleep-wake cycle desired or required by an individual’s physical environment or social or work schedules.
	• The circadian rhythm disruption leads to insomnia symptoms, excessive sleeping, or both.
	• The sleep-wake disturbances cause clinically significant distress or impairment in mental, physical, social, occupational, educational, or other important areas of functioning.

Prognosis and complications

With proper treatment and management, the prognosis for these sleep disorders is excellent. When environmental disrupters are eliminated, stress factors resolved, limits properly set, inappropriate sleep-onset associations replaced, and inciting behaviors modified, the associated sleep problems may disappear. It is not uncommon for multiple factors to be contributing to sleep difficulties; therefore, multiple interventions addressing these factors may be required to eliminate sleep disorders. If the patient remains symptomatic, if sleep quality remains suboptimal, or if the level of daytime functioning does not improve, then other diagnoses must be considered.

Without adequate treatment or with persistence of the causative external factors, the course is less predictable. In some cases, the patient may adapt to the inciting stressor or environmental condition. The factors that initially caused stress (eg, the death of a family member) may remain but with progressively decreased impact over time. With growth, development, and maturation, there may be progressively less need for a child to test limits, less desire to involve others in sleep-onset routines, or less demand for nighttime feedings.

Sleep disorders due to drugs or substances should resolve as the offending agent is eliminated. Sleep disorders caused by drugs or substances are unlikely to resolve with continued exposure, and associated medical problems may become paramount. Chronic neurologic, hepatic, or renal dysfunction may persist, leading to ongoing medical problems; these may subsequently become associated with other sleep disorders. Coma and death are also possible, depending on the substance involved and the duration of exposure. However, if the sleep disorder is induced by psychotropic agents, eg, antidepressants, the induced-sleep disorder may persist longer due to difficulty in controlling the psychiatric disorder. Given the complex links between sleep, health, and quality of life, it is critical to be recognize the effects of drugs on sleep (60).

Clinical vignette

AC, a two-year-old girl, presented with multiple episodes of crying at night. According to her parents, the child had a long history of sleeping problems, which first began at about six months of age when she developed dependency on the pacifier. At that time, through behavioral techniques, they were able to establish sleep without the pacifier. However, at the time of presentation, AC had developed a problem wherein she would wake up multiple times during the night and cry until her parents intervened. AC’s nightly ritual, which began at 7:00 PM, involved her parents reading stories and playing with puzzles. She usually went to bed by 8:00 PM. Her parents would then leave the room while AC was still awake, and she would fall asleep on her own. However, after a variable amount of time asleep, AC would awaken and cry loudly. Usually, when her parents went into her bedroom, they could easily soothe her: she would ask for her belly to be rubbed, for a drink of water, or for other things; when this was done, she would relax and return to sleep -- her parents were out of the room when she fell back asleep. If her parents did not intervene, AC would cry for hours at a time. Her parents reported that they were allowing her to cry and having success in extinguishing the behavior. However, she then got an ear infection, and they were afraid to let her cry. Since that time, they had not found success in weaning her from this behavior.

AC’s parents reported that during these episodes, although she would cry and scream, she was usually rapidly consolable. She exhibited no automatic behaviors, and the episodes did not run a spontaneous course; the crying would persist as long as the parents stayed out of the room. There were no episodes wherein AC appeared to get out of bed and stumble into objects or be out of touch with her surroundings. She had no daytime episodes that were similar when she was awake; however, she did take a daily 1- to 3-hour nap and would occasionally have a crying spell during the nap.

According to her parents, AC’s mother had a normal pregnancy and delivery, and AC had reached normal developmental milestones. She had no other significant health problems. Her parents reported that AC did not snore or have any other obvious respiratory difficulties during sleep. There were no abnormal motor activities during sleep.

Past medical history. Significant for recurrent ear infections, otherwise was unremarkable.

Medications. None at the time of presentation.

Allergies. No known drug allergies.

Family history. No family members had a similar sleeping disorder.

Exam. A complete exam was normal.

Impression. The patient had pediatric chronic insomnia due to poor limit-setting. The patient’s parents attempted behavioral intervention, but they had not been consistent and persistent enough to be successful. A carefully planned and consistently executed behavioral program would probably be successful in this child.

Biological basis

Environmental sleep disorders are the result of extrinsic factors. Gene-environment interaction through epigenetic pathways can modify the DNA (23; 29) and could be a determinant factor for the development of the environmental sleep disorders. Large prospective and multicenter studies using genome-wide association (GWAS) and epigenome-wide association studies (EWAS) will help to clarify the biological basis of this diseases.

Etiology and pathogenesis

In environmental and behavioral sleep disorders, various external factors perpetuate sleep disruption. In this group of sleep disorders, the pathogenesis and pathophysiology are nearly synonymous with the etiologies for these disorders. The effects of extrinsic variables on sleep occur on a neuropsychological and physiological level.

Chronic insomnia related to extrinsic factors. The etiology of chronic insomnia is variable, and a single causative factor often cannot be identified. Comorbid mental health disorders or medical conditions may predispose a patient to chronic insomnia. Developmental delay can also play a role in the development of chronic insomnia (03). Insomnia is affected by genetic susceptibility, major life changing events and stressors, and brain function. Predisposition to insomnia may involve brain circuits regulating emotion and arousal rather than those regulating circadian and homeostatic sleep regulation. Genetic predisposition to sleep arousal can be augmented by early adverse events. Once the genetic polymorphisms are set up to increase the risk of insomnia, early developmental or environmental conditions can modify their expression through epigenetic changes (61). Studies investigating the pathophysiology of insomnia suggest an increase in physiologic arousal systems, which may be due to a heightened sympathetic nervous system and hypothalamic-pituitary-adrenal axis (03). This may manifest itself as a state of hypervigilance during the day and difficulty initiating or maintaining sleep at night. There is typically no structural brain abnormality accounting for chronic insomnia.

Activities that result in poor sleep hygiene, such as use of caffeine, nicotine, or alcohol close to bedtime, social activities or exercising in the late-evening, use of electronic devices before bed, or stress, can all lead to chronic insomnia. Blue light is known to increase arousal at night and decrease melatonin production (44). This mechanism may contribute to chronic insomnia due to using devices before bed or keeping a television or computer on in the room while sleeping. Individuals with caregiver responsibilities may also develop habits and behavioral patterns that are disruptive to sleep. These behavioral tendencies contribute to the development and propagation of insomnia.

Children with chronic insomnia due to poor limit setting are capable of normal sleep. The arousal pathways in the central nervous system function normally but are stimulated intentionally by the child’s efforts to stay awake. The key factor is that the child is allowed, and perhaps encouraged, to stay awake by parents or caretakers who fail to enforce bedtimes appropriately and consistently in the face of the child's demands, requests, or stalling tactics. The parents' inability to properly set limits at night may also coexist with difficulty in limit-setting during the day. Environmental issues such as a new baby sharing the child's room or a move from a crib to a bed may also interfere with a child’s desire to fall asleep. Psychosocial factors such as depression, parents' own unresolved childhood conflicts, a crowded and noisy home, a sick family member, and inconvenient parental work schedules are also important to consider. A child's need to test limits at night may reflect normal control issues, poor daytime nurturing, or overheard nightly parental fighting.

As in chronic insomnia due to poor limit setting, patients with chronic insomnia due to sleep-onset associations have a normal arousal system. The system is triggered by an awareness that conditions habitually associated with the transition to sleep are not present, are being changed, or have been changed. The arousals are accompanied by efforts to reestablish such conditions to facilitate falling back to sleep. This may include trying to elicit a sibling or caregiver to reproduce the desired environment or activity. This behavior consequently delays the transition back to sleep and can cause difficulty with sleep onset or maintenance.

Ingestion of exogenous substances, including medications, may perpetuate this tendency for hyperarousal seen in chronic insomnia. This may cause insomnia by enhancing the effects of activating neurotransmitters. Stimulant medications increase the release and inhibit the reuptake of dopamine, norepinephrine, and serotonin. Another potential mechanism is that drugs or substances may hinder the actions of inhibitory neurotransmitters. Withdrawal of medications or substances may cause increased arousal, leading to chronic insomnia as well.

Short-term insomnia disorder (adjustment insomnia). This disorder is caused by acute stress. Factors may be related to changes or pressures at work, school, or home and may reflect upcoming deadlines or examinations. Even stress related to positive events, such as marriage or childbirth, can lead to transient insomnia. This stressor likely accentuates the central nervous system hyperarousability, although the pathophysiology of short-term insomnia has not been as well studied as chronic insomnia. A prior history of depression or anxiety may predispose a patient to short-term insomnia due to stress (03). Infections have been implicated in short-term insomnia. Mild short-term insomnia has been significantly associated with the common cold, even after adjusting for the symptoms of cough and rhinorrhea (28).

It is estimated that 40% of insomnia patients have a coexisting psychiatric condition, with depression being the most common. One study found that children with lower vagal tone were at increased risk of externalizing problems, exhibiting depression symptoms, and having higher body mass index; this was associated with increased sleep disruptions (ie, lower sleep efficiency, increased wake minutes, and fewer sleep minutes). These results indicate that lower vagal tone may function as a vulnerability factor for adjustment problems in the context of sleep problems.

Other sleep disorder due to sleep-disruptive environmental circumstances. Suboptimal factors in the sleeping environment, such as noise or light, uncomfortable temperature, or change in sleep setting, can induce a sleep disorder. External conditions such as noise or light lead to stimulation of the central nervous system. Light is the most potent zeitgeber, or time cue. Because of its activating effects, extraneous light can be particularly disruptive to sleep, causing difficulty with sleep onset or sleep maintenance.

Behaviorally induced insufficient sleep syndrome. This syndrome is caused by self-induced sleep deprivation. Causes are numerous and may include late bedtimes and early wake times, which may result from social behaviors or may be a function of school- or work-related obligations. Behaviorally induced insufficient sleep syndrome may occur because of another sleep disorder; it is not unusual to diagnose behaviorally induced insufficient sleep syndrome in a patient who meets criteria for another ICSD-3 diagnosis. The arousal pathways in the central nervous system function normally as in chronic insomnia due to behavioral factors. These pathways are not spontaneously hyperstimulated; rather, they are stimulated intentionally by efforts to remain awake.

Hypersomnia due to drug or substance use. Excessive daytime sleepiness has a multitude of possible causes (neurochemical, structural, secondary to medical or psychiatric disorders, or because of a primary sleep disorder). The use of a drug or other substance may potentiate an individual’s tendency for excessive daytime sleepiness. Excessive daytime sleepiness is particularly common with several prescription medications, such as benzodiazepines, narcotics, antiepileptics, antidepressants, and antihistamines to name a few. This effect is more prominent in elderly patients or those with multiple medical comorbidities. Combining multiple medications can also increase the risk of excessive daytime sleepiness. Some patients may find tolerance to the sedation of prescription medications over time (03). Illicit drugs, alcohol, or other toxins may also cause excessive daytime sleepiness. Substances may potentiate inhibitory neurotransmitters or inhibit excitatory neurotransmitters to cause hypersomnia. For example, ethanol blocks the NMDA receptor, which is one of the receptor subtypes for the excitatory neurotransmitter, glutamate. Drug-induced sleepiness is a major problem as it significantly worsens the waking function, including adversely impacting motor vehicle operation and related negative health consequences (48).

Other circadian rhythm sleep disorder due to drug or substance. Changes in sleep phase may result from the use of prescription medication, illicit drugs, alcohol, or other substances. These inciting agents cause mild to severe disruption of the sleep-wake cycles; the magnitude of effect may vary with duration and intensity of exposure. Possible mechanisms for this include triggering cellular damage to structures involved in sleep-wake regulation or affecting levels of neuropeptides that participate in sleep-wake regulation. Drug addiction has been implicated in epigenetic regulation of the circadian clocks. There is overlap between circadian networks and addiction-related pathways, which are regulated by DNA methylation (53).

Epidemiology

	• Symptoms of difficulty falling asleep or daytime sleepiness affect 35% to 50% of adults.
	• Difficulty with sleep onset or with sleep maintenance is associated with female sex, older age, attentive personality, low socioeconomic status, and comorbid medical and psychological conditions.

Difficulties with falling asleep or daytime sleepiness affect approximately 35% to 50% of the U.S. adult population, whereas the prevalence of insomnia disorder ranges from 12% to 20% using the criteria described in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-V) (22). This definition includes daytime impairment or distress and the additional requirements that insomnia symptoms persist for at least three nights per week for at least three months and do not exclusively occur in the presence of another sleep disorder, mental disorder, or the direct physiological effects of a substance or medical condition (22). Insomnia is frequently observed as a comorbid condition, with up to 40% to 50% of individuals with insomnia also presenting with a comorbid mental disorder (05). The reported prevalence of insomnia in children between 5 and 12 years old is approximately 19.3%, with a peak in girls aged 11 to 12 years old (14). Variations are likely due to differences in study methods, samples, and ages of the children. Insomnia is the most prevalent sleep disorder during adolescence, with a current prevalence of 9.4% and a 10.7% lifetime prevalence. Diagnosis on insomnia in adolescents is complex and needs to be evaluated in the context of social, behavioral, and biological changes (21).

Difficulty with sleep onset or with sleep maintenance are more common in women, in individuals of low socioeconomic status, and in those with comorbid medical and psychological conditions. Women are more likely to complain of insomnia than men in every age group. However, there are greater gender differences in prevalence than incident rates, suggesting that females have periods of insomnia of longer duration (57). Prevalence of insomnia increases with age, with insomnia symptoms in the elderly occurring in 30% to 48% (50). As people age, difficulty with sleep maintenance becomes more common than problems with sleep onset. These gender differences can already be observed in early childhood, whereas effects of socioeconomic status emerge only later in adolescence (38).

Prevalence data for extrinsic factor-related sleep disorders are difficult to ascertain. Sleep disturbances due to external factors are relevant and unknown variables associated with a decrease in sleep quality and, consequently, in quality of life. Multiple sleep disorders influenced by extrinsic factors may coexist in a given individual; for instance, a patient with chronic insomnia may have inadequate sleep hygiene, poor sleep due to stress, and behaviorally induced insufficient sleep syndrome. This complicating factor further accentuates the difficulties in collecting epidemiological data on sleep disorders due to extrinsic factors.

Prevention

	• Addressing poor sleep hygiene, inappropriate light disruption, environmental disruptions, and stress are important to improve potential modifiable factors to help improve quality of sleep.
	• Sleep disturbances due to substances can be averted by avoiding exposure to offending medications or substances.

Most people will, at various times, be exposed to many potential sleep disrupters.

Maintaining good sleep hygiene (avoiding caffeine before bed, not using devices or watching television prior to getting into bed, keeping a room dark, keeping a consistent bedtime) is key to preventing sleep problems. Environmental disrupters can sometimes be avoided or moderated. Adjusting room temperature, using a sound machine, putting in ear plugs, and using an eye mask are all examples of modifying the environment to promote sleep. A snoring partner might need to be evaluated for sleep apnea. Similarly, some stress can be avoided by judicious planning and carefully made decisions; stress that cannot be avoided can sometimes be reduced through stress management techniques.

Insomnia due to behavioral factors can be avoided by implementing appropriate limits and consistent bedtime routines. Consistency and adherence to parent or caregiver-determined limits can help deter behavioral insomnia in susceptible populations.

Sleep disturbances due to substances can be averted by avoiding exposure to toxic chemicals or substances. For example, implementation of workplace safety guidelines can protect employees from hazardous exposure. Cessation of illicit drug use, tobacco use, and alcohol and prescription drug abuse should be encouraged in all affected individuals. Prescription medications, particularly those with potential for abuse, should be dispensed at the lowest permissible dose for the shortest possible time period.

Differential diagnosis

The diagnosis of these disorders is complicated by the overlap that exists amongst these and other sleep disorders, such as chronic insomnia. In addition, environmental and behavioral sleep disorders may appear as a complication of comorbid sleep disorders. A thorough sleep history can help identify external factors that may be contributing to poor sleep in a patient. All patients with sleep complaints should be evaluated for medical conditions, such as sleep disordered breathing and restless leg syndrome. Screening for comorbid psychiatric conditions such as depression, anxiety, or mania should also be performed.

If the symptoms do not resolve with proper adjustment of external factors, other sleep disorders should be considered. Chronic insomnia may be confused with delayed sleep-wake phase disorder wherein a patient’s endogenous circadian rhythm is delayed, causing inability to fall asleep at the desired time. These patients fall asleep easily and sleep well when their chosen sleep time is aligned with their delayed circadian phase. This is opposed to those with chronic insomnia who cannot fall asleep or stay asleep regardless of the time the patient chooses to go to sleep. Chronic insomnia can sometimes be differentiated by asking patients what will happen if they are allowed to sleep based on their desired sleep-wake schedule. When patients with delayed sleep-wake phase disorder are forced to arise several hours earlier than biologically mandated, insufficient sleep will be present (03).

Advanced sleep-wake phase disorder should also be differentiated. In this case, patients wake up earlier than desired and have earlier sleep initiation than desired. This is more common in older adults. In contrast to patients with chronic insomnia, these patients also fall asleep easily and get adequate sleep when their chosen sleep time is aligned with their circadian rhythm. Sleep disruptive environmental circumstances and behaviorally induced insufficient sleep syndrome should also be considered in the differential for chronic insomnia.

A determination of the time and frequency of sleep difficulty should be undertaken to help differentiate short-term insomnia disorder from chronic insomnia. Shift work or jet lag may also present similarly to short-term insomnia disorder. Circadian rhythm disorders should be considered in the evaluation of both short-term insomnia disorder and behaviorally induced insufficient sleep syndrome.

In the evaluation of a patient with insomnia due to drug or substance use, comorbid medical or psychiatric disorders should be considered.

The evaluation of hypersomnia due to drug or substance abuse should incorporate the consideration of other causes of excessive daytime sleepiness. These include, but are not limited to, narcolepsy with or without cataplexy, idiopathic hypersomnia, Kleine-Levin syndrome, hypersomnia due to medical or psychiatric condition, or hypersomnia due to another sleep disorder. In medically complicated patients, excessive daytime sleepiness may be multifactorial and may be difficult to attribute to a single etiology.

Diagnostic workup

	• A detailed history is essential in revealing the relevant extrinsic factors or maladaptive behaviors impacting the patient’s sleep quality.
	• Subjective measures of sleep quality and duration include sleep diaries and sleep questionnaires.
	• Actigraphy, polysomnogram, and the multiple sleep latency test may be considered in the workup for other sleep disorders.
	• Serum and urine toxicology studies may aid in determining the role of other substances and cerebrospinal fluid lab studies.

The sleep disorders discussed in this article should occur or worsen with exposure to a particular extrinsic factor or maladaptive behavior and improve when the factor or behavior is eliminated, resolved, or has lost its effect. The best way to determine this is usually through a careful and detailed history. Evaluation should include a discussion of the patient’s dietary habits, exercise routine, and social schedule both during the week and on weekends. It is also important to obtain a detailed description of the patient’s bedtime routine, which may involve reading or watching television while in bed. Naps should also be accounted for. A description of the patient’s sleep environment may be helpful, such as if their bedroom is facing a busy road or bright streetlight. Transient stressors should be explored as well as any potential drug, toxin, or medication usage, which could be affecting sleep.

In children with sleep problems, bedtime requests and stall tactics should be described by parents as should conditions in which the child typically falls asleep. However, subjective reports may underestimate behaviors seen or environmental factors that could be modified. A new coding system for overnight interactions between a child with sleep disorders and their caregivers was piloted in three children at risk for chronic insomnia (27). This system, known as the Overnight Parent-Child Interaction Coding System (OPIC System) utilized coding of events seen on overnight video to objectively identify factors where behavioral interventions could be utilized. Following further validation, the OPIC system could serve as an additional tool for providers when offering treatment advice to parents of children with chronic insomnia.

Sleep diaries and actigraphy can be helpful in assessing the sleep patterns and duration of insomnia in children. Sleep diaries and questionnaires provide subjective measures of sleep duration and quality. However, actigraphy can provide a quantitative assessment of these parameters (12). Actigraphy can also be used on those challenging cases of sleep disorders where establishing a sleep pattern is important prior to starting other therapies like cognitive behavioral therapy for insomnia (CBT-I).

Standard sleep questionnaires completed by the patient and bed partner may be useful. Sleep charts or diaries can help the patient and clinician determine patterns over time. Administration of the Minnesota Multiphasic Personality Inventory, Beck Depression Inventory, Hamilton Depression Rating Scale, or Hamilton Anxiety Rating Scale may be useful as screening devices to detect an underlying mood disorder. Physical examination occasionally discloses findings of medical illness or drug abuse.

Most laboratory tests are only occasionally helpful. If restless legs syndrome is considered, iron studies may reveal iron deficiency. Nocturnal polysomnography should be performed if sleep-disordered breathing is suspected. Polysomnography should also be considered when a diagnosis is uncertain, when a comorbid primary sleep disorder is suspected, or when the expected response to treatment does not occur. In the appropriate clinical context, a multiple sleep latency test (MSLT) following polysomnography should be part of the diagnostic evaluation. The multiple sleep latency test allows for quantification of sleepiness and is useful in confirming a diagnosis of narcolepsy, with or without cataplexy. Cerebrospinal fluid analysis for hypocretin-1 level may be considered if narcolepsy is suspected (40). However, newer data suggest that alternate multiple sleep latency test parameters, such as daytime REM sleep duration, may better identify hypocretin-deficiency among patients with hypersomnolence and those with narcolepsy (40). Other serologies to evaluate for comorbid medical conditions confounding the sleep symptoms may be considered, or imaging procedures (such as brain MRI) if other features point to possible underlying neurologic issues.

Sleep disorders related to drug or substance use are diagnoses of exclusion. There should be a temporal relationship between the symptoms and the offending agent. A full workup as above should be undertaken with possible addition of a urine or serum toxicology screen, cerebrospinal fluid evaluation, and serologies pending the suspected substance the patient was exposed to.

Management

	• Management includes modifying external factors that disrupt sleep and focusing on behavioral interventions to improve sleep.
	• A multidimensional, nonpharmacological approach for insomnia is crucial for long-term symptom control.

A discussion of appropriate sleep hygiene measures and adequate sleep times is the cornerstone for the treatment of environmental or behavioral sleep disorder. Education about the nature of sleep and the myriad effects of disrupted or insufficient sleep may help patients make behavioral modifications that facilitate sleep.

Management is generally directed at removing or modifying the external factors responsible for producing sleep disruption. If this can be done, then improvement or even remission can be expected. If the symptoms do not improve with removal of the external factor, an alternate diagnosis should be considered. If the inciting trigger cannot be removed from the patient’s environment or a disruptive behavior cannot be completely eliminated, then management may be directed at modifying symptoms. General strategies, such as scheduled "worry time," progressive relaxation, biofeedback, cognitive behavioral therapy for insomnia (CBT-I), meditation, sleep limitation, and stimulus control methods (avoiding prolonged attempts of trying to fall asleep in bed) may be useful. CBT-I is an effective treatment for insomnia symptoms, even when depression and insomnia occur simultaneously (09). If medications are considered as part of the therapeutic regimen, the lowest effective dose should be utilized. If symptoms are not severe, or if they are expected to be transient, then reassurance and time may be sufficient therapy.

Chronic insomnia related to extrinsic factors. In patients with poor sleep hygiene, the clinician should provide patients with strategies for behavior modification so that the patient can fully eliminate habits that contribute to sleep disruption. Close follow-up may be required initially as the patient incorporates a new set of behaviors into the daily routine. Pharmacologic treatment is not usually necessary as symptoms should fully resolve with implementation of behaviors and habits that are conducive to sleep. A randomized controlled trial in 55 adolescents showed that treatment is possible through sleep extension and sleep hygiene advice (20). This, in turn, had beneficial effects on sleep, self-reported sleep problems, and depressive symptoms of adolescents with chronic sleep reduction.

Behavioral interventions are the key to treatment of chronic insomnia due to sleep-onset associations and difficulty with limit setting. Children should not be in bed longer than needed to get the recommended sleep duration (25). In children, evidence has shown that behavioral interventions provide long lasting effects in most children with sleep difficulty (41; 47). Initial treatments may include modifying a child’s sleep schedule by temporarily shortening the time in bed. This will increase the likelihood of a child falling asleep faster and, therefore, decrease resistance to sleep and overnight awakenings (47). The sleep time can gradually be shifted to a more routine schedule once the child falls asleep on their own and stays asleep through the night.

Children with a sleep-onset association disorder need to be taught new patterns to associate with sleep transitions. The first step in this process is for the parents or caregivers to decide on the setting in which they want the child to sleep (eg, alone, in the crib, without a bottle or pacifier). Next, they must teach the child to fall asleep with these new conditions enforced. Caregivers should provide support to the child during the first few nights of this transition. Caregivers must also create a ritual around bedtime that includes putting the child to bed drowsy but awake. The child must learn to fall asleep with external elements that are associated with sleep so that he or she will reclaim the circumstances that are associated with sleep during overnight awakenings. In other words, if the child goes to sleep on their own, they will go back to sleep on their own when they wake at night. Once the routine is completed, the parents should leave the room and follow a pattern of waiting time, increasing progressively, following techniques for the modification of conduct until the child manages to get to sleep on his or her own. Consistency by caregivers is an essential component to this process (47). It can often take three to six weeks for old habits to be broken and new habits to be formed.

Parents and caregivers of children with a limit-setting sleep disorder need to develop insight and understanding as to why they have difficulty setting limits. Caregivers may need help in establishing a concrete plan of limit-setting that they can carry out. Positive reinforcement can motivate older children (47). Close follow-up and support are critical. Formal parenting instruction or psychotherapy for parents or family is sometimes necessary. Some of the recommendations described in sleep-onset association disorder can be useful in this setting as well.

For patients with chronic insomnia due to drug or substance use, the offending agent must be reduced or eliminated to halt symptomatic progression. Counseling or therapy may need to be incorporated into the treatment regimen as well. For example, CBT-I is becoming first-line treatment for patients with alcohol use disorder and insomnia (26). Treatment should also be aimed at the various systemic effects of the substance; this depends on the nature of the substance, the time course and degree of exposure, and the severity of biological responses.

A multidimensional, nonpharmacological approach for insomnia is crucial for long-term symptom control. In routine general practice settings, psychological treatment for insomnia improved sleep quality, reduced hypnotic drug use, and improved health-related quality of life at a favorable cost among long-term hypnotic users with chronic sleep difficulties (30)

Short-term insomnia disorder (adjustment insomnia). Short-term sedation may be useful in the management of a patient with short-term insomnia disorder. Temporary anxiolytic therapy while the patient is facing a stressor may also be beneficial. Occasionally, through discussion and support, a patient may be helped to recognize and change the situation leading to stress. Short-term counseling may also help a patient deal with sources of stress that cannot be altered, such as from the death of a family member.

Other sleep disorder due to sleep-disruptive environmental circumstances. Patients with environmental sleep disorder are usually aware of the etiology of their sleep disturbance but lack the means of modifying their surroundings. Sometimes physician support is needed to reinforce a patient's decision to change bedrooms, move to another home, or buy a new mattress or air conditioner. Help may be required to enlist cooperation of roommates or family members. Recommendation of curtains, eye shades, ear plugs, and white noise generators are occasionally of value. Short-term sedation may permit sleep in well-defined situations, such as during airplane travel.

Behaviorally induced insufficient sleep syndrome. The clinician must educate the patient on the importance of obtaining a consistent and sufficient amount of sleep. Successful treatment may require the patient to adapt to a new school or work schedule; the provider may be called on to support the medical necessity of making such changes. Continued reassurance and support are helpful as the patient transitions to a new schedule and new set of behaviors that facilitates more sleep. Close follow-up should be arranged until the patient has modified behaviors to consistently obtain more sleep.

Hypersomnia due to drug or substance. Decontamination (activated charcoal), antidote administration, or elimination efforts (hemodialysis, exchange transfusion, chelation) may be appropriate in cases of life-threatening hypersomnia due to drug, substance or toxin use. Long-term discontinuation of the inciting agent is necessary for worsening hypersomnia. If there is a concern for addiction or dependence, a formal detoxification program should be considered. Alternative treatment is especially required if alcohol or hypnotic dependency is a concern.

Circadian rhythm disorder due to drug or substance. As with other sleep difficulties secondary to drug or substance use, discontinuation is a key component to treatment of the sleep disorder. Prolonged weaning periods might be required to prevent rebound or withdrawal. Modifications of lifestyle and environmental factors have been shown to have a positive effect on elderly patients’ sleep quality ratings (36). Hypnotic dependency can be managed by using alternative hypnotics that have lower risks of abuse and dependency.

Outcomes

The outcomes of environmental sleep disorders will depend on how soon the external factors are eliminated. If the external factors are completely eliminated, the outcomes and prognosis will be the resolution of the disorder. Sometimes the environmental factors are unknown, and sometimes they are not completely eliminated with treatment.

Among the environmental sleep disorders, chronic insomnia is one of the most studied and the most prevalent. Spontaneous remission rate of chronic insomnia in a 5-year cohort study with annual follow-up was found to be 29.3%, 50.6%, and 62.5% at 1-, 3-, and 5-year follow-up, respectively. However, 33.2% of those with remission worsened in the subsequent year (43). A meta-analysis of CBT-I for patients with insomnia found a 33% higher (95% CI 28% to 39%) remission rate for CBT-I compared with controls. Remission rates were 46% higher in the CBT-I group of patients with insomnia and no comorbidities, whereas in patients with comorbid medical conditions, the remission rate was 35% higher favoring CBT-I (18). To date, there are no studies evaluating the outcomes or prognosis of other extrinsic sleep disorders.

References

01: Abell JG, Shipley MJ, Ferrie JE, Kivimäki M, Kumari M. Recurrent short sleep, chronic insomnia symptoms and salivary cortisol: A 10-year follow-up in the Whitehall II study. Psychoneuroendocrinology 2016;68:91-9. PMID 26963375
02: American Academy of Sleep Medicine. ICSD-2 International Classification of Sleep Disorders. Diagnostic and coding manual. 2nd edition. American Academy of Sleep Medicine, 2005.
03: American Academy of Sleep Medicine. ICSD-3 International Classification of Sleep Disorders. 3rd edition. Darien, IL: American Academy of Sleep Medicine, 2014.
04: American Academy of Sleep Medicine. ICSD-3 International Classification of Sleep Disorders. 3rd ed., text revision. Darien, IL: American Academy of Sleep Medicine, 2023.
05: American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th edition. Arlington, VA: American Psychiatric Publishing, 2013.
06: American Sleep Disorders Association. International classification of sleep disorders: diagnostic and coding manual. Rochester (MN): American Sleep Disorders Association, 1997.
07: Angarita GA, Emadi N, Hodges S, Morgan PT. Sleep abnormalities associated with alcohol, cannabis, cocaine and opiate use: a comprehensive review. Addict Sci Clin Pract 2016;11(1):9. PMID 27117064
08: Arnulf I. Sleepwalking. Curr Biol 2018;28(22):R1288-9. PMID 30458142
09: Asarnow LD, Manber R. Cognitive behavioral therapy for insomnia in depression. Sleep Med Clin 2019;14(2):177-84. PMID 31029185
10: Bhat S, Chokroverty S. Sleep disorders and COVID-19. Sleep Med 2022;91:253-61. PMID 34391672
11: Billings ME, Hale L, Johnson DA. Physical and social environment relationship with sleep health and disorders. Chest 2020;157(5):1304-12. PMID 31870910
12: Brown KM, Malow BA. Pediatric insomnia. Chest 2016;149(5):1332-9. PMID 26378738
13: Bugueño M, Curihual C, Olivares P, et al. Quality of sleep and academic performance in high school students. Rev Med Chil 2017;145(9):1106-14. PMID 29424396
14: Calhoun SL, Fernandez-Mendoza J, Vgontzas AN, Liao D, Bixler EO. Prevalence of insomnia symptoms in a general population sample of young children and preadolescents: gender effects. Sleep Med 2014;15(1):91-5. PMID 24333223
15: Chen WL, Chen JH. Consequences of inadequate sleep during the college years: Sleep deprivation, grade point average, and college graduation. Prev Med 2019;124:23-8. PMID 31034864
16: Cochen De Cock V. Sleepwalking. Curr Treat Options Neurol 2016;18(2):6. PMID 26874839
17: Conroy DA, Arnedt JT. Sleep and substance use disorders: an update. Curr Psychiatry Rep 2014;16(10):487. PMID 10163422
18: Edinger JD, Arnedt JT, Bertisch SM, et al. Behavioral and psychological treatments for chronic insomnia disorder in adults: an American Academy of Sleep Medicine systematic review, meta-analysis, and GRADE assessment. J Clin Sleep Med 2021;17(2): 263-98. PMID 33164741
19: Desaulniers J, Desjardins S, Lapierre S, Desgagne A. Sleep environment and insomnia in elderly persons living at home. J Aging Res 2018;2018:8053696. PMID 30363712
20: Dewald-Kaufmann JF, Oort FJ, Meijer AM. The effects of sleep extension and sleep hygiene advice on sleep and depressive symptoms in adolescents: a randomized controlled trial. J Child Psychol Psychiatry 2014;55(3):273-83. PMID 24252173
21: de Zambotti M, Goldstone A, Colrain IM, Baker FC. Insomnia disorder in adolescence: diagnosis, impact, and treatment. Sleep Med Rev 2018;39:12-24. PMID 28974427
22: Doufas AG, Panagiotou OA, Panousis P, Wong SS, Ioannidis JP. Insomnia from drug treatments: evidence for meta-analyses of randomized trials and concordance with prescribing information. Mayo Clin Proc 2017;92(1):72-87. PMID 27842706
23: Flanagan JM. Epigenome-wide association studies (EWAS): past, present, and future. Methods Mol Biol 2015;1238:51-63. PMID 25421654
24: Fox JL, Scanlan AT, Stanton R, Sargent C. Insufficient sleep in young athletes? Causes, consequences, and potential treatments. Sports Med 2020;50(3):461-70. PMID 31679145
25: Friman PC, Schnoes CJ. Pediatric prevention: sleep dysfunction. Pediatr Clin North Am 2020;67(3):559-71. PMID 32443994
26: Geoffrey PA, LejoyeuxM, Rolland B. Management of insomnia in alcohol use disorder. Expert Opin Pharmacother 2020;21(3):297-306. PMID 31899990
27: Gilbraith L, Bull K, Hill CM. Video analysis of parent-child interactions in behavioral sleep disorders: development of a scoring algorithm. Front Psychiatry 2019;10:861. PMID 31824357
28: Gomi S. Short-term insomnia and common cold: a cross-sectional study. J Gen Fam Med 2019;20(6):244-50. PMID 31788402
29: Goyal D, Limesand SW, Goyal R. Epigenetic responses and the developmental origins of health and disease. J Endocrinol 2019;242(1):T105-19. PMID 31091503
30: Guo W, Wang J, Gao WB, Wu EL, Wu YT. [A comparison study of cognitive-behavioral therapy alone versus combination with tapered hypnotic agents in patients with chronic insomnia]. Zhonghua Nei Ke Za Zhi 2019;58(1):56-62. PMID 30605952
31: Hale L, Guan S. Screen time and sleep among school-aged children and adolescents: a systematic literature review. Sleep Med Rev 2015 Jun;21:50-8. Epub 2014 Aug 12. PMID 25193149
32: Hu N, Wang C, Liao Y, Dai Q, Cao S. Smoking and incidence of insomnia: a systematic review and meta-analysis of cohort studies. Public Health 2021;198:324-31. PMID 34507139
33: Janson E, Johannessen A, Holm M, et al. Insomnia associated with traffic noise and proximity to traffic -- a cross-sectional study of the Respiratory Health in Northern Europe III population. J Clin Sleep Med 2020;16(4):545-52. PMID 32022662
34: Kang EK, Kim SS. Behavioral insomnia in infants and young children. Clin Exp Pediatr 2021;64(3):111-6. PMID 32683806
35: Koo YS, Song JY, Joo EY, et al. Outdoor artificial light at night, obesity, and sleep health: Cross-sectional analysis in the KoGES study. Chronobiol Int 2016;33(3):301-14. PMID 26950542
36: Kuck J, Pantke M, Flick U. Effects of social activation and physical mobilization on sleep in nursing home residents. Geriatr Nurs 2014;35(6):455-61. PMID 25270432
37: Lee YJ, Park J, Kim S, Cho S-J, Kim SJ. Academic performance among adolescents with behaviorally induced insufficient sleep syndrome. J Clin Sleep Med 2015;11(1):61-8. PMID 25515277
38: Lewien C, Genuneit J, Meigen C, Kiess W, Poulain T. Sleep-related difficulties in healthy children and adolescents. BMC Pediatr 2021;21(1):82. PMID 33593333
39: Linh TTD, Ho DKN, Nguyen NN, Hu CJ, Yang CH, Wu D. Global prevalence of post-COVID-19 sleep disturbances in adults at different follow-up time points: A systematic review and meta-analysis. Sleep Med Rev 2023;71:101833. PMID 37597302
40: Lopez R, Barateau L, Laura Rassu A, et al. Rapid eye movement sleep duration during the multiple sleep latency test to diagnose hypocretin-deficient narcolepsy. Sleep 2023;46(1):zsac247. PMID 36222741
41: Meltzer L, Mindell J. Systematic review and meta-analysis of behavioral interventions for pediatric insomnia. J Ped Psych 2014;38(8):932-48. PMID 24947271
42: Mindell JA, Cook RA, Nikolovski J. Sleep patterns and sleep disturbances across pregnancy. Sleep Med 2015;16(4):483-8. PMID 25666847
43: Morin CM, Jarrin DC, Ivers H, Mérette C, LeBlanc M, Savard J. Incidence, persistence, and remission rates of insomnia over 5 years. JAMA Netw Open 2020;3(11):e2018782. PMID 33156345
44: Motamedzadeh M, Golmohammadi R, Kazemi R, Heidarimoghadam R. The effect of blue-enriched white light on cognitive performances and sleepiness of night-shift workers: A field study. Physiol Behav 2017;177:208-14. PMID 28495465
45: Nunes ML, Bruni O. Insomnia in childhood and adolescence: clinical aspects, diagnosis, and therapeutic approach. J Pediatr (Rio J) 2015;91(6 Suppl 1):S26-35. PMID 26392218
46: Olaithe M, Ree M, McArdle N, et al. Cognitive dysfunction in insomnia phenotypes: further evidence for different disorders. Front Psychiatry 2021;12:688672. PMID 34349682
47: Owens J, Moore M. Insmonia in infants and young children. Pediatr Ann 2017;46(9):e321-6. PMID 28892546
48: Pagel JF. Drug-induced hypersomnolence. Sleep Med Clin 2017;12(3):383-93. PMID 28778236
49: Paruthi S, Brooks LJ, D'Ambrosio C, et al. Recommended Amount of Sleep for Pediatric Populations: A Consensus Statement of the American Academy of Sleep Medicine. J Clin Sleep Med 2016;12(6):785-6. PMID 27250809
50: Patel D, Steinberg J, Patel P. Insomnia in the elderly: a review. J Clin Sleep Med 2018;14(6):1017-24. PMID 29852897
51: Riemann D, Baglioni C, Bassetti C, et al. European guideline for the diagnosis and treatment of insomnia. J Sleep Res 2017;26(6):675-700. PMID 28875581
52: Royant-Parola S, Londe V, Tréhout S, Hartley S. Nouveaux médias sociaux, nouveaux comportements de sommeil chez les adolescents. [The use of social media modifies teenagers' sleep-related behavior]. Encephale 2018;44(4):321-8. PMID 28602529
53: Saad L, Zwiller J, Kalsbeek A, Anglard P. Epigenetic regulation of circadian clocks and its involvement in drug addiction. Genes (Basel) 2021;12(8):1263. PMID 34440437
54: Silvestri R, Aricò I. Sleep disorders in pregnancy. Sleep Sci 2019;12(3):232-9. PMID 31890101
55: Simonelli G, Dudley KA, Weng J, et al. Neighborhood factors as predictors of poor sleep in the Sueno Ancillary Study of the Hispanic Community Health Study/Study of Latinos. Sleep 2017;40(1):1-8. PMID 28364454
56: Sowho M, Sgambati F, Guzman M, Schneider H, Schwartz A. Snoring: a source of noise pollution and sleep apnea predictor. Sleep 2020;43(6):zsz305. PMID 31837267
57: Suh S, Cho N, Zhang J. Sex differences in insomnia: from epidemiology and etiology to intervention. Curr Psychiatry Rep 2018;20(9):69. PMID 30094679
58: Sundbom F, Malinovschi A, Lindberg E, Almqvist C, Janson C. Insomnia symptoms and asthma control-Interrelations and importance of comorbidities. Clin Exp Allergy 2020; 50(2):170-177. PMID 31631397
59: van der Wall HEC, Doll RJ, van Westen GJP, et al. Using machine learning techniques to characterize sleep-deprived driving behavior. Traffic Inj Prev 2021;22(5):366-71. PMID 33960857
60: Van Gastel A. Drug-induced insomnia and excessive sleepiness. Sleep Med Clin 2018;13(2):147-59. PMID 29759266
61: Van Someren EJW. Brain mechanisms of insomnia: new perspectives on causes and consequences. Physiol Rev 2021;101(3):995-1046. PMID 32790576
62: Watson NF, Badr MS, Belenky G, et al. Recommended Amount of Sleep for a Healthy Adult: A Joint Consensus Statement of the American Academy of Sleep Medicine and Sleep Research Society. Sleep 2015;38(6):843-4. PMID 26039963
63: Williams AB, Dzierzewski JM, Griffin SC, Lind MJ, Dick D, Rybarczyk BD. Insomnia disorder and behaviorally induced insufficient sleep syndrome: prevalence and relationship to depression in college students. Behav Sleep Med 2019;18(2):275-86. PMID 0789063

Contributors

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

Authors

Roneil Gopal Malkani MD MS

Dr. Malkani of Northwestern University Feinberg School of Medicine has no relevant financial relationships to disclose.
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Mariam Mirza MD

Dr. Mirza of the University of Illinois at Chicago has no relevant financial relationships to disclose.
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Editor

Bradley V Vaughn MD

Dr. Vaughn of UNC Hospital Chapel Hill and University of North Carolina School of Medicine has no relevant financial relationships to disclose.
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Former Authors

Stephanie Bissonnette MPH DO
Carmen Taype-Roberts MD PhD
Michael J Howell MD
Richard Ferber MD (original author), Hrayr P Attarian MD, Maha Alattar MD, Anita Valanju Shelgikar, Shalini Paruthi MD, Raman Malhotra MD

Patient Profile

Age range of presentation: 0 month to 65+ years
Sex preponderance: male=female
Heredity: None, but genetic susceptibility to react to extrinsic factors may play a role.
Population groups selectively affected: Women and older adults

People with other medical conditions

People with known history of drug or substance abuse
Occupation groups selectively affected: School-age children

Industrial workers

High-stress professionals

ICD & OMIM codes

ICD-9: Alcohol-induced sleep disorders: 291.82

Drug-induced sleep disorders: 292.85

Insomnia: 327.0

Circadian rhythm sleep disorder: 327.3

Sleep behavior disorder: 327.4
ICD-10: Sleep disorders: G47

Disorders of initiating and maintaining sleep [insomnias]: G47.0

Disorders of the sleep-wake schedule: G47.2

Alcohol-induced sleep disorders: F10.182

Drug-induced sleep disorders: F11.182; F11.282; F11.982; F13.182; F13.982; F14.182; F14.282; F14.982; F15.182; F15.282; F15.982; F19.182; F19.282; F19.982

Insomnia: G47.00; G47.01; F51.05; G47.09

Circadian rhythm sleep disorder: G47.20

Sleep behavior disorder: G47.50

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Environmental and behavioral sleep disorders

Differential Diagnosis

inadequate sleep hygiene
insufficient sleep syndrome
alcohol-dependent insomnia
circadian rhythm sleep disorders
delayed sleep-wake phase syndrome
- advanced sleep-wake phase syndrome
- irregular sleep-wake pattern
- psychophysiological insomnia
- insomnia due to a psychiatric condition
- hypersomnia due to a medical condition
- sleep apnea syndromes
- sleep-onset disorder
- limit-setting disorder
- Prader-Willi syndrome
- Kleine-Levin syndrome
- gastritis
- stomach ulcer
- colic
- sleep-related gastroesophageal reflux
- neurologic causes of disturbed sleep
- asthma
- use of alcohol, hypnotics, or stimulants
- withdrawal from alcohol, hypnotics, or stimulants
- other sleep disorders associated with medical conditions
- idiopathic hypersomnia

Also Relevant

Drug-induced sleep disorders
Inadequate sleep hygiene
Irregular sleep-wake rhythm disorder
Shift work disorder
Sleep and alcohol use and abuse
- Sleep and medical disorders
- Sleep disorders
- Sleep, trauma, and anxiety

Clinical Categories

Sleep Disorders

Patient Handouts

Web References

Clinical Trials

NIH: Sleep Disorders

Environmental and behavioral sleep disorders

Introduction

Overview

Key points

Historical note and terminology

Table 1. Extrinsic Sleep Disorders

Clinical manifestations

Presentation and course

Table 2. Age-Appropriate Recommendations for Adequate Sleep

Table 3. ICSD-3 Criteria for Chronic Insomnia

Table 4. ICSD-3 Criteria for Insufficient Sleep Syndrome

Table 5. ICSD-3 Criteria for Circadian Rhythm Sleep-Wake Disorders

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

Outcomes

Special considerations

Pregnancy

Acknowledgment

Media

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes

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Also in This Category

Hypersomnolence

Fatal familial insomnia

Sleep and mental disorders

Sleep paralysis

Sleep and epilepsy

Narcolepsy

Confusional arousal

Restless legs syndrome

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