Introduction
Background
Insomnia is defined as repeated difficulty with the initiation, duration, maintenance, or quality of sleep that occurs despite adequate time and opportunity for sleep that results in some form of daytime impairment. Approximately one third of adults report some difficulty falling asleep and/or staying asleep during the past 12 months, with 17% reporting this problem as a significant one. Insomnia can be acute or chronic. Acute adjustment insomnia occurs in the context of an identifiable stressor (eg, personal loss, change in interpersonal relationships, bereavement, occupational stress, job loss) that acts as a precipitating factor. It typically lasts 3 months or less, and resolves as the stressor is no longer present or as the individual adapts to the stressor. The 1-year prevalence of adjustment insomnia in adults is approximately 10-15%.
Despite inadequate sleep, many patients with insomnia do not complain of excessive daytime sleepiness, such as involuntary episodes of drowsiness in boring, monotonous, nonstimulating situations. However, they do complain of feeling tired and fatigued with poor concentration. This may be related to a physiological state of hyperarousal (see Pathophysiology). In fact, despite not getting adequate sleep, patients with insomnia oftentimes have difficulty falling asleep even during daytime naps.
Chronic insomnia also has numerous health consequences. For example, patients with chronic insomnia report reduced quality of life comparable to other conditions such as diabetes, arthritis, and heart disease. Quality of life improves with treatment but still does not reach the level seen in the general population. In addition, chronic insomnia is associated with impaired occupational and social performance and an elevated absenteeism rate that is 10-fold greater than controls. Furthermore, insomnia is associated with higher healthcare use, including a 2-fold increase in hospitalizations and office visits.
Insomnia can also be a risk factor for depression and a symptom of a number of medical, psychiatric, and sleep disorders. In fact, insomnia appears to be predictive of a number of disorders, including depression, anxiety, alcohol dependence, drug dependence, and suicide. The annual cost of insomnia is not inconsequential with the estimated annual costs for insomnia at $12 billion dollars for healthcare and $2 billion dollars for sleep promoting agents.
In 2005, the National Institutes of Health held a State of the Science Conference on the Manifestations of Chronic Insomnia in Adults. This conference focused on the definition, classification, etiology, prevalence, risk factors, consequences, comorbidities, public health consequences and the available treatments and evidence for their efficacy. A summary of this conference can be obtained at the NIH Consensus Development Program home page. Prior to this conference, most cases of chronic insomnia were widely believed to be secondary to another medical or psychiatric condition and effective treatment of the primary condition was believed to effectively address secondary insomnia. However, at this 2005 conference, based on the review of the literature and the panel experts, the following was concluded:
This is an important point since insomnia is often only a secondary symptom that will resolve once the primary cause, whether it be medical or psychiatric, is treated. Consequently, this results in the underrecognition and undertreatment of insomnia. Furthermore, oftentimes if sleep difficulties are not the presenting complaint, there is too little time to address them at an office visit. There is also very little training in medical school on sleep disorders and their impact on patient overall health and quality of life. In fact, most providers rate their knowledge of sleep medicine as only fair. Finally, many providers are not aware of the safety issues, efficacy of cognitive behavioral and pharmacologic therapies, or when to refer a patient to a sleep medicine specialist.Most causes of insomnia are co-morbid with other conditions. Historically, this has been termed secondary insomnia. However, the limited understanding of the mechanistic pathways precludes drawing firm conclusions about the nature of these associations or directions of causality. Furthermore, there is concern that the term secondary insomnia may promote under treatment. Therefore, we propose the term comorbid insomnia.
Insomnia often persists despite treatment of the underlying medical or psychiatric condition and the persistence of insomnia can increase the risk of relapse of the primary condition in certain cases. In this regard, the clinician needs to understand that insomnia is a condition in its own right that requires prompt recognition and treatment to prevent morbidity and improve quality of life for their patients.
For related information, see Medscape's Insomnia and Sleep Health Resource Center. Also see Medscape's CME activity, Insomnia: Impact on Health and Quality of Life.
Pathophysiology
In the late 1980s, Spielman created a model of insomnia in terms of predisposing, precipitating, and perpetuating factors.
Predisposing factors
Genetic and neurobiologic factors likely determine a person’s risk of developing insomnia in the context of a precipitating factor (psychosocial, medical, or psychiatric). Many of these have not been identified. Sleep and wakefulness is an active, tightly regulated process that may differ between individuals who have different susceptibilities to exogenous influences.
Recent studies indicate differential genetic susceptibility to exogenous influences such as caffeine, light, and stress. For example, one study found that differences in the adenosine 2A receptor gene (ADORA2) determine differential sensitivity to caffeine’s effect on sleep. The ADORA2A 1083T>C genotype determined how closely the caffeine-induced changes in brain electrical activity (increased beta activity) during sleep resembled the alterations observed in patients with insomnia.
In addition, circadian clock genes (Clock, Per2) have been identified that regulate the circadian rhythm. For example, a mutation or functional polymorphism in the clock gene (Per2) can lead to circadian rhythm disorders such as advance sleep phase syndrome (sleep and morning awakening occur earlier than normal), and delayed sleep phase syndrome (sleep and morning awakening are delayed). Furthermore, a study examining the association between Clock gene polymorphisms and insomnia revealed a higher recurrence of initial, middle, and terminal insomnia in patients homozygous for the Clock genotype.
A missense mutation has been found in the gene encoding the GABAA beta 3 subunit in a patient with chronic insomnia. Polymorphisms in the serotonin receptor transporter gene may modulate the ability of an individual to handle stress or may confer susceptibility to depression. In depression, serotonin is an important neurotransmitter for arousal mechanisms. Furthermore, antagonism of the 5-HT2 receptor promotes slow wave sleep. Therefore, preliminary basic science evidence indicates a possible genetic predisposition to hyperarousal and insomnia.
Clinical research has also shown that patients with chronic insomnia show evidence of increased brain arousal. For example, studies have indicated that patients with chronic primary insomnia demonstrate increased fast frequency activity during NREM sleep, an EEG sign of hyperarousal, and evidence of reduced deactivation in key sleep/wake regions during NREM sleep when compared with controls. Furthermore, patients with insomnia have higher day and night body temperatures, urinary cortisol and adrenaline secretion, and ACTH than patients with normal sleep. A study of normal sleepers demonstrated that these changes were not due to sleep deprivation. Only a fraction of patients with medical and psychiatric conditions develop insomnia, which suggests that some patients have an inherent susceptibility (whether psychosocial, medical, or psychiatric) to develop insomnia in the context of a stressful event.
Precipitating factors
In retrospective studies, a large proportion of patients with insomnia (78%) can identify a precipitating trigger for their insomnia. Morin and colleagues showed that these patients demonstrate an increased response to stress as compared with controls. A number of factors can trigger insomnia in vulnerable individuals. These factors include depression, anxiety, sleep-wake schedule changes, medications, other sleep disorders, and medical conditions. In addition, positive or negative family, work-related, and health events are common insomnia precipitants.
Perpetuating factors
Insomnia, regardless of how it is triggered, is generally accepted to be perpetuated by cognitive and behavioral mechanisms. Cognitive mechanisms include misconceptions about normal sleep requirements and excessive worry about the ramifications of the daytime effects of inadequate sleep. As a result, these patients often become obsessive about their sleep or try too hard to fall asleep. These dysfunctional beliefs often produce sleep disruptive behaviors such as trying to catch up on lost sleep with daytime naps or sleeping in late, which in turn reduces their natural homeostatic drive to sleep at their habitual bedtime. Learned sleep-preventing associations are characterized by overconcern about inability to fall asleep.
Consequently, these patients develop conditioned arousal to stimuli that would normally be associated with sleep (ie, heightened anxiety and ruminations about going to sleep in their bedroom). A cycle then develops in which the more the patients strive to sleep, the more agitated they become, and the less they are able to fall asleep. They also have ruminative thoughts or clock watching as they are trying to fall asleep in their bedroom. Thus, conditioned environmental cues causing insomnia develop from the continued association of sleeplessness with situations and behaviors that are typically related to sleep.
Theoretical model of the factors causing chronic insomnia. Chronic insomnia is believed to primarily occur in patients with predisposing or constitutional factors. These factors may cause the occasional night of poor sleep but not chronic insomnia. A precipitating factor, such as a major life event, causes the patient to have acute insomnia. If poor sleep habits or other perpetuating factors occur in the following weeks to months, chronic insomnia develops despite the removal of the precipitating factor. Adapted from Spielman AJ, Caruso LS, Glovinsky PB: A behavioral perspective on insomnia treatment. Psychiatr Clin North Am. 1987 Dec;10(4):541-53.
Overview of mechanisms of normal sleep and wakefulness
A basic understanding of mechanisms of sleep and wakefulness is essential to understanding potential mechanisms of insomnia and how insomnia medications affect these pathways to promote sleep.
Both animal and human studies support a model of 2 processes that regulate sleep and wakefulness: homeostatic and circadian. The homeostatic process is the drive to sleep that is influenced by the duration of wakefulness. The circadian process transmits stimulatory signals to arousal networks to promote wakefulness in opposition to the homeostatic drive to sleep.
Sleep-wake cycle.
The suprachiasmatic nucleus (SCN) is entrained to the external environment by the cycle of light and darkness. The retinal ganglion cells transmit light signals via the retinohypothalamic tract to stimulate the SCN. A multisynaptic pathway from the SCN projects to the pineal gland, which produces melatonin. Melatonin synthesis is inhibited by light and stimulated by darkness. The nocturnal rise in melatonin increases between 8 and 10 am and peaks between 2 and 4 am, then declines gradually over the morning. Melatonin acts via specific melatonin receptors MT1 which attenuates the alerting signal and MT2 which phase shifts the SCN clock. The novel sleep-promoting drug ramelteon acts specifically at the MT1 and MT2 receptors to promote sleep.
Brain areas critical for wakefulness include the tuberomammillary nucleus (TMN) in the posterior hypothalamus that contains histamine neurons, which project stimulatory inputs to brainstem arousal centers such as the locus coeruleus (LC) (norepinephrine), the dorsal raphe nuclei (DRN) (serotonin), the ventral tegmental area (VTA) (dopamine), and the basal forebrain (acetylcholine), which project diffusely to cortical areas to promote arousal.
The TMN also inhibits sleep-promoting areas, such as the anterior hypothalamus. Similarly, the brainstem arousal regions inhibit sleep-promoting regions in the anterior hypothalamus. Adenosine, a neurotransmitter, accumulates in the brain during prolonged wakefulness and inhibits wake-promoting regions in the posterior hypothalamus and the basal forebrain. Acetylcholine in the basal forebrain also projects diffusely to cortical areas and the TMN to promote wakefulness.The ascending arousal system. Adapted from Saper et al. Hypothalamic Regulation of Sleep and Circadian Rhythms. Nature 2005;437:1257-1263.
The anterior hypothalamus, which includes the ventrolateral preoptic nucleus (VLPO) contains GABA and the peptide galanin, which are inhibitory and promote sleep. They project to the TMN and the brainstem arousal regions to inhibit wakefulness. GABA is the predominant inhibitory neurotransmitter in the central nervous system.Ventrolateral pre-optic nucleus inhibitory projections to main components of the arousal system to promote sleep.
Saper and colleagues proposed the flip-flop switch model of sleep-wake regulation.1 This flip-flop circuit consists of 2 sets of mutually inhibitory components. The sleep side is the VLPO and the arousal side includes TMN histaminergic neurons and brainstem arousal regions (the DRN serotonergic neurons, VTA dopaminergic neurons, and LC noradrenergic neurons). Each side of the switch inhibits the other. For example, when activation of one side is slightly stronger, the weaker side has increased inhibition, thus further tipping the balance toward the stronger side. This flip-flop switch allows for rapid state transitions.Schematic flip-flop switch model. Adapted from Saper C et al. Hypothalamic regulation of sleep and circadian rhythms. Nature 2005;437:1257-1263.
Hypocretin neurons in the posterolateral hypothalamus are active during wakefulness and project to all of the wakefulness arousal systems described above. Hypocretin neurons interact with both the sleep-active and the sleep-promoting systems and act as stabilizers between wakefulness-maintaining and sleep-promoting systems to prevent sudden and inappropriate transitions between the 2 systems.2 For example, patients with narcolepsy with cataplexy have a greater than 90% loss of hypocretin neurons, and they have sleep-wake state instability with bouts of NREM/REM sleep intruding into wakefulness.
Benzodiazepine receptor agonists (BZRAs) and nonbenzodiazepine receptor agonists (NBZRAs), for example, work through GABAA receptors to promote sleep by inhibiting brainstem monoaminergic arousal pathways, through facilitation of VLPO inhibitory GABAergic projections to arousal centers such as the anterior hypothalamus TMN, the posterolateral hypothalamic hypocretin neurons, and the brainstem arousal regions (see Medication for further information about BZRAs and NBZRAs).
In summary, sleep and wakefulness is a tightly regulated process with reciprocal connections that produce consolidated periods of wakefulness and sleep that are entrained by environmental light to occur at specific times of the 24-hour cycle.
Frequency
United States
In a 1991 survey, 30-35% of American adults reported difficulty sleeping in the past year and 10% reported the insomnia to be chronic and/or severe. Despite the high prevalence, only 5% of persons with chronic insomnia visited their physician specifically to discuss their insomnia. Only 26% discussed their insomnia during a visit made for another problem.
International
A study from Quebec indicated an overall prevalence of insomnia of approximately 20% of French Canadians. A study of young adults in Switzerland indicated a 9% prevalence of chronic insomnia. A World Health Organization (WHO) study conducted in 15 centers found a prevalence of approximately 27% for the complaint "difficulty sleeping."
Mortality/Morbidity
Consequences of chronic insomnia
- Patients with insomnia report decreased quality of life compared with normal controls in all dimension of the SF-36.
- Patients with insomnia report excessive fatigue as measure by the Fatigue Severity Scale and the Profiles of Mood Status (POMS).
- Patients with insomnia are more than twice as likely as the general population to have a fatigue-related motor vehicle accident.
- Increased occupational dysfunction and decreased work performance are likely due to chronic hyperarousal state or perceptions of sleep deprivation rather than actual sleep loss from insomnia. For example, unlike patients with chronic sleep deprivation from other causes, patients with insomnia report less excessive daytime sleepiness and less psychomotor and cognitive impairment.
Associations of insomnia with depression and anxiety
One of the early descriptions of an association between insomnia and depression and anxiety was by Ford and Kamerow.3 What is still unknown is the nature of the association. For example, does insomnia presage the development of an incipient mood disorder and/or do mood disorders independently predispose to insomnia.
After adjusting for medical disorders, ethnicity, and sex, patients with insomnia were 9.8 times more likely to have clinically significant depression and 17.3 times more likely to have clinically significant anxiety than persons who did not have insomnia.
Ohayon and Roth found that symptoms of insomnia were reported to occur before the first episode of an anxiety disorder 18% of the time, simultaneously 39% of the time, and after the onset of an anxiety disorder 44% of the time.4
In contrast, insomnia symptoms were reported to occur before a first episode of a mood disorder 41% of the time, simultaneously 29% of the time, and after the onset of a mood disorder 29% of the time.
Race
At this time, no data are available to suggest an association for or against race as a risk factor for insomnia.
Sex
The prevalence of chronic insomnia is 1.2-2.0 times greater in women than men. One study by Strine and colleagues indicated that women who have menstrual-related problems are more likely to have insomnia as compared with women without such problems.5 In fact, after adjustments were made for age, race and ethnicity, education, marital status, and employment status, women who had menstrual-related problems were 2.4 times as likely to report insomnia than women without such problems. At this time, whether social factors or neurobiologic factors contribute to the increased prevalence in women is not known.
Age
Chronic insomnia increases in frequency with age and is more common in the elderly. This is presumed due to greater psychosocial stressors, losses, and medical illnesses. Recent epidemiologic data indicate that the prevalence of chronic insomnia increases form 25% in the adult population to 50% in the elderly population.
Clinical
History
The history is the most important part of evaluating insomnia. It must include a complete sleep history, medical history, psychiatric history, social history, and careful medication review.
Sleep history
Determining the timing of insomnia, the patient's sleep habits (commonly referred to as sleep hygiene), and symptoms of sleep disorders associated with insomnia is important.
- Timing of insomnia: Patients should be asked about any difficulty falling asleep, frequent or early morning awakening, problems in sleep onset, and whether they feel sleepy when getting into bed.
- Sleep schedule: Patients must be asked what time they go to bed and rise from bed in the morning. Determine whether the sleep schedule is consistent and if the schedule has changed recently.
- Sleep environment: Patients should be asked about temperature, bed comfort, noise, and light levels. Ask whether the patient sleeps better in his or her own bed or in a chair or a foreign environment (like a hotel).
- Sleep habits: Patients with insomnia often have poor sleep hygiene. They should be asked about activities prior to bedtime (ie, relaxation or work), whether they read or watch TV in bed, and whether the TV or light is kept on during the night. Also, ask patients what they do if unable to fall asleep and whether they fall asleep after waking up in the middle of the night. Ask patients about daytime naps and whether they exercise and the time of exercise.
- Patients should be asked about symptoms of other sleep disorders such as obstructive sleep apnea (eg, snoring, witnessed apneas, gasping) and restless legs syndrome/periodic limb movement disorder (ie, restless feeling in legs on lying down, which improves with movement; rhythmic kicking during the night; sheets in disarray in the morning).
- Daytime effects: Patients should experience daytime effects if they truly are not sleeping at night. In fact, if a patient is having no daytime effects, he or she is probably getting adequate sleep and the complaint of insomnia is truly subjective. Common complaints are fatigue, tiredness, lack of energy, irritability, reduced work performance, and difficulty concentrating. These complaints should be distinguished from the complaint of excessive sleepiness, which is uncommon in insomnia. For example, if a patient complains of excessive daytime sleepiness (ie Epworth Sleepiness Scale Score >10), another sleep disorder should also be considered. (See Media file 12 for the Epworth Sleepiness Scale.)
Medical history
A thorough medical history and review of systems should be performed, with particular emphasis on those disorders mentioned in Causes.
Psychiatric history
A review of signs and symptoms of anxiety or depression should be sought. A 2-question case-finding instrument can help screen for depression.
Diagnostic algorithm for major depression.
Diagnostic criteria for generalized anxiety disorder.
Social history
For transient or short-term insomnia, inquire about new situational stresses such as a new job, new school, relationship change, or bereavement. For chronic insomnia, attempt to relate the onset of insomnia to past stresses or medical illnesses. Inquire about tobacco, caffeinated products, alcohol, and illegal drug use.
Medication history
Medications that commonly cause insomnia include beta-blockers, clonidine, theophylline (acutely), certain antidepressants (protriptyline or fluoxetine), decongestants, and stimulants. Also inquire about over-the-counter and herbal remedies that the patient may be taking.
Physical
The physical examination can provide clues to comorbid insomnia.
- A large neck size of 18 inches or greater in males, elevated BMI of 30 kg/m2, enlarged tonsils, Mallampati airway score of 3 or 4 (see Media file 2), low lying soft palate particularly in patients with hypertension or cardiac disease, and obstructive sleep apnea/hypopnea syndrome should be considered. Other features include enlarged tongue, retrognathia, micrognathia, or a steep mandibular angle.
- If patients have evidence of peripheral neuropathy (ie, stocking distribution loss of temperature sensation) with or without trophic changes, they should be asked about painful symptoms (ie, burning sensation) in their feet, and history of diabetes, alcohol abuse, and neurologic consultation should be requested.
- If patients complain of symptoms of restless legs syndrome or symptoms suggestive of a neurologic disorder, such as nocturnal seizures, Parkinson disease, or a neuromuscular disorder, a neurologic consultation should be requested.
- In patients with chronic pain syndromes or rheumatologic syndromes, referral to a pain management specialist and/or rheumatologist should be considered.
- If chest examination shows reduced breath sounds; clubbing or wheezing in the setting of clinical signs; and symptoms suggestive of chronic obstructive pulmonary disease, asthma, or obesity hypoventilation syndrome, pulmonary consultation should be requested.
Causes
Many clinicians often assume that insomnia is secondary to a psychiatric disorder, However, a large epidemiologic survey showed that half of insomnia diagnoses were not related to a primary psychiatric disorder. As mentioned earlier, an insomnia diagnosis does increase the future risk for depression or anxiety (see Morbidity).
Frequency of insomnia causes.
Classification of Insomnia
The International Classification of Sleep Disorders classifies insomnia into 11 categories, listed below.Adjustment insomnia (acute insomnia)
This occurs in the context of an identifiable stressor (eg, personal loss, change in interpersonal relationship, bereavement, occupational stress, job loss) that acts as a precipitating factor. It typically last 3 months or less and resolves as the stressor is no longer present or as the individual adapts to the stressor .
Chronic insomnia
The following are diagnoses of chronic insomnia and meet the criteria for chronic insomnia:
- Repeated difficulty with the initiation, duration, maintenance, or quality of sleep that occurs despite adequate time and opportunity for sleep that results in some form of daytime impairment.
- Number 1 must be present for at least 1 month.
Psychophysiologic insomnia (primary insomnia)
- The patient has evidence of conditioned sleep difficulty and or/heightened arousal in bed as indicated by one or more of the following:
- Excessive focus on and heightened anxiety about sleep
- Difficulty falling asleep at the desired bedtime or during planned naps, but no difficulty falling asleep during other monotonous activities when not intending to sleep
- Ability to sleep better away from home than at home
- Mental arousal in bed characterized either by intrusive thoughts or a perceived inability to volitionally cease sleep-preventing mental activity
- Heightened somatic tension in bed reflected by a perceived inability to relax the body sufficiently to allow the onset of sleep
- The sleep disturbance is not better explained by another sleep disorder, medical or neurologic disorder, medication use, or substance abuse disorder.
- One or more of the following criteria apply:
- The patient reports a chronic pattern of little or no sleep most nights, with rare nights during which relatively normal amounts of sleep are obtained.
- Sleep log data from one or more weeks of monitoring show an average sleep time often with no sleep at all indicated for several nights each week; typically daytime naps are absent following such nights.
- The patients typically show a mismatch between objective findings from polysomnography or actigraphy and subjective sleep estimates from self-reported sleep diary.
- At least one of the following is observed:
- The patient reports constant or near constant awareness of environmental stimuli throughout most nights.
- The patient reports a pattern of conscious thoughts or rumination throughout most nights while maintaining a recumbent posture.
- The daytime impairment reported is consistent with that reported by other insomnia subtypes but is much less severe than expected given the extreme level of sleep deprivation reported.
- The sleep disturbance is not better explained by another sleep disorder, medical or neurologic disorder, medication use, or substance abuse disorder.
- The patient has a coexisting medical condition known to disrupt sleep.
- The insomnia is clearly associated with the medical condition. The insomnia began near the time of onset or with significant progression of the medical condition and waxes and wanes with the severity of this condition.
- The sleep disturbance is not better explained by another sleep disorder, medical or neurologic disorder, medication use, or substance abuse disorder.
Insomnia due to mental disorder
- A mental disorder has been diagnosed according to the criteria of DSM-IV-TR.
- The insomnia is temporally associated with the mental disorder; however, in some cases, insomnia may appear a few days or weeks before the emergence of the underlying mental disorder.
- The insomnia is more prominent than that typically associated with the mental disorders, as indicated by causing marked distress or constituting an independent focus of treatment.
- The sleep disturbance is not better explained by another sleep disorder, medical or neurologic disorder, medication use, or substance abuse disorder.
Insomnia due to drug or substance abuse
- One of the following applies:
- The patient has current ongoing dependence on or abuse of a drug or substance known to have sleep disruptive properties either during periods of use or intoxication or during periods of withdrawal.
- The patient has current ongoing use of or exposure to a medication, food, or toxin known to have sleep-disruptive properties in susceptible individuals.
- The insomnia is temporally associated with the substance exposure, use, or abuse, or acute withdrawal.
- The sleep disturbance is not better explained by another sleep disorder, medical or neurologic disorder, medication use, or substance abuse disorder.
Insomnia not due to substance or known physiological condition, unspecified
This diagnosis is used for forms of insomnia that cannot be classified elsewhere in ICSD-2, but are suspected to be due to an underlying mental disorder, psychological factors, or sleep disruptive processes. This diagnosis can be used on a temporary basis until further information is obtained to determine the specific mental condition or psychological or behavioral factors responsible for the sleep difficulty.
Inadequate sleep hygiene
- Inadequate sleep hygiene practices are evident by the presence of at least 1 of the following:
- Improper sleep scheduling consisting of frequent daytime napping, selecting highly variable bed or rising times or spending excessive amounts of time in bed.
- Routine use of products containing alcohol, nicotine, or caffeine, especially in the period preceding bedtime.
- Engagement in mentally stimulating, physically activating, or emotionally upsetting activities too close to bedtime.
- Frequent use of the bed for activities other than sleep (eg, television watching, reading, studying, snacking, thinking, planning).
- Failure to maintain a comfortable sleeping environment.
- The sleep disturbance is not better explained by another sleep disorder, medical or neurologic disorder, medication use, or substance abuse disorder.
Idiopathic insomnia
A longstanding complaint of insomnia with insidious onset in infancy or childhood. No precipitant or cause is identifiable. There is a persistent course with no sustained periods of remission. This condition is present in 0.7% of adolescents and 1% of very young adults.
Behavioral insomnia of childhood
- A child's symptoms meet the criteria for insomnia based on parents or other adult caregivers observations.
- The child shows a pattern consistent with either sleep-onset association or limit-setting type of insomnia:
- Sleep onset association type
- Falling asleep is an extended process that requires special conditions.
- Sleep onset associations are highly problematic or demanding.
- In the absence of associated conditions, sleep onset is significantly delayed or sleep is otherwise disrupted.
- Nightime awakenings require caregiver intervention for the child to return to sleep.
- Limit-setting type
- The individual has difficulty initiating or maintaining sleep.
- The individual stalls or refuses to go to bed at an appropriate time or refuses to return to bed following a nighttime awakening.
- The caregiver demonstrates insufficient or inappropriate limit setting to establish appropriate sleeping behavior in the child.
- Sleep onset association type
Primary sleep disorders causing insomnia
- Restless legs syndrome (RLS) is a sleep disorder characterized by the following:
- An urge to move the legs, usually accompanied by uncomfortable and unpleasant physical sensations in the legs.
- The urge to move or the unpleasant sensations begin or worsen during periods of rest or inactivity such as lying or sitting.
- The urge to move or the unpleasant sensations are partially or totally relieved by moving, such as walking or stretching, at least as long as the activity continues.
- The urge to move or the unpleasant sensations are worse or only occur in the evening or the night.
- Obstructive sleep apnea/hypopnea syndrome: A minority of patients complain of insomnia rather than hypersomnolence. They frequently complain of multiple awakenings or sleep-maintenance difficulties. They may also have nocturia causing frequent nocturnal awakenings.
- Circadian rhythm disorders
- Advanced sleep phase syndrome: The patient feels sleepy earlier than their desired bedtime (ie, 8 pm) and they wake up earlier than they would like to (ie, 4-5 am). This condition is more common in the elderly. These patients typically complain of sleep maintenance insomnia.
- Delayed sleep phase syndrome: The patient does not feel sleepy until much later than the desired bedtime, and he or she wakes up later than desired or socially acceptable. On sleep diaries or actigraphy, these patients show a consistent sleep time with earlier wake times that correspond to school or work days, and delayed wake times on weekends, time off, and vacations. This condition often begins in adolescence and may be associated with a family history in up to 40% of patients. These patients report difficulty falling asleep at usually socially desired bedtimes, and complain of excessive daytime sleepiness during the school or work week.
- Shift work sleep disorder: A complaint of insomnia or excessive sleepiness is typically temporally related to a recurring work schedule that overlaps the usual sleep time. This can occur with early morning shifts (4-6 am), where the patient is anxious about waking up in time for their early shift particularly when they have a rotating shift schedule. Evening shifts that end at 11 pm can result in insomnia in that the patient may need some time to wind down from work before retiring to bed. Night shift can be associated with both sleep onset and maintenance insomnia due to exposure to sunlight on their drive home from work, daylight exposure in their bedroom, and social and environmental cues (picking up children at school, paying bills, household chores, etc).
- Irregular sleep-wake rhythm: This is typically seen in patients with poor sleep hygiene, patients who live or work alone with minimal exposure to light, activity, and social cues. These patients randomly nap throughout the day making it difficult, if not impossible, to fall asleep at a habitual bedtime with a consolidated sleep period.
More on Insomnia |
 Overview: Insomnia |
| Differential Diagnoses & Workup: Insomnia |
| Treatment & Medication: Insomnia |
| Follow-up: Insomnia |
| Multimedia: Insomnia |
| References |
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Further Reading
Keywords
insomnia, sleep disorder, sleep problem, sleep symptom, sleep complaint, sleeplessness, inability to sleep, transient insomnia, short-term insomnia, chronic insomnia, insomnia, sedative, hypnotic, melatonin, sleep loss
