{
  "id": "insomnia",
  "title": "Insomnia",
  "lang": "en",
  "source_lang": "en",
  "summary": "Insomnia is a common sleep disorder marked by persistent difficulty falling or staying asleep, with daytime impairment.",
  "category": "health",
  "subcategory": "diseases",
  "type": "concept",
  "aliases": [
    "Sleeplessness",
    "Agrypnia"
  ],
  "generated_at": "2026-10-09",
  "model": "pro/claude-haiku-5-5",
  "url": "https://aiwiki.page/en/insomnia/",
  "translations": {
    "zh-Hans": {
      "url": "https://aiwiki.page/zh/insomnia/",
      "json": "https://aiwiki.page/zh/insomnia.json"
    }
  },
  "sections": [
    {
      "heading": "",
      "text": "Insomnia is a persistent difficulty in initiating or maintaining sleep, or waking too early and being unable to return to sleep, that impairs functioning during waking hours. It is distinct from a single bad night: in clinical usage it refers to a recurring pattern, usually defined by frequency and duration thresholds, that is recognized as a sleep disorder in its own right and as a frequent feature of many mental and medical conditions. It is the most common sleep complaint in clinical practice and one of the most prevalent disorders in epidemiology and public health research. Its consequences extend beyond tiredness to attention, memory, emotional regulation, cardiometabolic health, and accident risk.\n\nThis entry examines insomnia from its definition and classification through its prevalence, the physiology of sleep regulation, its causes and comorbidities, and its consequences. It then reviews the main treatments, principally cognitive behavioral therapy for insomnia (CBT-I) as first-line care and pharmacological options with their risks, followed by insomnia across the lifespan, the history of its classification, and the unresolved debates in the field."
    },
    {
      "heading": "Definition and clinical features",
      "text": "Subjective complaint and objective sleep\n\nInsomnia is defined mainly by what the person reports. Current diagnostic manuals describe it as repeated difficulty with sleep initiation, maintenance, consolidation, or quality that occurs despite adequate time and opportunity to sleep and produces some form of daytime impairment. The DSM-5 places the emphasis on a predominant complaint of dissatisfaction with the quantity or quality of sleep, which is why the diagnosis rests on symptom history rather than on a laboratory test. Unlike most other sleep disorders, insomnia is the one condition for which polysomnography (PSG) is not required to confirm the diagnosis.\n\nSelf-report and objective recordings frequently disagree. In the literature this is called sleep state misperception, subjective-objective sleep discrepancy, or, in the ICSD-3 terminology, paradoxical insomnia. People with insomnia commonly underestimate their total sleep time and overestimate how long they take to fall asleep and how long they remain awake after sleep onset. In sleep clinics, discrepancies of this kind are seen in roughly 5–9% of insomnia cases, and the discrepancy is typically greatest in insomnia itself compared with other sleep complaints. Some researchers have argued that the mismatch reflects subtle changes in sleep physiology, such as cortical activation during sleep, that conventional PSG scoring does not capture, but findings have been inconsistent. A 2025 analysis of polysomnographic recordings suggested that insomnia with and without this discrepancy may involve different patterns of intrusions of wakefulness into sleep or of sleep into waking, which points to separate mechanisms. Terminology in this area remains contested, and some authors have proposed replacing labels such as \"subjective insomnia\" and \"paradoxical insomnia\".\n\nCore symptom types\n\nThe four principal nocturnal complaints are difficulty initiating sleep, difficulty maintaining sleep, early-morning awakening, and non-restorative sleep. Sleep-onset difficulty is commonly operationalised as taking more than 30 minutes to fall asleep. Sleep-maintenance difficulty is characterised by frequent awakenings or trouble returning to sleep after waking, and it is often the most common complaint in population surveys. Early-morning awakening means waking well before the desired time, typically at least two hours early in epidemiological definitions, without being able to fall back asleep. Non-restorative sleep describes waking unrefreshed even after a duration that seems adequate. In general-population studies, these items were typically counted as present when they occurred at least three mornings a week for a month or longer. Brief nocturnal awakenings alone are common, affecting about one-third of the general population, but they are unlikely to produce daytime impairment unless the person also has difficulty resuming sleep, which is the feature most strongly linked to daytime consequences and to help-seeking.\n\nDaytime manifestations\n\nInsomnia is diagnosed on the basis of its effects in waking hours as well as at night. Typical daytime features include fatigue and low energy, daytime sleepiness, inattention and poor concentration, slowed or \"foggy\" thinking, irritability and mood disturbance, and reduced performance at work, school, or home. Because the daytime and night-time symptoms interact, poor sleep produces daytime deficits that can in turn impair the following night's sleep, creating a repeating cycle. The DSM-5 requires that the sleep disturbance cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.\n\nDistinguishing insomnia from other sleep patterns\n\nOccasional nights of poor sleep, such as those caused by a stressful event, noise, or a late flight, do not in themselves constitute insomnia. Insomnia is also not defined by a particular number of hours. Some people sleep less than most others but feel rested and function normally, and this short sleep is not classed as a disorder. Conversely, a person who sleeps six hours but is distressed and impaired by it may meet criteria. Conventional thresholds, such as falling asleep in more than 30 minutes or sleeping less than six hours, are used as guides, not as diagnostic cut-offs. Sleep deprivation and insomnia can be contrasted by their underlying cause: in deprivation, the person has the physiological capacity to sleep but insufficient opportunity to do so, whereas in insomnia sleep is difficult to initiate or sustain even when time in bed is adequate."
    },
    {
      "heading": "Classification: acute, short-term, and chronic insomnia",
      "text": "Insomnia is commonly grouped by how long it lasts. Transient insomnia is the briefest form, and sources disagree on its upper limit: one definition describes it as present for one to several days, lasting less than one week, while most experts describe it as lasting less than four weeks. Acute, or short-term, insomnia runs longer, and clinicians diagnose acute insomnia when symptoms occur at least three times a week for one week to three months. Triggers are central to this picture. Acute episodes are often triggered by situational stressors, such as illness, work stress, or bereavement, and in most cases acute insomnia resolves once the stressor or temporary cause is removed. Persistence is the exception rather than the rule. One figure from a consumer sleep resource, which summarizes research, puts recovery from acute insomnia at about 75 percent, with about 6 percent going on to develop a chronic form.\n\nThe third edition of the International Classification of Sleep Disorders (ICSD-3), published in 2014, consolidated all insomnia disorders under three umbrella categories: chronic insomnia, short-term insomnia, and other insomnia disorder. Short-term insomnia disorder covers difficulties that fail to meet the minimal frequency and duration criteria of chronic insomnia disorder but are associated with clinically significant sleep dissatisfaction or perceived daytime impairment. Its criteria are otherwise close to those of the chronic form: they are identical except in terms of duration, which is under three months, and the lack of a frequency criterion. The text revision (ICSD-3-TR) simplified the scheme. Unlike earlier editions that delineated multiple subtypes, it primarily recognizes chronic insomnia disorder and short-term insomnia disorder. The ICD-11 classification follows ICSD-3 terminology in having codes for chronic insomnia, short-term insomnia, and \"insomnia disorders, unspecified\".\n\nThe chronic category carries the most clinical weight. Chronic insomnia is the most prevalent sleep disorder and a frequent concern during primary care visits. It is associated with excessive daytime sleepiness, a higher risk of automobile accidents, and multiple physical and psychiatric comorbidities in adults. The diagnosis is reserved for individuals whose sleep difficulties exceed minimal frequency and duration thresholds associated with clinically significant morbidity outcomes. The three-month threshold reflects a change in the DSM-5. Earlier criteria used a duration of one month, but the threshold was increased to three months, based on evidence that three months is a critical period, after which insomnia is more likely to persist and its morbidity becomes more noticeable. The cut-off is a pragmatic boundary rather than a biological one. Persistence remains substantial past that point: insomnia is often a chronic condition, with a 40% persistence rate over a five-year period. The duration rule also has a known gap, since some patients with chronic insomnia may experience recurrent episodes of sleep/wake difficulties lasting several weeks at a time over several years, yet not meet the three-month duration criterion for any single episode.\n\nEpisodes that fall short of full disorder criteria are handled differently. When there is no reported or observed daytime impairment or dissatisfaction with sleep, people who describe prolonged sleep latency, recurrent awakenings, or restricted sleep duration are not regarded as having an insomnia disorder that warrants clinical attention, other than education and reassurance. The \"other\" category is narrower. It should be assigned in rare cases that fail to meet criteria for chronic or short-term insomnia disorder yet have sufficient symptoms of insomnia to warrant clinical attention. In practice, acute insomnia may not require medical treatment if it resolves naturally. Clinical follow-up becomes more appropriate when symptoms persist; one guidance source advises seeking professional consultation if sleeplessness lasts beyond a few weeks, or if resulting daytime fatigue and mood changes become severe."
    },
    {
      "heading": "Diagnostic criteria across major classification systems",
      "text": "The DSM-5 places insomnia disorder first among its sleep-wake disorders, and its criteria start with a predominant complaint of dissatisfaction with sleep quantity or quality. That complaint must include at least one of three features: difficulty initiating sleep, difficulty maintaining sleep (frequent awakenings or trouble returning to sleep after waking), or early-morning awakening with inability to return to sleep. The disturbance must also cause clinically significant distress or impairment in social, occupational, educational, academic, behavioral, or other important areas of functioning. Time criteria are at least 3 nights per week and present for at least 3 months.\n\nAdequate opportunity for sleep\n\nThe DSM-5 requires that the difficulty occurs despite adequate opportunity for sleep. The ICSD-3 expresses the same idea by stating that the complaint cannot be explained purely by insufficient time allotted for sleep or by an unsuitable environment, where the room should be safe, dark, quiet and comfortable (The reported sleep/wake complaints cannot be explained purely by inadequate opportunity (i.e. enough time is allotted for sleep) or inadequate circumstances (i.e. the environment is safe, dark, quiet and comfortable) for sleep.). This criterion separates true insomnia from a short sleep schedule that a person has chosen or been assigned, so clinicians need to check the time and conditions available for sleep before diagnosing.\n\nICSD-3 and ICD-11\n\nThe third edition of the International Classification of Sleep Disorders was published in 2014 and consolidated all insomnia disorders under three umbrella categories: chronic insomnia, short-term insomnia, and other insomnia disorder. Its chronic-insomnia criteria were built on ICSD-2, with only the addition of the DSM's frequency criterion of three times per week, a duration criterion of at least 3 months, and an exclusion criterion for other sleep disorders. The overlap is not accidental: DSM-5 and ICSD-3 insomnia diagnostic criteria are similar due to collaborative efforts between the APA and the AASM classification task forces.\n\nThe ICD-11 was endorsed at the World Health Assembly in May 2019 and was set to take effect on 1 January 2022. Its insomnia codes follow ICSD-3 terminology in having codes for chronic insomnia, short-term insomnia, and \"insomnia disorders, unspecified\". The ICD-10 had separated organic from non-organic sleep disorders, but ICD-11 will follow the avenue paved by DSM-5 and ICSD-3. The result is that the ICSD-3, ICD-11, and DSM-5 abandoned all attempts at categorizing insomnias by presumed pathology, and put aside the primary/secondary and organic/nonorganic dichotomies.\n\nExclusion rules\n\nThe diagnosis is not made when the symptoms are not better explained by and do not occur exclusively during the course of another sleep-wake disorder. Symptoms also cannot be attributed to the effects of a substance (e.g., drug abuse and medication). Coexisting mental disorders and medical conditions do not adequately explain the predominant complaint of insomnia. Comorbidity itself is not excluded. Insomnia probably more frequently occurs as a co-morbid condition together with somatic and mental disorders, than it does occur in its isolated form, and DSM-5, ICSD-3 and ICD-11 pay respect to this by explicitly allowing co-morbidity. The ICSD-3 text revision adds that insomnia symptoms can also arise from substance use, and that a separate insomnia disorder diagnosis is warranted when the insomnia symptoms are persistent and result in distress or impairment."
    },
    {
      "heading": "Clinical assessment and differential diagnosis",
      "text": "Insomnia is diagnosed on clinical grounds, because no laboratory test establishes it. The core of the assessment is a structured clinical interview that establishes the symptom pattern: which complaint predominates (difficulty falling asleep, staying asleep, early waking, or non-restorative sleep), how often and for how long these occur, and what daytime consequences follow. The interview also covers medical, psychiatric and substance history, the patient's beliefs and worries about sleep, and the response to earlier treatments, including over-the-counter sleep aids and prescribed hypnotics. Where a bed partner or household member can contribute, their observations of snoring, breathing pauses, limb movements or nocturnal behaviour are often more informative than the patient's own account, since people who lie awake for long periods tend to misjudge how much they have slept.\n\nSleep diaries, questionnaires and actigraphy\n\nClinicians commonly ask patients to keep a sleep log for roughly two to four weeks before treatment begins. Recording bed and wake times, sleep duration, naps and daytime activities reveals irregular schedules and daytime napping that retrospective recall tends to miss, and it provides a baseline against which later change can be judged. Standardized questionnaires quantify severity and daytime impact, and brief screening instruments for depression and anxiety are often added. These tools are inexpensive and scalable, but they depend on self-report.\n\nActigraphy uses a wrist-worn device that records movement and ambient light over several days or weeks. Because people move far less during sleep than while awake, the activity pattern yields an indirect estimate of sleep timing and duration. In a laboratory comparison with polysomnography, actigraphy and sleep diaries both underestimated total sleep time and sleep efficiency and overestimated wake time, and actigraphy was more accurate than diaries overall. It was also sensitive enough to detect treatment effects, which is why it is used mainly to complement diaries. Its routine clinical value in insomnia is more limited; its most established roles are documenting circadian patterns, separating insomnia from circadian rhythm disorders, and tracking response to treatment, particularly in research and in children or older adults who cannot easily attend a sleep laboratory.\n\nWhen polysomnography is indicated\n\nPolysomnography records EEG alongside eye movements, muscle tone, breathing, oxygen saturation and leg movements. It is not routinely required for insomnia. It is indicated mainly to exclude sleep disorders that can resemble insomnia. The principal target is sleep apnea: loud snoring, witnessed breathing pauses or marked daytime sleepiness warrant a sleep study, because repeated airway obstruction fragments sleep. Periodic limb movement disorder and restless legs syndrome are the other main reasons, since the leg movements they cause produce awakenings that patients often attribute to a primary sleep problem. Referral is also appropriate for violent or injurious behaviour during sleep, which suggests a parasomnia, and when treatment has failed, because an unrecognized condition may explain the failure.\n\nScreening for treatable secondary causes\n\nBecause many cases have treatable secondary causes, assessment includes deliberate screening. Depression and anxiety are the most frequent, and brief questionnaires such as the PHQ-9 and GAD-7 are widely used in primary care; questions about alcohol use and, where relevant, bipolar symptoms are also standard. Chronic pain of many kinds, as well as respiratory, cardiac, thyroid, gastrointestinal, urinary and menopausal conditions, can disturb sleep, and pain control is generally addressed before the insomnia itself is treated. Medication review is equally important. Stimulants such as caffeine, amphetamines and cocaine classically disrupt sleep; some antidepressants, decongestants, asthma medicines, allergy and cold preparations and beta blockers can do so as well. Alcohol may shorten the time taken to fall asleep, but it tends to fragment the later part of the night, and its use is typically recorded as a contributing factor rather than a remedy. Routine blood tests are not usually needed. Thyroid function is checked when symptoms suggest thyroid disease, and iron studies, including serum ferritin, are obtained when restless legs symptoms are present."
    },
    {
      "heading": "Epidemiology and prevalence",
      "text": "Estimates of how many people have insomnia depend heavily on the definition used. Symptom-based surveys give the largest figures. One range reported by a review states that symptoms are present in about 33–50% of the adult population. Stricter criteria produce much smaller numbers. In a 2022 systematic review, Morin and Jarrin found that 10–15% of adults reported insomnia with daytime symptoms, while 6–10% met strict DSM or ICSD criteria. Earlier, Ohayon's 2002 review of DSM-based studies had reported a prevalence of 6%.\n\nStudies that apply a formal diagnostic standard to random general-population samples give more consistent results. A 2025 meta-analysis pooled a prevalence of 12.4% from studies using diagnostic interviews, and 16.3% from studies using self-report questions framed around DSM criteria. Questionnaire-based studies, which used different cut-offs, ranged from 7.5% to 32.3%. The same analysis found that prevalences differed significantly across regions, and higher-quality studies yielded lower rates than lower-quality studies. A single-population comparison illustrates the point: in the Tromsø Study's seventh survey, applying four sets of criteria to the same cohort produced figures from 8.5% under DSM-5 to 23.6% under DSM-IV-TR.\n\nFor chronic insomnia disorder specifically, a 2025 global estimate built by combining published prevalence data with United Nations population statistics put the figure at 16.2% of adults, roughly 852 million people. That estimate included a severe subgroup of about 7.9%. Because the figure was derived from aggregated studies rather than a single worldwide survey, it reflects the same definitional variation described above. Older textbook figures, which hold that roughly 10–15% of adults have chronic insomnia and a further 25–35% have transient or occasional insomnia, were based on inconsistent criteria, and their authors acknowledged that the estimates varied accordingly.\n\nInsomnia is consistently more common in women. A commonly cited figure is that insomnia is approximately 1.5 times more common in women than in men. Reviews of population studies give a range of about 1.3–2.0 times more common in women than in men. The gap is sensitive to the criteria used. Léger and colleagues showed that the more restrictive the criteria for insomnia, the more important the difference between sexes. In one French study cited in a review, the DSM-IV-based prevalence was 22% in women and 14% in men, and under the stricter severe-insomnia definition it was 12% and 6.3%. The female-to-male ratio also changes with age. One review reports that the ratio for insomnia symptoms is about 1.4, and rises to about 1.7 after age 45. Women are also less likely to remit. In the EPESE cohort of older adults, women were less likely to achieve remission (46% of women vs 52% of men), which suggests that the higher female prevalence may reflect fewer resolved cases rather than more new ones.\n\nIncidence and persistence are harder to measure than point prevalence, because they require repeated follow-up. In a prospective study of good sleepers aged 35 and older (67% female), daily diaries showed a one-year incidence of acute insomnia of 27.0%. Of those who developed acute insomnia, 72.4% went on to recover good sleep. A further 19.3% continued to experience persistent poor sleep, but did not meet criteria for chronic insomnia. The one-year incidence of chronic insomnia in the same sample was 1.8%. An earlier analysis of acute episodes estimated a transition rate of about 21% from acute to chronic insomnia, although the authors described it as tentative. Longer population follow-up points to persistence. In a Canadian five-year cohort, 13.9% of those without insomnia at baseline developed an insomnia syndrome during the 5-year follow-up and 37.5% of those with insomnia at baseline reported persisting insomnia. A three-year population-based study found that nearly half of the sample (46%) reported persistent insomnia at all time points, and that persistence was more likely when baseline severity was higher."
    },
    {
      "heading": "Normal sleep regulation and the physiology of wakefulness",
      "text": "Homeostatic and circadian control\n\nSleep timing in healthy adults is often described by the two-process model that Alexander Borbély proposed in 1982. Process S is the homeostatic sleep drive. It builds during time spent awake and dissipates during sleep, most visibly as slow-wave activity in non-REM sleep. Adenosine accumulation in the basal forebrain is one proposed mediator, though its exact role remains debated. Process C is the circadian component, an oscillation with a period close to 24 hours that continues independently of prior sleep. It is generated by the suprachiasmatic nucleus (SCN) in the anterior hypothalamus. Sleep is easiest to initiate when the homeostatic drive is high and the circadian signal favours sleep, and hardest in the late afternoon and early evening, when the circadian signal opposes it.\n\nThe SCN is synchronised to the day–night cycle mainly through light. Intrinsically photosensitive retinal ganglion cells, which contain the photopigment melanopsin, send signals to the SCN through the retinohypothalamic tract. Light in the early biological night delays the clock, while light in the late biological night advances it. The SCN also regulates melatonin release from the pineal gland through a multisynaptic pathway, so melatonin secretion rises in darkness and is suppressed by light exposure. Because of this, timing of light exposure shapes both sleep onset and the phase of the rhythm.\n\nWake-promoting and sleep-promoting systems\n\nWakefulness depends on an ascending arousal network that originates in the brainstem and hypothalamus and projects diffusely to the thalamus and cerebral cortex. Its components include noradrenergic neurons of the locus coeruleus, serotonergic neurons of the dorsal raphe, histaminergic neurons of the tuberomammillary nucleus, dopaminergic neurons of the ventral tegmental area and substantia nigra, and cholinergic neurons of the basal forebrain and brainstem. Orexin-producing neurons of the lateral hypothalamus also support stable wakefulness. These systems use different neurotransmitters, and their firing patterns differ across states.\n\nHistaminergic neurons fire fastest during waking and fall silent during sleep, which is consistent with the sedation produced by first-generation H1 antihistamines. Serotonergic and noradrenergic neurons are most active in waking, slow during non-REM sleep, and nearly silent during REM sleep. Cholinergic neurons of the pons, by contrast, become active during REM sleep, which helps explain the state's distinctive cortical activation. Dopaminergic signalling contributes to arousal and motivated wakefulness, although the precise contributions of its specific circuits are less fully mapped than those of histamine or noradrenaline.\n\nSleep onset depends on the ventrolateral preoptic area (VLPO) of the anterior hypothalamus, whose neurons are active during sleep and inhibit the arousal nuclei. Clifford Saper and colleagues proposed in 2001 that these inhibitory connections form a mutually inhibitory \"flip-flop\" switch, which accounts for the rapid transitions between sleep and waking.\n\nSleep architecture and EEG\n\nElectroencephalography, first recorded in humans by Hans Berger in 1924, is the basis for staging sleep. Sleep is scored in 30-second epochs. N1 is the transitional stage, with slowing of the background rhythm and vertex waves. N2 is marked by sleep spindles (bursts of roughly 12–14 Hz activity) and K-complexes. N3, the deepest non-REM stage, is defined by high-amplitude slow delta waves. The 2007 American Academy of Sleep Medicine manual merged the older stages 3 and 4 into N3, replacing the 1968 Rechtschaffen and Kales scheme.\n\nREM sleep was identified by Eugene Aserinsky and Nathaniel Kleitman in 1953, who described rapid eye movements accompanied by a low-voltage, mixed-frequency EEG. Surface EMG shows loss of muscle tone (atonia) during REM, while the cortical EEG resembles waking. Sleep proceeds in cycles of roughly 90 minutes, usually four to six per night. Slow-wave sleep is concentrated in the early part of the night, and REM periods lengthen toward morning. Individual variation in these proportions is considerable, and the staging criteria above are conventions for scoring rather than sharp biological boundaries."
    },
    {
      "heading": "Causes and risk factors",
      "text": "Predisposing factors\n\nMost explanations of insomnia build on the three-factor model that Arthur Spielman and colleagues proposed in 1987, which sorts contributing influences by their timing. It extends a diathesis-stress model to describe how acute insomnia can onset and move toward a chronic course through a combination of predisposing, precipitating, and perpetuating factors. Predisposing factors are the stable background vulnerabilities. Heritable traits are a central example, including a temperament that is easily woken by noise, a nervous system that stays on high alert, and a tendency toward anxiety or perfectionism. Research on biological hyperarousal, trait anxiety, perfectionism, and physiological hyperreactivity to stress keeps returning to these same traits. A predisposition rarely produces insomnia on its own; its main effect is to lower the threshold at which a stressor leads to lasting sleep trouble. Genetic findings are discussed in the neurobiology section.\n\nPrecipitating events\n\nPrecipitating factors are the events that start an episode. Common examples include major life stress (job loss, bereavement, relationship breakdown), acute illness or physical pain, a new baby or significant disruption to routine, trauma, shift work changes, or even a period of jet lag. These triggers are usually temporary, and for many people sleep recovers once they pass, within a few weeks. The sleep loss itself can be physiological: the stressor raises adrenaline and cortisol activity and keeps the brain alert at bedtime, so sleep is disrupted even after the initial worry has moved on.\n\nPerpetuating factors\n\nThe distinctive feature of the 3P model is that insomnia can outlast its trigger. Perpetuating factors are the behaviours and mental habits adopted in an attempt to fix sleep, which end up maintaining it. Chief among them are conditioned arousal, in which the bed becomes linked with worry, frustration, and clock-watching, and irregular sleep and wake times. Napping, attempts to \"catch up\" on lost sleep, and staying in bed while awake all contribute. Spending more time in bed awake is thought to weaken the homeostatic sleep drive, so the person becomes less sleepy at bedtime, which reinforces the expectation of poor sleep. Cognitive behavioural therapy for insomnia targets these maintaining processes directly.\n\nMedications and substances\n\nMany drugs can cause or worsen insomnia, often as a side effect rather than the intended action.\n\n- Caffeine: its exact mechanism has not been fully elucidated, but at typical intake it is generally understood to block central adenosine receptors, reducing sleepiness and increasing vigilance.\n- Stimulants: amphetamines and methylphenidate promote wakefulness more directly by increasing dopamine and noradrenaline transmission.\n- Alcohol: although it is sedating at first, it fragments sleep later in the night, and its withdrawal can independently produce insomnia; the same is true of alcohol-like central depressants such as barbiturates.\n- Antidepressants: serotonin-targeting drugs such as SSRIs often cause sleep disturbance, especially at the start of treatment. Bupropion is a notable case: insomnia is one of its main side effects, more so than with SSRIs, due to increased levels of dopamine and norepinephrine. Stopping some antidepressants abruptly can also bring on sleep problems.\n- Corticosteroids: excessive glucocorticoid levels also cause insomnia. Problems are more common with twice-daily or evening dosing than with morning dosing.\n- Other agents: blood pressure treatments such as beta blockers have been linked to disrupted sleep and vivid dreams, and nicotine withdrawal during smoking cessation is a recognised cause. Decongestants and theophylline-type bronchodilators can also keep people awake.\n\nIdentifying a medication or substance as a contributor matters clinically because it can often be adjusted or removed, which may resolve the insomnia without further treatment."
    },
    {
      "heading": "Comorbidity with mental and medical conditions",
      "text": "Insomnia is one of the most frequent co-occurring problems in psychiatric and medical care. Sleep disorders are often comorbid with mental disorders, for example major depressive disorder, bipolar disorder, post-traumatic stress disorder and generalized anxiety disorder. The overlap is strongest with depression, and the direction of the link has been the main subject of research.\n\nThe association runs in both directions, although the evidence is uneven. A systematic review of longitudinal studies published through December 2011 found that definitive conclusions regarding bidirectionality cannot be made for most sleep disturbances due to the small number and heterogeneity of cohort samples used across studies. Nevertheless, best available evidence suggests insomnia is bidirectionally related to anxiety and depression. A one-year prospective study in the general population found that baseline anxiety and baseline depression each predicted new cases of insomnia, while baseline insomnia predicted later episodes of high anxiety and high depression. Anxiety at baseline (OR=4.27) and depression at baseline (OR=2.28) were related to new cases of insomnia on follow-up. Insomnia at baseline was related to new episodes of high anxiety and high depression on follow-up. Insomnia is also frequently found alongside anxiety disorders and post-traumatic stress disorder, but there are few studies investigating potential mechanisms contributing to the comorbidity between insomnia and these diagnoses.\n\nFor depression, the question of precedence has been studied directly. In one clinical cohort, about half of participants said their insomnia began before their current depressive episode. Longitudinal work has treated insomnia as a predictor of depression, with one meta-analysis describing insomnia as an independent risk factor for emerging or recurrent depression. Insomnia that persists after a depressive episode is also common. Residual insomnia is one of the most commonly reported residual symptoms after remission from depression. In a cohort of patients who had completed at least 20 weeks of therapy, 22%, 26% and 17% suffered from initial insomnia, from middle insomnia, and from terminal insomnia. Residual insomnia is linked to recurrence: patients with residual insomnia experience relapse significantly earlier and have a poor prognosis. Antidepressants can contribute to the problem, since SSRIs, particularly fluoxetine, can lead to insomnia.\n\nInsomnia also co-occurs frequently with chronic pain. Musculoskeletal pain and insomnia each increase the risk of the other. In postmenopausal women, a bidirectional association has been reported, and insomnia was found to contribute to worse clinical outcomes, including the perception of pain. Among older adults with chronic pain, half to three-quarters also report insomnia. Obesity is another recurrent companion: these common comorbidities include obesity, insomnia, cardiovascular conditions, and anxiety and depressive symptoms. In an 11-year prospective study, obesity, poor sleep, and chronic disease all predicted persistent chronic widespread pain, except for depression. In the menopausal transition, core menopausal symptoms include musculoskeletal pain and insomnia, together with vasomotor symptoms. Insomnia may occur as a symptom of menopause or as a disorder on its own.\n\nWhether insomnia is a risk factor, a symptom, or a marker of shared causes remains unresolved. The evidence fits all three roles in different settings. Chronic pain and insomnia share similar symptoms and features, including age, obesity, female sex, catastrophizing, low physical activity, socioeconomic factors such as education, and anxiety and depressive symptoms, which points to common causes rather than a single direction of effect. For psychiatric illness, the prodromal view has gained ground: sleep problems are no longer viewed as an epiphenomenon of depression but as a predictive prodromal symptom. The implications for treatment order follow from this uncertainty. If insomnia drives mood disorders, treating it early could alter their course. If it is largely a symptom, treating the underlying condition should resolve it. Evidence from trials supports the first option in part: in people with depression and insomnia, CBT-I consistently improves insomnia symptoms and can also reduce depressive symptoms.\n\nClinical concern centres on insomnia that outlasts treatment of the comorbid condition. Some clinicians regard it as a separate problem. One account holds that people who toss and turn often come to view the bed as a cue for poor sleep, and develop an insomnia disorder that needs additional sleep-focused treatment. Patients whose sleep does not recover are at higher risk of recurrence. People whose sleep does not recover are more likely to experience another depressive episode than those whose sleep normalises. Evidence on which residual symptoms respond to specific therapies is limited: a few non-pharmacological treatment methods, such as CBT-I, Mindfulness-Based Cognitive Therapy and behavioral activation, have proven to mitigate residual insomnia."
    },
    {
      "heading": "Health consequences and functional impact",
      "text": "Insomnia's effects extend well beyond the night. Daytime impairment is part of the diagnostic definition, and its most consistent cognitive signature involves attention and memory. Insomnia has been linked to weaker memory, poorer concentration, slower psychomotor function and reduced alertness, and people with the disorder often find that sustaining performance takes more deliberate effort than it should. Among adolescents, insomnia has been associated with diminished cognitive performance, emotional dysregulation and lower stress tolerance (Among adolescents, insomnia is associated with diminished cognitive performance, emotional dysregulation, and lowered stress tolerance). Impairment also has a practical side: patients who have insomnia have more emergency department and physician visits, laboratory tests, and prescription drug use than those who do not.\n\nEpidemiological cohorts have connected insomnia with cardiometabolic disease, although the causal picture is still debated. In a Chinese cohort of about 487,000 adults aged 30 to 79, three insomnia symptoms were associated with increased risk of total CVD, with adjusted hazard ratios of 1.09, 1.07 and 1.13, and participants with all three symptoms had a higher risk of cardiovascular disease than those without them. The associations were stronger in younger adults and in people without baseline hypertension (Associations between 3 symptoms and CVD incidence were consistently stronger in younger adults or those without baseline hypertension). A meta-analysis of 17 cohort studies reported that insomnia significantly increased cardiovascular mortality (hazard ratio 1.33). The link with hypertension appears to run in both directions, according to a systematic review of prospective cohorts (the association between insomnia and hypertension might be bidirectional). A Mendelian randomization review reports that genetic liability to insomnia is associated with several cardiometabolic outcomes, which the authors read as a probably causal link (genetic liability to insomnia increases the risk of multiple cardiometabolic outcomes). Findings for type 2 diabetes rest largely on a single cohort, which found that combining polysomnography-measured sleep duration with insomnia identifies people at higher diabetes risk (combining polysomnography data on sleep duration with information on insomnia can identify individuals at higher risk for diabetes). Not all studies agree on the size of the effect. In another prospective analysis, sleep complaints produced only a slightly increased risk of cardiovascular disease, and the effect on hypertension was inconsistent.\n\nEmotional consequences are among the most clinically pressing. Patients often report problems with emotion regulation and impaired social interactions. Researchers have proposed that insomnia raises suicide risk through pathways of hyperarousal, hopelessness, and impaired emotion regulation. Clinical data support an association that persists beyond depressive symptom severity: insomnia is associated with an increased risk for suicide, even when accounting for the severity of other depressive symptoms. In one cross-sectional sample of patients with schizophrenia, the suicide-risk rate was 38% among those with insomnia compared with 19.8% among those without it. Fatigue after poor sleep may also reduce problem-solving ability and emotional control, which can increase vulnerability to impulsive behaviour (fatigue after sleep difficulties may impair problem solving and decrease emotion regulation).\n\nThe daytime costs fall on workplaces, roads and the wider economy. Insomnia has been shown to affect daytime functioning, including workplace productivity, as well as workplace and public safety, and the indirect costs reportedly exceed the direct costs of treatment (these daytime effects of insomnia are translated into indirect costs that are reportedly higher than the direct costs of this disorder). Workers with sleep disorder symptoms have a higher occupational injury rate than those without sleep problems, and a Swedish study linked trouble sleeping with a higher risk of fatal occupational accidents. Impaired performance also threatens road safety when drivers with excessive daytime sleepiness take on dangerous tasks such as driving (Impaired performance due to reduced or inefficient sleep creates public safety risks when individuals with excessive daytime sleepiness are involved in potentially dangerous daily activities such as driving)."
    },
    {
      "heading": "Neurobiological and stress-system research",
      "text": "The hyperarousal model\n\nMuch of the biological research on insomnia is organised around the hyperarousal model. This model proposes that chronic insomnia involves a trait-level excess of physiological, cognitive and cortical activation that persists across the 24-hour day, rather than a sleep problem confined to the night. In its physiological form, the model assumes that high arousal and sleep are mutually exclusive, so a person whose baseline arousal stays elevated before or during the usual sleep period will struggle to maintain sleep continuity. Early reports from the late 1960s and 1970s described raised body temperature, cortisol and adrenaline levels, heart rate and skin resistance in people with sleep complaints, and later studies have extended this list. Results remain inconsistent across studies, and the model is best understood as a framework that organises several partly overlapping lines of evidence rather than a settled mechanism.\n\nMetabolic rate, cortisol and the HPA axis\n\nThe most cited metabolic evidence comes from work by Bonnet and Arand in the 1990s, who measured oxygen consumption and carbon dioxide production at several points in the day and night and found significant 24-hour increases in metabolic rate in people with insomnia. Higher whole-body metabolism is consistent with the warmer core temperature reported in these groups. Some studies also suggest that the normal fall in core temperature before sleep onset is blunted, which may reflect impaired heat loss at the time of falling asleep.\n\nEndocrine evidence centres on the HPA axis, the chain running from the hypothalamus through the pituitary to the adrenal cortex, which ends in cortisol release. A 2022 systematic review and meta-analysis of case–control studies, which included 20 studies with 449 patients and 357 good sleepers, found moderately raised cortisol in insomnia, with a larger difference in studies that used blood samples. In some studies, nighttime urinary cortisol rose in proportion to the time spent awake, and higher cortisol at sleep onset has been read as evidence of HPA dysregulation. Intervention studies add a further layer. A small crossover trial of doxepin, and a separate small study of sleep restriction therapy, each reported reduced cortisol, but whether lowering HPA activity is part of how treatment works remains unclear. Sleep deprivation in healthy people more often lowers cortisol or leaves it unchanged, which is one reason researchers regard insomnia as a disorder of arousal rather than simply of sleep loss.\n\nBrain activity during wakefulness and sleep\n\nElectroencephalography has supplied some of the most consistent findings. Studies have reported increased beta and gamma power in the waking EEG of people with insomnia, and increased beta power across wakefulness, REM and non-REM sleep. Because beta and gamma activity are usually taken to index cortical arousal, these results have been used to argue for a 24-hour pattern. Positron emission studies have also shown greater cerebral glucose metabolism in people with insomnia during sleep, at the transition from wake to sleep, and particularly in brain arousal centres. Increased beta activity has been linked to subjective reports of longer sleep latency and poorer sleep quality.\n\nNeuroimaging findings and their limitations\n\nMagnetic resonance imaging and functional MRI studies have pointed to several candidate regions. A systematic review of 28 neuroimaging studies, covering 951 patients with insomnia disorder and 884 controls, found that the anterior cingulate cortex was the region most often reported, followed by the thalamus, insula, precuneus and posterior cingulate cortex. Reviewers concluded that the literature was too heterogeneous to weight the findings quantitatively. Structural studies have reported reduced grey matter in the prefrontal cortex and hippocampus, and a more recent systematic review of 93 studies interpreted such patterns as supporting the hyperarousal model. However, a large multi-cohort analysis found no significant associations between insomnia symptoms and regional cortical or subcortical volumes after correction for multiple comparisons, and a meta-analysis concluded that no consistent brain alterations could be identified. Functional studies have reported attentional bias toward sleep-related stimuli, reduced prefrontal activation during working-memory and verbal tasks, and altered amygdala reactivity. Connectivity studies have found atypical default mode and salience network activity. Limitations common to this field include small samples, heterogeneous definitions and tasks, cross-sectional designs, and difficulty separating insomnia from comorbid depression or anxiety.\n\nGenetics and heritability\n\nFamily and twin studies indicate that insomnia is moderately heritable. A longitudinal twin study of adults estimated heritability at 59% in women and 38% in men, suggesting that genetic influences differ by sex. A 2021 meta-analysis of twin studies, which included 12 papers, produced a pooled estimate of about 40%, with stronger heritability in females and when symptoms were reported by parents rather than by the individuals themselves. Heterogeneity between studies has been attributed to differences in sex composition, age, informant and the definition of insomnia used. In children and adolescents, the heritability of clinically significant insomnia ranged from 14% to 38% across waves of a longitudinal study, with new genetic influences emerging later in childhood. Genome-wide association studies have identified numerous variants associated with insomnia symptoms, but each variant has a small effect, and the biological pathways they point to, including those involving stress-hormone signalling and the circadian system, have not been firmly established. Genetic findings also overlap with those for depression and anxiety, which suggests shared rather than insomnia-specific mechanisms.\n\nSubjective complaints and objective measurement\n\nA persistent puzzle is that people who complain of severe insomnia often show sleep on polysomnography or actigraphy that is shorter or more fragmented than they report, but not always as disrupted as their experience suggests. Some people report sleeping very little while objective recordings show substantially more sleep, a discrepancy that has been studied under the labels of sleep-state misperception or paradoxical insomnia. Researchers have struggled to find an objective counterpart to the distress described by patients. One group of authors has argued that objective markers are more likely to appear in measures of affect and arousal, such as amygdala activity and emotional memory, than in sleep recordings alone. This raises open questions: whether the cognitive and emotional features of insomnia are the primary abnormality or a consequence of poor sleep; whether the hyperarousal measured during the day reflects the cause of sleep difficulty or a response to it; and whether any single biomarker can capture a condition defined largely by the individual's own report."
    },
    {
      "heading": "Cognitive behavioral therapy for insomnia (CBT-I)",
      "text": "Core components\n\nCBT-I is a structured psychological program that targets the behaviors and thought patterns that maintain disrupted sleep. It is generally regarded as the first-line treatment for chronic insomnia, and it does not depend on medication. Common components of CBT-I include stimulus control, sleep restriction, relaxation techniques, cognitive restructuring, and sleep hygiene education.\n\nSleep restriction shortens the time a person spends in bed so that it roughly matches actual sleep, which increases sleep pressure and consolidates sleep. Its dose is tuned with sleep efficiency, the time spent sleeping expressed as a percentage of time spent in bed. The prescribed window is adjusted once efficiency reaches 90% or falls below 85% (bedtime and waketime are adjusted accordingly).\n\nStimulus control aims to re-link the bed with sleep. Patients use the bed only for sleep and sex, get out when they cannot fall asleep, and return only when drowsy. The time-awake threshold for getting up varies between protocols; one guide advises leaving after ten minutes, while another gives twenty. During treatment, the bed is only used for sleep and sex. Clients are instructed to get out of bed when it's difficult to fall asleep or when they lie awake for more than 10 minutes, and a different protocol uses twenty minutes as the cutoff.\n\nCognitive restructuring targets maladaptive beliefs about sleep and exaggerated worry about the daytime consequences of poor sleep, which can add to arousal and anxiety. Relaxation training usually includes progressive muscle relaxation, breathing exercises, or mindfulness exercises. Sleep hygiene education addresses environmental and lifestyle factors, but the American Academy of Sleep Medicine clinical practice guideline recommends against sleep hygiene as a single-component therapy for adults with chronic insomnia disorder.\n\nCourse, sleep diary, and goal\n\nA typical course runs over six to eight sessions, and the first meeting usually involves a longer intake in which the sleep diary is started and the patient learns how insomnia is maintained. The diary is the main monitoring tool, because it supplies the efficiency figures used to adjust sleep restriction. Across the course, the central aim is to associate the bed with sleeping and limit its association with stimulating behavior.\n\nDelivery formats\n\nCBT-I has been delivered face to face, individually or in groups, by telephone, through written self-help materials, and over the internet. A network meta-analysis of 241 trials suggested that cognitive restructuring, third-wave components, sleep restriction, stimulus control, and in-person format may be beneficial. Internet-delivered versions have been studied extensively: their effects were comparable to those found for face-to-face CBT-I, and were generally maintained at 4–48 wk follow-up. A meta-analysis also found that longer treatment duration and higher degree of personal clinical support were associated with larger effect sizes. In a randomized trial of people with comorbid depression, therapist-delivered CBT-I produced far higher remission than written material alone, with 61.1% of CBT-I participants in clinical remission from their insomnia and depression, compared with 5.6% of the self-help group.\n\nDurability and the state of the evidence\n\nBenefits often persist after treatment ends. A meta-analysis of digital CBT-I found that the improvements were sustained at short-term follow-up and 1-year follow-up. A pilot study cited durability of up to 24 months in its background review, though not every trial reaches that horizon. Not all patients achieve full remission: in one pilot, among patients who did not achieve full remission after the first course of digital CBT-I, 44.4% and 62.5% of participants experienced a reduction in their ISI scores to <8 following the second course of treatment and at the 3-month follow-up.\n\nComponent-level research has complicated the picture. A component network meta-analysis reported that sleep restriction therapy seems to improve subjective perception of sleep continuity (SOL, WASO, SE) and sleep quality, while stimulus control therapy improves subjective total sleep time. The same analysis found little to no evidence indicating any enhancement of objective sleep parameters by any of the CBT-I components. Most reported gains therefore rest on self-reported sleep rather than on objective measures such as sleep recordings.\n\nAdaptations for comorbid populations\n\nBecause 85% of individuals with depression also experience chronic insomnia, several trials have tested CBT-I in people with both conditions. In the TRIAD trial, combining antidepressant treatment with CBT-I was superior to CTRL in reducing insomnia severity, but the overall difference in depression remission between the treatments was not statistically significant. A later double-blind trial found that CBT-I had specific effects on insomnia relative to a control treatment, and that adding a depression-focused psychological therapy did not improve depression outcomes; its authors suggested that CBT-I should always be offered to patients with insomnia and depression comorbidity, possibly as the first-hand choice. Digital adaptations have also been tested in comorbid groups; one randomized trial of 140 participants, most of them women, measured depressive symptoms as its primary outcome.\n\nAdaptations for older adults have been tested as well. A fully automated internet program was evaluated in a randomized trial of 311 adults aged 55 to 95, in which nearly half of participants who received the fully automated SHUTi OASIS intervention no longer experienced insomnia at the 1-year follow-up. Such digital programs are often considered a way to extend access to online delivery, though the question of access is still open."
    },
    {
      "heading": "Pharmacological treatments",
      "text": "Place of medication in treatment guidelines\n\nMedication remains the most widely used treatment for insomnia, but clinical guidelines place it after psychological treatment. The American College of Physicians (ACP) advises that all adults with chronic insomnia disorder receive cognitive behavioral therapy for insomnia (CBT-I) first, and it leaves the decision to add a drug, after CBT-I has failed, to a shared discussion of benefits, harms and costs (ACP recommends that all adult patients receive CBT-I as the initial treatment for chronic insomnia disorder. (Grade: strong recommendation, moderate-quality evidence) Recommendation 2: ACP recommends that clinicians use a shared decision-making approach, including a discussion of the benefits, harms, and costs of short-term use of medications, to decide whether to add pharmacological therapy in adults with chronic insomnia disorder in whom CBT-I alone was unsuccessful.). The American Academy of Sleep Medicine (AASM) built its 2017 pharmacological guideline on a systematic review of individual drugs, graded with the GRADE method, and most of its drug-specific recommendations are weak or conditional (These new recommendations are based on a systematic review of the literature on individual drugs commonly used to treat insomnia, and were developed using the GRADE methodology.). It suggests considering medication for people who cannot access CBT-I, whose symptoms persist despite CBT-I, or who need a temporary supplement to it (The guideline recommends clinicians consider prescribing medications to patients with chronic insomnia who cannot participate in CBT-I, whose symptoms persist despite trying CBT-I, or who need a temporary adjunct to CBT-I.). A later AASM guideline on combined treatment suggests adding medication to CBT-I rather than using medication alone, but it advises against adding medication to CBT-I that is already effective, and both suggestions rest on low-certainty evidence (In adults with chronic insomnia disorder, the AASM suggests the use of combination treatment with CBT-I plus insomnia medication over insomnia medication alone. (Conditional recommendation, low certainty of evidence).).\n\nHypnotic drug classes\n\nBenzodiazepines and non-benzodiazepine Z-drugs act on the GABA<sub>A</sub> receptor, the latter with selectivity for certain receptor subunits intended to reduce side effects. Benzodiazepines increase the frequency with which the GABA<sub>A</sub> chloride channel opens, which underlies their hypnotic, sedative and anxiolytic effects (From a molecular point of view, BZDRs enhance the inhibitory effect of γ-aminobutyric acid at the γ-aminobutyric acid A subunit receptor by increasing the frequency of chlorine channel opening). Zolpidem has been the most frequently prescribed hypnotic worldwide over recent years (Over the last 5 years zolpidem has been the most frequently prescribed hypnotic worldwide). Z-drugs are licensed only for short-term use, and the restriction reflects a growing risk-benefit imbalance with longer treatment, including rapid tolerance and a risk of addiction (The time restriction on BDLM use is attributable to their effect-risk profile, where negative impact multiplies with prolonged duration of treatment and benefits decrease or stay steady at best).\n\nOrexin receptor antagonists form a newer class. Suvorexant was approved by the US FDA in 2014, lemborexant in 2019, and daridorexant has been approved in both the US and Europe (Currently, three orexin receptor antagonists—suvorexant, lemborexant, and daridorexant—are FDA approved for the treatment of insomnia. Suvorexant is a nonselective orexin receptor antagonist approved in 2014 for the treatment of both sleep-onset and sleep-maintenance insomnia. Lemborexant, which was approved for the treatment of insomnia in 2019, is a more selective orexin-2 receptor antagonist). Rather than enhancing sedation, these agents inhibit the wake-promoting orexin system (Dual orexin receptor antagonists (DORAs) such as daridorexant, lemborexant, and suvorexant, represent a novel approach to insomnia treatment by inhibiting wakefulness rather than enhancing sedation.). Some doses of these drugs are associated with more daytime somnolence than placebo (some doses of these DORAs are associated with a higher incidence of somnolence compared to placebo.). Melatonin receptor agonists such as ramelteon are FDA approved for chronic use, and the AASM has issued conditional recommendations for ramelteon in sleep-onset insomnia (Ramelteon, eszopiclone, and controlled-release zolpidem are FDA approved for chronic use.; The AASM issued a CPG on pharmacological treatment of chronic insomnia in 2017 and provided conditional recommendations for medications to manage sleep onset insomnia (triazolam, ramelteon, zaleplon), sleep maintenance insomnia (doxepin, suvorexant), and combined sleep onset and maintenance insomnia (temazepam, zolpidem, eszopiclone).).\n\nAntihistamines, off-label agents and adverse effects\n\nSedating antihistamines such as diphenhydramine are common over-the-counter sleep aids, but their anticholinergic effects make them unsuitable for older adults because of the risks of falls and confusion (Sedating antihistamine medications such as diphenhydramine have significant anticholinergic effects and are also contraindicated in older adults because of risk of falls and confusion.). Some antidepressants and antipsychotics with antihistamine properties show short-term benefit, but their tolerability has been documented as a concern (Drugs with antihistamine properties, including certain antidepressants and antipsychotics, exhibit short-term efficacy but have documented tolerability). The AASM found little evidence that sedating antidepressants such as trazodone treat chronic insomnia, though they may be considered in people with psychiatric comorbidity (The task force found little evidence to support the use of sedating antidepressants to treat chronic insomnia. These medications may be appropriate for people with psychiatric comorbidities.). Low-dose doxepin is among the drugs with a conditional recommendation for sleep-maintenance insomnia (doxepin, suvorexant). Hypnotic drugs carry a range of warnings: observational studies have linked them to fractures and dementia, and FDA labeling warns of daytime impairment, complex sleep behaviors such as sleep driving, and worsening depression in depressed patients (Infrequent but serious adverse events, such as fractures and dementia, have been reported for hypnotic drugs in observational studies. FDA label warnings include daytime impairment, \"sleep driving,\" behavioral abnormalities, and worsening depression in depressed patients.).\n\nOlder adults, tapering and deprescribing\n\nGuidance for older adults is more restrictive. The American Geriatrics Society Beers Criteria, in its 2023 update, places benzodiazepines and Z-drugs on the list of medications to avoid, because they raise the risk of cognitive impairment, delirium, falls and fractures (According to the 2023 AGS Beers criteria, all benzodiazepines (short-, intermediate-, and long-acting) should not be used for insomnia in older adults.; Benzodiazepines and Z-drugs are on the list because they increase the risk of cognitive problems, delirium, falls, accidents, and fractures.). Longer-acting benzodiazepines such as diazepam carry an added risk of drug accumulation because of slow metabolism (Longer-acting agents such as diazepam and chlordiazepoxide are concerning because of their slow metabolism and the consequent risk of accumulating toxic levels.). Abrupt withdrawal of a sedative-hypnotic can cause rebound insomnia, which is more likely with larger doses and short-acting agents, and tapering at smaller doses reduces it; the AASM notes that concurrent CBT-I helps these measures (Rebound insomnia may develop when a sedative-hypnotic is abruptly withdrawn. This is more likely to occur with larger doses and with the short-acting agents. Using smaller doses and tapering the drug can avoid rebound insomnia. The AASM guideline states that these measures are aided by concurrent CBT for insomnia (CBT-I).). Deprescribing in older adults has been supported by tools such as the STOPPFall screening aid, developed in 2020 by a European expert group for people at high fall risk (In 2020, a European expert group developed the STOPPFall tool, an explicit screening tool and deprescribing aid in older adults with high fall risk.). Medication is therefore generally positioned as a short-term or adjunctive option, with tapering planned from the outset and CBT-I used where it is available."
    },
    {
      "heading": "Other non-pharmacological approaches and digital interventions",
      "text": "Apart from CBT-I delivered by a therapist, several non-drug options are used for insomnia, and the strength of their evidence varies widely. Sleep hygiene advice, which covers habits such as caffeine timing, bedroom conditions, and regular routines, is among the most commonly offered. Its effects as a stand-alone treatment are small and uncertain. A 2025 meta-analysis of 42 RCTs encompassing 4245 adults found a pooled reduction in Insomnia Severity Index scores of about 3.4 points, but the majority of included trials (85.71 %) had a high overall risk of bias. An earlier 2018 review concluded that sleep hygiene education was clearly less effective than CBT-I, and it left open whether it should be offered before CBT-I in primary care. Current guidance treats it mainly as an adjunct, since education alone is not sufficient to ensure effectiveness in treating insomnia.\n\nBright light therapy is the best-studied approach in the circadian-related group. A 2023 meta-analysis of studies with a total of 685 participants found that light therapy for insomnia compared with control conditions significantly improved wake after sleep onset, a difference of roughly 11 minutes by actigraphy. Timing matters: morning light exposure advanced sleep–wake rhythms and evening exposure led to a delay. The same authors noted that the studies' heterogeneity and publication bias limit the interpretation. A separate 2024 meta-analysis of 10 randomized trials reported some efficacy in improving sleep quality in insomnia, and its authors asked for larger trials. In shift workers, light exposure produced significantly small to medium effects on sleepiness and large treatment effects on circadian phase shift, which suggests that the clearest benefit lies in resetting the body clock rather than in directly producing sleep. Chronotherapy, which deliberately moves sleep and wake times over several days, is discussed mainly for circadian-related insomnia. The evidence for it in the general insomnia population is less developed than for light, and this section does not assign it a firm effect size.\n\nDigital CBT-I (dCBT-I) developed in response to a gap in access. CBT-I is effective but limited by cost and therapist availability, and access to in-person CBT-I remains limited due to a shortage of trained providers and structural barriers. A 2025 systematic review of fully automated programs covered 29 randomized controlled trials (RCTs) involving 9475 participants and found moderate to large effects on insomnia severity compared with control groups. Smartphone formats have been tested in several settings. One Dutch trial of an app that packaged a sleep diary, a relaxation exercise, sleep restriction exercise, and sleep hygiene and education was fully automated. A Chinese trial in young people with insomnia and subclinical depression found that the app-based CBT-I group has higher remission rates of insomnia disorder than the controls at post-intervention (52% versus 28%). Engagement was reasonably high in that trial: 296 (84%) completed all six sessions. A meta-analysis focused on adolescents found that dCBT-I trials showed significant improvement in adolescent insomnia, whereas educational, sleep hygiene and holistic promotion interventions yielded more variable results.\n\nSeveral cautions apply to this literature. Many app trials compare the intervention with a waitlist control, which cannot separate the specific treatment from expectation or attention effects. Samples are not always clinical; one Austrian app trial consisted predominantly of participants with subclinical symptom severity, without a formal diagnosis of insomnia. Uptake outside research settings is also uncertain, and digital tools may reach younger, more digitally confident users more readily than older adults or people on low incomes, a pattern discussed under the digital divide. Measures of adherence and long-term use are reported unevenly across studies.\n\nLess established approaches, including many commercial smartphone sleep products, wearable-linked coaching tools, and various complementary remedies, have few randomized trials, often small samples, and outcome measures that rely heavily on self-report. In such cases the evidence-based standard of comparison is an open question rather than a settled finding, and claims of benefit should be read against the quality of the underlying trials."
    },
    {
      "heading": "Insomnia across the lifespan and in special populations",
      "text": "Childhood and adolescence\n\nReviews place the share of typically developing children affected by insomnia at up to one in three, and above 80% among children with neurodevelopmental disorders or chronic medical illness (Pediatric insomnia is common, impacting up to a third of typically-developing, healthy children, and over 80% of children with neurodevelopmental disorders or chronic medical conditions.). Estimates for infants and toddlers run from roughly 20 to 30 percent, and up to a third of adolescents are affected (the prevalence of insomnia ranges from 20 to 30% in infants and toddlers [3,4], and up to one-third of adolescents).\n\nIn young children, the characteristic problem is often not an inability to sleep in principle but a reliance on particular conditions for falling asleep. Behavioral insomnia of childhood is linked to dependence on conditions the child cannot reproduce alone, such as caregiver-set limits or a parent's presence (Behavioral Insomnias of Childhood (BIC) are linked to dependence on specific conditions for initiating sleep that the child cannot reproduce without assistance). The two recognized forms are the sleep-onset association type, in which a child needs a specific cue such as rocking or a parent in the room to fall asleep, and the limit-setting type, in which bedtime resistance reflects inconsistent limits. Both forms lead to the same practical problem: a child who wakes at night cannot return to sleep without caregiver involvement. Clinical criteria for children therefore include resistance to going to bed and difficulty sleeping without a parent's presence, together with daytime impairment (children/adolescents must have the following based on child or parent report (1) difficulty falling asleep or staying asleep, resistance to going to bed when directed, and/or difficulty sleeping without parental presence or parental support). In older children and adolescents, the pattern tends to shift toward late sleep onset, associated with changes in circadian timing during puberty and with evening schedules. Daytime consequences extend to academic performance, mood, and social functioning (Insomnia among children and adolescents is ubiquitous and takes a great toll on youth and their families, impacting academic achievement, mood, social functioning, and a variety of developmental outcomes.).\n\nOlder adults\n\nPolysomnographic studies of aging repeatedly show shorter total sleep, lower sleep efficiency, less slow-wave sleep, and more time awake after sleep onset (In polysomnographic studies, four consistent changes related to aging are observed: decreased total sleep time, sleep efficiency, and slow‐wave sleep; and increased waking after sleep onset.). Reviews disagree on timing. One holds that most age-related sleep architecture changes occur in early and mid-years, whereas another reports that most of these changes plateau at age 60.\n\nWhether insomnia itself becomes more common with age has a more qualified answer. Prevalence is higher in older people, with one source describing a rise from about 10% in people aged 15–24 to about 20% at 75 and older (the prevalence of insomnia doubles from 10% in individuals aged 15-24 to 20% in those aged 75 or older). However, the incidence of insomnia is higher in older adults than younger adults, but is most often associated with other age-related conditions, rather than age per se. Older patients also present differently: sleep‐maintenance insomnia and early awakening are more common complaints than sleep‐onset insomnia. Medication is an important contributor. Chronic sedative-hypnotic use is associated with a reduction in time spent in deep sleep (N3) and REM sleep while increasing duration in N2 sleep, which compounds age-related changes. Clinical guidance also stresses that sleep problems in the elderly are not a normal part of aging.\n\nPregnancy, the postpartum period, and menopause\n\nA 2024 meta-analysis pooling 44 studies estimated a prevalence of 43.9% for insomnia symptoms during pregnancy (Forty-four studies, encompassing a total of 47,399,513 participants, were included in the analysis. The overall prevalence of insomnia symptoms during pregnancy was 43.9%.). The rate rises as pregnancy advances. In one prospective cohort, prevalence was 6.1% pre-gestational, 44.2% in first trimester (T1), 46.3% in second (T2) and 63.7% in third trimester (T3). Pregnancy also brings an increase of respiratory sleep problems, restless legs syndrome, sleepiness, short sleep duration, fragmentation and poor sleep quality. Hormonal shifts, nocturia, back pain, and fetal movement add to the disruption, and anxiety about delivery is one of the factors linked to later sleep problems (High EPDS scores and anxiety in pregnancy, fear of delivery, previous depression, primiparity, and higher educational level were risk factors for both postpartum insomnia and depression.).\n\nThe postpartum picture is shaped by sleep fragmentation and by the emotional load of early parenthood. In the Akershus Birth Cohort Study, the prevalence of insomnia remained stable at 60 % at the first two time periods, and remained high at 41 % at year 2 postpartum. Subjective and objective measures can diverge here. After delivery, one study found that sleep duration was reduced by 49 minutes (to 6.5 hours), and mean sleep efficiency was reduced from 84% to 75%, yet self-reported insomnia scores improved. Prior insomnia is a consistent predictor, as previous insomnia was the strongest predictor of current insomnia. Prevalence also varies widely by setting. A community study in southern Ethiopia reported insomnia was prevalent among 23.2% (95% CI: 19.3%, 27.4%) of mothers who had given birth within the previous 12 months.\n\nDuring menopause, the decline in estrogen is linked to vasomotor symptoms such as night sweats and hot flushes, which fragment sleep. Mood changes and altered thermoregulation are additional contributors, and the overlap with depressive symptoms complicates attribution.\n\nShift workers and people with Parkinson disease\n\nShift work requires sleep at times that conflict with the circadian clock. Daytime sleep is typically shorter and more fragmented by light and noise, and cumulative sleep loss is common. These schedules are classified separately as shift work disorder, a circadian rhythm sleep-wake disorder, but insomnia complaints overlap substantially with it. In diagnostic terms, the criterion of adequate opportunity for sleep becomes central, since a rotating schedule may limit the opportunity to sleep in the first place.\n\nIn Parkinson disease, sleep disturbance is common and multifactorial. Insomnia in this group often involves frequent nocturnal awakening, nocturia, and night-time motor symptoms such as rigidity or dystonia. Restless legs syndrome and REM sleep behavior disorder, which can precede motor symptoms by years, further complicate the picture. Daytime sleepiness may arise from dopaminergic medication, which can make the distinction between primary insomnia and sleep disruption caused by the disease itself difficult to draw."
    },
    {
      "heading": "History of classification and research",
      "text": "Descriptions of prolonged sleeplessness appear in some of the oldest surviving texts, and the ancient Greek vocabulary for it is still visible in modern terminology. The Greek noun ἀγρυπνία (agrypnía), meaning sleeplessness or watchfulness, comes from the adjective ἄγρυπνος, \"sleepless, wakeful,\" and was used by the physician Hippocrates and by Plato. Latin later supplied insomnia, which became the standard European term. In a medical dictionary published in 1892, the older Greek-derived term agrypnia was divided into subtypes: agrypnia excitata (sleeplessness from mental excitement), agrypnia pertoesa (sleeplessness from bodily unease), and agrypnia senilis (the sleeplessness of old age). Some of these categories anticipated modern ideas, such as cognitive arousal and abnormal sensory processing as factors that maintain insomnia. English lexicography also recorded the word early; the early 1620s dictionary compiler Henry Cockeram used insomnia as a synonym for \"watching,\" meaning an inability to sleep.\n\nModern sleep medicine developed mainly in the twentieth century. Nathaniel Kleitman at the University of Chicago had studied sleep and circadian rhythms since the 1920s and published the reference work Sleep and Wakefulness in 1939. In 1953, Kleitman and his student Eugene Aserinsky reported rapid eye movement (REM) sleep, identified from eye-movement recordings, and linked it to dreaming: participants woken during REM recalled dreams far more often than those woken in other stages. William Dement, another Kleitman student, described the cyclical organisation of night-time sleep in the mid-1950s, and Michel Jouvet later characterised REM sleep as \"paradoxical sleep\" distinct from light sleep. These findings overturned the view that sleep was a passive state, and full-night recordings became routine by the late 1950s. From the early 1960s, researchers applied the same tools to sleep pathology; sleep apnoea was described in 1965, and the first clinical sleep laboratory was reportedly established at Stanford in 1970. These laboratories, which relied on electroencephalography and related measures, allowed clinicians to test for sleep disorders objectively rather than relying only on patients' reports. The discovery of REM sleep is commonly regarded as a founding moment for the field, and its clinical branch is often described as sleep medicine.\n\nDiagnostic classification followed a parallel path. For much of the twentieth century, insomnia was usually treated as a symptom of another condition, such as depression, pain, or medical illness, and it was often described in general terms. Later editions of the international and American classification systems moved towards explicit criteria, specifying how often sleep difficulty occurs, how long it persists, and how much daytime impairment accompanies it. This shift from descriptive labels to operational thresholds made it possible to compare studies and to ask whether insomnia could be a disorder in its own right, a question that remains debated. The criteria discussed in the diagnostic sections above reflect this process of refinement.\n\nTreatment history shows a similar change. For decades, hypnotic medication, initially barbiturates and later benzodiazepines and related drugs, was the most common response to insomnia. Behavioural methods were developed and tested over several decades and were eventually assembled into the multicomponent package known as cognitive behavioural therapy for insomnia (CBT-I). Guideline bodies then moved CBT-I into the first-line position. In 2016 the American College of Physicians recommended CBT-I as the first-line treatment for chronic insomnia, citing its efficacy and safety, and the European Sleep Research Society issued a comparable guideline in 2017. The American Academy of Sleep Medicine's 2017 pharmacological guideline noted that it had not previously issued formal drug guidance, even though medication remained the most common approach, and it stated that CBT-I was a standard primary intervention for chronic insomnia. Medication continued to be recommended in some circumstances, but the consensus shifted towards treating CBT-I as the starting point, with hypnotics positioned as adjuncts or second-line options."
    },
    {
      "heading": "Debates and unresolved questions",
      "text": "Primary disorder or symptom of other conditions\n\nResearchers still disagree about whether chronic insomnia is a disorder in its own right or mainly a feature of other illnesses. Insomnia has traditionally been viewed and treated as a symptom rather than a disease, with most therapies aimed at underlying medical factors. Critics argue that this framing can be too narrow. One review concluded that treating insomnia as a mere by-product of other disorders can be unfounded, and this view may deprive many patients of treatment, which might not only cure their insomnia, but may also reduce symptoms associated with the assumed 'primary' disorder. The question is harder for conditions such as depression. Insomnia is now seen as a risk factor for depression, not only a symptom of it, yet the reasons for this change in classification (from symptom to risk factor) have yet to be clearly articulated. Clinicians must therefore decide whether a coexisting condition causes the sleep problem or merely coexists with it, since the answer determines what is treated first.\n\nOverdiagnosis from broad survey questions\n\nPrevalence estimates depend heavily on how the question is asked. A 2025 meta-analysis found a pooled prevalence of 12.4% in studies that used clinical interviews to apply DSM criteria, compared with 16.3% in studies relying on self-report, and questionnaire-based studies with different cut-offs ranged from 7.5% to 32.3%. The authors note that many survey items are almost never validated and oftentimes do not assess any daytime consequences. In the Tromsø study, the proportion classified as having insomnia ranged from 8.5% under DSM-5 to 23.6% under DSM-IV-TR, and over half the participants classified as having insomnia using the DSM-IV-TR and ICSD-3 criteria did not report having impaired daytime functioning at least three days per week. Self-assessment instruments also generally lack exclusion criteria and may capture individuals who do not fully meet all diagnostic requirements regarding symptom severity and duration. Whether rising reported rates reflect a real increase in disorder or a measurement artefact remains open.\n\nLong-term safety and tapering of hypnotics\n\nEvidence on long-term safety is limited for several hypnotic classes. For Z-drugs, one national guideline states that use of zolpidem and zopiclone beyond 4 weeks is not recommended due to the lack of long-term safety data. By contrast, eszopiclone has demonstrated safety for up to 12 months in primary insomnia patients. For benzodiazepines, most guidelines recommend that benzodiazepines and Z-drugs used continuously for more than 4 weeks should be withdrawn, if the patient is agreeable, yet long-term use remains common. Discontinuation is difficult because of physical dependence, and the most severe withdrawal effects are suicidality, akathisia and protracted withdrawal syndromes which can last for months or years.\n\nNo single tapering method has been established. Current guidelines vary, with some suggesting linear reductions and some proportionate reductions. Hyperbolic reduction schedules have been proposed, though randomized trials comparing them with linear schedules were still awaited in one review. A 2025 joint guideline recommends starting low and going slow (e.g., beginning with a 5–10% reduction in total daily dose every 2–4 weeks), with pace adjusted to each patient, and it advises against using general anaesthetics such as propofol or ketamine for tapering. Pharmacological tapering aids, including liquid or compounded formulations, are often needed at low doses.\n\nAccess to CBT-I and consumer sleep technology\n\nCognitive behavioural therapy for insomnia is the recommended first-line treatment in many national guidelines, but the gap between recommendation and practice is substantial. An Australian qualitative study reported that current Australian general practice guidelines recommend cognitive behavioural therapy for insomnia (CBTi) as first line treatment for insomnia, however research suggests that most general practice consultations for insomnia result in a prescription for hypnotic or sedative medicines. The same study noted that little is known about the capacity of general practitioners to manage insomnia. Open questions include how many clinicians are trained to deliver CBT-I, how far they can meet demand, and whether digital delivery through internet or smartphone programmes can close the gap without leaving out people with limited digital access or low health literacy.\n\nConsumer sleep devices raise a parallel question. Their estimates of sleep duration and continuity are easy to obtain, but it is contested whether they can support diagnosis or only self-monitoring, and whether their data should guide clinical decisions when they diverge from objective measures. Resolving these issues will require validation studies, clear standards for clinical use, and attention to how such tools change help-seeking and prescribing."
    }
  ],
  "links": [
    "mental-disorder",
    "medicine",
    "epidemiology",
    "public-health",
    "cognitive-behavioral-therapy",
    "electroencephalography",
    "depression",
    "pain",
    "light",
    "neurotransmitter",
    "anxiety-disorders",
    "epinephrine",
    "dopamine",
    "ethanol",
    "serotonin",
    "hypertension",
    "post-traumatic-stress-disorder",
    "type-two-diabetes",
    "internet",
    "digital-divide",
    "smartphone",
    "evidence-based-medicine"
  ],
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  ],
  "license": "https://creativecommons.org/licenses/by/4.0/"
}