Insomnia

Insomnia Disorder is a sleep-wake disorder in the DSM-5-TR defined by dissatisfaction with sleep quantity or quality, associated with difficulty initiating sleep, difficulty maintaining sleep, or early-morning awakening with inability to return to sleep. The disturbance occurs at least 3 nights per week for at least 3 months, despite adequate opportunity for sleep, and causes clinically significant distress or functional impairment. References: DSM-5-TR, StatPearls (NCBI Bookshelf).

Insomnia Disorder is a sleep-wake disorder in the DSM-5-TR defined by dissatisfaction with sleep quantity or quality, associated with difficulty initiating sleep, difficulty maintaining sleep, or early-morning awakening with inability to return to sleep. The disturbance occurs at least 3 nights per week for at least 3 months, despite adequate opportunity for sleep, and causes clinically significant distress or functional impairment. Insomnia is the most common sleep complaint worldwide. It carries ICD-11 code 7A00. The DSM-5-TR eliminated the old primary/secondary insomnia distinction, recognising insomnia as a disorder in its own right regardless of co-occurring conditions. Chronic insomnia drives substantial healthcare utilisation, workplace absenteeism, and accident risk. It is a modifiable risk factor for depression, anxiety, cardiovascular disease, and cognitive decline. This information is for psychoeducation only.

Three patterns of sleep difficulty: (1) Sleep-onset insomnia — taking >20-30 minutes to fall asleep (normal sleep latency is 10-20 minutes). (2) Sleep-maintenance insomnia — frequent or prolonged awakenings during the night, with >30 minutes total wake time after sleep onset. (3) Early-morning awakening — waking >=30 minutes before the desired time and being unable to return to sleep, with total sleep time <6.5 hours. Daytime consequences include fatigue (distinct from sleepiness), difficulty concentrating, mood disturbance (irritability, dysphoria), reduced motivation, increased errors and accidents, tension headaches, and gastrointestinal distress. Paradoxical insomnia (sleep-state misperception) occurs when individuals report severe insomnia but polysomnography shows near-normal sleep — the subjective experience of wakefulness during objectively recorded sleep. Hyperarousal is a hallmark: patients often feel "tired but wired," unable to nap during the day despite significant nighttime sleep loss. Bed partners may observe restlessness, frequent position changes, or clock-watching behaviour.

Female sex: women are 1.4 times more likely to develop insomnia than men, with increased risk during perimenopause and menopause (hot flashes, hormonal changes). Age: prevalence increases with age; ~30-48% of older adults report insomnia symptoms. Psychiatric comorbidity: depression, anxiety, PTSD, and substance use disorders all increase insomnia risk 2-5 fold. Insomnia also predicts future onset of depression (relative risk ~2.0). Medical conditions: chronic pain (arthritis, fibromyalgia, neuropathy), COPD, heart failure, GERD, nocturia, and hyperthyroidism. Shift work: rotating and night shifts disrupt circadian alignment. Personality traits: neuroticism, rumination, perfectionism, and a tendency toward cognitive hyperarousal.

Substances: caffeine (half-life 5-6 hours), nicotine (stimulant), alcohol (fragments sleep architecture), and medications (SSRIs, beta-blockers, corticosteroids, decongestants, stimulants). Behavioural factors: irregular sleep schedules, excessive time in bed, daytime napping >30 minutes, and screen use before bed.

Spielman's 3P model provides the dominant explanatory framework. Predisposing factors: genetic vulnerability (heritability ~40%, per twin studies), trait hyperarousal, female sex, and neurobiological tendency toward cortical hyperexcitability. Precipitating factors: acute stressors (job loss, bereavement, illness, relationship conflict), medical events, or schedule disruption that trigger initial sleep difficulty. Perpetuating factors: maladaptive behaviours and cognitions that maintain insomnia after the precipitant resolves — spending excessive time in bed, napping, using the bed for non-sleep activities, clock-watching, catastrophising about sleep consequences ("if I don't sleep 8 hours I can't function"), and safety behaviours (cancelling activities to recover sleep). The hyperarousal model posits that chronic insomnia reflects a 24-hour state of elevated physiological and cognitive arousal. Evidence includes elevated whole-body metabolic rate, increased cortisol (especially evening cortisol), elevated high-frequency EEG beta power during NREM sleep, and increased brain glucose metabolism (PET studies) during sleep compared to good sleepers.

Approximately 30-40% of adults report insomnia symptoms annually. When strict DSM-5-TR/ICSD-3 criteria are applied (frequency >=3 nights/week, duration >=3 months, plus daytime impairment), 6-10% meet criteria for Insomnia Disorder. Women are affected roughly 1.4:1 compared to men. Prevalence increases with age, with highest rates in adults over 65. Insomnia co-occurs with other psychiatric disorders in ~40-50% of cases: major depressive disorder (~40%), generalised anxiety disorder (~30%), PTSD, and substance use disorders. Medical comorbidities are present in ~75% of insomnia patients. Shift workers have 2-3 times the risk. Insomnia is the strongest modifiable risk factor for depression — a meta-analysis of longitudinal studies showed insomnia doubles the risk of developing new-onset depression. Economic costs in the US exceed $100 billion annually, primarily from lost workplace productivity, healthcare utilisation, and accidents.

The hyperarousal model is supported by multiple lines of evidence. Neuroendocrine: evening and nighttime cortisol levels are elevated in chronic insomnia, indicating HPA axis hyperactivity. The normal evening cortisol nadir is blunted. Neuroimaging: PET studies show increased whole-brain glucose metabolism during both wakefulness and NREM sleep in insomnia patients versus controls — the brain fails to reduce metabolic activity during sleep. fMRI shows increased activation in the amygdala and anterior cingulate cortex during pre-sleep periods. EEG: increased beta and gamma power (high-frequency activity) during NREM sleep, reflecting cortical hyperarousal; reduced slow-wave activity. Neurotransmitter systems: the flip-flop switch model involves reciprocal inhibition between wake-promoting centres (lateral hypothalamus orexin/hypocretin neurons, locus coeruleus norepinephrine, tuberomammillary histamine, basal forebrain acetylcholine) and sleep-promoting centres (ventrolateral preoptic area GABA/galanin neurons). In insomnia,

the balance tips toward sustained wake signalling. GABA levels in the anterior cingulate and occipital cortex (measured by MR spectroscopy) are reduced in primary insomnia. Circadian disruption: although the central clock in the suprachiasmatic nucleus is generally intact, phase misalignment between circadian drive and desired sleep time can perpetuate insomnia.

Assessment requires: (1) Detailed sleep history — bedtime, lights-out time, estimated sleep latency, number and duration of awakenings, final wake time, rise time, and total estimated sleep time. Ask about each night of the week, as patterns often differ between work and free days. (2) Sleep diary maintained for 1-2 weeks — the gold standard for characterising insomnia patterns and calculating sleep efficiency (time asleep / time in bed x 100; normal >=85%). (3) History of daytime consequences — fatigue, concentration difficulty, mood, function. (4) Screening for comorbid sleep disorders: snoring and witnessed apnoeas (OSA), leg jerking (periodic limb movement disorder), restless legs (RLS), parasomnias. (5) Psychiatric screening: PHQ-9 (depression), GAD-7 (anxiety), PC-PTSD-5. (6) Medical history: pain conditions, respiratory disease, nocturia, menopause. (7) Substance review: caffeine intake (including timing), alcohol, nicotine, cannabis, and medications that impair sleep. (8) Validated scales: Insomnia Severity Index (ISI, scores 0-28; >=15 = moderate clinical insomnia), Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Scale (ESS), Sleep Condition Indicator (SCI). Physical exam: BMI (obesity increases OSA risk), neck circumference, oropharyngeal exam, thyroid palpation.

DSM-5-TR criteria: (A) Predominant complaint of dissatisfaction with sleep quantity or quality, with >=1 of: difficulty initiating sleep, difficulty maintaining sleep (frequent or prolonged awakenings), or early-morning awakening with inability to return to sleep. (B) Sleep disturbance causes clinically significant distress or impairment in social, occupational, educational, academic, behavioural, or other functioning. (C) Sleep difficulty occurs on >=3 nights per week. (D) Sleep difficulty is present for >=3 months. (E) Sleep difficulty occurs despite adequate opportunity for sleep. (F) Not better explained by another sleep-wake disorder (narcolepsy, breathing-related sleep disorder, circadian rhythm sleep-wake disorder, parasomnia). (G) Not attributable to physiological effects of a substance. (H) Coexisting mental or medical conditions do not adequately explain the insomnia complaint.

Specifiers: "Episodic" (>=1 month but <3 months), "Persistent" (>=3 months), "Recurrent" (>=2 episodes within 1 year). Specify if comorbid with a non-sleep mental disorder, medical condition, or another sleep disorder. ICD-11 code: 7A00.

Sleep diary (1-2 weeks) is the recommended first-line assessment tool. Key metrics derived: total sleep time, sleep efficiency, sleep latency, wake after sleep onset (WASO), and number of awakenings. Wrist actigraphy provides objective estimates of sleep-wake patterns over 1-2 weeks and is useful for characterising circadian rhythm irregularities; however, it overestimates sleep in insomnia patients. Polysomnography (PSG) is NOT routinely indicated for insomnia diagnosis but should be ordered when obstructive sleep apnoea (snoring, witnessed apnoeas, obesity), periodic limb movement disorder, or other comorbid sleep disorders are suspected. The ISI (Insomnia Severity Index) tracks treatment response — a decrease of >=8 points or post-treatment score <8 indicates remission. Laboratory tests when clinically indicated: TSH (hyperthyroidism), ferritin (restless legs if <50 ng/mL), CBC, liver and renal function. The STOP-BANG questionnaire screens for OSA. Cognitive assessment may be warranted in older adults to distinguish insomnia from early neurodegenerative disease.

Obstructive sleep apnoea (OSA): repeated upper airway collapse causes arousals; patient may report insomnia symptoms (especially sleep-maintenance) but snoring, witnessed apnoeas, and excessive daytime sleepiness point to OSA. Can co-occur with insomnia (COMISA — Co-Morbid Insomnia and Sleep Apnoea). Restless legs syndrome (RLS): uncomfortable urge to move legs, worse in evening/at rest, relieved by movement — causes sleep-onset difficulty that mimics insomnia. Circadian rhythm sleep-wake disorders: delayed sleep phase (cannot fall asleep until very late, then sleeps normally — common in adolescents), advanced sleep phase (falls asleep very early, wakes very early — common in elderly). Inadequate sleep hygiene: poor sleep habits without the frequency/duration/distress criteria. Depression: early-morning awakening with inability to return to sleep; insomnia and depression frequently co-occur and exacerbate each other. Substance/medication-induced sleep disorder: caffeine, stimulants, alcohol withdrawal, corticosteroids, SSRIs. Anxiety disorders: cognitive hyperarousal and worry at bedtime cause sleep-onset insomnia. Narcolepsy: excessive daytime sleepiness, cataplexy, and disrupted nighttime sleep.

Treatment of Insomnia follows a stepped-care approach with cognitive-behavioural therapy for insomnia (CBT-I) as the first-line treatment. CBT-I: Cognitive-Behavioural Therapy for Insomnia is recommended as the first-line treatment by multiple guidelines (AASM, ACP, NICE) and is effective for both acute and chronic insomnia. Core components include: Sleep Restriction Therapy (limiting time in bed to match actual sleep time, then gradually extending as sleep efficiency improves above 85%); Stimulus Control (using the bed only for sleep and intimacy, getting

out of bed when unable to sleep within 15-20 minutes, maintaining a fixed wake time regardless of sleep quality); Cognitive Restructuring (challenging unhelpful beliefs about sleep such as catastrophising about consequences of poor sleep, unrealistic sleep expectations, attentional bias toward sleep-related threat); Sleep Hygiene Education (consistent wake time, comfortable sleep environment, limiting caffeine after noon and alcohol within 3 hours of bed, avoiding screens 1-2 hours before bed); and Relaxation Training (progressive muscle relaxation, diaphragmatic breathing, mindfulness). CBT-I is delivered in 4-8 sessions and produces durable improvements that persist after treatment ends, with effect sizes (d = 0.7-1.1) for sleep latency, WASO, and sleep efficiency. Digital CBT-I (e.g., Sleepstation, Sleepio, CBTI Coach app) shows comparable efficacy and improves access when therapists are unavailable. Brief Behavioural Therapy for Insomnia (BBTI) — 4 sessions focusing on sleep restriction and stimulus control — is effective in primary care settings. Pharmacotherapy: Medication is considered when CBT-I is insufficient, unavailable, or when short-term relief is needed. Options include: melatonin receptor agonists (ramelteon 8 mg) for sleep onset difficulty — no abuse potential, safe for older adults; dual orexin receptor antagonists (suvorexant 10-20 mg, lemborexant 5-10 mg) for sleep onset and maintenance — block wake-promoting orexin signalling, lower dependence risk; low-dose doxepin (3-6 mg) for sleep maintenance in adults and older adults; short-term use of non-benzodiazepine hypnotics (zolpidem 5-10 mg, eszopiclone 1-3 mg, zaleplon 5-10 mg) for acute insomnia — Z-drugs act on GABA-A alpha-1 subunit; and melatonin (0.5-5 mg, 1-2 hours before bed), particularly useful in circadian rhythm disorders and older adults with reduced endogenous melatonin. Benzodiazepines are generally avoided for chronic insomnia due to tolerance, dependence, rebound insomnia, next-day sedation, falls in elderly, and cognitive impairment. The 2019 AGS Beers Criteria strongly recommends against benzodiazepines and Z-drugs in older adults. Antihistamines (diphenhydramine, doxylamine) are not recommended for chronic use due to anticholinergic effects, tolerance, and next-day impairment. Addressing Comorbidities: Treatment of underlying conditions (depression, anxiety, chronic pain, sleep apnoea, restless legs syndrome) often improves insomnia. Medication review to identify drugs that impair sleep (stimulants, certain antidepressants like bupropion and venlafaxine, corticosteroids, beta-blockers, theophylline) is important. COMISA (comorbid insomnia and sleep apnoea) benefits from combined CPAP plus CBT-I.

With CBT-I, approximately 70-80% of patients show significant improvement, and 40-50% achieve insomnia remission (ISI <8). Treatment gains from CBT-I persist at 6-12 month follow-up, distinguishing it from pharmacotherapy where benefits cease upon discontinuation. Natural course without treatment: ~50-70% of individuals with chronic insomnia still have insomnia 1-3 years later. Chronic insomnia follows a fluctuating course, with periods of exacerbation during stress and partial remission during stable periods. The "short sleep" phenotype (insomnia plus objectively short sleep <6 hours on PSG) carries worse health prognosis, including higher cardiovascular and metabolic risk. Poor prognostic factors: longer duration before treatment, severe psychiatric comorbidity, chronic pain conditions, older age, and ongoing substance use. Patients who complete CBT-I have lower relapse rates (15-20% at 2 years) compared to those treated with medication alone (~50% relapse after discontinuation).

Psychiatric: insomnia doubles the risk of new-onset major depression (meta-analytic finding). It also increases risk for anxiety disorders, substance use disorders (especially alcohol as a self-medication strategy), and suicidal ideation (independent of depression). Cognitive: chronic sleep loss impairs working memory, attention, executive function, and consolidation of declarative memory. In older adults, chronic insomnia accelerates cognitive decline and may increase dementia risk. Cardiovascular: short-sleep insomnia associates with a ~29% increased risk of hypertension, elevated risk of coronary artery disease, heart failure, and stroke. Metabolic: insomnia increases risk of type 2 diabetes (~17% higher risk), obesity (via disrupted leptin/ghrelin signalling and increased appetite), and metabolic syndrome. Immune: sleep deprivation reduces natural killer cell activity and vaccine response. Occupational: workplace accidents, absenteeism, and presenteeism; insomnia is associated with 7.8 additional lost workdays per year. Motor vehicle accidents increase 2.5-4.5 fold with significant sleep deprivation. Chronic pain: insomnia lowers pain thresholds and amplifies pain perception, creating a bidirectional insomnia-pain cycle.

Good sleep practices reduce insomnia risk: maintain a consistent wake time 7 days per week (the single most important sleep hygiene behaviour); keep the bedroom dark, quiet, and cool (18-20°C); limit caffeine to morning hours; avoid alcohol as a sleep aid (it fragments sleep architecture in the second half of the night); exercise regularly but not within 2-3 hours of bedtime; limit screen exposure before bed (blue light suppresses melatonin). Patient education points: 7-9 hours of sleep is the recommended range for adults (National Sleep Foundation), but individual needs vary; spending excessive time in bed trying to "catch up" on sleep worsens insomnia; the bed should be for sleep and intimacy only; if unable to sleep after 15-20 minutes, get up and do something calming until sleepy; worry about sleep itself is one of the biggest perpetuating factors — sleep is a natural process that cannot be forced; CBT-I is more effective than medication long-term and has no side effects; over-the-counter sleep aids (antihistamines, melatonin) should not be used as a long-term solution without medical guidance.

Insomnia has been recognised since antiquity. The word derives from Latin "in" (not) + "somnus" (sleep). Ancient Egyptian and Greek texts describe sleeplessness and its treatments (opium, alcohol, valerian). Before the 20th century, insomnia was considered a symptom rather than a disorder. Nathaniel Kleitman established the first sleep laboratory at the University of Chicago in 1925. The discovery of REM sleep by Aserinsky and Kleitman in 1953 launched modern sleep medicine. Spielman introduced the 3P model (predisposing, precipitating, perpetuating factors) in 1987, which remains the theoretical foundation for CBT-I. Bootzin developed stimulus control therapy in 1972. Spielman developed sleep restriction therapy in 1987. Arthur Morin and colleagues formalised CBT-I as a multi-component treatment in the 1990s. DSM-III (1980) distinguished primary insomnia from insomnia secondary to other conditions. DSM-5 (2013) abandoned the primary/secondary distinction, recognising Insomnia Disorder as an independent diagnosis warranting treatment regardless of comorbidities. The American College of Physicians endorsed CBT-I as first-line treatment in 2016.

Sleep deprivation is normalised in many cultures. Phrases like "I'll sleep when I'm dead" reflect attitudes that devalue rest. The 24/7 economy, shift work, and constant digital connectivity erode sleep opportunities. Cultural differences in sleep practices include: siesta cultures (afternoon napping is common in Mediterranean, Latin American, and some Asian countries); co-sleeping norms (common in many non-Western cultures); and monophasic versus biphasic sleep expectations. The "clean sleep" and "sleep optimisation" movement has gained consumer attention, generating a $432 billion global sleep economy (mattresses, apps, wearables, supplements). Over-the-counter melatonin sales in the US exceed $1 billion annually, despite limited evidence for chronic insomnia. Socioeconomic disparities affect insomnia: individuals in lower-income brackets have higher insomnia rates, partly due to noise, shift work, economic stress, and reduced access to CBT-I. Racial/ethnic minorities have higher insomnia prevalence and less access to evidence-based treatment. Stigma around sleep medication use varies by culture — some view it as shameful weakness, others as routine self-care.

Active research areas: (1) Digital CBT-I — automated online programmes (Sleepio, Sleepstation) show large-scale efficacy; research on AI-personalised CBT-I is ongoing. (2) Pharmacology — next-generation orexin antagonists with improved selectivity; daridorexant (FDA-approved 2022) for insomnia with next-day functional improvement. (3) Biomarkers — high-density EEG and PET imaging to identify hyperarousal subtypes; cortisol awakening response as a treatment predictor. (4) Insomnia subtypes — cluster analyses have identified 5 insomnia subtypes based on life history and personality traits, with different treatment responses. (5) COMISA research — integrated CBT-I + CPAP protocols for patients with both insomnia and obstructive sleep apnoea. (6) Transcranial stimulation — transcranial direct current stimulation (tDCS) and transcranial magnetic stimulation (TMS) targeting prefrontal cortex to modulate arousal. (7) Gut-brain axis — emerging evidence linking gut microbiome composition to sleep quality. (8) Insomnia and dementia risk — longitudinal studies examining whether treating insomnia reduces Alzheimer's disease risk.

APA. (2022). Diagnostic and Statistical Manual of Mental Disorders (5th ed., text rev.; DSM-5-TR). APA Publishing. Sadock BJ, Sadock VA, Ruiz P. (Eds.). (2024). Kaplan & Sadock's Comprehensive Textbook of Psychiatry (11th ed.). Wolters Kluwer. StatPearls [Internet]. Insomnia. NCBI Bookshelf. StatPearls Publishing. Morin CM, Espie CA. (2003). Insomnia: A Clinical Guide to Assessment and Treatment. Springer. WHO. (2022). ICD-11 for Mortality and Morbidity Statistics. Geneva: World Health Organization.

StatPearls Insomnia: https://www.ncbi.nlm.nih.gov/books/NBK526136/ AASM (American Academy of Sleep Medicine): https://aasm.org Sleep Foundation: https://www.sleepfoundation.org NICE Insomnia Guidelines: https://www.nice.org.uk CBT-I Coach App (VA): https://mobile.va.gov/app/cbt-i-coach WHO ICD-11 code 7A00: https://icd.who.int Crisis: 988 (US Suicide & Crisis Lifeline); Text HOME to 741741 (Crisis Text Line) Note: Educational only. Not a substitute for professional care.