Sleep disorders

• Sleep is as biological as breathing, and sleep disorders are disorders of the control systems that govern when, how deeply, and how safely we sleep.
• The International Classification of Sleep Disorders, third edition (ICSD-3), groups all sleep disorders into the major families: insomnia, sleep-disordered breathing (including sleep apnoea), central disorders of hypersomnolence (including narcolepsy), circadian rhythm sleep-wake disorders, parasomnias, sleep-related movement disorders (including restless legs syndrome (RLS)) and other sleep disorders. Patients often have more than one.
• Insomnia is the most common complaint in sleep medicine; it is diagnosed from the history, and its first-line treatment is cognitive behavioural therapy for insomnia (CBT-I), not tablets. Hypnotics, when used, are short-term bridging agents at the lowest effective dose for the shortest duration. ^[1][6]
• Narcolepsy is a chronic neurological disorder of daytime sleepiness, usually with cataplexy and unstable night sleep; strong AASM 2021 recommendations support modafinil, pitolisant, sodium oxybate and solriamfetol. ^[2]
• Parasomnias split by sleep stage: night terrors and sleepwalking arise from deep non-REM sleep and are common in children; REM sleep behaviour disorder arises from REM sleep, occurs mainly in older men, and often precedes Parkinsonian or Lewy body disease. ^[4]
• Restless legs syndrome is diagnosed at the bedside using four criteria and, in 2025 AASM guidance, is treated by correcting iron deficiency and using alpha-2-delta ligands rather than dopamine agonists. ^[3]
• Circadian disorders are disorders of timing, not of sleep itself: the treatment of delayed sleep-wake phase disorder is timed melatonin and timed light, given at the correct phase. ^[5]

By the end of this page you should be able to:

1. List the ICSD-3 families of sleep disorders and give one example of each.
2. Take a sleep history, screen with STOP-Bang where apnoea is possible, and recognise the red flags that distinguish narcolepsy, RLS, parasomnias and circadian disorders.
3. State the diagnostic criteria for chronic insomnia and for RLS, and the thresholds that govern iron supplementation and periodic limb movements.
4. Explain why CBT-I is first-line for chronic insomnia and describe its core components.
5. Choose and dose first-line pharmacotherapy for narcolepsy and for REM sleep behaviour disorder, including drug safety points.
6. Manage night terrors, sleepwalking and sleep talking in children and adults, and counsel on bedroom safety.
7. Plan timed melatonin and light therapy for delayed sleep-wake phase disorder.
8. Recognise the sleep apnoea cross-check and know when to refer or admit.

A sleep disorder is a condition in which the normal processes of sleep (its timing, duration, depth, continuity, or motor control) are disturbed enough to cause distress or impairment in waking life. Sleep itself is not a single state: over a night it alternates between non-REM (N1, N2, N3 "slow-wave" sleep) and REM sleep, governed by the circadian clock and by homeostatic sleep pressure. A disorder can strike either system, or the boundary between sleep and wakefulness.

The ICSD-3 (used alongside DSM-5-TR and ICD-11 in practice) classifies sleep disorders into the major families. ^[1]

• Insomnia. Chronic insomnia disorder and short-term insomnia disorder.
• Sleep-related breathing disorders. Obstructive sleep apnoea, central sleep apnoea, sleep-related hypoventilation, sleep-related hypoxaemia.
• Central disorders of hypersomnolence. Narcolepsy type 1 and type 2, idiopathic hypersomnia, Kleine-Levin syndrome, and hypersomnia due to medical, psychiatric, drug, or insufficient sleep causes.
• Circadian rhythm sleep-wake disorders (CRSWD). Delayed sleep-wake phase (DSWPD), advanced sleep-wake phase (ASWPD), non-24-hour (N24SWD), irregular sleep-wake (ISWRD), shift work and jet lag.
• Parasomnias. Non-REM-related (sleepwalking, sleep terrors, confusional arousals, sleep-related eating), REM-related (REM sleep behaviour disorder (RBD), nightmare disorder, sleep paralysis) and others.
• Sleep-related movement disorders. Restless legs syndrome, periodic limb movement disorder, bruxism and others.
• Other sleep disorders. Insufficient sleep, environmental and unclassified disorders.

A pragmatic bedside grouping is just as useful for learning: disorders of initiating and maintaining sleep (insomnia and its mimics), disorders of excessive daytime sleepiness (narcolepsy, apnoea, circadian), disorders of unwanted behaviours in sleep (parasomnias), and disorders of timing (circadian).

Insomnia is the most common sleep complaint in general practice and psychiatry. Occasional, short-term insomnia affects roughly 30% to 50% of people; chronic insomnia disorder, defined as above, affects an estimated 5% to 10% in industrialised nations, and far more in medical and psychiatric populations and in older adults. ^[1] Most sleep disorder epidemiology therefore collapses into insomnia epidemiology.

• Sex and age. Women report insomnia more often than men, and prevalence rises with age; prevalence of chronic insomnia in older adults may reach the upper end of the published range.
• Comorbidity is the rule, not the exception. Chronic insomnia frequently coexists with depression, anxiety, chronic pain, RLS, sleep apnoea, and with the medicines used for those conditions. Under current NICE and AASM thinking insomnia is treated as a condition in its own right even when one of these is present, because each worsens the other. ^[1][6]
• Narcolepsy is uncommon and typically begins in the second decade. The AASM hypersomnolence guideline treats narcolepsy type 1 and type 2 together for most recommendations because trials aggregate them. ^[2]
• RLS is clinically significant in 2% to 3% of adults and 0.5% to 1% of children; it is about 50% more common in women and more common in people of northern European origin. Genetics is strong: about half of affected people have an affected first-degree relative. ^[3]
• RBD is commoner than once thought: community surveys in older adults suggest about 1 in 20 may be affected, with age the strongest risk factor. It is seen in older men far more than women. ^[4]
• Circadian disorders are underdiagnosed: delayed sleep-wake phase disorder is the commonest intrinsic circadian disorder and is especially common in adolescents and young adults.

Sleep disorders are rarely random. The most useful mental model is "predisposition, precipitant, perpetuating factors" (the "three P's" used in insomnia practice). Understanding which apply directs treatment.

Insomnia

• Predisposition: a tendency towards arousal — hyperactivity of the stress systems, anxiety trait, a light, anxious sleep style, a family history of poor sleep.
• Precipitants: bereavement, illness, shift work, a time-zone change, pain, depression, medication (steroids, antidepressants, decongestants, caffeine, alcohol), noisy or unsafe sleeping environment, a new baby.
• Perpetuating (the maintenance machinery): irregular bedtimes, spending too long in bed awake, napping to catch up, watching the clock, caffeine in the afternoon, alcohol as a nightcap, benzodiazepines used nightly. This is the machinery that CBT-I dismantles. ^[1][6]
• Medical and psychiatric drivers: chronic pain, gastro-oesophageal reflux, asthma, depression and anxiety disorders, post-traumatic stress disorder, neurodegenerative disease. Treating these is part of insomnia care, but the insomnia often still needs its own treatment. ^[1]

Narcolepsy. The cause is not established in detail; in narcolepsy type 1 there is a loss of the orexin (hypocretin) neurons of the lateral hypothalamus, felt to be most often immune-mediated (the strong link to HLA-DQB1*06:02, and onset after infections or vaccination, supports this), producing EDS with cataplexy and unstable REM-sleep timing. Narcolepsy type 2 has EDS without cataplexy or documented orexin deficiency; some progress to type 1, some do not.

Parasomnias. Non-REM parasomnias (night terrors, sleepwalking, confusional arousals, sleep-related eating) are disorders of arousal from deep slow-wave sleep. They run in families, peak in childhood when slow-wave sleep is deepest and most abundant, and are set off by anything that fragments or deepens sleep: sleep deprivation and recovery sleep, fever, alcohol, sedatives, obstructive sleep apnoea, RLS, stress and irregular schedules. They usually resolve in adolescence.

REM sleep behaviour disorder is different in mechanism: it is a failure of REM atonia (the glycinergic/GABAergic inhibition of spinal motor neurons during REM). It is most often (eventually) a prodrome of an alpha-synucleinopathy — Parkinson disease, dementia with Lewy bodies or multiple system atrophy — and can also be drug-induced (most commonly SSRIs, SNRIs, tricyclics, beta-blockers) or secondary to narcolepsy or structural brain disease. ^[4]

Circadian disorders. These arise from a mismatch between the internal clock (coupled to light entering the eyes) and the required social schedule. Delayed sleep-wake phase (DSWPD) and advanced sleep-wake phase (ASWPD) are usually intrinsic chronotypes exaggerated by behaviour and late light exposure; non-24-hour disorder (N24SWD) and irregular sleep-wake disorder (ISWRD) are usually consequences of blindness or of neurodevelopmental/neurodegenerative disease breaking the clock's entrainment. Shift work and jet lag are the extrinsic forms.

RLS. Genetic (164 polymorphisms reported), brain iron deficiency (MRI and CSF studies in people with RLS show reduced brain iron even when peripheral iron is normal), and dopaminergic dysfunction. Secondary causes matter: pregnancy, iron deficiency, chronic kidney disease (especially end-stage renal disease), diabetes, peripheral neuropathy, Parkinson disease, and medicines that worsen RLS (antihistamines, most antidepressants, antidopaminergics, antiemetics such as metoclopramide). Alcohol, caffeine and nicotine aggravate it. Obstructive sleep apnoea is on the list of exacerbating factors and should be treated in anyone with RLS. ^[3] A sleep apnoea cross-check is therefore part of every RLS work-up.

Insomnia. The working model is hyperarousal: people with chronic insomnia show increased cortical and autonomic activity day and night, a higher metabolic rate, and altered connectivity in arousal networks, so sleep is not the absence of effort but the active down-regulation of arousal. To sleep, the brain must release the "wake" networks (orexin, histamine, noradrenaline, serotonin, acetylcholine) and let the ventrolateral preoptic (VLPO) sleep-active neurons take over. Anything that pushes the wake side (stress, caffeine, pain, grief, worry) raises the threshold; anything that weakens the sleep side (ageing, light, anxiety) lowers the drive. Key consequence: the conditioned arousal learned by lying awake in bed, and the distorted perception of sleep (people with insomnia often underestimate objective sleep, the so-called sleep-state misperception). This is why staying in bed awake to "catch up" backfires.

Narcolepsy. Orexin stabilises the flip-flop switch between sleep and wake; when it is lost, the switch becomes unstable, so wake intrudes into sleep and (especially REM) sleep intrudes into wake. Cataplexy is an intrusion of REM-atonia into waking, triggered by emotion (laughter, surprise, anger). The same instability produces hypnagogic/hypnopompic hallucinations and sleep paralysis.

Apnoea physiology produces sleep fragmentation and is the subject of the dedicated sleep apnoea page; it is enough here to say that breathing pauses fragment sleep architecture and repeatedly rouse the patient, so an apnoea patient and an insomnia patient can look identical by day. Screen whenever sleep is poor.

RLS. Reduced brain iron lowers the threshold of the sensory and motor systems, and the dopaminergic (A11) descending pathways that modulate spinal sensory input are implicated. Symptoms are circadian (dopamine is lowest at night) and positional (movement brings relief because it changes proprioceptive input and activates sensorimotor networks).

RBD. Pontine REM-atonia generators (glutamatergic sublaterodorsal nucleus; glycinergic/GABAergic spinal interneurons) fail, so REM sleep carries full motor output. Lesion studies and the prodromal neurodegenerative course support a brainstem origin.

Circadian. The suprachiasmatic nucleus generates a rhythm slightly longer than 24 hours; light (especially short-wavelength morning light) entrains it. Melatonin (from the pineal in response to darkness) is both a marker of phase and, when given at the right time, a phase-shifting signal. Mis-timed melatonin or light shifts phase the wrong way.

Always ask the same six questions, in the patient's own words. What is the complaint? When did it start? What has changed? Does it occur every night or in bursts? Is it better on holiday or at weekends (a pointer to circadian and environmental causes)? What does the bed partner see?

Insomnia. Difficulty falling asleep, staying asleep, waking early; restorative sleep is poor and daytime impairment is present. Ask for a sleep diary of one to two weeks: bedtime, lights-out, sleep latency, awakenings, wake time, nap frequency. Distinguish acute stress insomnia from chronic; the "rule of three" (at least three nights per week for at least three months with daytime consequences) is the ICSD-3 threshold. Ask about sleep hygiene, caffeine and alcohol timing, medicines (SSRIs, venlafaxine, bupropion, thyroid, beta-agonists, corticosteroids, decongestants), snoring, restlessness, mood and anxiety, pain and reflux. Ask the partner about snoring and kicks. ^[1]

Hypersomnia and narcolepsy. EDS is not the same as tiredness: narcoleptic patients fall asleep in seconds to a minute, often into REM, in monotonous situations (meetings, lectures, driving, eating), and take a nap that feels refreshing but short-lived. Ask about sleep attacks, cataplexy (sudden loss of muscle tone triggered by emotion — the knees buckle, the jaw drops, the head falls forward, without loss of consciousness, often in response to laughter), sleep paralysis, hypnagogic/hypnopompic hallucinations, and disturbed night sleep (frequent awakenings, vivid dreams, periodic limb movements). Ask about weight, snoring, and other medical causes.

Parasomnias. Non-REM parasomnias. Night terrors: a scream, sitting up in bed with eyes open, autonomic surge (tachycardia, sweating, dilated pupils, flushed skin), inconsolability, no recall the next morning, occurrence in the first third of the night from slow-wave sleep. Sleepwalking: rising from bed, open eyes, blank stare, complex but usually clumsy behaviour, difficulty navigating, return to bed or awakening disoriented; amnesia for the event; can last minutes; dangerous (falls, leaving the house, turning on ovens). Sleep-related eating disorder: eating while asleep with poor recall and sometimes injury. Confusional arousals: waking bewildered for minutes.

REM sleep behaviour disorder: vivid, often violent dream enactment (punching, kicking, defending oneself from an attacker), occurring in the second half of the night when REM is longest; the patient can usually recall the dream; injurious and alarming for the partner; can be mistaken for nightmares, nocturnal seizures, post-traumatic stress disorder or alcohol blackouts. Acting out the dream is the danger. ^[4]

Circadian. The patient says "I can't fall asleep until 3 a.m. and then I can't wake for school", but sleep quality and duration are normal when allowed to sleep at their preferred times. Late-sleepers report sleep-onset insomnia and morning inability to wake; early-sleepers report evening sleepiness and early waking. Ask for a workday/free-day comparison: the difference between sleep-onset times is the marker of "social jetlag".

RLS. An urge to move the legs, a deep aching, crawling, or electric sensation, worst when lying down in the evening, relieved only by movement, sometimes felt in the arms; severe cases disrupt sleep onset every night and cause insomnia. Ask the four criteria; ask about iron deficiency, renal disease, pregnancy, medicines, family history and snoring. Ask the partner about kicks (periodic limb movements). ^[3]

General examination in sleep disorders is short but targeted.

• Build and habitus: obesity, neck circumference, jaw size, tongue, tonsils, and Mallampati oropharyngeal crowdedness (point toward apnoea).
• Neurological: cranial nerves, motor tone, tremor, eye movements, parasomnias signs; the "clean" normal MSE of the narcoleptic paradox.
• Mental state examination: mood and anxiety, suicidality, cognition, insight. In insomnia secondary to depression/anxiety, treat both conditions. In suspected mania or psychosis, refer.
• Sleep-state examination: observe a nap opportunity in selected hypersomniacs (multiple sleep latency testing is deferred to the laboratory).
• Signs of iron deficiency or renal disease: pallor, dermatological signs, oedema in RLS work-ups.
• Blood pressure and BMI.

There are no pathognomonic physical signs for insomnia, narcolepsy, circadian or parasomnia disorders; the diagnosis is overwhelmingly clinical, supported by targeted tests.

Most sleep complaints are insomnia on the surface and something else underneath. The key separates is shown.

Doctors often forget that a sleep apnoea patient can complain of insomnia, and that many insomnia patients turn out to have occult apnoea once a partner is asked. Sleep apnoea is covered in detail on the separate MedGrasp page "Obstructive sleep apnoea and obesity hypoventilation syndrome"; this page keeps only the cross-check: whenever a patient has poor sleep plus snoring, witnessed apnoeas, or resistant hypertension, screen with STOP-Bang and test accordingly, and avoid prescribing sedatives, opioids or hypnotics until apnoea is excluded. ^[3]

Aetiology drives tests; most sleep disorders are diagnosed from the history and a written sleep diary. Use tests to confirm, grade severity, or exclude mimics.

• Sleep diary (time in bed, estimated sleep latency, number and duration of awakenings, wake time, naps, caffeine/alcohol) is essential for insomnia and circadian disorders.
• Actigraphy (wrist movement, worn continuously) supports circadian disorders, where AASM practice sees actigraphy as desirable when feasible, and helps document irregular sleep. ^[5]
• Polysomnography (PSG, level 1): the laboratory overnight study of sleep stages (EEG), eye movements, chin/leg EMG, airflow, respiratory effort, oxygen saturation, position and ECG. Gold standard for diagnosing RBD (REM without atonia), RLS/periodic limb movements, central hypersomnias and sleep-related breathing, and for titrating positive airway pressure. PSG is not required for uncomplicated insomnia. ^[4]
• Home sleep apnoea test (HSAT) is the first-line test for sleep apnoea in uncomplicated adults; the formal diagnostic branch is on the sleep apnoea page.
• Multiple sleep latency test (MSLT) after a night PSG: used to evaluate narcolepsy and hypersomnia by measuring mean sleep latency and sleep-onset REM periods (SOREMPs).
• CSF orexin-A (hypocretin-1), where available, in suspected narcolepsy type 1 (low levels support the diagnosis).
• Iron studies in every clinically significant RLS: ferritin and transferrin saturation (calculated from iron and total iron binding capacity), drawn in the morning after avoiding iron-containing supplements or foods for at least 24 hours. ^[3]
• Renal function and pregnancy test where relevant in RLS.
• Epworth Sleepiness Scale (8 brief items on daytime sleepiness) and STOP-Bang (screening questionnaire for sleep apnoea) as adjuncts.
• Blood pressure, BMI, neck circumference and screening blood tests (glucose, lipids, thyroid) for metabolic comorbidity.

Not all patients need all tests. An uncomplicated chronic insomnia in an otherwise well person needs a good history, a two-week diary, a STOP-Bang screen, an Epworth, and iron studies if RLS is suspected; PSG is reserved for the cases listed above.

CBT-I is not a relaxation tape. It is a structured, skills-based therapy with five components, each aimed at a specific perpetuating mechanism.

1. Stimulus control. The bed is for sleep (and sex) only. If unable to sleep after a short time, get up, do something quiet in dim light, and return only when sleepy. This re-conditions the bed as a sleep cue.
2. Sleep restriction. Temporary reduction of time in bed to the actual sleep time, then gradual re-extension as sleep efficiency recovers. This builds sleep pressure and consolidates sleep; a short-term dip in daytime function is expected and warned about.
3. Cognitive therapy. Targets performance anxiety, catastrophic beliefs ("if I do not sleep tonight, I will get cancer"), and sleep effort.
4. Sleep hygiene and behavioural optimisation. Regular rise time every day, no clock-watching, limit caffeine after midday, avoid alcohol at night, exercise earlier in the day, keep the bedroom dark, cool and quiet, stop screens in the hour before bed.
5. Relaxation training. Progressive muscle relaxation, paced breathing, imagery.

CBT-I is more effective than hypnotics at 6 and 12 months, with no tolerance or dependence, which is why it is first-line for chronic insomnia in NICE NG215 (2022) and the AASM 2017 pharmacologic guideline, and why the ACP guideline gives a strong recommendation for CBT-I as initial treatment. ^[1][6] Selected components can be delivered in brief primary-care consultations when full CBT-I is unavailable or when a patient is not ready. Digital CBT-I (for example NHS-endorsed Sleepio or Sleepstation) is an acceptable alternative where local services have not commissioned face-to-face therapy. ^[6]

CBT-I can be delivered to patients with comorbid conditions (pain, depression, apnoea, cancer) and it usually improves the comorbidity's symptoms at the same time. It is contraindicated or modified in bipolar disorder during manic phases, in epilepsy, and in anyone whose occupation makes sleep restriction unsafe (heavy goods drivers, machinery operators) — in those, stimulus control, cognitive work and relaxation carry the load.

When medicines are needed. Hypnotics are not recommended as routine first-line for chronic insomnia. NICE NG215 (2022) frames them as short-term agents, reviewed within 4 weeks, at the lowest effective dose for the shortest possible time, with the risks of dependence, tolerance and withdrawal explained before starting. The AASM 2017 guideline gives weak (conditional) suggestions, not strong recommendations, for individual agents, because the evidence quality is generally low. ^[1][6]

Medicines by role (weak recommendations, chosen for the symptom rather than the person when CBT-I fails or is unavailable):

• Sleep-onset or sleep-maintenance insomnia: zolpidem, eszopiclone, zaleplon, triazolam or temazepam (the temazepam recommendation in the 2017 guideline was based on 15 mg doses). ^[1]
• Maintenance insomnia in particular: suvorexant (an orexin receptor antagonist that lowers the wake signal rather than sedating globally) and low-dose doxepin. ^[1]
• Sleep-onset insomnia only (no next-day hangover): ramelteon. ^[1]
• Not recommended for insomnia (weak against): trazodone, tiagabine, diphenhydramine (antihistamines), melatonin, L-tryptophan and valerian. Trazodone without depression has poor evidence and cardiotoxic, priapism and orthostatic risks; over-the-counter antihistamines have anticholinergic cognitive risks, especially in older adults. ^[1]
• Low-dose modified-release melatonin is used for poor-quality sleep in older adults in some formularies (commonly off-label), but trial evidence for routine chronic insomnia is insufficient.

Deprescribing protocol: explain the dependence risk, taper gradually in small decrements (slower for long-term benzodiazepine use), add CBT-I components in parallel, switch to intermittent rather than nightly use, and review sleep and withdrawal symptoms. Avoid abrupt stopping after prolonged use because of rebound insomnia, anxiety and, for benzodiazepines, withdrawal seizures. Daridorexant (a dual orexin receptor antagonist, approved in the UK 2024) is the first medicine licensed specifically for chronic insomnia disorder and marks a move toward targeted, non-dependence-forming treatment. ^[6]

Red flags for hypnotics: avoid or use only with great caution in older adults, pregnancy, obstructive sleep apnoea, severe hepatic impairment, depression with suicidality, and anyone who drives or operates machinery. Hypnotics are central nervous system depressants and must never be combined with alcohol or opioids.

Management rests on three pillars: strategic napping and sleep hygiene, wake-promoting medication for excessive daytime sleepiness (EDS), and anticataplectic medication for type 1 narcolepsy.

• Non-drug measures: brief planned naps timed before periods of high sleepiness, a regular sleep schedule, avoiding alcohol and sedatives, weight management, and graded exercise. Driving and occupational safety counselling is mandatory and documented: untreated narcolepsy impairs driving like alcohol; licensing authorities usually require documented control before driving resumes, especially for commercial drivers. ^[2]
• Narcolepsy type 1 (with cataplexy): if EDS remains, add a wake-promoting agent.
• Orexin deficiency: treatment trials of orexin-replacement therapy are ongoing; none has yet reached routine practice.

AASM 2021 recommendations (strong) for EDS in adults with narcolepsy: modafinil, pitolisant, sodium oxybate and solriamfetol; conditional suggestions for armodafinil, dextroamphetamine and methylphenidate. ^[2]

• Modafinil (FDA Schedule IV): the usual first-line wake-promoting drug. The DailyMed label recommends 200 mg orally once daily in the morning for narcolepsy, with no consistent evidence of additional benefit above 200 mg; doses up to 400 mg/day have been tolerated. It halves with severe hepatic impairment and may lower oral contraceptive efficacy. Common adverse effects include headache, nausea, anxiety, insomnia, dry mouth and cardiovascular effects in predisposed people. Avoid combining with large caffeine loads. ^[7]
• Armodafinil (conditional AASM 2021): the R-enantiomer, dosed each morning per label.
• Solriamfetol (strong 2021, Schedule IV): dopamine/noradrenaline reuptake inhibitor for EDS, titrated each morning per label; avoid with monoamine oxidase inhibitors and use caution with hypertension, cardiac disease, or renal impairment.
• Pitolisant (strong 2021): histamine H3 inverse agonist, taken on waking per label; may prolong QTc and reduces oral contraceptive efficacy; use caution in hepatic disease.
• Sodium oxybate/Xyrem (strong 2021): the only approved treatment for cataplexy and a powerful EDS treatment. It is dosed at bedtime and during the night for twice-nightly formulations, titrated from a low dose per product label to the maximum tolerated; patients must take it in bed, and it carries a boxed warning for CNS depression and respiratory depression; it is available only through a risk evaluation and mitigation strategy (REMS) programme in certified pharmacies. Never combine with alcohol or sedatives. ^[2]
• Anticataplectic alternatives: venlafaxine, fluoxetine, or tricyclics (clomipramine, protriptyline) in low dose; SSRIs/SNRIs are the pragmatic first-line where sodium oxybate is unavailable, but they worsen insomnia and can cause RLS. Their doses are titrated per standard formularies.
• Dextroamphetamine and methylphenidate are conditional options for refractory or very sleepy patients, with Schedule II controls and abuse potential, and they raise heart rate and blood pressure.
• Children and adolescents: in AASM 2021, sodium oxybate and modafinil are the only conditional paediatric recommendations; pitolisant is not established in children; all need specialist sleep-medicine input. ^[2]

Safety notes: sodium oxybate is contraindicated in succinic semialdehyde dehydrogenase deficiency (rare). Both modafinil and sodium oxybate can worsen sleep-disordered breathing; rule out apnoea before and during treatment. Pitolisant and modafinil reduce oral contraceptive efficacy — add non-hormonal contraception.

Management is mostly non-pharmacological. Reassure families (these are not seizures and not psychiatric illness), deal with triggers, and protect the patient and others.

• Sleep safety: lock doors and windows, remove or pad sharp furniture and firearms, lower the bed, place a soft mat on the floor, sleep on the ground floor if possible, separate beds if violent, and consider scheduled ("anticipatory") awakening shortly before the usual event time — practical advice that reduces recurrence in children.
• Trigger treatment: restore sleep (more regular schedule, no sleep deprivation), treat fever, sleep apnoea or RLS if present, avoid alcohol and sedatives at night, reduce stress and manage any comorbid epilepsy.
• Scheduled nocturnal arousals before the typical time of the event can be effective in frequent night terrors in children.
• Consider pharmacotherapy only for frequent, injurious or highly disruptive cases: low-dose clonazepam at bedtime (small randomised support referenced in the parasomnia best-practice literature) or an SSRI for associated depression/anxiety. Evidence is limited and AASM guidance for RBD, below, suggests cautious benzodiazepine use, especially in older adults.
• Children: non-REM parasomnias are common (up to one-third of children sleepwalk), almost all resolve by adolescence. No medicine should be used as first-line; parental reassurance and safety outweigh everything else.

Do not confuse sleep terrors with nightmares (REM, recall present), seizures (post-ictal confusion, tongue bite) or psychogenic dissociation. If the events are violent, atypical, or start in adulthood, take a neurological and sleep history and arrange EEG or PSG.

AASM 2023 guidance recommends conditionally, for both isolated and secondary RBD: clonazepam, immediate-release melatonin, pramipexole, and rivastigmine (the last for RBD with mild cognitive impairment). A good-practice statement based on expert consensus underpins everything else: create a safe sleeping environment, remove guns and throw-able objects, pad furniture, place a mat by the bed, and have bed partners sleep separately or place a pillow between them. ^[4]

Dosing from the guideline discussion:

• Clonazepam: most patients respond to 0.25 to 1.0 mg at bedtime; in older or cognitively impaired patients start at 0.25 mg and watch for morning sedation, falls, delirium and worsening sleep-disordered breathing. Beers-criteria concern applies. ^[4]
• Immediate-release melatonin: start 3 mg at bedtime and titrate in 3 mg increments up to 15 mg (higher data are not available); melatonin is unregulated and USP-verified preparations give the most consistent dosing. It is mildly sedating and a good first choice for older patients. ^[4]
• Pramipexole: start 0.125 mg at bedtime, titrate slowly up to 2.0 mg nightly; most helpful when PSG shows abundant periodic limb movements; dopaminergic adverse effects include nausea, hypotension, impulse-control disorder and augmentation of RLS. ^[4]
• Rivastigmine transdermal patch: start 4.6 mg per 24 h, increase to 13.3 mg daily, for RBD in people with mild cognitive impairment. ^[4]
• Drug-induced RBD (often SSRIs, SNRIs, tricyclics, beta-blockers): if clinically possible, withdraw the offending drug slowly rather than add an RBD drug. ^[4]
• Combination therapy (clonazepam plus melatonin) is common in practice when monotherapy is inadequate, but is not addressed in the guideline.

Counsel every RBD patient about the neurodegenerative risk (most commonly dementia with Lewy bodies or Parkinson disease) without being fatalistic: not all progress, of whom many live years with manageable RBD, and longitudinal follow-up with a movement-disorders team is arranged. Avoid deep brain stimulation for RBD itself (AASM conditional recommendation against). ^[4]

Management is timing, not sedation.

• Common work-up: a sleep diary plus wrist actigraphy (continuous, including free and work days), plus (when possible) dim-light melatonin onset (DLMO) to anchor chronotype. Diagnosis of DSWPD/ASWPD requires symptoms for at least 3 months; N24SWD requires documented progressive shift over at least 14 days; ISWRD requires non-circadian bouts documented over at least 7 days. ^[5]
• DSWPD in adults: AASM 2015 suggests strategically timed melatonin (weak for), and post-awakening bright light with behavioural components (children and adolescents strongly supported; adults less so).
• Practical melatonin pattern for DSWPD: melatonin taken well before the desired sleep onset time at a low dose and titrated, with light exposure kept low in the evening (dim light, blue-blockers after sunset) and bright (ideally blue-enriched) light soon after natural waking. The melatonin dose matters less than the timing; PRC data above 5 mg are not available. ^[5]
• ASWPD: evening bright light, to delay sleep timing.
• N24SWD (blind adults): melatonin timed at a fixed clock time each day, titrated until entrainment.
• ISWRD in dementia: reduce daytime napping, morning bright light, and structured daytime activity and night-time care. Melatonin is weakly suggested against in demented elderly, and hypnotics (sleep-promoting medications) are strongly recommended against. ^[5]
• Shift work disorder: anchor sleep with a dark, quiet bedroom; strategic light during the shift and darkness after; short-acting hypnotic sparingly for daytime sleep; modafinil/armodafinil approved for shift-work EDS in some countries; melatonin at the start of daytime sleep may help; weigh long-term cardiovascular and safety risks.
• Jet lag: light exposure timed to the new time zone; short courses of timed melatonin may help, especially eastward travel.
• What does NOT help: prescribing a nightly benzodiazepine for someone whose problem is phase, not sleep pressure.

Step 1: Address exacerbating factors (alcohol, caffeine, antihistamines, serotonergic/antidopaminergic drugs, untreated sleep apnoea). Treat iron deficiency. Pregnancy-specific profiles apply. ^[3]

Step 2: Check iron studies (ferritin, transferrin saturation, morning sample, 24 hours without iron supplements or iron-rich foods). Supplement iron if ferritin 75 ng/mL or less, or transferrin saturation below 20%; use only IV iron if ferritin is 75 to 100 ng/mL; treat children when ferritin is under 50 ng/mL. Iron studies are repeated to guide further treatment. ^[3]

Step 3: If symptoms are frequent (more than half the days of the week, or causing difficulty initiating sleep), AASM 2025 strongly recommends an alpha-2-delta ligand: gabapentin enacarbil, gabapentin (started low in the evening and titrated; renal adjustment) or pregabalin, titrated to the lowest effective dose. ^[3] Doses and titration come from local formularies; gabapentin and pregabalin dosing for RLS is off-label in most jurisdictions and must follow product labels.

Step 4: If iron correction is needed acutely or oral iron is not tolerated/utilised, strong/conditional recommendations in AASM 2025 cover IV ferric carboxymaltose (strong), IV low-molecular-weight iron dextran and ferumoxytol (conditional), with ferrous sulfate as an oral conditional option; extended-release oxycodone (conditional) for refractory RLS, and bilateral peroneal nerve stimulation (conditional). ^[3]

Step 5: Dopamine agonists are no longer standard treatment in AASM 2025 because of augmentation (progressive worsening of intensity, duration and earlier onset over months to years, often treated by dose escalation). Pramipexole, ropinirole, rotigotine and levodopa are conditionally recommended against standard use, but may be chosen when short-term relief is prioritised over long-term adverse effects. Cabergoline is strongly not recommended. ^[3]

PLMD is diagnosed when periodic limb movements exceed 15 per hour in adults or 5 per hour in children, cause clinically significant sleep disturbance or daytime dysfunction, and no other condition (RLS, apnoea, RBD, narcolepsy) explains them. Evidence for specific pharmacotherapy is sparse (AASM 2025 recommends against triazolam and valproic acid in PLMD based on adverse-effect balance). Non-drug optimisation (iron, sleep schedule, avoid caffeine/alcohol) is first. ^[3]

• Insomnia: depression and anxiety (bidirectional), reduced work productivity, accidents, chronic pain amplification, analgesic and hypnotic dependence, and, in older men with objectively short sleep, hypertension and cardiovascular risk. Immune and metabolic effects of short sleep are also concerning.
• Narcolepsy: road traffic and occupational accidents (the major modifiable risk), obesity and metabolic syndrome, depression, impaired education and employment, social isolation; stimulant misuse risk and drug interactions; sodium oxybate abuse liability despite REMS controls.
• RBD: injury to the patient (lacerations, fractures, subdural haematoma) and to bed partners; the biggest long-term complication is the development of a neurodegenerative alpha-synucleinopathy in a substantial proportion of patients, over years to decades.
• RLS: severe insomnia, daytime sleepiness, depression, and augmentation with dopaminergic therapy. PLMD may be followed in its own right.
• Circadian disorders: academic and occupational failure, chronic sleep restriction, low mood, and in shift work, cardiovascular and metabolic risk.
• OSA comorbidity (see sleep apnoea page) amplifies all of the above; treating apnoea improves sleep quality and outcomes.

• Short-term insomnia resolves when the precipitant resolves; a minority becomes chronic.
• Chronic insomnia is often persistent but is very treatable: CBT-I gives durable improvement in sleep and daytime function in most patients.
• Narcolepsy is lifelong. Early diagnosis and treatment (wake-promoters and, where cataplexy is present, sodium oxybate) restores quality of life and functioning in the large majority; driving and work usually continue with treatment and documentation.
• RLS is chronic and fluctuates (symptom-free intervals of weeks to months); brain iron repletion helps some patients; alpha-2-delta ligands control symptoms in most but a minority becomes refractory. Augmentation, once established, is difficult; rotate or specialist care.
• Non-REM parasomnias usually resolve by adolescence. Adult-onset sleepwalking or new sleep terrors deserve neurological evaluation.
• RBD is usually persistent but often mild for years and treatable for symptom control; prognosis depends on evolution to neurodegenerative disease.
• Circadian disorders: type and chronicity vary; delayed sleep phase in adolescents often improves with age; non-24-hour disorder in blind patients requires ongoing timed treatment.

• Universal screening is not indicated for sleep disorders, but a low threshold is wise in hypertension, resistant hypertension, obesity, type 2 diabetes, heart failure, atrial fibrillation, stroke, depression and anxiety; ask a brief sleep question at every opportunity.
• Insomnia prevention: sleep education, stress management, avoiding routine benzodiazepine prescription for normal sleep variability, keeping a regular wake time, daylight exposure.
• Apnoea prevention (weight, alcohol avoidance, nasal breathing) is on the sleep apnoea page; treat apnoea before prescribing hypnotics.
• RLS prevention: maintain iron sufficiency, manage renal disease, review aggravating drugs, pregnancy folate/iron supplementation.
• RBD early detection in high-risk groups: older men with potential dream enactment; videoconfirmation; neurology follow-up.
• Occupational and driving screening: shift workers, commercial drivers, pilots and people with sleep apnoea all need structured programmes with documented fitness-to-drive assessments.

Pregnancy. Insomnia is common in pregnancy and is not an indication for nightly benzodiazepines; start with CBT-I components and sleep hygiene, and if drug treatment is unavoidable use the lowest dose for the shortest time with obstetric liaison. RLS is very common in pregnancy (iron demand and hormonal changes) and is managed with iron repletion first (ferritin targets often higher than general population targets in pregnancy) plus non-drug measures; dopaminergic and alpha-2-delta drugs are avoided where possible and used only after risk-benefit discussion. Obstructive sleep apnoea risk rises with gestational weight and fluid; screen with STOP-Bang and manage with CPAP if positive. Narcolepsy medicines (modafinil, sodium oxybate, pitolisant, solriamfetol) carry animal-data fetal-harm concerns; decisions must be individualised with obstetrics and sleep medicine. ^[2][3]

Children. Sleep is shorter and more plastic. Night terrors and sleepwalking are common and usually benign. Insomnia in children is usually behavioural (sleep-onset association, limit-setting disorder, bed-time resistance) and managed with behavioural modification and routines, not hypnotics. Obstructive sleep apnoea in children is usually adenotonsillar and managed surgically. Narcolepsy can start in childhood; paediatric recommendations exist for sodium oxybate and modafinil (AASM 2021) and both require specialist care. RLS can be diagnosed from about 5 years old but mimic growing pains; iron first. Circadian disorders in adolescents (delayed phase) are common and respond to evening light avoidance, morning bright light and timed low-dose melatonin. Melatonin prescription practices vary by country; counsel on product quality.

Older adults. Insomnia prevalence rises but so does the harm from sedatives: falls, confusion, delirium, anticholinergic burden. CBT-I remains effective, including in the over-75s; reduce or deprescribe hypnotics where possible. Parasomnias in the elderly should prompt cognitive and movement-disorder assessment. RLS may be refractory and associated with neuropathy and renal disease. Iron studies are mandatory; dosing of any drug starts low and goes slow. Avoid drugs on the Beers criteria and check for drug-disease interactions (see insomnia section).

Immunocompromised patients are not a specific insomnia group, but nocturnal discomfort, medication effects and hospital environments disrupt sleep; preserve sleep hygiene and treat underlying causes.

• A two-week sleep diary and a careful history cost nothing and diagnose most insomnia and circadian disorders.
• STOP-Bang, neck circumference and Epworth are free bedside tools; home pulse oximetry plus a simple overnight oximeter recording screens well for apnoea where PSG is unavailable.
• Iron status (at minimum a ferritin) is cheap and high-value in RLS; if ferritin is unavailable in practice, a trial of iron in suspected iron deficiency with RLS is reasonable.
• CBT-I can be delivered in primary care via written protocols, brief behavioural advice and digital applications, where therapy services do not exist; sleep restriction should be omitted if the patient drives or has bipolar illness.
• Avoid prescribing long-term benzodiazepines or sedating antihistamines for poor sleep; they are cheap today and costly in falls, dependence and cognitive harm.
• Refer severe narcolepsy, violent RBD, refractory RLS and uncertain parasomnias to the nearest sleep or neurology service for PSG and MSLT.

• Sleep disorders are common (chronic insomnia in 5% to 10% of adults in industrialised nations) and usually multiple: take a sleep history and screen for apnoea, RLS and mood in everyone.
• Classify into the seven ICSD-3 families, then ask whether the problem is sleep itself, sleepiness, behaviour, or timing.
• Insomnia is a clinical diagnosis from history and a written sleep diary; PSG is only for suspected breathing, movement or REM-atonia sleep disorders.
• CBT-I is the first-line treatment for chronic insomnia and beats hypnotics at 6 and 12 months, without dependence; NICE NG215 and the AASM 2017 guideline both put it first.
• Hypnotics, when used, are short-term, lowest effective dose, reviewed at 4 weeks, with dependence risks explained first; AASM 2017 gives only weak suggestions, and not for (among others) melatonin, trazodone or antihistamines.
• Narcolepsy (type 1 with cataplexy and usually low orexin) needs wake-promoting medication plus anticataplectic therapy; AASM 2021 strongly recommends modafinil, pitolisant, sodium oxybate and solriamfetol for EDS, with paediatric recommendations only for sodium oxybate and modafinil. ^[2]
• Modafinil 200 mg each morning is the conventional first-line dose; sodium oxybate is effective for cataplexy but is a controlled, possibly respiratory-depressant drug, given only through REMS pharmacies.
• Non-REM parasomnias (night terrors, sleepwalking) are normal-developmental in children; management is trigger control, safety and scheduled awakenings, not medicines.
• REM sleep behaviour disorder is dream enactment with lost REM atonia; it injures patients and bed partners and often heralds neurodegeneration; AASM 2023 conditionally recommends clonazepam (0.25 to 1.0 mg at bedtime), melatonin (start 3 mg, titrate to 15 mg), pramipexole or rivastigmine in selected cases, plus meticulous bedroom safety.
• Circadian disorders are disorders of timing: treat with phase-corrected melatonin and light according to the rhythm's phase, not with nightly hypnotics.
• RLS is diagnosed by four bedside criteria; check iron, treat iron when ferritin is 75 ng/mL or less, and use alpha-2-delta ligands (gabapentin enacarbil, gabapentin, pregabalin) first; dopamine agonists are no longer standard because of augmentation (AASM 2025).
• PLMD needs over 15 limb movements per hour in adults or 5 per hour in children to meet criteria.
• Always cross-check sleep apnoea in any sleep complaint: snoring, witnessed apnoeas and resistant hypertension are the easy clues.

• Obstructive sleep apnoea and obesity hypoventilation syndrome
• Depression
• Anxiety disorders
• Paediatric neurology and sleep problems in children
• Parkinson disease and neurodegeneration
• Iron-deficiency anaemia
• Chronic pain and insomnia
• Psychotropic prescribing in psychiatry