Paediatric OSA affects 1–4% of children (peak age 2–8 years) and is the most commonly missed medical cause of sleep disturbance in children. It is frequently attributed to "behavioural sleep problems" without a sleep history. The key clinical clues are: witnessed breathing pauses during sleep, habitual snoring (>3 nights/week), mouth breathing, restless sleep, sweating during sleep, morning headache, and daytime behaviour or attention problems (OSA may contribute, but should not be presented as a diagnostic explanation for them). Adenotonsillar hypertrophy is a common cause, but tonsil size alone does not diagnose OSA, and the outcome of adenotonsillectomy depends on age, obesity, craniofacial/neuromuscular comorbidity and severity. Nocturnal frontal lobe epilepsy (NFLE) is the most important epilepsy diagnosis to consider in apparent parasomnias — it is highly stereotyped, occurs in clusters, and presents as bizarre hypermotor movements (thrashing, cycling, vocalisation) in the first half of the night. Unlike true parasomnias, NFLE episodes are very stereotyped (identical each time), brief (seconds to minutes), may occur multiple times per night, and can be associated with post-ictal confusion. Video recording of the episodes is extremely valuable for differential diagnosis — parents should be encouraged to use a smartphone to record episodes.

Behavioural insomnia of childhood — sleep association disorder is the most common sleep problem presenting to GPs in infants and toddlers. The mechanism is that the child has learned to associate falling asleep with a specific stimulus (parental presence, feeding, rocking) and cannot re-initiate sleep independently at the natural end of each 90-minute sleep cycle during the night. The child wakes and signals — as they do during the day when they need something — because they have never learned to self-settle. Treatment is a consistent behavioural sleep plan agreed with the family (e.g. graduated checking, parental presence fading, camping out), not medication. The sleep diary is the most important initial clinical tool — it quantifies sleep architecture, identifies behavioural patterns, and forms the baseline for measuring treatment response. Two weeks of diary data identifies whether the problem is sleep onset, maintenance, early waking, or a combination, which determines which behavioural intervention is most appropriate. Delayed sleep phase syndrome in teenagers is a genuine circadian rhythm disorder — melatonin secretion is physiologically delayed in adolescence (circadian phase delay), making it biologically difficult for teenagers to fall asleep before 11pm–midnight. This is exacerbated by blue light exposure from screens (suppresses melatonin), irregular schedules, and caffeine. It is frequently misattributed to "laziness" or "poor sleep hygiene" alone, when there is a genuine biological component.

Night terrors and nightmares are frequently confused by parents but have completely different mechanisms and management. Night terrors: NREM sleep (deep sleep, first third of night) — child is behaviourally awake (eyes open, screaming) but neurologically deeply asleep. The partial arousal from deep sleep causes the terrified behaviour without conscious awareness or memory. Attempting to wake the child prolongs and intensifies the episode. Parents should be instructed to ensure the child's safety, remain calm, and allow the episode to resolve without intervention. Nightmares: REM sleep (second half of night, after midnight in most children) — full awakening with recall of frightening dream content and immediate response to comfort. The bedtime pass technique for limit-setting sleep disorder is an evidence-based behavioural intervention — the child is given a physical "pass" (a card or ticket) at bedtime. The pass can be used once to leave the bedroom for a brief sanctioned interaction with a parent (a hug, a drink of water). If the child uses the pass, it must be returned and cannot be used again. Having the pass can reduce bedtime curtain calls, even though the pass is rarely used — the child's anxiety is reduced by knowing they could leave the room if they wanted to. The behavioural principle is escape extinction with a safety valve.

Iron deficiency is one of the most overlooked treatable causes of paediatric sleep disruption — ferritin <50 μg/L is associated with restless legs syndrome (RLS) in children, frequent night waking, and increased periodic limb movements in sleep. A ferritin threshold of <50 μg/L is used in some paediatric sleep and restless-legs pathways but is not a universal NICE primary-care standard. If RLS is suspected, check FBC and ferritin and discuss iron replacement with paediatrics/sleep medicine if ferritin is low or borderline — paediatric dosing and duration are weight-based and iron toxicity is serious. The FBC may be normal. RLS in children presents as growing pains (bilateral leg discomfort, worse at night, relieved by movement) — it is frequently dismissed as "growing pains" without further investigation. The BEARS screening tool takes 2 minutes to complete in a consultation and systematically covers all aspects of paediatric sleep in an age-appropriate way. It is available free online and on most RCPCH resources. BEARS is a screening framework rather than a diagnostic test; using it at the start of a sleep consultation structures the history and identifies the dominant problem domain (bedtime, daytime, awakening, regularity, snoring) which then directs the management strategy.

The most important referral decision in paediatric sleep is recognising OSA and referring to ENT — because unlike behavioural sleep problems (which respond to GP-led intervention), OSA requires surgical or CPAP intervention that only ENT can provide. Delaying OSA diagnosis and treatment has significant consequences: sustained intermittent hypoxia during the key brain development years (ages 2–8) may contribute to neurocognitive, attention and behavioural difficulties. OSA can contribute to attention and behavioural problems in some children, which may improve with treatment, but it should not be presented as a diagnostic explanation for ADHD. Health Visitor sleep support services are the most appropriate first referral for infant/toddler behavioural insomnia — they provide structured support for behavioural sleep plans, sleep hygiene, and parental coping, and are far more accessible than CAMHS. Local commissioned children's sleep services vary by area — the GP should be familiar with local pathways. The Sleep Charity (thesleepchari​ty.org.uk) provides a national helpline and resources for parents and professionals.

Behavioural interventions, including graduated extinction, have good evidence for reducing night wakings and improving parental wellbeing, but evidence and acceptability vary between methods and families — some prefer parental presence fading, camping out or other responsive approaches. The widely cited concern that "crying it out" causes emotional or psychological damage is not supported by any longitudinal research — studies following children into adulthood show no difference in attachment, emotional adjustment, or behaviour between children who underwent graduated extinction and those who did not. The key is parental consistency — inconsistent application (responding on some nights but not others) reinforces the behaviour through intermittent reinforcement, making it harder to extinguish. The biggest barrier to success is parental consistency, which requires GP support and reassurance. The scheduled waking technique (proactive awakenings) for night terrors and sleepwalking works by disrupting the deep NREM stage 3 sleep that precedes the partial arousal. By briefly waking the child about 15 minutes before the usual episode time, the normal sleep architecture for that cycle is disrupted, preventing the typical parasomnia trigger. It is an option when episodes are predictably timed, but evidence and practicality vary.

In UK practice melatonin is used (usually specialist-initiated) as a treatment option for insomnia in children with neurodevelopmental conditions (primarily ASD and ADHD) where non-pharmacological approaches have been tried and failed. The evidence base (including the MENDS trial — Gringras et al., BMJ 2012) supports efficacy specifically in neurodevelopmental populations. For children without neurodevelopmental conditions, the evidence is weaker and melatonin is not recommended as routine treatment. The Circadin product (prolonged-release melatonin 2 mg) has a UK marketing authorisation specifically for insomnia in patients over 55 — its paediatric use is off-label except for Slenyto (melatonin 1 mg and 5 mg prolonged-release), which has a specific paediatric licence for ASD and Smith-Magenis syndrome in children 2–18 years. Shared care arrangements between paediatrics and GPs for melatonin prescribing vary by ICB — GPs should follow their local shared care protocol. Antihistamines are the most commonly used but completely inappropriate pharmacological "remedy" for childhood sleep problems — the evidence shows they are not effective for sleep induction in children, can cause paradoxical excitability in toddlers, and cause hangover sedation that impairs daytime cognitive performance.

The social jet lag phenomenon (irregular wake times on weekends vs weekdays) is one of the most modifiable contributors to adolescent sleep problems and school performance. A 2019 meta-analysis showed that social jet lag >2 hours (waking 2 hours later on weekends than weekdays) is associated with significantly worse academic performance, higher rates of depression, and increased obesity risk. The mechanism is the same as transmeridian jet lag — the circadian clock is shifted to a later phase by the late weekend wake time, making Monday morning waking feel like 5am to the body. The practical advice is to keep weekend wake times reasonably close to weekday wake times. Energy drinks in children and teenagers are a significant and underaddressed public health concern — most UK retailers voluntarily stopped selling high-caffeine energy drinks to under-16s in 2018, and the government confirmed in July 2026 that a statutory ban on sales to under-16s in England will be introduced (expected April 2027). Despite this, many teenagers still consume energy drinks, which contain 160 mg of caffeine per 500 ml plus synergistic stimulants (guarana, taurine). Asking about energy drink consumption is a high-yield sleep hygiene question for adolescents that is frequently omitted.

Regular melatonin review, with any cessation trial led by the specialist, is important — melatonin prescriptions for children with ASD and ADHD are frequently continued indefinitely without review. The natural history of sleep problems in many neurodevelopmental conditions is improvement with age (as children mature and their sleep architecture becomes more adult-like). Melatonin should be reviewed regularly for ongoing need and benefit, with any dose reduction or cessation trial led by the specialist and individualised, per the local shared-care protocol. Many GPs perpetuate melatonin prescriptions from a specialist initiation years previously without review — this does not reflect good practice and denies the child an opportunity to demonstrate whether they still need the medication.