📋 Key Information Summary
- Insomnia is the most prevalent sleep disorder in Australia, affecting approximately 20% of adults; cognitive behavioural therapy for insomnia (CBT-I) is first-line treatment, ahead of pharmacotherapy.
- Obstructive sleep apnoea (OSA) affects an estimated 5–10% of Australian adults and is strongly associated with obesity, cardiovascular disease, and motor-vehicle accidents.
- Central sleep apnoea (CSA) is less common and typically secondary to heart failure, opioid use, or high-altitude exposure; treat the underlying cause first.
- Polysomnography (sleep study) remains the gold standard for diagnosing OSA, CSA, narcolepsy, and parasomnias; home sleep studies are suitable for uncomplicated suspected OSA.
- Continuous positive airway pressure (CPAP) is first-line therapy for moderate-to-severe OSA; mandibular advancement splints are an alternative for mild-to-moderate disease or CPAP-intolerant patients.
- Narcolepsy type 1 (with cataplexy) is caused by orexin/hypocretin deficiency; diagnosis requires a multiple sleep latency test (MSLT) showing mean sleep latency ≤8 minutes with ≥2 sleep-onset REM periods (SOREMPs).
- Modafinil is first-line pharmacotherapy for narcolepsy-related excessive daytime sleepiness; sodium oxybate is used for cataplexy and disrupted nocturnal sleep.
- Parasomnias include disorders of arousal (sleepwalking, night terrors) and REM sleep behaviour disorder (RBD); RBD in older adults is a strong prodromal marker for synucleinopathies (Parkinson disease, dementia with Lewy bodies).
- Sleep hygiene education is a foundational component of management for all sleep disorders but alone is insufficient for chronic insomnia.
- Excessive daytime sleepiness increases road-transport risk; clinicians must consider mandatory reporting obligations under state/territory legislation (e.g., Austroads fitness-to-drive guidelines).
- Aboriginal and Torres Strait Islander Australians experience higher rates of sleep-disordered breathing and shorter sleep duration, driven by socioeconomic disadvantage and chronic disease burden.
- Melatonin (prolonged-release) is PBS-listed for insomnia in adults ≥55 years; short-term benzodiazepines and Z-drugs should be limited to ≤4 weeks due to dependence risk.
Introduction & Australian Epidemiology
Sleep disorders encompass a broad range of conditions that impair the timing, quality, or quantity of sleep, leading to daytime dysfunction and reduced quality of life. The International Classification of Sleep Disorders, Third Edition (ICSD-3) categorises sleep disorders into insomnia disorders, sleep-related breathing disorders, central disorders of hypersomnolence, circadian rhythm sleep–wake disorders, parasomnias, and sleep-related movement disorders. This guideline focuses on the four most clinically significant presentations encountered in Australian general practice: insomnia, obstructive and central sleep apnoea, narcolepsy and idiopathic hypersomnia, and parasomnias.
In Australia, sleep disorders represent a major public-health burden. The 2022 Sleep Health Foundation national survey estimated that 33–45% of Australian adults report inadequate or poor-quality sleep on a regular basis. Chronic insomnia disorder affects approximately 15–20% of the adult population, with higher prevalence in women, older adults, and those with comorbid psychiatric illness. Obstructive sleep apnoea is diagnosed in 5–10% of adults, though the true prevalence may be higher when including undiagnosed disease; the increasing prevalence of obesity (affecting 31% of Australian adults in 2022, AIHW data) is a major driver. Narcolepsy is rare, with an estimated prevalence of 20–50 per 100,000, while REM sleep behaviour disorder occurs in approximately 1–2% of older adults.
The economic impact is substantial. The Sleep Health Foundation has estimated that sleep disorders cost the Australian economy over billion annually in healthcare expenditure, productivity losses, and accident-related costs. Untreated OSA alone contributes significantly to cardiovascular morbidity, motor-vehicle accidents, and workplace injuries.
Insomnia & Basic Principles of Management
Chronic insomnia disorder, as defined by ICSD-3 and DSM-5, is characterised by difficulty initiating or maintaining sleep, early-morning awakening, or non-restorative sleep occurring at least three nights per week for at least three months, causing clinically significant distress or functional impairment. The condition is not attributable to another sleep disorder, medical condition, mental disorder, or substance use.
Classification
| Type | Duration | Typical Cause | Management Approach |
|---|---|---|---|
| Acute / short-term | <3 months | Stressful life event, jet lag, acute illness | Reassurance, sleep hygiene, short-term hypnotic if needed |
| Chronic insomnia | ≥3 months | Hyperarousal, conditioned arousal, comorbidities | CBT-I first-line; pharmacotherapy second-line |
| Comorbid insomnia | Variable | Psychiatric, pain, respiratory, medication-related | Treat comorbidity + CBT-I; avoid reflex hypnotic prescribing |
Non-Pharmacological Management — CBT-I
Cognitive behavioural therapy for insomnia (CBT-I) is the recommended first-line treatment for chronic insomnia in adults of all ages, endorsed by the American Academy of Sleep Medicine (AASM), the European Sleep Research Society, and the Australasian Sleep Association (ASA). CBT-I is superior to pharmacotherapy in the long term and does not carry dependence or rebound-insomnia risks.
Core CBT-I components include:
- Sleep restriction therapy: Limiting time in bed to actual sleep time, then gradually increasing as efficiency improves.
- Stimulus control: Use the bed only for sleep and intimacy; leave the bedroom if unable to sleep within ~20 minutes.
- Cognitive restructuring: Challenging maladaptive beliefs about sleep (e.g., catastrophising about sleep loss).
- Sleep hygiene education: Consistent wake time, limiting caffeine and alcohol, minimising screen exposure before bed, optimising bedroom environment.
- Relaxation training: Progressive muscle relaxation, mindfulness-based techniques.
Pharmacological Management
Pharmacotherapy should be considered when CBT-I is insufficient, unavailable, or when insomnia is severe and causing acute functional impairment. Short-term use (≤4 weeks) is recommended for most hypnotic agents. Long-term use requires specialist review.
Sleep Apnoea (Obstructive & Central)
Obstructive Sleep Apnoea (OSA)
OSA is characterised by repeated episodes of complete (apnoea) or partial (hypopnoea) upper-airway obstruction during sleep, resulting in oxyhaemoglobin desaturation, sleep fragmentation, and excessive daytime sleepiness. It is the most common form of sleep-disordered breathing.
Risk factors: Obesity (BMI ≥30), increased neck circumference (>43 cm males, >38 cm females), male sex, age >50 years, craniofacial abnormalities, tonsillar/adenoid hypertrophy (paediatric), family history, alcohol and sedative use, smoking, nasal obstruction, and supine sleeping position.
Severity Classification (AASM Criteria)
Diagnosis
- In-laboratory polysomnography (PSG): Gold standard; monitors EEG, EOG, EMG, airflow (nasal pressure + oronasal thermistor), respiratory effort (thoraco-abdominal belts), SpO₂, ECG, body position, and leg movements. Available at accredited sleep laboratories across Australian capital cities and major regional centres.
- Home sleep apnoea testing (HSAT): Limited-channel devices (typically airflow, respiratory effort, SpO₂) suitable for adult patients with high pre-test probability of moderate-to-severe OSA and no significant comorbidities (e.g., heart failure, neuromuscular disease, suspected hypoventilation). The Australasian Sleep Association supports HSAT as a cost-effective pathway for uncomplicated OSA.
- MBS item numbers: In-laboratory PSG — MBS item 12203 (sleep study); home-based studies may be billed under practice-based arrangements or state-funded sleep-service programmes.
Management of OSA
Central Sleep Apnoea (CSA)
CSA results from intermittent loss of ventilatory drive during sleep, without upper-airway obstruction. It is less common than OSA and usually secondary to:
- Heart failure — Cheyne–Stokes respiration is the most common pattern of CSA in Australia, occurring in 25–50% of patients with heart failure with reduced ejection fraction (HFrEF).
- Opioid and sedative use — suppresses central respiratory drive.
- Brainstem/upper cervical cord pathology — stroke, tumour, Chiari malformation.
- High-altitude exposure — transient CSA due to hypoxic ventilatory response instability.
Treatment of CSA centres on managing the underlying condition. Supplemental oxygen, acetazolamide, and phrenic-nerve stimulation are emerging therapies used in specialist settings.
Narcolepsy & Idiopathic Hypersomnia
Narcolepsy
Narcolepsy is a chronic neurological disorder of central hypersomnolence caused by loss of orexin (hypocretin)-producing neurons in the lateral hypothalamus. Prevalence in Australia is estimated at 20–50 per 100,000, with onset typically in adolescence or early adulthood. Diagnosis is often delayed by 8–15 years.
| Feature | Narcolepsy Type 1 (NT1) | Narcolepsy Type 2 (NT2) |
|---|---|---|
| Core symptom | Excessive daytime sleepiness (EDS) | EDS without cataplexy |
| Cataplexy | Present — sudden bilateral loss of muscle tone triggered by emotions (laughter most common) | Absent |
| CSF orexin-A | ≤110 pg/mL (low/undetectable) | Normal (>200 pg/mL) |
| HLA association | HLA-DQB1*06:02 positive (>98%) | HLA-DQB1*06:02 positive (~50%) |
| MSLT criteria | Mean sleep latency ≤8 min + ≥2 SOREMPs (or 1 SOREMP + CSF orexin ≤110 pg/mL) | Mean sleep latency ≤8 min + ≥2 SOREMPs |
Diagnosis
- Epworth Sleepiness Scale (ESS): Screening tool; score ≥10 suggests pathological sleepiness. Validated in Australian populations.
- Overnight PSG followed by MSLT: Must be performed the day after PSG (which should show ≥6 hours total sleep and exclude other causes). PSG excludes OSA and other sleep disorders; MSLT measures mean latency to sleep and SOREMPs across 4–5 nap opportunities at 2-hour intervals.
- CSF orexin-A measurement: Lumbar puncture for CSF hypocretin-1 level — highly specific for NT1 when ≤110 pg/mL. Available at major Australian tertiary hospitals.
- HLA typing: HLA-DQB1*06:02 — supportive but not diagnostic (present in ~20% of the general population).
Management of Narcolepsy
Treatment of Excessive Daytime Sleepiness
Treatment of Cataplexy
Idiopathic Hypersomnia
Idiopathic hypersomnia (IH) is characterised by excessive daytime sleepiness with prolonged, unrefreshing nocturnal sleep (≥10 hours) and severe sleep inertia (difficulty waking). Unlike narcolepsy, there is no cataplexy and MSLT shows mean sleep latency ≤8 minutes with <2 SOREMPs. CSF orexin-A is normal. The condition is less responsive to standard wake-promoting agents than narcolepsy. Treatment includes modafinil, dexamphetamine, or low-dose clarithromycin (off-label, modulates GABA-A receptors) under specialist supervision. Flumazenil (IV or sublingual) has shown benefit in some refractory cases but is not widely available.
Parasomnias (Sleepwalking, Night Terrors, REM Sleep Behaviour Disorder)
Parasomnias are undesirable physical events or experiences that occur during sleep entry, within sleep, or during arousal from sleep. They are classified by the sleep stage in which they arise.
Non-REM Parasomnias (Disorders of Arousal)
| Feature | Sleepwalking (Somnambulism) | Night Terrors (Sleep Terrors) |
|---|---|---|
| Sleep stage | N3 (slow-wave sleep) — first third of night | N3 (slow-wave sleep) — first third of night |
| Age group | Peak prevalence 4–8 years; ~4% of adults | Peak 4–12 years; ~2% of adults |
| Presentation | Ambulation during sleep; eyes open but blank expression; limited responsiveness; amnesia for the event | Sudden arousal with intense fear, screaming, autonomic activation (tachycardia, diaphoresis); inconsolable; amnesia for the event |
| Precipitants | Sleep deprivation, fever, stress, alcohol, sedatives, noise, full bladder | Same as sleepwalking; also overtiredness in children |
| Management | Safety measures first; reassurance; treat triggers; scheduled awakenings (paediatrics); low-dose clonazepam if frequent/injurious | Parental reassurance; safety; avoid precipitants; scheduled awakenings; rarely requires pharmacotherapy |
REM Sleep Behaviour Disorder (RBD)
RBD is characterised by loss of normal REM-sleep atonia, resulting in dream-enacting behaviours that may be violent and cause injury to the patient or bed partner. Unlike non-REM parasomnias, patients typically recall dream content and the episodes occur in the latter half of the night (when REM sleep predominates).
Critical clinical significance: RBD is now recognised as a prodromal marker of alpha-synucleinopathies. Longitudinal studies demonstrate that 80–90% of patients with idiopathic RBD will eventually develop Parkinson disease, dementia with Lewy bodies, or multiple system atrophy, with a median interval of 10–15 years from RBD onset. All patients with newly diagnosed RBD should be referred to a neurologist for baseline assessment and longitudinal monitoring.
Diagnosis of RBD
- Polysomnography: Demonstrates REM sleep without atonia (RWA) on EMG — increased phasic or tonic chin/limb EMG activity during REM. This is the diagnostic hallmark.
- Clinical history: Dream-enacting behaviours (talking, shouting, punching, kicking) reported by bed partner. Most patients are males aged >50 years.
- Exclude mimics: Obstructive sleep apnoea (can cause REM-related arousals mimicking RBD), non-REM parasomnias, nocturnal seizures, PTSD-related nightmares.
Management of RBD
Investigations — Overview
Special Populations
Pregnancy
Paediatrics
Elderly (≥65 years)
Renal Impairment
Hepatic Impairment
Immunocompromised
Aboriginal and Torres Strait Islander Health
📚 References
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