Hypersomnia

Hypersomnia is excessive daytime sleepiness or prolonged nocturnal sleep, with inability to stay awake and alert in the major waking episodes of the day, resulting in lapses into sleep or unintended naps. It must be separated from fatigue (lack of energy without propensity to sleep), tiredness from insufficient sleep, depression, and sleep disorders, because the causes, tests and treatments differ.

It is a safety problem, since drowsy driving and workplace accidents are common, so driving and occupational risk must be assessed, a treatable cause found (insufficient sleep, sleep apnoea, drugs, medical or psychiatric disease), and central disorders of hypersomnolence identified.

Definition. Excessive sleepiness on at least 3 days each week for at least 3 months, despite a main sleep period of at least 7 hours. It is shown by any of the following:

• recurrent lapses into sleep or napping on the same day
• a nonrestorative main sleep period of 9 hours or more
• difficulty being fully awake after abrupt awakening (sleep inertia)

Excessive daytime sleepiness is commonly defined as an Epworth Sleepiness Scale score over 10 (scale 0 to 24).

Classification

• Insufficient sleep syndrome (the most common cause in adults), shift work and circadian disorders.
• Sleep related breathing disorders: obstructive sleep apnoea, central sleep apnoea, and obesity hypoventilation syndrome.
• Central disorders of hypersomnolence: narcolepsy type 1 (cataplexy or low cerebrospinal fluid hypocretin), narcolepsy type 2, idiopathic hypersomnia, and Kleine-Levin syndrome.
• Hypersomnia due to a medical disorder (hypothyroidism, encephalitis, brain tumour or injury, genetic disorders, Parkinson disease).
• Hypersomnia due to a medication or substance.
• Hypersomnia associated with a psychiatric disorder (depression, bipolar disorder, atypical features, seasonal).
• Periodic limb movement disorder and restless legs syndrome with fragmented sleep.
• Medical and neurological hypersomnia (hypothyroidism, hepatic and renal failure, hypercapnia, anaemia, hypoxia, infection, epilepsy, brain lesions).

Epidemiology. Excessive daytime sleepiness affects about 10 to 20% of adults. Obstructive sleep apnoea affects up to 10 to 20% of adults (moderate to severe in about 10%). Narcolepsy affects 25 to 50 in 100000 people, with onset typically between 10 and 25 years, and a diagnostic delay of years. Idiopathic hypersomnia is rarer. Kleine-Levin syndrome affects adolescent boys mainly.

Mechanisms. Loss of hypocretin (orexin) producing neurons in the lateral hypothalamus in narcolepsy type 1 (autoimmune in people with HLA-DQB1*06:02) leads to unstable wake and sleep states, REM sleep intrusions (cataplexy, sleep paralysis, hypnagogic hallucinations), and short sleep latency. Sleep fragmentation from apnoea or limb movements reduces sleep quality. Sleep deprivation raises homeostatic sleep pressure. Drugs and brain lesions affect arousal circuits.

Key distinctions. Sleepiness (tendency to fall asleep) must be separated from fatigue, which is a state of exhaustion without an increased tendency to fall asleep. Daytime sleepiness with sudden muscle weakness triggered by laughter suggests narcolepsy type 1. Heavy snoring, witnessed apnoeas and obesity suggest sleep apnoea. A history of chronic short sleep that resolves on holidays suggests insufficient sleep.

Long unrefreshing sleep with severe sleep inertia and no cataplexy suggests idiopathic hypersomnia. Episodic sleep of days to weeks with cognitive change and hyperphagia suggests Kleine-Levin syndrome.

History

• Sleepiness: onset, duration, severity, time of day, situations of dozing (reading, television, meetings, driving, talking), unplanned sleep attacks, refreshing or unrefreshing naps, and sleep inertia (confusion on waking).
• Driving and occupation: drowsy driving, near misses, crashes, safety critical jobs (drivers, pilots, machine operators), and legal obligations.
• Sleep schedule: bed and wake times on work and free days, total sleep, shift work, sleep debt, and long sleep on weekends.
• Cataplexy: sudden bilateral loss of muscle tone with preserved consciousness triggered by laughter, joking or surprise (knees buckling, jaw drop, head drop), lasting seconds to minutes.
• Other REM phenomena: sleep paralysis, vivid hypnagogic or hypnopompic hallucinations, fragmented night sleep, automatic behaviour, and REM sleep behaviour disorder.
• Sleep apnoea: snoring, gasping, witnessed pauses, nocturia, morning headache, dry mouth, hypertension, and weight gain.
• Restless legs and limb movement symptoms.
• Mood and psychiatric symptoms: depression, bipolar disorder, seasonal pattern, atypical depression with hypersomnia and appetite increase, and psychosis.
• Medical history: hypothyroidism, diabetes, kidney and liver disease, heart failure, epilepsy, head injury, stroke, encephalitis, HIV, Parkinson disease, multiple sclerosis, brain tumour, and genetic conditions (Prader-Willi, myotonic dystrophy).
• Drugs: sedating antihistamines, benzodiazepines, Z drugs, opioids, gabapentinoids, antiepileptics (phenobarbital, valproate, carbamazepine), antipsychotics, tricyclic antidepressants, mirtazapine, trazodone, beta blockers, clonidine, methyldopa, dopamine agonists (pramipexole, ropinirole), muscle relaxants, cannabis and alcohol. Recent stopping of stimulants.
• Onset after infection, vaccination, head injury or weight gain.
• Family history of narcolepsy and sleep disorders.
• Hyperphagia, hypersexuality, derealisation and episodic course (Kleine-Levin).

Examination

• Weight, body mass index, neck circumference, blood pressure, pulse, and oxygen saturation.
• Upper airway: Mallampati class, tonsil size, retrognathia, nasal obstruction.
• Cardiorespiratory: heart failure, cor pulmonale, hypoventilation signs, and right ventricular heave.
• Endocrine: goitre, slow reflexes, bradycardia, dry skin, macroglossia, and cushingoid or acromegalic features.
• Neurological: cranial nerves, visual fields (pituitary), pupillary reaction, tone, tremor, deep tendon reflexes (myotonia), gait, and cognition.
• Mental state: mood, apathy, psychomotor slowing, and suicidal thoughts.
• Hepatic and renal signs: flap, jaundice, pallor, and oedema.
• Bedside tests: Epworth Sleepiness Scale (0 to 24; 11 to 12 mild, 13 to 15 moderate, 16 to 24 severe), STOP-BANG, Stanford Sleepiness Scale, glucose, oxygen saturation, PHQ-9, a 2 week sleep diary, and an assessment of driving fitness.

Red flags

• Falling asleep at the wheel, near miss or crash, or safety critical occupation.
• Sudden muscle weakness with emotion (cataplexy), sleep paralysis with hallucinations.
• Severe obesity with hypercapnia, daytime hypoxia, cor pulmonale, or morning headache (obesity hypoventilation).
• Reduced level of consciousness, stupor, or coma.
• Headache, visual field defect, diplopia, vomiting, or papilloedema (intracranial mass or raised pressure).
• Recent head injury, stroke, encephalitis, seizure or focal signs.
• Fever, meningism, or recent travel (infection, cerebral malaria, trypanosomiasis).
• Myxoedema features (bradycardia, hypothermia, hyponatraemia) or hypercalcaemia.
• Hepatic or renal failure with flap, asterixis or uraemic symptoms.
• Opioid, sedative or alcohol use, or poisoning.
• Severe depression with suicidal ideation, catatonia, or stupor.
• Episodes of sleeping for days with cognitive or behavioural change in a teenager (Kleine-Levin syndrome).
• Hypersomnia in pregnancy with hypertension (pre-eclampsia) or anaemia.
• Sudden weight gain, endocrine signs, or early onset in childhood (hypothalamic lesion, craniopharyngioma, rapid onset obesity with hypoventilation).

Special groups

• Children and adolescents: narcolepsy often starts with sudden severe sleepiness, weight gain and cataplexy with facial hypotonia (cataplectic facies). Poor school performance and mood symptoms are common. Assess for sleep apnoea due to adenotonsillar hypertrophy, delayed sleep phase and insufficient sleep. Use age specific doses.
• Pregnancy: sleepiness is common. Exclude anaemia, hypothyroidism, sleep apnoea and pre-eclampsia, and avoid wake promoting drugs.
• Older adults: sleepiness may signal dementia, depression, medication effect, sleep apnoea, heart failure, or Parkinson disease.
• Shift workers: shift work disorder, with planned naps and light exposure.
• Region specific: African trypanosomiasis (sleeping sickness) and cerebral malaria in endemic areas, neurocysticercosis, tuberculous meningitis, HIV, and heavy khat or sedative use.

Lifestyle and circadian

• Insufficient sleep syndrome and chronic sleep restriction.
• Shift work disorder and jet lag.
• Delayed sleep phase disorder.
• Poor sleep habits and long sleeper (normal variant).

Sleep related breathing and movement disorders

• Obstructive sleep apnoea.
• Central sleep apnoea, including Cheyne-Stokes breathing in heart failure.
• Obesity hypoventilation syndrome.
• Periodic limb movement disorder and restless legs syndrome.
• Chronic insomnia with daytime sleepiness.

Central disorders of hypersomnolence

• Narcolepsy type 1 and type 2.
• Idiopathic hypersomnia.
• Kleine-Levin syndrome.
• Hypersomnia associated with a psychiatric disorder (depression, bipolar disorder, seasonal affective disorder).

Neurological

• Traumatic brain injury and post concussion syndrome.
• Stroke (thalamic, brainstem), brain tumour, and hypothalamic or pituitary lesion.
• Encephalitis, post infectious hypersomnia, and sleeping sickness.
• Parkinson disease, Lewy body disease, multiple system atrophy, and Alzheimer disease.
• Multiple sclerosis and myotonic dystrophy.
• Epilepsy, postictal states, nonconvulsive status.
• Prader-Willi syndrome and Niemann-Pick disease type C.
• Autoimmune encephalitis and neuromyelitis optica.
• Raised intracranial pressure and hydrocephalus.

Metabolic, endocrine and systemic

• Hypothyroidism.
• Hyperglycaemia or hypoglycaemia, and diabetic ketoacidosis.
• Hypercalcaemia, hyponatraemia, hypernatraemia and uraemia.
• Hepatic encephalopathy.
• Anaemia, iron deficiency and vitamin B12 deficiency.
• Hypercapnia from COPD or neuromuscular disease.
• Adrenal insufficiency and Cushing syndrome.
• Heart failure, chronic infection (tuberculosis, HIV), cancer, and chronic fatigue.
• Sepsis.

Drugs and substances

• Sedatives and hypnotics (benzodiazepines, Z drugs, barbiturates).
• Sedating antihistamines, antipsychotics, tricyclic antidepressants, mirtazapine, and trazodone.
• Opioids, gabapentin, pregabalin, and muscle relaxants (baclofen).
• Antiepileptics, beta blockers, clonidine, and dopamine agonists.
• Alcohol, cannabis, and withdrawal from stimulants (cocaine, amphetamine, khat) or caffeine.
• Carbon monoxide and other toxins.

Mimics

• Fatigue without sleepiness (anaemia, hypothyroidism, depression, fibromyalgia, chronic fatigue syndrome, heart failure, cancer).
• Cataplexy mimics: syncope, atonic seizures, periodic paralysis, hyperekplexia, and functional weakness.
• Apathy in dementia or frontal disease.
• Catatonia and stupor.

Step 1. Establish sleepiness and risk. Document the Epworth Sleepiness Scale, the circumstances of dozing, driving risk and occupational risk. Advise on driving immediately, since legal duties may require reporting to licensing bodies. Obtain a sleep diary for at least 2 weeks (with actigraphy where possible) to quantify sleep time and detect insufficient sleep or a circadian pattern.

Step 2. Clinical screening for the main causes. Screen with STOP-BANG for obstructive sleep apnoea, assess for restless legs, review all drugs and substances, and screen for depression (PHQ-9), bipolar disorder and thyroid disease. Elicit cataplexy and other REM phenomena. Confirm that sleep opportunity is at least 7 hours on most nights for 2 weeks (sleep extension test: if symptoms resolve, insufficient sleep is the cause).

Step 3. First line tests

• Full blood count, ferritin, urea, creatinine, electrolytes, calcium, glucose or HbA1c, liver tests, and thyroid stimulating hormone.
• Vitamin B12, folate, vitamin D, creatine kinase (myotonic dystrophy), and HIV and syphilis serology where risk exists.
• Serum bicarbonate (27 mmol/L or more suggests chronic hypoventilation), then arterial blood gas for hypercapnia.
• Urine or serum drug screen when sedative or substance use is possible.
• Pregnancy test in women of reproductive age.
• ECG and chest radiograph when cardiopulmonary disease is possible.
• Overnight oximetry for suspected sleep apnoea (screening).

Step 4. Sleep studies

• Polysomnography, attended overnight, for suspected sleep apnoea with comorbid disease, hypoventilation, limb movements, parasomnia and as the night before a multiple sleep latency test. It should show at least 6 hours of sleep.
• Home sleep apnoea testing for uncomplicated suspected obstructive sleep apnoea. Apnoea-hypopnoea index: 5 to 14 mild, 15 to 29 moderate, 30 or more severe.
• Multiple sleep latency test: 5 nap opportunities at 2 hour intervals the day after polysomnography.
• It follows at least 1 week of sleep diary or actigraphy confirming at least 7 hours of sleep, and stopping REM suppressing drugs such as antidepressants, ideally for 2 weeks or 5 half lives.
• Narcolepsy is diagnosed with a mean sleep latency of 8 minutes or less and 2 or more sleep onset REM periods (including one on the polysomnography the night before).
• Idiopathic hypersomnia is supported by a mean sleep latency of 8 minutes or less without 2 sleep onset REM periods, or a total sleep time of 11 hours or more in 24 hours (extended recording).
• Maintenance of wakefulness test (4 sessions of 40 minutes) to assess ability to stay awake and treatment response for safety critical work (mean latency under 8 minutes is abnormal, 40 minutes is normal).
• Cerebrospinal fluid hypocretin-1 (orexin) by lumbar puncture: 110 pg/mL or less (or under a third of the normal mean) supports narcolepsy type 1, when cataplexy is absent and polysomnography is difficult.
• HLA-DQB1*06:02 typing: present in about 90% of narcolepsy type 1, and in about 25% of the general population, so it is supportive but not diagnostic.

Step 5. Targeted tests

• MRI brain with pituitary and hypothalamic sequences for focal signs, headache, visual loss, hormonal abnormalities, or atypical hypersomnia.
• Electroencephalogram (sleep deprived) for suspected seizures or encephalopathy.
• Spirometry, lung volumes and maximal inspiratory pressures for neuromuscular or lung disease.
• Echocardiography for heart failure and pulmonary hypertension in sleep apnoea.
• Lumbar puncture (cell count, protein, oligoclonal bands, autoimmune and infectious tests) for encephalitis, and thick blood films and serology for trypanosomiasis and malaria in endemic areas.
• Genetic tests (Prader-Willi, myotonic dystrophy, Niemann-Pick type C) in children and young adults with a suggestive phenotype.
• Cortisol, prolactin, growth hormone axis, and gonadotropins when pituitary disease is suspected.
• Neuropsychology and cognitive testing for suspected dementia.

Interpretation. Combine history, diaries and objective testing. Many patients with sleep apnoea also have insufficient sleep, and both need treatment. The multiple sleep latency test has limited reliability, so repeat it when suspicion remains and results are borderline. Drugs, sleep deprivation and untreated sleep apnoea invalidate the test.

Limits. The Epworth scale is subjective and correlates poorly with objective sleepiness. Sleep studies are not widely available in all regions. Sleep onset REM periods occur in sleep deprivation, shift work, apnoea and REM suppressant withdrawal.

Immediate. Advise the patient not to drive or operate machinery until sleepiness is controlled, document this advice, and follow legal duties to inform licensing authorities where required. Arrange a safe plan for work. Rule out emergencies (altered consciousness, hypercapnic respiratory failure, intracranial lesion, hypothyroid crisis, hepatic encephalopathy, hypoglycaemia, poisoning).

General measures

• Regular sleep schedule with 7 to 9 hours in bed, regular wake time, and extension of sleep opportunity.
• Planned short naps (15 to 20 minutes, up to 2 daily) in narcolepsy, and avoiding naps beyond 30 minutes.
• Avoid alcohol, sedatives, heavy meals before driving, and shift work where possible.
• Weight loss, exercise, and caffeine in measured amounts (up to 200 to 400 mg daily) as short term support.
• Education about safety, driving, and employment protections. Patient organisations and counselling for children in school (accommodations).

Treatment of the cause

• Insufficient sleep: sleep extension to 8 to 9 hours for 2 weeks with review.
• Obstructive sleep apnoea: continuous positive airway pressure (auto titrating 4 to 20 cmH2O, with a mask fit and adherence of 4 hours or more on most nights; sleepiness improves in weeks).
• Weight loss (loss of 10% of body weight reduces the apnoea-hypopnoea index by about 25 to 30%), positional therapy, and mandibular advancement device for mild to moderate disease.
• Hypoglossal nerve stimulation or surgery for selected patients.
• Tirzepatide 2.5 mg subcutaneously weekly increasing every 4 weeks to 10 or 15 mg for adults with obesity and moderate to severe sleep apnoea.
• Residual sleepiness after effective treatment of apnoea is treated with wake promoting drugs. Avoid sedatives, opioids and alcohol.
• Obesity hypoventilation: noninvasive ventilation (bilevel positive airway pressure) with titration, oxygen supplementation, weight loss, and specialist referral.
• Hypothyroidism: levothyroxine 1.6 micrograms/kg orally once daily on an empty stomach in healthy adults (25 to 50 micrograms daily in older adults and in heart disease, increased every 4 to 6 weeks), with thyroid stimulating hormone monitoring at 6 to 8 weeks.
• Anaemia and iron deficiency: ferrous sulphate 200 mg orally once or twice daily for 3 months after normalisation. Vitamin B12 deficiency: hydroxocobalamin 1 mg intramuscularly on alternate days for 2 weeks, then every 3 months.
• Depression: treat with psychological therapy and an antidepressant (bupropion or an activating SSRI such as fluoxetine for atypical features). Bipolar depression: specialist treatment.
• Drug induced hypersomnia: reduce the dose, switch, or stop the drug (sedating antihistamines, benzodiazepines, gabapentinoids, antipsychotics). Do not stop antiepileptics abruptly.
• Hepatic encephalopathy: lactulose 20 to 30 mL orally 2 to 3 times daily to give 2 to 3 soft stools daily, and rifaximin 550 mg twice daily. Uraemia: dialysis assessment.
• Restless legs and periodic limb movements: iron if ferritin is under 75 micrograms/L, and gabapentin or pregabalin as the first line drugs.
• Epilepsy, tumour, stroke and encephalitis: specific treatment, with neurology and neurosurgery.
• African trypanosomiasis: specialist treatment with fexinidazole (1800 mg once daily for 4 days then 1200 mg once daily for 6 days, with food) for stage 1 or non severe stage 2, and eflornithine with nifurtimox for severe stage 2 disease.

Narcolepsy and idiopathic hypersomnia (specialist directed)

• Sleep schedule, planned naps, and cataplexy trigger awareness.
• Wake promoting drugs:
  • Modafinil 100 mg orally every morning, increased by 100 mg every 1 to 2 weeks to 200 to 400 mg daily (single morning dose or split morning and midday). Maximum 400 mg daily (100 to 200 mg in severe hepatic impairment, and in older adults start at 100 mg).
  • Modafinil induces CYP3A4 and reduces the effect of hormonal contraceptives (use a method with no interaction, and continue for 2 months after stopping).
  • Monitor for rash (stop at once if any rash occurs because of Stevens-Johnson syndrome risk), headache, anxiety, insomnia, and blood pressure. Avoid in pregnancy.
  • Armodafinil 150 mg orally every morning, up to 250 mg daily, with the same cautions.
  • Pitolisant 4.5 mg orally every morning for 1 week, then 9 mg for 1 week, then 18 mg, maximum 36 mg daily, for narcolepsy with or without cataplexy.
  • Reduce the maximum to 18 mg in moderate hepatic or kidney impairment (avoid in severe). Avoid with QT prolonging drugs and with strong CYP2D6 inhibitors; monitor ECG in cardiac disease. Pitolisant reduces the effect of hormonal contraceptives.
  • Solriamfetol 75 mg orally every morning, increased after 3 days to 150 mg (maximum 150 mg daily).
  • In kidney impairment, with estimated glomerular filtration rate 30 to 59 mL/min start 37.5 mg daily, maximum 75 mg; 15 to 29 mL/min maximum 37.5 mg daily; under 15 mL/min avoid.
  • Solriamfetol raises blood pressure and heart rate, so avoid in uncontrolled hypertension and recent cardiovascular events.
  • Methylphenidate 5 to 10 mg orally twice daily (maximum 60 mg daily), dextroamphetamine 5 to 10 mg orally in the morning increasing weekly to a maximum of 60 mg daily (divided doses). Second line, with cardiac and misuse risk.
• Sodium oxybate 2.25 g orally at bedtime and 2.25 g 2.5 to 4 hours later (total 4.5 g).
• Increase by 1.5 g each night (0.75 g for each dose) at weekly intervals to the effective dose of 6 to 9 g each night in 2 divided doses (maximum 9 g). Sodium oxybate treats cataplexy, sleepiness and fragmented sleep.
• Take it while in bed, avoid alcohol and other sedatives, avoid in succinic semialdehyde dehydrogenase deficiency, depression with suicidal thoughts, severe respiratory disease and sleep apnoea untreated, and reduce the dose by half in hepatic impairment.
• It contains much sodium (monitor in heart failure and hypertension). Monitor for respiratory depression, sleepwalking, confusion, nausea, and misuse.
• A low sodium formulation (calcium, magnesium, potassium and sodium oxybates) and a once nightly extended release formulation also exist.
• Cataplexy: sodium oxybate or pitolisant, venlafaxine modified release 37.5 mg daily increased to 75 to 150 mg, fluoxetine 20 to 40 mg daily, or clomipramine 10 to 75 mg at night. Avoid abrupt stopping because of rebound cataplexy (status cataplecticus).
• Sleep paralysis and hallucinations: usually treated with the wake promoting drugs and sodium oxybate, with explanation.
• Treat comorbid sleep apnoea, depression, and weight gain. Offer pregnancy planning advice, since drugs differ in risk.

Kleine-Levin syndrome. Supportive care and safety during episodes; lithium carbonate (start at 400 mg orally at night, titrated to a serum level of 0.6 to 1.0 mmol/L) for prevention in specialist care. Modafinil may shorten episodes. Avoid alcohol and sleep deprivation.

Special populations

• Pregnancy and breastfeeding: stop wake promoting drugs when planning pregnancy, where possible, and use scheduled naps, iron and sleep apnoea treatment. Sodium oxybate and modafinil lack safety data.
• Children and adolescents: specialist care. Modafinil is not licensed under 18 years in many places (off label use under specialist direction).
• Sodium oxybate is used in some centres (weight based, divided in 2 doses): 20 to under 30 kg start 2 g nightly, maximum 6 g; 30 to under 45 kg start 3 g, maximum 7.5 g; 45 kg or more start 4.5 g, maximum 9 g.
• Older adults: low starting doses, cardiovascular assessment before stimulants, and review of drugs and sleep apnoea.
• Kidney and liver impairment: reduce modafinil and armodafinil to a maximum of 100 to 200 mg daily in severe hepatic impairment.
• Reduce pitolisant to a maximum of 18 mg daily in moderate hepatic or kidney impairment.
• Reduce solriamfetol to a maximum of 75 mg daily at estimated glomerular filtration rate 30 to 59 mL/min and 37.5 mg daily at 15 to 29 mL/min (avoid under 15 mL/min).
• Safety critical workers: treatment and objective testing (maintenance of wakefulness test) before return.

Monitoring.

• Epworth Sleepiness Scale at each visit, with a goal of under 11 (a fall of 4 points or more is a clinically important change).
• Driving and work function.
• Adherence to continuous positive airway pressure (download data).
• Weight, blood pressure and heart rate (stimulants, solriamfetol).
• Mood and suicidality (sodium oxybate, pitolisant).
• Liver tests, ECG for pitolisant in cardiac disease, and misuse.
• Repeat the maintenance of wakefulness test for safety critical roles.

Referral and escalation. Sleep medicine for all patients with suspected narcolepsy, idiopathic hypersomnia, Kleine-Levin syndrome, sleep apnoea with complications, hypoventilation, or treatment failure. Endocrinology, neurology and neurosurgery for hypothalamic and pituitary lesions and other neurological causes. Psychiatry for mood disorders. Respiratory medicine and ENT for sleep related breathing disorders. Occupational health and driving licensing authorities for safety critical roles. Paediatric sleep services for children.

Admission criteria. Reduced level of consciousness, hypercapnic respiratory failure, suspected intracranial mass or encephalitis, severe metabolic derangement, poisoning, and suicidal ideation. Admission for polysomnography is outpatient in most cases.

Discharge and follow up. Written driving and safety advice. Review in 2 to 4 weeks after starting treatment, then every 3 to 6 months. Safety net advice: return for falling asleep while driving or at work, sudden weakness with emotion, worsening headache, visual loss, confusion, breathlessness, swelling, a new rash on modafinil, or low mood with suicidal thoughts.