Section 1: Epidemiology and aetiology.
We spend one-third of our lifetime asleep, yet scientists are only now beginning to learn about the complexity of the neuroanatomical/neurochemical networks of sleep and the genetics of the sleep-wake cycle.
For 10-15 per cent of adults the biological state of sleep is disturbed, leading to impaired psychological, cognitive and physical functioning.
Sleep is an active process. The sleep-wake cycle of humans is slightly longer than 24 hours and has to be entrained to a 24-hour cycle. This is achieved by behaviours such as the time we go to school, work, eat, and so on. However, the two most important entrainers of the cycle are light and melatonin, with a negative feedback loop.
When the suprachiasmatic nucleus in the hypothalamus receives the light signal via the photopigment melanopsin in the retina, responsive to short wavelength (blue) light, there is suppression of secretion of melatonin from the pineal gland.
As the environmental light decreases in the evenings, melatonin starts to be secreted, followed by fall in core body temperature, conducive to sleep.2
A number of hormone secretion cycles are closely related to sleep, including growth hormone, which peaks in the early part of sleep, and cortisol, which peaks at the end of night sleep.
The two well-recognised sleep states are non-rapid eye movement (NREM) sleep, alternating in 90-minute cycles with the more primitive rapid eye movement (REM) sleep.
In general, physiological parameters, such as heart rate, respiration and BP, fall in NREM sleep and are relatively unstable in REM sleep.
Insomnia is the most common sleep complaint in primary care; 10-15 per cent of referrals to sleep centres are for insomnia.
|ICSD 2 Classification of sleep disorders1|
Section 2: Insomnia
Psychophysiological insomnia is often described as primary insomnia. Patients have heightened arousal during the day, complain of a racing mind at bed time, and have developed a negative association with sleep and bed time/the bedroom.1
The insomnia leads to impaired daytime functioning, and a risk of developing secondary depression.
Patients worry about not being able to sleep in the night and fear night time. They will often report feeling sleepy at bed time, but alert as soon as they go to bed.
Management of insomnia includes addressing underlying problems. Because secondary depression is common, a low dosage sedative antidepressant such as trazodone, amitriptyline or mirtazapine may be helpful. Hypnotics may be necessary for a short period.
Pharmacological treatment should be a short-term solution, with the focus on educating patients on sleep.
A slow-release melatonin preparation has recently been licensed for patients with insomnia over the age of 55. There is some evidence that there is reduction in melatonin secretion with age, and replacement will help with initiation and maintenance of sleep in older patients.
A common feature of patients with insomnia is the excess effort they make to sleep, which is counterproductive.
It often helps to move the focus from night time to daytime activities, especially activities they enjoy.
Several studies have shown cognitive behavioural therapy (CBT), which should include sleep restriction, to be the most effective psychological therapy for insomnia. 3,4
Primary sleep disorders
A small number of patients with insomnia have a primary sleep disorder. It is important not to miss these. The two common disorders are restless leg syndrome (RLS) and sleep-wake cycle disorders.
RLS is a sensorimotor disorder characterised by intense discomfort, mainly in the legs but can involve the arms, appearing in the evening when at rest. It produces an irresistible urge to move the limbs.1
The prevalence is 5-15 per cent, but only 10 per cent of these have persistent severe symptoms needing definitive treatment.
Secondary RLS is common in patients with anaemia, especially during pregnancy and in end stage renal disease.
Mild RLS may respond to iron supplements, if the serum ferretin level is <50 microgram/litre. Management of RLS includes applying physical counterstimuli, such as stretching, massage, hot baths and ice packs, and avoiding caffeine, chocolate and sodium glutamate.
Disorders of the sleep-wake cycle may present with difficulty in initiating or maintaining night sleep or difficulty in waking in the morning and daytime sleepiness.
Delayed sleep phase syndrome (DSP), occurs when the intrinsic sleep onset time is delayed, usually to more than two hours.
These patients may go to bed early, but despite good sleep hygiene cannot fall asleep until the early hours of the morning.1
Treatment includes appropriately timed melatonin to advance sleep onset,5 morning bright light (blue light) exposure to push sleep toward night time, or chronotherapy, a programme in which bed time is progressively delayed by three hours a day over seven days, until the desired bed time is reached.
Advanced sleep phase syndrome (ASP) is often seen in the elderly, who complain of early morning waking. Their circadian clock is advanced so that sleep onset occurs earlier than conventional sleep onset time for age.
Increasing evening bright light exposure, and lifestyle changes such as avoiding alcohol and encouraging an increase in evening social activity,will help delay the circadian phase.
Shift workers may also suffer insomnia or daytime sleepiness.
Section 3: Excessive daytime sleepiness
Excessive daytime sleepiness is defined as the inability to stay awake and alert during the day with unintentional lapses into drowsiness and sleep.1 Sleepiness must be persistent and chronic before a primary sleep disorder is considered.
The severity of symptoms can be measured subjectively by scales such as the Epworth sleepiness scale (ESS), the multiple sleep latency test (MSLT), which measures the propensity to fall asleep during the day in a sleep-inducing environment, and the maintenance of wakefulness test (MWT), which measures the ability to stay awake in a sleep-inducing environment.
Patients with an ESS score of 11 or more should be referred for further assessment.
Obstructive sleep apnoea
Obstructive sleep apnoea (OSA) is characterised by repetitive episodes of complete or partial apnoea in sleep, from upper airway obstruction, resulting in episodes of oxygen desaturation in sleep and sleep fragmentation.
Bed partners usually report loud snoring, or gasping and choking in sleep with frequent movements.
Patients report unrefreshing sleep, and progressive increase in daytime fatigue and sleepiness. Systemic hypertension is a common finding with OSA.1
The prevalence of OSA in adults aged 30-60 years of age is about 4 per cent in men and 2 per cent in women. OSA can occur in any age group, but with increasing prevalence from middle age to older age adults.
Obesity is the most common predisposing factor for OSA, but craniofacial structural abnormality such as maxillomandibular malformation is also common. Menopause, smoking, large neck size, enlarged adenoids and tonsils, and endocrine disorders, such as acromegaly and hypothyroidism, are also associated with increased prevalence of OSA. It is common in adults with Down's syndrome.1
Absence of a history of snoring or thin build does not exclude OSA.
The mainstay of treatment is continuous positive airway pressure (CPAP) at night, in addition to lifestyle changes. Surgery for OSA remains controversial.
Narcolepsy is characterised by excessive daytime sleepiness typically associated with cataplexy, sleep paralysis, hypnagogic hallucinations and disturbed sleep.6
The prevalence of narcolepsy is 0.02-0.18 per cent in western countries. Age of onset is usually between 15 and 25 years of age.
Management of narcolepsy includes general advice on sleep hygiene, weight control and lifestyle.
Most patients will need treatment with either modafinil or amphetamine-based drugs such as dexamfetamine or methylphenidiate.6
Sodium oxybate is a very effective treatment option, targeting night sleep with a positive effect on both cataplexy and excessive daytime sleepiness.
Idiopathic CNS hypersomnia
Idiopathic CNS hypersomnia is a less well-understood central cause of excessive daytime sleepiness despite sufficient sleep. Co-morbid mild depression can be present.
Treatment is with stimulant medication as in narcolepsy, but patients often do not tolerate these drugs. Spontaneous resolution of symptoms can occur, hence it is important to keep these patients under review.
Section 4: Parasomnias
Parasomnias are undesirable physical events or experiences that occur during entry into sleep, within sleep or during arousals from sleep. They encompass abnormal sleep-related movements, behaviours, emotions, perceptions, dreaming and autonomic nervous system functioning. 1
Parasomnias are common in childhood and often remit spontaneously. They become a clinical disorder when the behaviour is frequent and disruptive, causes injury or affects the physical and psychosocial health of the patient.
NREM arousal parasomnias occur on arousal from deep sleep and include sleep walking and night terrors.
Precipitants for the sleep-related behaviour include febrile illness, sleep deprivation, alcohol, OSA, medication and environmental disturbance.
However, the most common trigger is emotional stress; some young people may appear relaxed and in control, able to suppress negative emotions, with sleep opening the doors kept shut during the conscious state.7
Sleep-related sex and eating behaviour can occur as a NREM arousal parasomnia, with patients unaware of their behaviour in sleep.
Management should target the triggers sustaining these behaviours; low-dosage clonazepam is recommended for regular or intermittent use in patients at risk of injury during the parasomnia.
REM sleep disorder
REM sleep behaviour disorder (RSBD) is characterised by violent motor activity including kicking and thrashing limb movements in sleep, often leading to injury to patient or partner.
Typically patients report a change in dream content with increasingly violent dreams. Sleep studies show loss of the normal muscle atonia in REM sleep that protects us from acting out our dreams.7
RSBD usually starts after the age of 50 and is highly associated with neurodegenerative disorders categorised as synucleinopathies, including Parkinson's disease, Lewy body dementia and multisystem atrophy.
Sleep studies are indicated when RSBD is suspected.
The behaviour can be modified by treatment with clonazepam alone or in combination with melatonin.
1. American Academy of Sleep Medicine. International classification of sleep disorders, 2nd ed: Diagnostic and coding manual, American Academy of Sleep Medicine, Westchester, IL 2005.
2. Borbely A A. A two process model of sleep regulation. Hum Neurobiol 1982; 1: 195-204.
3. Soeffing J P, Lichstein K L, Nau S D et al. Psychological treatment of insomnia in hypnotic-dependant older Adults. Sleep Medic 2008; 9: 165-71.
4. Edinger J D, Olsen M K, Stechuchak K M et al. Cognitive behavioral therapy for patients with primary insomnia or insomnia associated with mixed psychiatric disorders. Sleep 2009; 32(4): 499-510.
5. Arendt J, Van Somerson E J, Appleton R et al. Clinical update: melatonin and sleep disorders. Clin Medic 2008; 8(4): 381-3.
6. Zeman A, Britton T, Douglas N et al. Narcolepsy and excessive daytime sleepiness. BMJ 2004, 329: 724-8.
7. Zaiwalla Z. Parasomnias. Clin Medic 2005; 5: 109-12.
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