Sleep disorders

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chapter 43 Sleep disorders

INTRODUCTION AND OVERVIEW

As the quantity and quality of our sleep influences how we feel and function during the day, there is increasing awareness of the significant impact that disorders of sleep have on patients and society as a whole. Sleep disorders affect not only our day-to-day functioning, but also have medical morbidity and mortality consequences, as well as societal and economic costs. For example, both obstructive sleep apnoea and periodic limb movements with concomitant sleep disruption lead to excessive daytime sleepiness which in turn is associated with driving and industrial accidents. The most common sleep disorder, insomnia, is associated with daytime fatigue and impaired memory, alertness, motor performance and mood. Furthermore, recent research has found that sleep loss may have significant effects on mental health and the cardiovascular, immune and endocrine systems, contributing to hypertension, increased risk of cerebrovascular accident, obesity and diabetes.

There are many types of sleep disorders, with different aetiologies, presentations and treatments. Generally, sleep disorders can be classified into one of four groups: hypersomnias, parasomnias, insomnia and sleep–wake schedule disorders. Some sleep disorders need to be referred to a specialised sleep disorders clinic for diagnosis and treatment. Other sleep problems can be diagnosed and managed within general practice and will be emphasised in this chapter.

In the first part of this chapter we provide a brief introduction to the sleep process. In the second part, we outline sleep disorders such as obstructive sleep apnoea, narcolepsy and sleep-related movement disorders, bruxism and the parasomnias, which require referral to a specialised sleep centre. In the final part we describe the diagnosis and management of the more common but heterogenous sleep disorders of insomnia and sleep–wake schedule disorders. More detailed accounts of all these areas are available.1

THE NATURE OF SLEEP

It seems that the general public, as well as those with sleep disorders, believe that normal sleep is a long, continuous period of unconsciousness/inactivity. When asked to draw a graph to represent normal sleep, most people draw a U-shaped curve, with many hours of continuous deep sleep in the middle of the sleep period. This belief not only is incorrect, but will be worrisome when the person experiences awakenings in the middle of the night, and may lead to the development of insomnia.

Sleep research over the past 50 years has confirmed some interesting and very important facts about the nature of the sleep process. A state of sleep was discovered during which the sympathetic nervous system (‘fight-or-flight’ mechanism) was activated. It has variously been called activated, paradoxical and dreaming sleep, but now officially is termed rapid eye movement or REM sleep. One of its interesting characteristics is that it occurs in about four or five discrete episodes (only a few minutes long initially, up to 30–40 minutes in duration later) spaced about 90 minutes apart during a normal sleep period. But most of our sleep (80%) occurs between these REM sleep episodes. This non-REM state of sleep has been subdivided into different stages based on the variety of EEG cortical activity, from light (easily awoken, sleep not perceived) Stage 1 sleep to the deepest or behaviourally non-responsive Stage 4 sleep. The 90-minute non-REM/REM sleep cycles repeat four or five times during the nocturnal sleep period in a roller-coaster type pattern, as illustrated in Fig 43.1.

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FIGURE 43.1 A typical journey through the stages of sleep, as indicated by the solid red line, in the sleep period of a healthy young adult. Note that stages 3 and 4 are more prominent early, and REM sleep and brief awakenings later in the period.

An intriguing aspect of this typical sleep pattern is the spontaneous lightening of sleep at the end of each deep sleep phase. As a result of this 90-minute cycle of lighter sleep throughout the sleep period, awakenings out of this lighter sleep are normal events. Even children and adolescents who normally sleep ‘soundly’ have these awakenings but they are usually brief and not recalled. Normal ageing results in sleep becoming lighter, with more awakenings that are more likely to be remembered. Therefore, awakenings are a normal part of the sleep period, particularly in more mature individuals, but need not have any detrimental impact on daytime functioning.

Another curious aspect of sleep is that we cannot directly perceive our own sleep. Therefore, judgments about time spent sleeping are often incorrect. Our minds are usually active, with some fleeting images and thoughts, during sleep. When we awaken we may be aware of only the last vestiges of this activity because earlier thoughts are not stored in long-term memory. People with chronic insomnia are more likely to attribute these thoughts, incorrectly, to the state of being awake.2 Therefore two awakenings—for example, an hour apart—may seem to be a continuous hour of wakefulness rather than two brief, separate awakenings, thus leading to an underestimation of total sleep time. Because multiple awakenings become more common with age, there is an increased vulnerability to underestimating sleep time, concern about sleep and the likelihood of developing insomnia.

BIOLOGICAL DETERMINERS OF SLEEP PROPENSITY

Sleep homeostasis

Sleep acts like other basic biological drives regulating such processes as nutritional balance (hunger/eating), in that sleep drive or pressure builds steadily the longer we are awake (go without sleep) and decreases or is satisfied by sleeping. Young adult humans strike a balance of sleep and wakefulness in a ratio of about one to two, or about 8 hours asleep to 16 hours awake on average. Some individuals naturally require less sleep (6–7 hours), while others show signs of insufficient sleep if they do not get at least 8–9 hours.

Circadian rhythms

Independent of the sleep homeostasis mechanism, another major influence on sleepiness/alertness arises from our circadian (circa = about, dia = a day) or 24-hour rhythms.3 Virtually all our physiological, biochemical and hormonal measures show circadian variation—that is, variation from peak to trough (minimum) and back to peak, taking about 24 hours to complete a full cycle. To some extent they are influenced directly by the 24-hour external environment (night/day) and our behaviour. However, free of all these influences they are shown to be endogenous. The circadian timing of these rhythms is controlled by a small nucleus in the hypothalamus of the brain, the suprachiasmatic nucleus (SCN). For example, the SCN signals the peripheral vasculature to vasodilate at about 8 pm, starting the process of decreasing core body temperature to its trough at about 4–5 am. The SCN signals the pineal gland to start manufacturing and secreting the hormone melatonin at about 9 pm and to stop its activity at about 4 am. Likewise, many other biological rhythms are kept in synchrony, a main function of which is to maximise sleepiness at night and alertness during the day, for us diurnal-adapted humans.

Maximum circadian alertness occurs at about the time of core temperature peak (6–9 pm for most individuals) and maximum circadian sleepiness is at the trough of core temperature (about 4–5 am). A few hours later (9–11 am), alertness increases again. Thus most individuals would have a circadian sleep-conducive zone from about 11 pm to about 7 am. The variation of circadian temperature, melatonin and sleepiness for a normal sleeper is illustrated in Fig 43.2.

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FIGURE 43.2 For a normally good sleep between 11 pm and 7 am, the figure shows the associated circadian variation of core body temperature (dashed line), melatonin (dotted line), and sleep propensity (solid line).

However, this ‘sleepy’ zone is bracketed by ‘alert’ zones (one normally in the early evening and one in the later morning), which can be problematic if the timing of the circadian system comes adrift. For example, if the circadian timing is delayed by 2–3 hours, the evening alert zone may span the time when sleep is intended (e.g. 11 pm) and thus inhibit sleep. Alternatively, an early-timed circadian rhythm may wake an individual prematurely before sufficient sleep is obtained.4

The SCN, serving as the central body clock, receives its main sensory input from the optic nerve, arising from retinal ganglion cells. Retinal light stimulation, particularly at the blue end of the spectrum, is capable of re-timing the SCN clock. Considerable research has shown that light stimulation before the core body temperature minimum produces a delay of the circadian timing and, conversely, light stimulation after the core temperature minimum results in a shift of the clock to earlier times. Therefore, a sleep difficulty resulting from circadian timing gone astray may be treated with appropriately timed light stimulation. For example, sleep-onset insomnia arising from a circadian delay can be treated with morning bright light, and the opposite timing problem, early morning awakening insomnia arising from an abnormally early timed circadian rhythm, can be treated with evening bright light.

Although the SCN signals the pineal gland to secrete melatonin during the night, the SCN is also sensitive to melatonin feedback and can be influenced in its timing if melatonin is administered exogenously outside the normal sleep period. Melatonin administered several hours before typical sleep onset (e.g. 5–7 pm) can advance the circadian rhythm (reset to an earlier time). Conversely, melatonin administered late in the typical sleep period (e.g. 5–8 am) can delay circadian rhythms along with the circadian sleep-conducive period. Thus both bright light and exogenous melatonin can be used in a ‘push–pull’ manner to readjust circadian timing. (These sleep disorders and treatments are elaborated upon later, in the sections on insomnia and circadian rhythm sleep disorders.)

NORMAL PSYCHOLOGICAL AND BEHAVIOURAL DETERMINERS OF SLEEP PROPENSITY

Sleep propensity can also be influenced by a myriad normal psychological and behavioural variables, including learned responses, perceptions of danger/safety, ingestion of stimulants/sedatives and physical activity/inactivity. For example, if the tendency to fall asleep while watching a favourite television program happens frequently, it can become a learned or conditioned sleeping response. The opposite tendency, for people with insomnia to become alert when attempting to fall asleep despite being sleepy before bedtime, is also a conditioned response. An awakening at night may be perceived as a potential threat for its negative impact on meeting obligations the following day. The brain’s threat response or ‘fight-or-flight’ system will be activated, resulting in increased physiological activation and alertness inhibitory to sleep. Furthermore, if this perceived threat and subsequent fight-or-flight response occurs frequently enough in the same circumstances, it can become a conditioned response to that occasion of awakening and, therefore, occur automatically regardless of any subsequent daytime obligations. This process describes the putative conditioned or learned basis of ‘psychophysiological insomnia’ assumed to be present in most cases of chronic insomnia.

THE IMPACT OF SLEEP UPON HEALTH

An adequate amount of good-quality sleep on a regular basis is crucial to physical and mental wellbeing. It should be considered one of the ‘big three’ health promoters, in addition to nutrition and exercise. However, unlike eating and exercise, over which we have direct control, sleep cannot be forced. In fact, trying hard to sleep can be counter-productive. Providing the right behavioural and mental conditions for sleep is the best approach to prevent the development of sleep disorders.

Chronic sleep problems can have a negative impact on health but, equally, chronic health problems can affect sleep. For example, factors predicting the later development of insomnia include being overweight (35% more likely than average), physical inactivity (42%), alcohol dependence (75%) and having a joint or lower back disorder (195%).5 Having a major psychiatric disorder increases the risk eight-fold. Managing the sleep problem in such situations therefore requires attention to the underlying health problem.

The mismanagement of sleep problems and the overuse of sedatives can also have a negative impact upon health.6,7 Only a small proportion of patients taking sleeping pills regularly will note improvement in their insomnia in the long term. A higher proportion will report that their insomnia is worsened by them, despite the fact that the person soon finds themselves unable to sleep without them. Sleep medications can also be associated with a worsening of depression and reduced energy. Using pharmacological methods alone for management of long-term insomnia is an inadequate and incomplete solution.8 Sleeping tablets also accumulate in the body, particularly in the elderly for whom the half-life of the drugs is far longer, and are associated with other problems such as falls, drowsiness and lowered life expectancy.

LIFESTYLE FACTORS AND SLEEP

Education

As the problems associated with poorer sleep become more recognised, educating people from an early age as to what constitutes healthy sleep (as illustrated in Fig 43.1), and helping a person with sleep problems to understand the ways in which they can improve sleep, is an increasingly important role for the general practitioner.

Stress management

The two-way links between poor sleep and poor mental health are now well established. Depression and anxiety produce effects on various stress hormones including cortisol and catechols, which also have a negative impact on sleep patterns.9 The vicious circle of stress leading to poor sleep, lowered mood and more stress is a common one in our community.

It has been a common assumption in medical circles that sleep disturbance is secondary to depression, which is true, but evidence also suggests that it goes the other way as well. If a detailed chronological history is taken from a patient with depression, it is often found that sleep disturbance precedes the onset of lowered mood.10–12 Because a patient may present with concerns about the mood, the underlying role of sleep may be undervalued. Chronic insomnia nearly trebles the risk of depression, and in one study was found to be second only to recent bereavement as a risk factor and was a more significant risk factor than having had a previous episode of depression.13 Another study put the risk for depression at four times greater for women and twice as great for men if they suffered from long-term insomnia.14

Some studies suggest that, if people with depression undertake effective behavioural strategies for improving sleep, the depression will resolve in 57% of people and be improved by more than 40% in another 13%.15 These kinds of findings have been replicated in other studies on other behavioural interventions for insomnia in those with depression.16

Therefore, the management of sleep problems always needs to take mental health into account, and the holistic management of mental health problems always needs to include sleep.

Exercise

Being active during the day and exercising regularly will tend to improve sleep at night and wakefulness in the day.17,18 Some people find that vigorous exercise close to bedtime has a negative effect on sleep, because of sympathetic nervous system (SNS) activation. A solution can be to exercise earlier or to have a period of quiet activity between exercising and going to bed.

In the absence of chronic fatigue syndrome or other significant medical conditions, there are many people who oversleep and yet feel chronically tired. It would be easy to believe that the solution is to get more sleep, whereas it is likely that a better solution would be to include more activity in one’s daily life and not to sleep past what the body and mind need. (This will be explored in more detail later.)

Nutrition

An increasing number of people these days try to boost their available energy with stimulants such as caffeine and ‘energy drinks’. Unfortunately, these can exacerbate the original problem. Quality sleep is the optimal and natural way to replenish energy and is of central importance to our mental and physical health. Minimising caffeine and avoiding it entirely for up to 6 hours before bedtime, and avoiding alcohol abuse, are two of the simplest steps to help many people improve their sleep.

Tryptophan is a precursor to melatonin, so tryptophan-rich foods such as seaweed products or milk can boost melatonin levels, as can calorie restriction and foods rich in calcium, magnesium, vitamin B6 and niacinamide.

Connectedness

A number of potential sources of distress (e.g. loss of job, marital difficulties, bereavement) will normally trigger the ‘flight-or-flight’ mechanism and lead to shortened sleep and more awakenings. Rather than ruminating about the sleep problem, it may be more effective to resolve the underlying issue with problem-solving behaviour or counselling. The sleep problem, if of short duration, is likely to resolve in response to this approach.

However, a sleep problem can remain long after the precipitating problem has gone. This suggests the presence of conditioned insomnia, which can be addressed by the non-drug techniques discussed later.

Environment

Obviously, a noisy, light or unsettled environment is not conducive to good sleep patterns. For example, living on a main road or near an industrial area or major building works, or having a noisy dog next door, can be problematic for some people. Ear plugs and eye shades can be useful in these conditions. Most important is to avoid becoming angry or distressed about the noise, as this is more likely to disturb sleep than the noise itself.

Having adequate sunlight during the day and avoiding bright light close to bedtime or if you happen to wake during the night is important for having adequate melatonin levels at night.19,20

SLEEP DISORDERS

A large range of sleep disorders will be evident in general practice. It is important to be attentive to the clinical signs of these various disorders in order to provide appropriate diagnosis and treatment. Some sleep disorders are diagnosed and managed better at specialist sleep disorders units, and others can be managed within general practice using a range of behavioural and cognitive techniques.

SLEEP DISORDERS REQUIRING REFERRAL

In this section we outline a range of sleep disorders that are best referred to a specialist unit for confirmation of diagnosis and initial treatment. Table 43.1 summarises the most common clinical symptoms and how they relate to the different sleep disorders outlined below.

TABLE 43.1 Clinical symptoms, possible diagnosis and clinical management decisions

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Sleep disorders such as obstructive sleep apnoea, periodic limb movements in sleep, restless legs syndrome, narcolepsy, parasomnias and REM sleep behaviour disorder are diagnosed by clinical symptoms and overnight polysomnography (PSG) and should be referred to a sleep disorders unit for diagnosis and initial management. Overnight PSG involves an appointment to sleep in a motel-like room in a sleep disorders unit, usually associated with a hospital. Various sensors are attached to the skin of the head to measure brain waves (EEG), eye movements (EOG) and muscle tension (EMG), the finger or earlobe for blood oxygen saturation; a nasal cannula is used to measure nasal pressure during respiration, chest and abdominal pressure transducers measure breathing, and a sleep position sensor is used. These sensors are connected by thin wires to a box at the bed head and recorded on computer for subsequent analysis. Although this procedure appears intrusive, most patients obtain close to their usual sleep. (Contacts for these services can be found in the Resources list.)

Obstructive sleep apnoea

Obstructive sleep apnoea (OSA) is characterised by repetitive episodes of upper airway collapse and obstruction of airflow during sleep. These events can result in reductions in blood oxygen saturation and are usually terminated by brief arousals from sleep.21

Prevalence

OSA can occur in any age group, but in adults the prevalence rate for mild OSA has been estimated at 24% in men and 9% in women, and for moderate to severe OSA, 4% in men and 2% in women.21,22 The prevalence rate increases with age, with a higher rate in overweight middle-aged males and in women after menopause.

Diagnosis

Clinical symptoms include excessive daytime sleepiness and fatigue despite apparently adequate sleep time. Other clinical symptoms that are usually reported by the bed partner are heavy snoring and/or choking sounds, cessation of breathing for short periods (10–30 seconds) with resumption by gasping for breath. The patient may complain of a dry mouth and headache on awakening in the morning. An overnight PSG will report abnormalities of sleep architecture, the number of respiratory events per hour of sleep time and amount of oxygen desaturation.

Management

Lifestyle changes such as avoiding alcohol in the evening, losing weight, quitting smoking and using special pillows or devices to avoid sleeping on one’s back can help in treating OSA. If appropriate, one conservative treatment is an oral appliance to keep the airway open during sleep. If these conservative methods are ineffective in preventing obstruction of airway and decreasing daytime sleepiness, continuous positive airway pressure (CPAP) is usually recommended by the sleep physician. This involves wearing a nasal mask attached to an air pump to produce a mild positive airway pressure and is usually successful at maintaining airway patency and allowing unobstructed breathing during sleep. In some cases surgical procedures are recommended.

Obstructive sleep apnoea in children

OSA is surprisingly common in children (1–10%) and presents some clinical symptoms similar to those of adults (e.g. snoring, choking, daytime sleepiness) with additional daytime symptoms of hyperactivity, difficulty concentrating, excessive irritability, behaviour problems, meal refusals, failure to thrive and enuresis. The overlap of many clinical symptoms with those of attention deficit hyperactivity disorder (ADHD) can lead to an incorrect ADHD diagnosis and potentially inappropriate pharmacotherapy. Overnight PSG can provide a differential diagnosis. The most common aetiology of OSA in children is enlarged tonsils and adenoids. Adeno-tonsillectomy is, therefore, the most common and successful treatment for OSA and its associated symptoms in these children.

Narcolepsy

Narcolepsy, a disorder of excessive daytime sleepiness, is a rare, chronic, neurological disorder with prevalence rates in the United States and Europe of approximately 1 in 2000 people.23 Age of onset is typically adolescence or young adulthood.

Diagnosis

Narcolepsy is characterised by excessive and overwhelming daytime sleepiness temporarily relieved by a brief sleep. An adequate bed period at night but somewhat disrupted sleep is usually reported. Narcolepsy may be accompanied by cataplexy that is characterised by sudden weakening of large skeletal muscles provoked by emotional response, for example, elation, laughter, surprise or anger.21 The loss of muscle tone may range from a mild sensation of weakness to complete paralysis and collapse. Hypnagogic hallucinations and sleep paralysis are also associated with ‘narcolepsy with cataplexy’. An overnight PSG and a daytime multiple sleep latency test are commonly used in the diagnosis of this disorder.

Management

Sleep physicians may use stimulants during the day and hypnotics at night to control excessive daytime sleepiness, and antidepressants to ameliorate cataplexy. Lifestyle changes that may be useful include a regular bedtime schedule, and avoiding caffeine and alcohol within 6 hours before bedtime. Short, regular daytime naps are also recommended to ameliorate the sleepiness symptoms. This may require negotiation with schools and employers to modify class/work schedules, with the added benefit of informing those in the patient’s social environment of the presence of a medical, rather than motivational, condition.

Sleep-related movement disorders

Sleep-related movement disorders include the conditions of restless legs syndrome (RLS), periodic limb movements in sleep (PLMS) and sleep-related bruxism, all of which can affect sleep quality and daytime functioning.

Restless legs syndrome

Restless legs syndrome (RLS) is a sensorimotor disorder characterised by uncomfortable sensations in the legs, such as aching or internal itchy or burning feelings, that causes an irresistible urge to move the legs. These unpleasant feelings are most noticeable and problematic in the evening or whenever the person is trying to relax, but then often decline during the early morning period, suggesting a circadian influence. RLS can therefore prolong sleep onset and contribute to insomnia. PSG findings have demonstrated fragmented non-REM and REM sleep in individuals with RLS.24

Prevalence

RLS is reported by 5–10% of the population and occurs up to two times more commonly in women than in men.21 A recent survey found that clinically significant RLS, occurring at least twice a week and causing moderate distress, occurs in almost 3% of the population.25 RLS is generally idiopathic, and in 40–60% of cases there is a familial association. RLS may also be symptomatic of such associated conditions as peripheral neuropathies, uraemia, iron deficiency, diabetes, Parkinson’s disease and pregnancy.26

Diagnosis

RLS can be diagnosed by the presence of clinical symptoms and further evaluated using an immobilisation test, which is generally carried out in a sleep disorders unit.

Management

Treatment options include both behavioural and pharmacological approaches. Lifestyle changes of possible benefit include a balanced diet and avoiding caffeine, nicotine and alcohol in the evening. RLS appears to respond to dopaminergic agonists as short-term therapy.27 Because RLS is strongly associated with periodic limb movements in sleep (see below), the diagnoses and treatment of both would best rely on PSG and sleep physician respectively at a sleep disorders unit.

• Hot baths help some patients.
• Exercise early in the day.
• Magnesium supplementation may reduce symptom severity.28
• Assess for and correct iron deficiency (restless legs may be associated with iron deficiency).

Periodic limb movements in sleep

Periodic limb movements in sleep (PLMS) are characterised by periodic episodes of repetitive (every 20–40 seconds) short bursts (0.5–5 seconds) of limb movements that occur during sleep.21 They arise from dorsiflexion of the ankle and toes and a partial flexion of the knee. PLMS may sometimes occur in the arms. Although typically the individual is unaware of these movements, they can be associated with a cortical arousal or an awakening and hence lead to sleep onset and/or sleep maintenance problems and concomitant daytime sleepiness and fatigue.21

Prevalence

The prevalence of PLMS is estimated to be 4–11% in adults, with PLMS occurring in 80–90% of people with RLS.21,29 A large cross-sectional European study found that factors associated with PLMS are female gender, shift work, caffeine intake and stress.30

Diagnosis

Although clinical symptoms may be acutely evident to a bed partner, who may suffer from sleep disturbance from the frequent movements, diagnosis should be confirmed with PSG measured as the number of PLMS per hour of total sleep time.21

Management

Lifestyle measures that target the associated factors include reducing caffeine and nicotine intake, and stress management. One study has shown that magnesium supplementation can help. Most treatments use the newer dopaminergic medications that have been found to fully suppress PLMS. However, these potent drugs should be used cautiously as they are not free of side effects, including daytime augmentation of RLS symptoms.21

Sleep-related bruxism

Sleep bruxism (SB) is characterised by grinding or clenching of the teeth during sleep and is usually associated with cortical arousals but rarely full awakenings.21 It is associated with temporomandibular pain, headaches and tooth wear.

Prevalence

Prevalence is highest in childhood (14–17%) and then decreases over the lifespan to about 3% in older adults.21 A large cross-sectional survey found that risk factors for SB include OSA, loud snoring, heavy alcohol consumption, caffeine consumption (> 6 cups), smoking, anxiety and stress.31

Diagnosis

The condition is diagnosed from EMG during a clinical PSG. Bruxism occurs more frequently in the lighter stages (Stages 1 and 2) of sleep.

Management

The management of SB includes pharmacological (clonazepam), psychological and occlusal therapeutic approaches.32 Occlusal splints, fitted by a dentist, appear to be a more symptomatic treatment option. Psychological therapies have used biofeedback, relaxation, hypnosis, counselling, sleep hygiene and lifestyle changes. A recent study compared the effectiveness of an occlusal splint to cognitive–behavioural treatment (CBT) for sleep bruxism.32 The CBT comprised progressive muscle relaxation, nocturnal feedback and stress-management training. Both groups experienced significant reductions in SB activity and associated symptoms as well as improved psychological measures.

Parasomnias

Parasomnias are undesirable physical events or experiences that occur during entry into sleep, within sleep or during arousal from sleep. They involve sleep-related behaviours and experiences over which there is no conscious, deliberate control.21 These events can be injurious to the patient and others and can produce a significant disruption of the sleep–wake pattern. This section discusses the more common parasomnias including NREM disorders such as sleep terrors and sleepwalking, and parasomnias associated with REM sleep such as nightmares and REM sleep behaviour disorder (RBD).

According to the International Classification of Sleep Disorders21 only RBD requires PSG for a diagnosis, although an overnight sleep study can confirm a clinical diagnosis of other parasomnias and rule out other disorders, such as epilepsy. Diagnosis of other parasomnias requires a clinical interview with the individual and a family member to elucidate the description, timing, frequency and duration of the behavioural event.

Non-REM: sleep terrors and sleepwalking

Sleep terrors and sleepwalking are disorders caused by partial arousal from slow-wave sleep and therefore typically occur 1 to 3 hours after sleep onset, when slow-wave sleep is usually most prominent.33 Apart from diminished alertness, both are associated with amnesia for the event. They are common in childhood and decrease in incidence during early adolescence, when slow-wave sleep declines.

Sleep terrors are accompanied by a cry or piercing scream and behavioural manifestations of intense fear such as dilated pupils and pallor of the skin.21 Sleepwalking (somnambulism) consists of a series of complex behaviours such as walking about in a lowered state of consciousness, and impaired judgment.21

As both sleep terrors and sleep walking are associated with irregular sleep schedules, sleep deprivation and psychosocial stress, helpful actions include increasing time in bed and a regular sleep pattern.33 Adults experiencing sleepwalking and sleep terrors may also have a past or current history of depression or anxiety; however, control of these psychiatric disorders does not control the parasomnias.21 A recent study has found that sleep-disordered breathing is associated with parasomnias, with respiratory effort leading to a number of arousal reactions occurring in slow-wave sleep.34 Referral to a sleep disorders unit and PSG may be indicated in this instance.

REM: nightmares

Nightmares are characterised by awakening primarily from REM sleep, experienced as disturbing mentations.35

Prevalence and diagnosis

Up to 50% of children between 3 and 5 years of age experience nightmares severe enough to disturb their parents.21 In adults, 50–85% report experiencing at least an occasional nightmare.21 Because nightmares typically arise during REM sleep, they usually occur in the latter half of the night when REM propensity is high. Numerous studies have indicated that nightmares are associated with increased life stress, anxiety and other psychopathologies. Nightmares can also be associated with alcohol abuse and some medications that initially suppress REM sleep, and when these are stopped, REM rebound may occur, with often bizarre and frightening nightmares.

Management

Stress management techniques and cognitive behaviour therapy for anxiety may be recommended, as well as avoidance of chronic sleep restriction and excessive alcohol consumption before bed.

REM sleep behaviour disorder

REM sleep behaviour disorder seems to be caused by a failure of the normal muscle paralysis of REM sleep and is characterised by abnormal behaviours such as physically active (often violent) episodes, usually associated with dream recall. When aroused to reality, the patient will report that they had a violent dream and reinterpreted the present environment in terms consistent with the dream. RBD is more likely to occur in the latter half of the night when REM sleep is more frequent.

Prevalence

RBD is uncommon but tends to affect mainly men aged 50 years and older, and may be idiopathic or associated with other neurological disorders.21,36

Diagnosis

Differential diagnosis of RBD is made from PSG by the presence of abnormal REM sleep behaviours or failure of EMG suppression during REM sleep.

Management

Following diagnosis, medication such as clonazepam may be indicated. Ensure adequate sleep to avoid curtailing REM sleep with its potential subsequent REM rebound, which may exacerbate RBD.

INSOMNIA

In this final section we describe the common sleep disorders that may be managed in general practice.

Insomnia is defined as chronic difficulty with initiation, consolidation or duration of sleep, resulting in daytime impairment.21 It is the most common sleep disturbance in the general population and is said to be the third-highest complaint seen by the GP. Epidemiological surveys have yielded prevalence rates of 20–40% in the adult population, with 10–20% experiencing severe or frequent insomnia.37 Insomnia is often comorbid with other disorders (e.g. chronic pain, depression, anxiety) and therefore the GP needs to be alert for sleep problems when treating other physical and psychological disorders. Although insomnia may have been originally secondary to other health problems, if of long duration the insomnia is likely to be self-sustaining and require its own treatment.

Table 43.2 describes the three main types of insomnia complaints seen by the GP—that is, sleep onset, sleep maintenance and/or early morning awakening insomnia. These are illustrated in Fig 43.3, with examples of different sleep patterns from a typical sleep diary. Some patients may have a combination of insomnia diagnoses—for example, they may present with sleep onset insomnia but have a combination of psychophysiological insomnia as well as a delayed circadian rhythm, or they may have sleep maintenance insomnia as well as sleep onset insomnia.

TABLE 43.2 Clinical symptoms of insomnia subtypes and suggested treatment options

Clinical symptoms of insomnia type Treatment suggestions
Sleep onset insomnia  
Psychophysiological insomnia (PI) (Fig 43.2a)
• Long time taken to fall asleep (> 30 min) at desired bedtime
• Sometimes fall asleep when sleep is not intended
• May sleep better away from home
• Anxious about sleep, mentally/physically aroused after going to bed
• Some daytime impairment (tired, fatigued, irritable)

Stimulus control therapy
Cognitive therapy
Relaxation therapy
Good sleep practices

Delayed sleep phase disorder (DPSD) (Fig 43.2b)
• Normal sleep duration but later sleep pattern
• Long sleep latency at normal bedtime (e.g. 11 pm) but shorter latency at later time (e.g. 2 am)
• Able to sleep late in the morning if given opportunity
• Difficulty trying to awaken at desired time (e.g. 7 am)
Stimulus control therapy
Morning bright light
Dim light in evening
Good sleep practices
Sleep maintenance insomnia (Fig 43.2c,d)
• Usually no difficulty falling asleep at desired time
• Waking in middle of the night feeling anxious/alert
• Difficulty falling back to sleep
• Some daytime impairment (tired, fatigued, irritable)
Bedtime restriction
Cognitive therapy
Evening bright light
Good sleep practices
Relaxation therapy
Sleep onset and sleep maintenance (Fig 43.2e)
• Long sleep latency (> 30 min)
• Waking in the middle of the night, difficulty falling back to sleep
• Some daytime impairment (fatigue, distress)
Bedtime restriction
Cognitive therapy
Good sleep practices
Relaxation therapy
Early morning awakening insomnia (Fig 43.2f)
• Early evening sleepiness (falling asleep in front of TV)
• Able to fall asleep quickly at usual bedtime
• Early morning awakening (e.g. before 5 am) and unable to fall back to sleep
• Some daytime impairment
Evening bright light
Dim light in morning
image

FIGURE 43.3 Examples of typical sleep patterns for different subtypes of insomnia diagnoses: (a, b) sleep onset insomnia, (c, d) sleep maintenance insomnia, (e) sleep onset and sleep maintenance insomnia and (f) early morning awakening insomnia

Management

Still the most common medical treatment for insomnia is hypnotics and, more recently, antidepressants. However, these have negative consequences such as tolerance, dependence, withdrawal rebound insomnia and altered sleep physiology, as well as side effects such as amnesia, psychomotor slowing, cognitive impairment and unusual night-time behaviours. Particularly in the older population, hypnotics tend to exacerbate all the normal cognitive/behavioural impairment of ageing as well as potentially interacting with a patient’s other medications. Medication may provide temporary symptomatic relief only and does not address the causes of insomnia. In recent studies, cognitive behaviour therapy for chronic insomnia has been shown to be comparable to pharmacotherapy in the short term and more effective in the long term.38,39 Cognitive/behaviour and light therapies aimed at correcting the underlying aetiologies are suggested to produce greater long-term effectiveness. However, it is important to correctly identify the subtype of insomnia and its likely aetiology in order to provide the most appropriate treatment. Figure 43.3 and Table 43.2 can be used as a guide to this process. Identify the pattern of insomnia in Figure 43.3, then check the treatment suggestions in Table 43.2, which are elaborated in detail below.

In addition, insomnia non-drug treatment programs conducted in most major cities worldwide successfully use evidence-based therapies such as stimulus control, bedtime restriction and cognitive therapy and bright light to treat the different insomnia subtypes. (See the Resources list at the end of this chapter for websites of sleep clinics and practitioners.)

Non-drug, evidence-based insomnia treatments

Good sleep practices (sleep hygiene)

A good bedtime routine includes the following measures:

• Avoid vigorous exercise at least 2 hours before bedtime.
• Avoid caffeine drinks (stimulants) within 6 hours before bedtime.
• Avoid alcohol before bedtime, as it can lead to night-time awakening.
• Nicotine (smoking and patches) increases alertness. Smoking reduction or withdrawal can improve sleep as well as general health.
• Avoid going to bed hungry or after a big meal.
• Have a ‘wind down’ period (30–60 minutes) for relaxing in dim light before bed.
• Avoid a fixed bedtime or going to bed too early. Use feelings of sleepiness, not fatigue, as your guide for bedtime.
• Get rid of the bedroom clock if checking the time is a habit that is associated with worry about your sleep.
• Have a fixed wake-up time.

Short ‘power-naps’ (less than 20 minutes) may be rejuvenating when experiencing daytime sleepiness. A longer sleep (longer than 20–30 minutes), where one goes into deep sleep, often results in shorter and broken sleep that night. Furthermore, when we come out of a longer, deep sleep during the day or early evening, we can experience a period of lethargy for up to an hour after awakening, referred to as sleep inertia, which can counteract the rejuvenating purpose of daytime sleep.

Stimulus control therapy

Difficulty falling asleep may be due to an association that has developed between bedtime and difficulties with falling asleep. The process of getting ready for bed and going to bed may become stimuli that trigger negative emotions such as anxiety, frustration, worry—known as ‘conditioned insomnia’.

To extinguish these responses:

• Reserve the bedroom for sleep or sexual activity—no TV, computers, eating or arguing.
• Go to bed only when feeling sleepy, as opposed to going to bed because you feel exhausted or tired or believe it should be bedtime.
• If you are unable to fall asleep within a short time (e.g. 15–20 mins) or are feeling anxious or alert, get out of bed and go to another room and read or watch TV under dim lights. Return to bed again only when feeling sleepy.
• Keep repeating the above step until you fall asleep quickly.
• Keep a regular time for arising from bed, even on weekends, and get some light stimulation after arising.

In the first few nights/weeks this is likely to result in many times out of bed before rapid onset of sleep. In winter months it would be helpful to keep another room warm, to encourage you to get up when needed. Gradually, as sleep pressure builds and conditioned insomnia declines, sleep will occur more quickly, with fewer out-of-beds required.

Bedtime restriction

People who experience sleeplessness during the night often stay in bed longer in the hope of ‘catching up’ on lost sleep. This exacerbates the problem, as it usually increases time spent awake in bed. Spending too long in bed results in shallow and fragmented sleep, anxiety and daytime tiredness, and reinforces the conditioned insomnia.

By restricting the amount of time spent in bed, sleep will become consolidated due to an increase in sleep homeostatic pressure. To do this:

• Estimate the patient’s average total sleep time (e.g. 6 hours).
• Set a period in bed for only that amount of time (e.g. 6 hours).
• Choose a regular wake-up time to suit personal circumstances and then set a regular bedtime (e.g. 12 am to 6 am).
• Avoid daytime naps, to help increase sleep pressure.
• Assess the sleep pattern after a week and, if sleep is more consolidated with few awakenings, gradually extend time in bed by 15–30 minutes each week until daytime sleepiness/fatigue abates.

Cognitive therapy

Unhelpful and unrealistic thoughts and beliefs about sleep can lead to anxiety, and emotional and somatic arousal, which all interfere with the sleep process.

Cognitive therapy involves:

• explaining the normal sleep process (e.g. awakenings are normal)
• replacing unhelpful thoughts with more realistic, helpful thoughts and beliefs (e.g. feeling tired after a fragmented sleep is normal, but despite taking more effort, the following day can still be successful, and recovery sleep the following night is likely).

Relaxation techniques

• Learn a relaxation technique, such as diaphragmatic breathing, visualisation, meditation. All these involve focusing on a non-provocative idea/image in order to keep worrisome thoughts at bay. When extraneous thoughts re-enter consciousness, be mindful of that (don’t be discouraged, it will happen) and regain your focus on your relaxation image/idea. Practise this relaxation technique until proficient before using it in bed for sleep.
• Do something relaxing in the hour before bed—no computer work, computer games, business or arguments.
• If you have a lot on your mind, it can be helpful to spend a few minutes (e.g. 15–30 minutes in the early evening) planning the next day or thinking about the day’s activities.

Morning bright light

Morning bright light will advance a delayed circadian rhythm and lead to an earlier sleep pattern.4 For example, if a patient wishes to sleep between 11 pm and 7 am but is unable to fall asleep until 3 am and has difficulty waking earlier than 11 am, they may have delayed sleep phase disorder.21 To advance the sleep period back to the preferred earlier time, we suggest the following protocol:

1. Establish the patient’s ad lib wake-up time (sleep-in time, e.g. 11 am).
2. Commence light therapy sessions. The patient is exposed to 1 hour of bright light, possibly outdoor light, 30 minutes before this time (e.g. 10.30 am). Note: an artificial light device in the morning may be necessary during winter.
3. Gradually advance wake-up time and morning light exposure by 15–30 minutes each day until the preferred wake-up time is reached (e.g. 10 am, 9.30 am, 9 am, 8.30 am …).
4. Avoid bright light in the evenings—no computer or stimulating activity.
5. Keep a regular sleep/wake schedule, to prevent relapse delay of sleep phase.

Evening bright light

The abnormally early timed circadian rhythm and sleep pattern can be delayed by exposure to bright evening light.4 The patient with an early timed circadian rhythm (advanced sleep phase21) will struggle to stay awake until the desired or conventional bedtime and may experience frequently unintentional naps in the evening before retiring to bed. They will also experience early morning awakening. For example, the patient may have overwhelming sleepiness at 8 pm, prolong bedtime until 10 pm but despite this, still wake at 4 am and be unable to fall back to sleep. We suggest the following:

• Develop a habit of spending up to 60 minutes outdoors late in the day or early evening. An artificial light device may be used in winter with light exposure for 1 hour before bedtime.
• Do some light exercise early in the evening (walking, stretching).
• Avoid morning sunlight or other bright light within 1–2 hours after waking (may need to wear dark glasses).

Melatonin

Melatonin may be useful for those with a circadian rhythm sleep disorder. Because melatonin can re-time the circadian rhythm, it can be useful for treating the insomnias with a circadian mistiming component. In severe sleep onset insomnia, low-dose melatonin (0.5–1.0 mg) may be helpful if taken in the early evening (e.g. 6–8 pm). This will shift the underlying circadian rhythm to an earlier time and result in the ability to fall asleep earlier.

When early sleep onset with premature early morning awakenings is the problem, evening bright light and low-dose (0.3–0.5 mg) melatonin taken in the early morning (e.g. 3–5 am) can help to delay the abnormally early rhythms and allow longer sleep in the morning. It should be noted that pure melatonin, which is necessary for this effect, can only be obtained by prescription in Australia. In the United States, it is available in health food stores.

Herbal treatments

Common herbal treatments for insomnia include:

• Valerian (Valeriana officinalis)—usually used in combination with other herbal treatments. Not all research results are positive, but results from several well-conducted placebo-controlled studies suggest that valerian reduces sleep latency and increases sleep quality in poor sleepers if taken for more than 2 weeks.40
• Lavender—a number of controlled trials and observational studies suggest that inhalation of ambient lavender oil has a relaxing effect and can reduce anxiety and improve mood, concentration and sleep.41
• Lemon balm—often prescribed in combination with other herbs such as valerian in the treatment of insomnia.42

CONCLUSION

It is important to be alert to the clinical symptoms of sleep disorders in medical practice as these disorders will often not be the presenting problem. Many of these disorders are prevalent and cause significant morbidity. However, the field of sleep disorders has made, and will continue to make, considerable advances in diagnosis and treatment. Many of the suspected disorders would best be managed by referral to a specialist sleep disorders unit, while some of the most prevalent can be managed by the general practitioner using a variety of proven non-drug therapies.

RESOURCES

American Academy of Sleep Medicine. http://www.aasmnet.org.

Australasian Sleep Association. http://www.sleep.org.au.

Australasian Sleep Association, information on sleep disorders. http://www.sleepaus.on.net/factsheets.html.

Australasian Sleep Association, insomnia treatment services (in each Australian state). http://www.sleepaus.on.net/servicesinsomniatreatments.php.

British Sleep Society. http://www.sleeping.org.uk/.

European Sleep Research Society. http://www.esrs.eu/cms/front_content.php.

Lack L, Wright H, Bearpark H. Insomnia: how to sleep easy. Sydney: Media 21; 2003.

Morin CM, Espie CA. Insomnia: a clinical guide to assessment and treatment. New York: Kluwer Academic/Plenum, 2003.

Poceta JS, Mitler MM. Sleep disorders: diagnosis and treatment. New Jersey: Humana Press, 1998.

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