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.

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.

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.

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.)