ABC of Sleep Medicine (ABC Series)

Chapter 5

Insomnia

OVERVIEW

·        Accurately defining chronic insomnia as a sleep disorder is problematic since it is so common and widely heterogeneous in its nature

·        Primary chronic insomnia almost certainly has long-term health consequences and is strongly associated with depression, hypertension and a variety of physical or somatic symptoms

·        Chronic insomnia is most commonly precipitated by a trigger or life event in predisposed subjects and is subsequently fuelled over months or years by maladaptive thoughts and habits

·        Psychophysiological insomnia accounts for most cases of primary insomnia and is thought primarily to reflect excessive cognitive arousal

·        Mild insomnia may respond to simple advice on sleep hygiene together with relaxation therapy

·        Structured cognitive behaviour therapy (CBT) tailored for insomnia is a the best proven treatment for severe or resistant cases

·        Pharmacological treatment for chronic primary insomnia is controversial although it has a role in selected cases, possibly in combination with other strategies

·        A number of sedative drugs are used as surrogate hypnotic agents even though overall sleep quality is often not improved due to their adverse or inhibitory effects on deep non-REM sleep

Dissatisfaction with overnight sleep is such a common complaint that it is often overlooked or, at best, incompletely assessed. Indeed, if specifically asked about sleep quality, approximately one-third of those visiting a general practitioner will report problems, a proportion that rises to two-thirds of those attending psychiatry services. Insomnia is reported more in females and generally increases with age.

Transient or short-term insomnia, usually triggered by a recognisable life event or stressor, is a universally recognised phenomenon. However, the underlying mechanisms or causes of chronic insomnia are often more obscure. Furthermore, the pathways for managing significant insomnia presenting to primary care are generally very poorly developed, creating frustration for patients and physicians alike.

Defining chronic insomnia as a formal sleep disorder is challenging, especially as it is a heterogeneous complaint. Broadly, subjects can report difficulty with any aspect of sleep, whether it is initiation, duration, consolidation or quality. The problem persists despite a desire to sleep normally with adequate time and opportunity for satisfactory sleep.

Most authorities would suggest an approximate benchmark of 30 minutes either trying to achieve sleep or a similar time spent awake after sleep onset as reflecting significant insomnia. The problem needs to have been present most nights of the week for over one month and, importantly, to have resulted in a degree of daytime impairment. Typical daytime symptoms include lethargy, malaise and cognitive blunting, especially in tasks involving attention or concentration. In severe cases, the problem completely dominates a subject's life such that vocational, social or school performance is severely compromised.

Importantly, insomnia is recognised as a reliable independent risk factor for developing depression and hypertension. Furthermore, numerous somatic symptoms, such as increased muscle tension, gastrointestinal upset and headache, are often intimately associated with insomnia.

Although the distinction may often be blurred, it is useful to consider insomnia either as a primary phenomenon, reflecting an intrinsic sleep disorder, or as having an extrinsic cause largely due to factors such as the environment, drugs or other medical conditions. Broadly speaking, an important clue that insomnia is a primary rather than a co-morbid phenomenon is that subjects report a complete inability to nap under any circumstances during the day, despite persistently restricted or poor quality nocturnal sleep. At its simplest, a subject with primary insomnia can be considered ‘tired but wired’.

Mechanisms of insomnia

There are at least four interacting factors that can contribute to insomnia in clinical practice.

Homeostatic factors

It should be emphasised that normal sleepiness is a true drive state that builds exponentially with prolonged wakefulness and which can only be satiated by sleep itself. If the sleep drive is ‘weak’ for some reason or, perhaps more commonly, if someone is overly aroused or ‘wakeful’, insomnia may result. Although the neurochemistry of arousal and sleep onset systems in the brain is increasingly understood, consistent or objective abnormalities in insomniacs are difficult to demonstrate with current technology, even in severe cases. This may partly be due to the heterogeneous nature of the condition.

Inhospitable environment

A large number of adverse environmental factors may interfere with sleep and might not be readily recognised by an insomniac (Box 5.1). Alternatively, it is not uncommon for a person to recognise a possible cause for their insomnia but be unaware that there may be a potential remedy. Successful treatment of a bed partner's severe snoring is a relatively common example.

Box 5.1 Common environmental causes of insomnia

Loud noises

Bed partner (snoring, coughing, sleep-talking) or pets (e.g. barking); 

music, television, telephone;

traffic, trains, mechanical sounds (e.g. a lift)

Extreme temperature

Heat (no air conditioning in hot climates); 

cold (insufficient bedcovers or their removal during night)

Bedding materials

Bed or pillow uncomfortable;

Allergy to washing powder or feathers in pillow

Light

Bright light during summer in high latitudes; 

Normal sunlight during the day if working night shifts

Body positioning

Seated position (e.g. when using public transport); 

Cramped bed if subject or partner significantly obese

Movement

Vibration or turbulence if sleeping on public transport; 

Body movements (e.g. leg kicks from partner)

Up to 20% of people are aware there may be excessive noise in the sleeping environment. This may not be enough to fully wake subjects but might produce lighter and less refreshing sleep. Almost certainly, subjects vary in their ability to ‘gate’ extrinsic predictable noises at night, explaining why many find it possible to sleep peacefully next to train lines.

Maladaptive coping mechanisms and behaviours

Many potentially reversible behaviours, habits or beliefs exist to promote or worsen insomnia (Box 5.2).

Box 5.2 Maladaptive behaviours that can compromise sleep quality

·        Engaging in stimulating activities up to the point of bedtime

·        Using the bedroom for activities other than sleep

·        Inconsistent sleep–wake rhythm through the week

·        Excessive checking of the clock during the night

·        Consuming foods before bed that might promote acid reflux and heartburn

·        Inappropriate caffeine intake

·        Using alcohol habitually as a sleep aid

·        Inadequate physical activity or exercise during the day

It is obvious that both the body and mind need to be in a relaxed state before sleep can be initiated. This can often be overlooked with increasing trends for people to engage in work or other arousing activities right up to the intended time of sleep onset. The consequent inability to suddenly fall asleep then creates frustration and fuels further problems.

Insomniacs will often lose confidence that they can fall asleep in their bedrooms by a process of negative conditioning. Such patients will report significant sleepiness late evening whilst relaxing in the living room which disappears immediately they enter the bedroom. The failure of the bedroom to cue sleep occurs particularly in those who habitually use the room for activities such as studying or paying bills, for example. Paradoxically, compared to good sleepers, subjects with this type of insomnia generally spend an inordinate large amount of time in the bedroom across 24 hours but a much smaller proportion of it actually asleep (Figure 5.1).

Figure 5.1 Graph demonstrating the average time a group of typical insomniacs spends in bed (around nine hours) compared to time asleep (6.5 hours). This contrasts with good sleepers who spend 8.5 hours in bed, 7.5 hours of which are estimated asleep.

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Excessively sedentary lifestyles or very irregular sleep–wake schedules across a working week and weekend can also contribute to insomnia and not readily be recognised by the subject as provoking factors.

Awareness of the passage of time through the night and persistent checking of the time can lead to distress and increased alertness.

Responsiveness to caffeine is variable from person to person. Some may experience fragmented nocturnal sleep even with 100 mg or less taken in the morning, equivalent to a large cup of coffee.

Stress response

Attitudes and the ability to cope with normal stressors show a tremendous amount of individual variability. Recent evidence suggests that insomniacs are comparatively overreactive both to stress and potentially disruptive environmental stimuli such as extremes of temperature. This increased reactivity may be compounded by any underlying anxiety or mood disorder.

Psychophysiological insomnia

This is by far the commonest form of chronic primary insomnia, reflecting an interaction of psychological and physical factors. Although the precise neurobiology remains obscure, underlying theories of how it develops have been well rehearsed.

At some level, the subject is considered to have an underlying, partly genetic, predisposition to developing insomnia, perhaps reflecting an ill-defined tendency for cognitive ‘over-arousal’. Typically, sleep will be relatively normal until an event or medical condition triggers sleep disruption. Common examples include child birth, bereavement of a family member or an arduous shift work schedule. The ensuing preoccupation with insomnia then dominates the picture, months or years after the initial trigger has disappeared. As a result, the increased effort a subject puts into the normally automatic process of sleep initiation becomes counterproductive and actively contributes to sleep disruption. For many, intrusive ruminations and concerns over impaired performance during the subsequent working day following disrupted nocturnal sleep may further inhibit the ability to sleep.

A proportion of insomniac subjects appear to overestimate or overreact to their perceived poor sleep quality. A minority may even display so-called ‘paradoxical insomnia’, formerly known as sleep–wake misperception. In this, objective measures of sleep quantity and quality are within normal limits, in contrast to the subject's report or expectations.

Managing primary insomnia

Any initial assessment of insomnia should clarify the nature, longevity and severity of the problem. This is usually not time consuming and requires only a few directed questions, primarily to rule out potentially treatable co-morbid conditions or other sleep disorders. Not uncommonly, conditions such as restless legs syndrome and ‘clock’ problems, such as delayed sleep phase syndrome, may masquerade as primary insomnia.

In sleep clinics, if the history is clear for primary or psychophysiological insomnia, diagnostic tests are rarely useful or required and may even be counterproductive or produce misleading data. In particular, when undergoing polysomnography, some subjects sleep particularly badly if closely monitored overnight whereas others find they sleep more easily when away from their normal bedroom environment. Wrist actigraphy (Chapter 3) is occasionally used to explore sleep–wake cycles at home over a period of weeks, particularly if there are suspicions of paradoxical insomnia.

Sleep diaries or logs can be very useful in identifying and monitoring progress in insomnia patients in whom there is poor sleep hygiene or inappropriate scheduling (Figure 5.2). A diary should be simple, possibly using a graphical format over 24 hours. Ideally, it should show estimates of sleep and wake onset compared to time in bed as well as the timing of medication, including coffee consumption. The best information is obtained when a diary is filled out prospectively for at least two weeks.

Figure 5.2 Example of a simple self-completed sleep diary filled out prospectively over a week. Closed and open circles refer to times of going to bed and arising in the morning, respectively; the lines are the estimated sleep time; C = cup of coffee.

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Sleep hygiene

A central tenet of any treatment for insomnia is the concept of good ‘sleep hygiene’, although relatively few patients or, indeed, physicians have a full understanding of all the factors involved. The two key elements comprise optimisation of the sleeping environment and improving routines or attitudes conducive to good sleep.

With regard to improving conditions in the bedroom, insomniacs should generally be encouraged to experiment with adaptive strategies to improve sleep continuity if they have not already done so. Although obviously ‘toxic’ to good sleep, problems such as excessive noise or an uncomfortable bed may be difficult to resolve, particularly if a bed partner is responsible. However, some may respond to simple measures such as ear plugs. In others, however, this may focus attention on ‘internal’ noises, such as breathing, and be counterproductive. The temperature of the bedroom may impede quality sleep if above 24°C or disturb sleep onset if particularly low. A dark bedroom is clearly more conducive to sleep although some find complete darkness disturbing.

Many subjects with mild chronic insomnia may respond to advice on potential maladaptive routines or attitudes that have developed before sleep onset. In general, at least 30 minutes should be devoted to ‘winding down’ or relaxing before attempting to sleep. Avoiding large meals, caffeinated drinks and exercise within two hours of intended sleep onset is also important. Gentle regular exercise, however, perhaps early in the evening, has been shown to improve sleep quality in middle-aged and older adults.

In those who have ‘conditioned insomnia’ and find the bedroom hyper-arousing, it is recommended that no more than 15 minutes should be spent trying to sleep. They may be advised to leave the bedroom and engage in an alternative relaxing or potentially boring activity, such as watching television, reading or listening to music in an adjacent room, until they are once again sleepy. Keeping any bedroom clocks from easy viewing through the night is also preferable.

A consistent sleep–wake schedule is highly recommended in those prone to insomnia. A regular waking time, seven days a week, helps to optimise circadian rhythms. Daytime naps should generally be discouraged.

Approaches to moderate or severe insomnia

There are many long-standing or seemingly intractable insomniacs who have optimised their sleep hygiene and devoted considerable efforts to improving their sleep but remain severely symptomatic. Relaxation techniques can often be helpful if delivered in a systematic or structured way. Reading materials or audio tapes with cues designed to encourage peaceful thoughts and release muscle tension are widely available. Techniques similar to yoga, focusing on diaphragmatic breathing, for example, may also help. Others might gain more benefit from visual imagery in which the subject is instructed to conjure up tranquil scenes elaborated to encompass all the sensory domains for 15 minutes or so.

Relatively simple techniques to alter maladaptive behaviours interfering with sleep onset may be offered. For those who have excessive worry or intrusive ruminations at night, dedicating around 30 minutes in the late afternoon to list and examine concerns and stressors may diminish the energy and time spent worrying at night. Any new problems that lead to nocturnal awakenings are simply added to the ‘worry list’ the next day.

An alternative widely used technique involves sleep restriction (Box 5.3). Subjects are instructed to estimate sleep time the previous night and then limit their time in bed to this amount on subsequent nights until their sleep efficiency increases and they are able to increase sleeping time by small increments.

Box 5.3 Sleep restriction guidelines in the treatment of primary insomnia

·        Subjects use a sleep diary for at least two weeks to estimate average total sleep time (TST)

·        Time in bed (TIB) is reduced until it equals estimated TST but not less than four hours (some advocate this be done abruptly, others suggest a gradual reduction of TST over two weeks or so)

·        Treating clinicians may specify a precise bedtime and arising time initially

·        Patients monitor their quality and quantity of sleep each night for several weeks by estimating sleep efficiency (SE), the proportion of TIB spent asleep as a percentage

·        Once SE has reached a target level for a week (between 80 and 90%, depending on subject), TIB is increased by 15–30 minutes

·        The process is repeated until a goal of 7.5 hours of good quality sleep is achieved

·        Excessive daytime sleepiness may be experienced initially but naps should be discouraged

·        Sleep latency and time awake after sleep onset should decrease in parallel with increases in TST and SE

Formal cognitive behaviour therapy for insomnia (CBT-I) is held by many to be the ‘gold standard’ for the most severely affected patients (Box 5.4). Despite good evidence for long-term efficacy, the resources for delivering this type of therapy are generally poorly developed. CBT-I combines all the advice and approaches to insomnia previously described together with attempts at ‘cognitive restructuring’, typically over a course of treatment lasting six sessions. Simplistically, poor sleepers are encouraged to think and behave like good sleepers. It is emphasised that their problems are largely correctable and best perceived as a ‘bad habit’. Emphasis is usually placed on how good sleepers fall asleep automatically and how any forceful effort to sleep is invariably counterproductive. CBT-I can be delivered in groups or individually, usually with a manual.

Box 5.4 A typical structured six-week CBT programme for insomnia

Week 1

 detailed assessment and measurement of the insomnia problem; 

definition of realistic goals of treatment

Week 2

 education on sleep and its function with particular reference to insomnia

Week 3

 sleep hygiene and relaxation

Week 4

 scheduling a new sleep pattern

Week 5

 dealing with a racing mind and unhelpful thoughts

Week 6

 putting it all together

Pharmacological therapy

(Individual drugs used to treat insomnia are discussed more fully in Chapter 11.)

Many patients hold unrealistically high expectations that a simple drug therapy will solve their insomnia. Others may be fiercely resistant to hypnotic use which is seen as an absolute last resort.

In recent years, there has been a cultural change in attitudes to the routine use of hypnotic drugs and few areas of clinical pharmacology are more controversial, particularly for treatment periods of more than a few weeks. Fears of tolerance, physical dependence, withdrawal and other side effects, such as morning hangover, have clearly influenced both guidelines and prescribing practice. Drug expense is also a limiting factor. Many perceive the pendulum against prescribing may have swung too far and that fears of true ‘addiction’ are overstated. Unfortunately, there is a notable lack of positive data from long-term controlled drug trials to guide management. However, evidence that long-term use of hypnotics is necessarily harmful in all cases is also limited.

In general, if it is decided to recommend a course of hypnotic drug therapy, certain principles are worth emphasising. Firstly, realistic treatment goals and an ‘exit strategy’ for drug discontinuation should be established. However, overly strict protocols and limiting courses of treatment to only a few days can be counterproductive, increasing anxiety and poor sleep overall. If sleep onset is the main complaint, the lowest dose of a short-acting drug, for example Zolpidem, should be considered. If sleep maintenance is the major concern, a longer-acting agent such as Zopiclone or temazepam might be preferable.

Although many drugs used for insomnia may increase sleep continuity or total time asleep, relatively few improve actual sleep quality. Rather, the relative proportion of light non-REM (stage 2) sleep is increased, which may enhance a sense of morning ‘hangover’, necessitating dose reduction or a change in agent. Furthermore, some subjects misinterpret sensations of increased drowsiness on waking as a need for higher doses of hypnotics before bed.

Melatonin is available as a long-acting preparation licensed for use in primary insomnia. It is recognised as safe, especially at the extremes of age. It is unlikely to help severe insomnia, however, and is probably most effective for those who cannot switch to sleep at a conventional hour but who sleep relatively well thereafter. Such subjects may have an intrinsic abnormality of the internal ‘clock’ mechanism, delayed sleep phase syndrome (DSPS). Melatonin taken at a low dose of 0.5 mg or less, two or three hours before intended sleep, may be used to ‘advance’ the clock to a conventional hour of sleep onset.

If a particular hypnotic drug is successful, intermittent courses or having a supply at home for ‘rescue’ therapy can be useful. There are differing views as to whether combining hypnotics with CBT-I is a useful approach given that some will tend not to engage fully in a training package if a ‘simple’ drug therapy is also available.

Even in the absence of overt depressive symptoms, antidepressants, particularly tricyclics at low dose, are often used empirically as hypnotic agents. However, the evidence that commonly used antidepressants help primary insomnia is very limited. Indeed, sleep quality may be hampered, particularly if there is evidence for restless legs syndrome or periodic limb movements, as these are generally enhanced by most antidepressants. Furthermore, selective serotonin reuptake inhibitors (SSRIs) tend to cause arousal in some and rarely improve sleep parameters when formally measured.

When a mood disorder is identified, sedating antidepressant agents, such as Mirtazepine, Trazadone or Agomelatine, may be useful for any associated insomnia. Furthermore, if anxiety appears to be excessive, limited evidence suggests that pregabalin or paroxetine before bed may be helpful.

Antipsychotic drug therapies, including atypical neuroleptics, often cause drowsiness and have been used by some as surrogate hypnotic agents. There is little evidence that these drugs have a useful role in primary insomnia and side effects such as weight gain often outweigh any useful effects on sleep quality.

Antihistamines are generally sedative and available without prescription. Formal evidence that they help primary insomnia is lacking but short courses may be of help with mild sleep onset insomnia. Other ‘over the counter’ remedies are frequently used in the absence of good quality evidence for efficacy.

Further reading

Espie, C.A. (2006) Overcoming insomnia and sleep problems: a self-help guide using cognitive behavioural techniques. Robinson, London.

Espie, C.A., Inglis, S.J., Tessier, S. and Harvey, L. (2001) The clinical effectiveness of cognitive behaviour therapy for chronic insomnia: implementation and evaluation of a sleep clinic in general medical practice. Behav Res Ther39, 45–60.

Hauri, P. (1997) Can we mix behavioural therapy with hypnotics when treating insomniacs? Sleep20, 1111–1118.

Morgan, K., Kucharczyk, E. and Gregory, P. (2011) Insomnia: evidence-based approaches to assessment and management. Clin Medicine11, 278–281.

National Institute for Health and Clinical Excellence (2004) Guidance on the use of zaleplon, zolpidem and zopiclone for the short-term management of insomnia. Technology Appraisal Guidance 77, National Institute for Health and Clinical Excellence (NICE), London.

Wilson, S.J., Nutt, D.J., Alford, C. et al. (2010) British Association for Psychopharmacology consensus statement on evidence-based treatment of insomnia, parasomnias and circadian rhythm disorders. J Psychopharmacol24, 1577–1601.



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