ABC of Sleep Medicine E-Book

Paul Reading

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Serie: ABC Series
• Sprache: Englisch

Seitenzahl: 184

Veröffentlichungsjahr: 2012

Beschreibung

ABC of Sleep Medicine

ABC of
Sleep Medicine

About the ABC of Sleep Medicine

Patients presenting with sleep-related symptoms are common in primary care, but assessing and managing these conditions can be difficult. ABC of Sleep Medicine is a practical illustrated guide to sleep disorders which will give health professionals confidence in this complex area of diagnosis and management.

It explains the differences between normal and abnormal sleep, and looks in depth at individual disorders such as sleep apnoea, insomnia, narcolepsy, restless legs syndrome and the parasomnias, as well as sleep disorders as a comorbidity of neurodegenerative and psychiatric disease. Common sleep disorders in children are addressed in detail before concluding with an overview of pharmacological treatments and how commonly used drugs might affect sleep.

This brand new addition to the ABC series will be a valuable resource for general practitioners, practice and specialist nurses, psychiatrists, and medical trainees in both primary care and neurology.

About the ABC series

The new ABC series has been thoroughly updated, offering a fresh look, layout and features throughout, helping you to access information and deliver the best patient care. The newly designed books remain an essential reference tool for GPs, GP registrars, junior doctors and those in primary care, designed to address the concerns of general practitioners and provide effective study aids for doctors in training.

Now offering over 70 titles, this extensive series provides you with a quick and dependable reference on a range of topics in all the major specialities. Each book in the new series now offers links to further information and articles, and a new dedicated website provides you with even more support.

The ABC series is the essential and dependable source of up-to-date information for all practitioners and students in general practice. To receive automatic updates on books and journals in your specialty, join our email list. Sign up today at www.wiley.com/email

Leseprobe

Table of Contents

Series Page

Title Page

Copyright

Preface

Chapter 1: Normal versus Abnormal Sleep

The importance of sleep

Defining sleep

How much sleep is needed?

The effects of age

When is daytime sleepiness abnormal?

Normal nocturnal motor phenomena during sleep

Conclusions

Chapter 2: Diagnosing Sleep Disorders

Tests for sleep-related breathing disorders

Polysomnography

Objective tests of sleepiness and wakefulness

Actigraphy

Chapter 3: Excessive Daytime Sleepiness

Introduction

Causes

Narcolepsy

Secondary narcolepsy

Idiopathic hypersomnolence

Circadian misalignment

Chapter 4: Sleep Apnoea Syndromes

Diagnosing obstructive sleep apnoea

Treating obstructive sleep apnoea

Central sleep apnoea

Complex sleep apnoea

Chapter 5: Insomnia

Mechanisms of insomnia

Psychophysiological insomnia

Managing primary insomnia

Chapter 6: Secondary (co-morbid) Insomnia

General medical conditions

Neurological conditions

Rare causes of severe insomnia

Chapter 7: The Parasomnias

Parasomnias at the wake–sleep transition

Parasomnias from deep non-REM (slow wave) sleep

Parasomnias from REM sleep

Other parasomnias

Chapter 8: Sleep Disorders in Children

What is the problem and whose is it?

Normal sleep in children

The sleepless child

The child that snores

Chapter 9: Sleep in Neurodegenerative Disease

Parkinson's disease

Complex parkinsonian disorders

Alzheimer's disease

Motor neuron disease

Chapter 10: Sleep in Psychiatric Disease

Depression

Anxiety disorders

Psychotic disorders

Drug dependency

Chapter 11: Drugs Used in Sleep Medicine

Agents to promote wakefulness

Agents to induce or improve nocturnal sleep

Potential sleep-related side effects of commonly used drugs

Index

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Library of Congress Cataloging-in-Publication Data

Reading, Paul.

ABC of sleep medicine / Paul Reading.

p. ; cm.

Includes bibliographical references and index.

ISBN 978-0-470-65946-5 (pbk.)

I. Title.

[DNLM: 1. Sleep Disorders–pathology. 2. Sleep–physiology. WL 108]

616.8′498–dc23

2012035462

A catalogue record for this book is available from the British Library.

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.

Cover design by: Meaden Creative

Preface

At a personal level, everyone recognises the importance of good quality sleep. From a medical perspective, however, only recently has the potential adverse impact of a disordered sleep–wake cycle on cognitive, mental and even physical health been realised. The consequences of excessive daytime sleepiness are also increasingly defined, especially with respect to driving and other potentially dangerous activities. Perhaps surprisingly, the precise biological reasons why every animal has a basic need for regular sleep are still speculative and the fascinating state of rapid eye movement (REM) sleep remains a particular enigma. However, it is abundantly clear that sleepiness is a true drive state and, ultimately, as important as hunger or thirst for optimal health and survival.

Partly because it cuts across numerous more established specialities, the emerging discipline of sleep medicine remains in its infancy and is generally poorly addressed in medical schools. As a consequence, many physicians in primary and secondary care lack confidence in addressing sleep-related symptoms, despite significant advances in our understanding and treatment options for the majority of sleep disorders over the last decade. A further confound is a widely held and mistaken belief that sleep disorders invariably require complex and expensive techniques for confident diagnosis. With the exception of sleep-related breathing disorders, the majority of sleep disorders can actually be adequately managed without an absolute need for detailed investigations.

This book has been written as a primer for understanding the fascinating phenomenon of sleep and its commoner disorders. The aim has been to provide a readable text for non-specialists, covering the full range of recognised sleep disorders that might present to general physicians and sleep clinics. Throughout, it is emphasised that a full sleep–wake history, potentially corroborated by close family members, together with a basic knowledge of sleep neurobiology, will usually allow an accurate diagnosis and potential treatment options. The full range of diagnostic sleep investigations is also discussed in some detail, outlining when they are appropriate but also highlighting pitfalls in interpretation. Of course, it is often difficult to know whether sleep-related symptoms reflect a defined disorder or simply result from social or psychological factors; grey areas undoubtedly remain. However, symptomatic ‘red flags’ are highlighted which may indicate the need for more specialist attention.

A particularly difficult area in sleep medicine is the scarcity of a controlled evidence base to guide treatment protocols. As an inevitable consequence, the reader should be aware that many suggestions for medications mentioned in this text are personal recommendations, based largely on anecdotal evidence. Furthermore, it should be noted that it is rare for a drug to have a formal licence for use in sleep medicine.

Sleep clinics, at least in the United Kingdom, are increasing in numbers but remain variable in their ability to address the whole gamut of sleep disorders. The majority are primarily concerned with managing the important condition of obstructive sleep apnoea but lack expertise in neurological or psychological aspects of sleep disorders. A working knowledge of the whole spectrum of sleep disorders is therefore essential for primary care physicians, especially since symptoms of impaired sleep or reduced daytime alertness are amongst the commonest complaints. Not infrequently, a potentially disabling and treatable condition such as narcolepsy may be missed if an incomplete history is elicited. This book will hopefully introduce non-specialists to sleep medicine and increase confidence in how to approach sleep-related symptoms, removing some of the mystique surrounding this fascinating and important area of medicine.

Paul Reading

Chapter 1

Normal versus Abnormal Sleep

OVERVIEW

Sleep almost certainly serves a vital function at the cellular level and is an absolute requirement for every animalIn large population studies across the globe, chronically poor or insufficient sleep appears to correlate with increased mortality, arterial disease, diabetes and possibly cancer ratesSleep is highly orchestrated into discrete cycles of non-rapid eye movement (non-REM) and rapid eye movement (REM) stagesVivid dreams most often occur from the REM sleep stageIncreasing age dramatically alters sleep quality and consolidationIf insufficient deep non-REM sleep is obtained during a night, subjects will generally awake unrefreshedREM sleep is a very active brain state which has been proposed to facilitate memory consolidation and emotional processing although its true function ultimately remains obscureAt least 90% of the adult population benefit from 7–8 hours of good sleep per nightAround 5% of the population can be considered excessively sleepy during the day although increased sleepiness may not be recognised as such and may be expressed through other symptomsDuring nocturnal sleep, a variety of bodily movements is experienced normally

The importance of sleep

Virtually everyone acknowledges that significantly disturbed sleep has profound and immediate adverse effects on mental, cognitive and even physical well-being. However, the true long-term importance of good sleep for optimal general health may not yet be fully recognised.

The fact that every animal has evolved to have an absolute need for regular sleep in order to survive clearly suggests that it performs some vital and, as yet, ill-defined function. Intuitively, sleep appears to facilitate restoration and repair. Almost certainly, however, it has much more than a simple passive or restful role. In many respects, sleep is an active brain state and is not merely the absence of wakefulness. Indeed, during rapid eye movement (REM) sleep, the brain is as metabolically active as during wakefulness. As a consequence, some authorities have termed REM sleep as ‘paradoxical sleep’.

In recent animal models, it appears that being awake for just a few hours vigorously activates metabolic ‘cell stress’ or adaptive biochemical pathways. This response to prolonged wakefulness is seen particularly in nerve cells that appear to be protecting themselves from damage and potential early death or apoptosis. It is therefore conceivable that any excess of wakefulness is the potentially damaging factor rather than a lack of sleep per se.

It is clearly difficult to study the long-term consequences of bad sleep in humans. Of interest, however, a large prospective four-year study of healthy elderly subjects suggested that the only reliable predictor of death or subsequent dependency from a large number of demographic details was a complaint of disordered sleep, particularly in males.

A renowned sleep researcher (William Dement) famously stated that ‘Sleep is of the brain, for the brain and by the brain’, emphasising the adverse effects of poor sleep predominantly on brain function and mental health. Conversely, virtually every central nervous system and mental health disorder has the potential to disturb the sleep–wake cycle. Furthermore, chronic poor quality or insufficient sleep may actively fuel many common conditions, such as generalised pain syndromes and affective disorders. This strongly suggests that sleep has a ‘bi-directional’ relationship with many common conditions (Figure 1.1).

Figure 1.1 Chronically poor quality or insufficient sleep is rarely an isolated problem. For example, pain and anxiety may well impede good sleep but sleep restriction or impairment can also increase sensitivity to pain and raise anxiety levels.

In many situations, it is possible that direct attention both to sleep quantity and quality may have indirect and positive effects on an unexpected range of health issues. In this respect, the established epidemiological links between chronic sleep deprivation (less than six hours a night) and diabetes, hypertension, vascular disease or even cancer are increasingly germane. The difficult and important question of whether increasing quantity or quality of sleep in ‘at risk’ populations will positively affect outcome remains to be established.

Defining sleep

The loose behavioural definition of sleep as a temporary and reversible state of altered consciousness and perceptual disengagement has been superseded by electrophysiological criteria.

Although simplistic, it is valid to consider three distinct and mutually exclusive brain states, namely wakefulness, rapid eye movement (REM) sleep and non-REM sleep (Figure 1.2). Switches between these states should occur automatically, quickly and relatively seamlessly. A large proportion of sleep disorders is associated with inefficient, faulty or incomplete states of transition.

Figure 1.2 The brain can be considered as normally existing in the three mutually exclusive states of WAKE, non-REM or REM sleep. Orchestrated transitions between these states occur automatically and relatively quickly over the 24-hour period. In many sleep disorders, particularly the parasomnias, the switch between states may be inefficient or incomplete.

Non-REM sleep can be divided into light (stages 1 and 2) or deep phases (stages 3 and 4) on the basis of the surface cerebral electroencephalogram (EEG) (Figure 1.3). Around 20% of the night is spent in the curious state of REM sleep, in which most of the cerebral cortex and limbic system is extremely active, as confirmed by recent functional brain imaging studies. In contrast to this enhanced metabolic activity, there are descending inhibitory neural impulses from the brainstem that innervate the vast majority of peripheral muscles during REM sleep, rendering the subject floppy (atonic) and areflexic.

Figure 1.3 Representative electroencephalographic (EEG) traces of the 4 stages of non-REM sleep. The arrow indicates a K-complex, one of the hallmarks of light non-REM sleep. Large amplitude delta (slow) waves dominate the trace in deep non-REM sleep (stages 3 and 4).

In recently revised criteria for sleep staging, light non-REM sleep (stages 1 and 2) has been designated as N1 whereas deep non-REM (stages 3 and 4) is N2. This revision has not been completely accepted internationally at the time of writing.

REM sleep loosely correlates with the normal phenomena of dreams or nightmares, usually recalled briefly if a subject is awoken from this stage of sleep. However, less vivid or bizarre ‘sleep mentation’, usually without a narrative thread, is also frequently reported if arousals from sleep occur from non-REM sleep stages.

An ideal nocturnal sleep in young adults consists of four or five cycles of REM/non-REM sleep with deep non-REM sleep dominating the first third of the night and REM sleep the last third (Figure 1.4). Minor arousals from sleep are common, especially with increasing age, and often not registered or recalled.

Figure 1.4 A typical hypnogram of a young adult showing discrete cycles of non-REM and REM sleep through the night. Deep non-REM sleep predominates in the first third whereas REM sleep is most dense in the last third. Brief awakenings are often not recognised. If they occur during REM sleep, a vivid dream would be expected.

How much sleep is needed?

There is clearly a degree of individual variation in the optimum length of the nocturnal sleep period but probably 90% of adults require at least seven hours of good quality sleep. For most people, sleeping regularly for six hours or less produces objective signs of reduced vigilance, even if subjective sleepiness is minimal.

Although sleepiness is the obvious consequence of acute sleep deprivation, increasingly, a number of studies have demonstrated neuropsychological effects (Table 1.1). The majority of these can be interpreted in terms of temporary frontal lobe dysfunction. Many have commented that the sleep-deprived brain of a young adult functions in a similar way to the brain in extreme old age.

Table 1.1 A selected list of the neuropsychological effects secondary to acute sleep deprivation.

Main neuropsychological effect of acute

Year of study

sleep deprivation

Increased reaction times

1988

Perseveration and reduced flexibility

1999

Impaired sense of humour

2006

Increased risk taking

2007

Impaired moral judgement

2007

Reduced emotional intelligence

2010

Increased ‘negativity’ with enhanced memory for adverse events

2010

Increased distractibility

2010

Although underlying mechanisms are unclear and precise interpretation is difficult, several enormous population studies have consistently reported increased mortality, vascular disease and diabetes in those reporting less than five hours of sleep per night when followed up for several years. Intriguingly, those sleeping for more than 9.5 hours a night similarly have reduced longevity.

Increasingly, it is realised that the nature of sleep may be as crucially important as its quantity, although precise definitions of sleep quality are poorly defined. The absolute amount of deep non-REM (slow wave) sleep through the night may predict how refreshed a subject feels in the morning but other measures, such as the time spent awake after sleep onset, may also be used as surrogate markers of quality.

The true function of REM sleep remains a mystery. Most awakenings from REM sleep are associated with vivid dreams that often have a bizarre narrative, incorporating elements of recent events or more distant memories. Psychoanalytic explanations of dreams in terms of ‘wish fulfilment’ have largely been superseded by more biological explanations. However, it remains unclear whether it is the dream itself or the underlying neurobiological processes behind REM sleep that are more important.

A common thread with much recent research on REM sleep function concerns memory processing or consolidation. In brief, one influential view is that the brain restructures or consolidates certain forms of memory through a form of rehearsal when ‘off-line’ during REM sleep. It is likely that processing of emotional memories is a particularly important function. Many cognitive tasks seem to improve after a period of sleep and some evidence even supports the notion that unexpected insights into mathematical problems occur during the unconscious state of sleep.

The study of dreams, oneirology, has a rich history. Many theories regarding dream function and REM sleep have been generated. Some interesting facts concerning REM sleep are listed in Box 1.1.

Box 1.1 Interesting facts about REM or ‘paradoxical’ sleep

Almost one third of the first few months of life are spent in a form of REM sleep.In animal experiments, preventing rats from entering REM sleep for around four weeks has fatal consequences.There are profound autonomic changes during REM sleep causing ‘instability’ of pulse rate and blood pressure. In theory, this might predispose certain individuals to cardiac arrhythmias during REM sleep.Thermoregulation is absent during REM sleep. If the environment is too hot or cold, arousals from sleep are particularly likely during the REM stage.Many drugs, including alcohol, suppress REM sleep. If stopped abruptly after prolonged intake, such drugs lead to rebound symptoms, including vivid dreaming or even visual hallucinations.Depressed patients enter REM sleep more quickly.The majority of antidepressant drugs suppress or delay REM sleep.Domestic animals have significantly more REM sleep than their feral counterparts.

It is often overlooked that sleepiness, like thirst or hunger, is a true drive state which builds up during prolonged wakefulness and will only be satiated by sleep itself. The neurobiological substrates of sleepiness and the underlying homeostatic mechanisms remain poorly understood although accumulation of the neurochemical adenosine in certain key areas, such as the basal forebrain, may be crucial. Indeed, caffeine works to offset the sleep drive by inhibiting adenosine receptors in these areas.

Superimposed on the homeostatic sleep drive are circadian factors which confer additional levels of somnolence at certain times of the day, irrespective of the immediate sleep history. These ‘dips’ in alertness, seen particularly at 3.00 p.m. and 4.00 a.m., may have consequences for behaviour and explain the rise in sleep-related traffic accidents at these times.

The fascinating field of chronobiology has provided a sound scientific basis for understanding the mechanisms of our internal clocks. Remarkably, the molecular machinery at a subcellular level has been largely established and hardly differs across all species studied from fruit flies to humans. The suprachiasmatic nucleus, a small area in the hypothalamus comprising around 25 000 neurons, has been established as the ‘master clock’, with the capacity to influence all circadian rhythms throughout the body (Figure 1.5).

Figure 1.5 The suprachiasmatic nucleus in the hypothalamus is circled with magnification of the cellular component. This small area of the brain contains around 25 000 neurons but is the ‘master’ timekeeper of all circadian rhythms in the body.

The effects of age

The quantity and, particularly, the quality of sleep change enormously across the normal lifespan. Newborns typically spend over half of the 24-hour period in a state resembling REM sleep. They have wakeful episodes lasting two or three hours interspersed with similar relatively short sleep periods across the day–night period. In the first two years, a prolonged nocturnal sleep usually becomes established, invariably encouraged by parental input, with afternoon naps remaining the norm until around five years of age.

The commonest pattern through teenage life is for sleep onset to become progressively later. Although lifestyle factors and habits may fuel this tendency, there is also evidence that most teenagers have internal clock mechanisms predisposing them to become ‘night owls’. The most obvious practical consequence of this pattern is extreme difficulty arising at a conventional hour for educational purposes.

Beyond adolescence, however, the brain's internal clock tends to ‘advance’. With each subsequent decade, the natural desire to sleep typically occurs around 30 minutes earlier.

The most striking age-related change in sleep patterns relates to a progressive deterioration in sleep consolidation. Several minor arousals, usually later in the night, might be considered normal in early middle-age. In the healthy elderly, frank sleep fragmentation is extremely common. The depth of slow wave sleep (non-REM stages 3 and 4) also reduces dramatically with age, with the earliest changes evident in males as young as 25.