University of Groningen. Insomnia in perspective Verbeek, Henrica Maria Johanna Cornelia

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1 University of Groningen Insomnia in perspective Verbeek, Henrica Maria Johanna Cornelia IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from it. Please check the document version below. Document Version Publisher's PDF, also known as Version of record Publication date: 2004 Link to publication in University of Groningen/UMCG research database Citation for published version (APA): Verbeek, H. M. J. C. (2004). Insomnia in perspective: diagnosis, treatment and education Groningen: s.n. Copyright Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons). Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. Downloaded from the University of Groningen/UMCG research database (Pure): For technical reasons the number of authors shown on this cover page is limited to 10 maximum. Download date:

2 Chapter 1 Introduction Aristotle wrote a monograph about insomnia ( De Insomnia ) in the Greek Antiquity. After that time, our knowledge about sleep remained unchanged until the middle of the last century. For centuries, sleep had been considered a passive happening, where only the depth of sleep could change. Dreams were considered as guardians of sleep in that external stimuli that could wake the sleeper were thought to be taken up by the brain and made into dreams. In this way dreams were thought to protect the sleeper against unimportant interruptions that otherwise would wake the sleeper. According to Freud, dreams are the royal way to unconsciousness (Freud, 1942). In 1953, the discovery of rapid eye moments (REMs) during a period of sleep in which dreams occur (now called REM sleep), led to a completely different idea about sleep. Sleep is now seen as an active process in which different kinds of sleep occur, each with its own characteristics and functions. The social aspect of sleep was recognized after the industrial revolution because employers had an interest in well-rested workers. The eighthour working day and altered ideas about housing (each family member having their own room if possible) led to different sleep behavior. Together with the discovery of electric light in 1913, the collective habit of going to bed with the birds disappeared. Besides prosperity, our altered way of life brought more sleep problems. In 1979, the Association of Sleep Disorders Centres (ASDC) in the USA proposed a classification system for sleep disorders based on four groups: - insomnias (disorders of initiating and maintaining sleep) - hypersomnias (disorders of excessive sleep) - dyssomnias (disorders of the circadian rhythm) - parasomnias (disorders during sleep). This classification was of great importance. Sleep disorders were no longer seen merely as a symptom of a somatic disease or mood disorder. This classification system was updated in 1990 and again in Since sleep disorders were added in 1987 as a distinct diagnostic category in the Diagnostic and Statistical Manual of Mental Disorders (DSM), sleep complaints can also be considered to be within the domain of psychotherapists (DSM-IV-R, 2001). In 1993 the Dutch College of General Practitioners (Nederlands Huisartsen Genootschap, or NHG) published Sleeplessness and Hypnotics, guidelines for general practitioners on the diagnosis and treatment of insomnia and updated them again in 1999 (Knuistingh Neven et al., 1993, 1999). The guidelines highlight that General Practitioners (G.P.s) generally should prevent chronic use of hypnotics. Attention for the economic consequences of sleep disorders has developed only recently. In 1988, the American Sleep Disorders Association stated that the accidents with nuclear power stations in Three Mile Island and Chernobyl were attributable to human error. The people running the stations failed to take into account the fact that the risk of error as a result of sleepiness is highest between 1.00 and 6.00 a.m., with the risk probably heightened by the monotonous computer 7

3 work of the operators. The costs of poor sleep both direct costs related to treatment and indirect costs related to accidents and loss of productivity were estimated by Stoller (1994) for the United States of America between 92 and 107 billion dollars. In this chapter, the backgrounds of sleep and the different disorders are discussed. The focus lies on the diagnosis and treatment of insomnia, because this disorder has a high prevalence and is the main topic of this thesis. 1.1 Characteristics of sleep Sleep is a daily recurring phenomenon that serves to allow an individual to recover from exertions and gain energy for new activities. Even after years of fundamental research, the exact functions of sleep are still not fully understood. Sleep is a complex mixture of physiological and behavioral processes. The question of Why do we sleep? is therefore difficult to answer. The common assumption is that sleep serves to rest and restore both mind and body. However, there are studies that show that the body does not need sleep for restoration. The synthesis of proteins and division of cells are dependent on nourishment, circadian rhythm and rest. We do not need sleep for that. Another theory about the function of sleep is that during sleep our brain is put partly on non-active, making it possible to execute tasks that are difficult when fully awake (e.g. information processing, erasing superfluous memories and brain connections that are rarely used). For the time being, this theory is speculative Sleep stages and sleep cycles The most important procedure for monitoring sleep is polysomnography (PSG). This procedure consists of an electroencephalogram (EEG), electromyogram (EMG) and an electro-oculogram (EOG). In the EEG, electrical signals from the brain are registered by electrodes placed on the scalp. In the EEG, waves are seen of a certain frequency (number of waves per second) and amplitude (height or size). The brain activity is fast during wakefulness, and it slows down during sleep. In this way sleep and wake may be distinguished from each other. Two types of sleep are identified by the EEG: rapid-eye-movement (REM) and non-rapid-eyemovement (NREM) sleep. NREM sleep is further subdivided into four stages: from stage 1 (very light sleep) to stage 4 (deepest stage of sleep). During NREM sleep most physiological functions are slowed down (e.g. heart rate and respiration rate). The five sorts of sleep are described below. NREM1 is a transition stage between wake and sleep. During this stage, slow eye movements (SEM) are seen and the frequency of the EEG slows down. NREM1 takes only 2 5% of the total amount of sleep (10 20 minutes). NREM2 follows this short period of NREM1 sleep. In this stage a more intense stimulus is necessary to wake a person. Many chronic insomniacs do not experience NREM2 as real sleep. NREM2 is defined as the beginning of sleep and lasts minutes in the first sleep cycle. The total amount during the night is 45 55% ( minutes). 8

4 NREM3 follows and this stage is characterized as a gradual shifting to slow and high waves; it is the transition to NREM4 sleep. During the night, the total amount of NREM3 sleep is only 3 8% (15 40 minutes). NREM4 produces slow and high waves during more than 50% of the time. The duration of NREM4 sleep in the first sleep cycle is minutes. The total amount of NREM4 sleep is 15 20% of total sleep time (75 90 minutes). The amount of NREM4 sleep decreases with age. REM sleep, which is also called dream sleep, follows NREM4 after a short transition to lighter sleep. REM sleep is characterized by fast waves, as if a person is awake. To an observer it is clear that there is sleep: there is atonia of the muscles of the limbs. Rapid eye movements are seen under the closed eyes. Dreams occur mostly during REM sleep. During the first sleep cycle the duration of REM sleep is short; in total it takes % of the total sleep time ( minutes). Figure 1: Hypnogram of normal sleep of an adult NREM and REM sleep alternate during the night in the sequence described above. The sequence of light sleep, deep sleep and dream sleep is called a sleep cycle. The duration of one sleep cycle varies from 90 to 120 minutes. The total night sleep is built up of four to five of these sleep cycles, which can be shown clearly in a so-called hypnogram (figure 1). In figure 1 a shift during the night is evident. Deep sleep (NREM3 and NREM4) is predominant in the first part of the night, whereas the proportion of NREM2 and REM sleep is much greater in the last part of the night. Short periods of wake occur in the last part of the night. These periods are of short duration and are often not remembered the following day. The amount of wake during sleep is 5% of total sleep time. Horne postulated that only a part of a normal night of sleep is essential (core sleep) and that the remaining sleep exists primarily as a buffer (optional sleep) (Horne, 1987). Core sleep covers the first 3 sleep cycles, where nearly all deep sleep and a great part of REM sleep take place. Although the quality of sleep 9

5 dependent. Newborn babies spend about 50% of their sleep time in REM sleep. The percentage of REM sleep is stabilized by late adolescence (about 20 25%) and remains essentially unchanged until late life, when a slight decrease is seen. The proportion of stage 2 sleep remains fairly consistent across age groups. As people grow older, besides an increase in stage 1 sleep, the predominant change is that less deep sleep (especially NREM4) is seen. Slow-wave sleep diminishes gradually and fairly consistently from childhood to old age. Subjectively, these changes are experienced as lighter and more fragmented sleep, which may account for the increased prevalence of insomnia complaints in late life. 1.2 Sleep disorders The International Classification of Sleep Disorders (ICSD) was introduced in 1979 as a tool for clinical practice and research in sleep-disorders medicine. The first classification was based on symptoms. In 1990 and 1997 this classification was revised and based on the etiology. A total of 88 sleep wake disorders are described and classified in four main groups. 1. Dyssomnias The dyssomnias are the disorders that produce either difficulty initiating or maintaining sleep, or excessive sleepiness. This section is subdivided into three groups of disorders: Intrinsic sleep disorders (either originating or developing within the body) Extrinsic sleep disorders (either originating or developing from causes outside the body) Circadian-rhythm sleep disorders (related to the timing of sleep within the 24-hour day) 2. Parasomnias The parasomnias are disorders that intrude into the sleep process and are not primarily disorders of sleep and wake states per se. These disorders are manifestations of central nervous system activation, usually transmitted through skeletal muscle or autonomic nervous system channels. They are subdivided into four groups: Arousal disorders Sleep-Wake transition disorders Parasomnias usually associated with REM sleep Other parasomnias 3. Sleep disorders associated with mental, neurological, or other medical disorders This section lists those disorders that are not primarily sleep disorders but have either sleep disturbance or excessive sleepiness as a major feature of the disorder. There are three groups: Associated with mental disorders Associated with neurological disorders Associated with other medical disorders 4. Proposed sleep disorders This section lists those disorders for which there is insufficient information available to confirm existence of the disorder. 11

6 1.3 Insomnia Insomnia is characterized by difficulty with initiating, maintaining, or obtaining good quality sleep. One-third of all adults report some type of occasional insomnia. The prevalence of chronic insomnia is 9 10% (Roth, 1999; Swinkels, 1993). Individuals with insomnia typically report daytime symptoms such as fatigue, mood disturbances, memory dysfunction and reduced quality of life (Riedel&Lichstein, 2000). These daytime consequences of insomnia are associated with increased absenteeism, higher health-care utilization, psychiatric and medical care, and risk of alcohol and/or medication abuse. Insomnia therefore represents a risk factor for a variety of dysfunctions (Walsh & Üstün, 1999). Among patients with an insomnia complaint who were referred from primary care to sleep disorder centers, insomnia related to mental disorders was the most frequent diagnosis (46%), with primary insomnia being the next most frequent sleep diagnosis (22%)(Hajak, 2000). According to the International Classification of Sleep Disorders (ICSD, 1997), the most common types of primary insomnia are psycho-physiological insomnia, sleep state misperception, idiopathic insomnia, inadequate sleep hygiene, and hypnotic-dependent sleep disorder. Without going into detail about the specific criteria of each of these diagnoses, the common features of chronic primary insomnia according to both the ICSD and the DSM- IV-R (2001) are as follows: primary complaint of sleep onset and/or sleep maintenance insomnia and/or early morning awakening or non-refreshing sleep during a period of at least six months the sleep complaints lead to dysfunction during the day (social, work) the sleep disorder does not occur exclusively in the course of narcolepsy, sleeprelated breathing disorder, circadian-rhythm disorder or parasomnia the sleep disorder does not occur exclusively in the course of a psychiatric disorder (depression, general anxiety disorder) the sleep disorder is not the result of direct physiological effects of drugs or medicine or a somatic disorder there are indications of learned sleep-preventing associations (trying too hard to sleep, conditioned arousal to bedroom or sleep-related activities). It is important that this definition focuses not only on complaints during the night, but also on the relation with functioning during the day. This concerns mainly tiredness, irritability, sleepiness and problems with cognitive functioning. If there are no problems in functioning during the day, we do not speak of a sleep disorder. In chronic insomnia, often there has been a stressor that led to the insomnia, but this cannot usually explain why the complaints continue to exist. Other factors like predisposition, maladaptive habits and dysfunctional cognitions about sleep are responsible for perpetuation of the complaints. 1.4 Diagnosis Insomnia is a subjective complaint about duration, efficiency and quality of sleep. Therefore, it is very important that the physician listen to the story of the patient in 12

7 a clinical interview and as well as provide for a sleep log registration. In certain cases, polysomnography or actigraphy may be necessary or useful Clinical interview A detailed review of the sleep problem is conducted with the patient during the clinical interview. The most important components of the clinical interview are a detailed sleep history and a careful functional analysis of its controlling variables. A sleep history includes assessment of the nature of the sleep complaint; the patient s typical sleep wake schedule; the impact of disturbed sleep on daytime functioning; the natural history of insomnia; medication use; dietary, smoking, and exercise habits; screening for other sleep disorders; and a medical history. The functional analysis investigates predisposing, precipitating and perpetuating factors (maladaptive habits and dysfunctional cognitions). A clinical interview assessed by a G.P. will be shorter than one assessed by a psychologist. To obtain a preliminary impression of the complaint, the following questions may be helpful: - How long have you been suffering from sleep problems? (acute or chronic) - How many nights per week do you suffer from sleep problems? - What are the consequences during the day? (Do you feel tired and sleepy?) - Do you have problems falling asleep? If yes, how long does it take? - Do you awake earlier than you wish? When? - How often do you awake during the night? How long are you awake? What wakes you up? - What do you think is the cause? - Is there a somatic cause? (pain, itching, sleep apnea, periodic limb movement, restless legs) - Is there a psychiatric cause? (depression, fear) - Do you work in shifts? Are there changes in schedules? - Do you use alcohol before going to sleep? - How much coffee, tea or cocoa do you drink in the evening? - Which medicines do you use? - What have you done to obtain a better sleep? The complaint I sleep so poorly may be a symptom of a psychiatric or organic disorder. Problems with initiating sleep are often seen in patients with anxiety disorders, and early awakening is a classical symptom of depression. The differential diagnosis is often difficult because of the co-morbidity: both insomnia and a mood disorder may occur Sleep log As insomnia is a subjective complaint, self-monitoring of sleep has proven an invaluable assessment tool. A sleep log may be a useful supplement to the clinical interview. A typical sleep log requires daily recording (for one to two weeks) of the following parameters: bedtime, arising time, sleep-onset latency (SOL), minutes of wake after sleep onset (WASO), number of awakenings (AWAK), time of last awakening, naps, medication, caffeine and alcohol intake, and some indices of sleep quality. An example of a sleep log is shown in figure 2. 13

8 Figure 2: Example of a sleep log Assessment of subjective sleep by way of a sleep log has several advantages, both for the patient and his/her physician: - Maintaining a sleep log helps establish a baseline of the initial severity of the sleep problem, both for the patient and the physician. Patients may realize after a few days of self-monitoring that they get more sleep than they initially thought. Enhanced awareness may decrease the patient s anxiety over sleep loss, and consequently may alleviate the subjective complaints. - Sleep diaries provide a better understanding of how sleep patterns change over time and can pinpoint situational and temporal factors contributing to these variations. - The sleep log is an excellent tool for monitoring progress over the course of treatment. - The influences of medication, caffeine, alcohol and lifestyle become clear. - A sleep log appeals to the responsibility of the patient; his/her subjective sleep is the basis for treatment. The sleep complaints are taken seriously. - Compliance with keeping the sleep log provides a test of expected compliance with the intervention. The main drawbacks of sleep log monitoring have to do with validity. Insomniacs have a tendency to overestimate sleep-onset latency and to underestimate total sleep duration in comparison to EEG measurement (Carskadon et al., 1976). However, daily monitoring estimates of specific sleep parameters (SOL, WASO) 14

9 yield a reliable and valid relative index of insomnia, even though they do not reflect the absolute values obtained from polysomnography. Furthermore, daily estimates are less subject to exaggeration than a single, global and retrospective measure. Sleep logs are inexpensive compared to polysomnography. Although subjective sleep is measured, one or two weeks of daily registration of subjective sleep gives a more representative view of one s sleep than do one or two nights of PSG, often in laboratory conditions. This is particularly important in light of the extensive nightto-night variability in the sleep patterns of chronic insomniacs. Thus, daily sleep log monitoring is the most practical, most economical, and most widely used method for assessing insomnia Polysomnography Nocturnal polysomnography is recognized as the golden standard for sleep measurement and provides the most comprehensive assessment of a sleep disorder. It is the only assessment modality yielding data about sleep stages, and is therefore the only method that can generate a hypnogram (figure 1). A PSG evaluation involves all-night electrographic monitoring of sleep (EEG, EOG, EMG), ECG, leg movements, respiration and oxygen desaturation. PSG is essential for diagnosing and documenting the severity of sleep-related breathing disorders, periodic-limb-movement disorder, and narcolepsy. Despite the wealth of information provided by nocturnal PSG, its role in the assessment and differential diagnosis of chronic insomnia is controversial. It is unlikely that one night of sleep laboratory evaluation will yield valid and reliable information of insomnia severity. The well-known first-night-effect (worsening of sleep), or the more common reverse first-night-effect in insomniacs, limits its clinical usefulness with these patients. The American Sleep Disorders Association (ASDA) published practice parameters for the use of PSG in the evaluation of insomnia in 1995 and updated them again in 2003 (Littner et al., 2003). Insomnia is diagnosed clinically primarily with a detailed medical, psychiatric, and sleep history. PSG is not indicated for the routine evaluation of insomnia. PSG is indicated when either a sleep-related breathing disorder or periodic limb movement disorder is suspected, initial diagnosis is uncertain, treatment fails, or arousals occur with violent or injurious behavior. We add that PSG is also useful in determining the level of discrepancy between the subjective complaint and actual, objective sleep as seen in sleep-state misperception Actigraphy Professionals have sought ways other than PSG for measuring sleep objectively. The great night-to-night variability in insomnia makes it time-consuming and expensive to measure with PSG. Therefore actigraphy is often used for clinical and research evaluation of sleep disorders. The wrist actigraph is a small portable device that is worn on the wrist and senses physical motion; it generates an internal signal each time it is moved (accelerated). This ambulatory monitoring system uses a microprocessor to record and store this signal along with actual clock time. Data are recovered and processed through microcomputer software. An 15

10 algorithm is used for estimating sleep-onset latency (SOL), wake after sleep onset (WASO), and total sleep time (TST). Global measurements of sleep duration and wake time as estimated from wrist actigraphy are highly correlated with PSG recordings in good sleepers. However, mixed results have been obtained with insomniacs, especially when absolute values of SOL, WASO and TST are compared. These discrepancies are particularly pronounced with patients with low levels of behavioral activity while awake (e.g. depressed patients) and patients with high levels of behavioral activity while asleep (e.g. non-refreshed sleep). 1.5 Treatment strategies Basis of treatment Several interventions have been developed for the treatment of chronic insomnia. The theoretical foundation upon which these interventions are based is broad. In general, the development of insomnia can be explained by physiological hyperarousal, cognitive hyper-arousal and conditioning. * physiological hyper-arousal The approach using physiological hyper-arousal as an explanatory model comes from studies that showed that among poor sleepers the measures for physiological hyper-arousal are higher than for good sleepers. Insomniacs have higher heart rates, body temperature, basal skin resistance, phasic vasoconstriction, and frontalis EMG activation than normal sleepers. Moreover, compared with good sleepers, insomniacs have higher metabolic rates during night and day (Bonnet et al., 1995&1998, Lamarche et al., 1997). When evaluated as a single component treatment for insomnia, relaxation methods produce moderately-sized effects (Morin et al., 1994). Based on research, one cannot say that physiological arousal plays a causal role in insomnia. * cognitive hyper-arousal The explanation of cognitive hyperactivity links up with the experience of many insomniacs who see worrying as a cause of their sleep problem (Lichtstein & Rosenthal, 1980). Measurements for cognitive arousal, like the pre-sleep arousal scale, show a significant correlation between cognitive arousal and sleep variables (Nicassio et al., 1985). A study about specific pre-sleep intrusive thoughts that delay sleep showed three factors: active problem-solving, present-state monitoring and environmental reactivity (Wicklow & Espie, 2000). So besides the arousal aspect, the content of the cognitions is also important. Often this concerns catastrophic interpretations of sleeping behavior. One common example is the demand of many people to get eight hours of sleep. They think that sleeping less will automatically give them serious problems. Interventions for altering these cognitions include thought-stopping and rational emotive training. * conditioning Bootzin and Nicassio (1978) explain the maintenance of insomnia through conditioning. Whereas normally stimuli around the sleep situation (bed, bedroom, 16

11 rituals before going to bed) function as an introduction to become sleepy, these stimuli have an opposite effect in people with sleep problems. Because of the prolonged association with unpleasant experiences such as unintentionally being awake, these stimuli evoke behavior that is incompatible with sleep. The most important one is probably worrying about how not sleeping will influence the following day. Other behaviors that are often seen are reading in bed, watching television and eating. Interventions that influence these are stimulus control and sleep restriction (see Non-pharmacological treatment). * the operant factor Not sleeping may also have an unintentional positive effect. This operant factor may contribute to continued existence of the complaint. The following case is a nice example of this from practice. Mrs. X is 67 and has been awakening for years between 1.00 and 2.00 am. Because she cannot fall back to sleep, she rises and gets herself a nice sandwich with butter and jam. In this way she feels better and falls back to sleep easily. She suffers from heart problems and therefore she has to maintain a strict diet. Butter and jam are not allowed. The positive consequences of being awake during the night (eating forbidden foods), makes it probable that the next night she will also awaken. * multi-factorial model Besides the hypotheses mentioned above, which all identify one cause of insomnia, it has come to be assumed that in insomnia there is a complex interaction between physiological, cognitive and behavioral factors (Espie, 1991). With regard to treatment, this means that often a single intervention is insufficient. A model that describes more factors that affect insomnia is given in figure 3. 17

12 is more important than quantity (the amount of hours), not many people are satisfied with only 5 hours of sleep Sleep and the arousal system The feeling of being wide awake depends on more than a good night s sleep; the possibility to relax both mentally and physically is at least as important. We make a distinction between somatic, cognitive and emotional arousals (see also Basis of treatment). We cannot expect to feel rested after five hours of sleep if our arousal system is out of balance. In our 24-hour society, in which everything has to happen faster, time for relaxation both mentally and physically is scarce. Relaxation and exertion are out of balance. This affects sleep in a negative way: restlessness is taken into the night Sleep history and circadian factors In addition to being influenced by the arousal system, the duration and quality of sleep are also dependent upon prior sleep history (the longer one has been awake, the greater the sleep deficit and the faster sleep onset occurs) and circadian factors. Chronobiological research has identified several circadian (meaning about a day ) rhythms. The best known is that of day and night. The sleep wake cycle follows a circadian periodicity that is dependent upon both intrinsic and extrinsic influences. The intrinsic factor is our biological clock, which determines whether we are morning or evening types. Our individual need for sleep (long or short) is also an intrinsic factor. Our sleep is also influenced by extrinsic time cues ( Zeitgebers ); e.g. the light dark cycle, work times, social contacts and mealtimes Individual differences There can be large differences in inter-individual sleep behavior. Evening types prefer to go to bed late and rise late. Morning types would rather go to bed early and rise early. A morning type will never become an evening type (and vice versa). Our biological clock can only make adaptations of a few hours. There are also differences in the composition, depth and duration of sleep. Short sleepers, for example, need only five hours of sleep to feel well rested, while long sleepers need double the time (nine to ten hours) Sleep and age Total sleep time is highest in infancy and gradually declines, leveling off in young adulthood. Average sleep time per 24-hour cycle decreases from about 16 hours during infancy to hours in early childhood and about 7 9 hours in the midtwenties. As people grow older (above 45 years of age), sleep becomes more fragmented. This means that people may awake more easily during the night and that they sleep less deeply. However, for people above 60 years of age, daytime napping is a common practice and when this diurnal sleep is added to nighttime sleep, the amount of sleep per 24-hour period remains fairly stable from middle age to late life. Napping in old age, however, cannot simply be equated with unfulfilled sleep need, because both cultural and social factors undoubtedly play a role. The proportion of time spent in NREM en REM sleep stages is age 10

13 Figure 3: A model of insomnia (from Insomnia: psychological assessment and management. CM Morin, The Guilford Press New York, 1993) Non-pharmacological treatment The complex symptomatology of sleep complaints and the frequent absence of clear cause effect relations have led to the development of multi-modal interventions. Each method contains educational, behavioral and cognitive elements. In The Netherlands, Klip et al. investigated multi-component treatment of chronic insomniacs in the 1970s (Klip et al. 1978). The most frequently applied and investigated non-pharmacological treatment of chronic insomnia is the cognitive behavioral treatment (CBT) (Hauri, 1997; Morin et al., 1999; Edinger et al., 2001). CBT has become the first choice of treatment. Treatment modules have a certain composition and are easy to explain to patients. Self-monitoring The sleep log as discussed previously is the most commonly used method for selfmonitoring. Every morning the patient records several sleep parameters (see Sleep log). Self-monitoring requires an active role of the patient; he/she has to show what the sleep was like. In this way patients feel they are taken seriously. Psycho-education Psycho-education includes information about sleep stages (figure 1), core and optional sleep, the changes of sleep during the lifespan (1.1.5 Sleep and age) and lifestyle. Insomniacs often make high demands ( I have to sleep eight hours or If I don t sleep by 12 o clock I will not sleep the whole night ). Discussing individual 18

14 differences (short versus long sleepers, evening versus morning types) can bring these demands to a more realistic level. When these dysfunctional cognitions are strong, cognitive therapy may be indicated; this will be discussed later. Sleep hygiene Sleep hygiene involves many guidelines and measures of an ordinary character. Because they seem so ordinary, they often are not taken seriously by the patient. Consistent implementation, however, often leads to good results. These guidelines are given to the patient after the first consultation and before more intensive treatment is given. They return in a more intensive way in the various components of cognitive behavioral treatment, which are discussed later in this chapter. The most commonly used guidelines are: - Keep regular times to go to bed and to rise. In the weekends, the time to rise may shift a maximum of two hours compared to week days. - Reduce the time in bed to a maximum of eight hours. - Save the bed for sleeping and sexual activity. Get up if you cannot fall asleep within minutes. Go to another room and relax (e.g., read or watch television). Only go back to bed when relaxed. - Reduce reading and watching television in bed to a maximum of 30 minutes. - Relax before you go to sleep: unwind and avoid intensive mental and physical activities during the last hour before bedtime. - Do not nap during the evening; a short nap during the day (maximum 30 minutes) is no problem as long as it does not cause deterioration of nighttime sleep. - Turn our alarm clock away from you to avoid watching the time all the time. Knowing what time it is only produces restlessness. - Avoid caffeine after 6 pm (coffee, black tea, coca-cola, chocolate). - Do not use alcohol as a nightcap. One to two glasses spread over the evening is no problem. - Exercise during the day is desirable. * Sleep environment Ideally, the sleep environment (bedroom, bed, blankets, and pillows) is neutral. A hard bed can lead to many body movements, more frequent awakenings and more NREM1. For couples, it is useful to know that sleeping alone leads to more NREM4 and less REM sleep. The feeling of safety when sleeping together also has advantages. Knowing the time because of an illuminated alarm clock may be the evidence that the insomniac is awake for hours and the time to sleep is much too short. Therefore, hide illuminated alarms to avoid clock-watching during the night. A hot bedroom may interrupt sleep and even induce nightmares. The ideal temperature is about degrees Celsius. If the bedroom is not illuminated fully, bedroom sounds should be low and consistent. A high level of noise increases the level of arousal and disrupts sleep (Hofman, 1994). When sleeping in a noisy environment, use earplugs or tune the radio between two FM stations for white noise. 19

15 * Food Going to bed with a full stomach leads to increased activity of the digestive organs, which prevents the decrease of physiological activity that is necessary before sleep. An empty stomach is also not beneficial to a good sleep. Dairy products may be used as a remedy to this, since the tryptophan in those products has a mild sleep-inducing effect. In moderate quantities (one to two glasses), alcohol may be used as a nightcap. Sleep-onset latency is shortened, but total sleep time does not really increase. In larger quantities, alcohol may initially deepen sleep and decrease the percentage of REM sleep early in the night, but this is usually followed in the latter part of the night by a REM rebound, impairment of sleep continuity and early morning awakening. Coffee, tea and cocoa contain stimulating materials that can disrupt sleep certainly the sleep of insomniacs. The same applies for soft drinks with caffeine or quinine. * Exercise The relation between exercise and sleep is complicated. Intensive exercise in the evening may deepen sleep in the latter part of the night, but may also increase sleep-onset latency. Exercise during the day does not really affect sleep. Moderate exercise in the beginning of the evening (e.g. jogging) may shorten sleep-onset latency and increase NREM4 in the first sleep cycle. * Rituals Going to bed is associated with specific behavior that normally is performed in a fixed order. For a good sleeper, this behavior contributes to a healthy sleep. Poor sleepers associated this behavior with poor sleep. It may be necessary to build up a new ritual. For example, turn off the television one hour before bedtime, listen to your favorite music, take a shower, and do not hold intensive discussions in bed. Combined with other guidelines, this can contribute to good circumstances for sleeping. Behavioral component Insomnia sufferers frequently develop strategies for coping with their sleep difficulties. Spending excessive amounts of time in bed, sleeping late in the morning, and routine daytime napping often help people to cope with the shortterm detrimental effects of insomnia. In the long run, however, these same coping strategies interfere with sleep and perpetuate insomnia problems. The behavioral therapy component involves a combination of stimulus control and sleep restriction procedures. These procedures are designed to eliminate sleep-incompatible behaviors, to regulate the sleep wake schedule, and to consolidate sleep over a shorter period of time spent in bed. * Stimulus control The goals of applying stimulus control are to help the insomniac to learn to fall asleep quickly and to maintain sleep by strengthening the association with the bed as being a cue for sleep, and weakening the association with it as being a cue for waking activities (Bootzin and Nicassion 1978). 20

16 They suggest the following procedures to the patient: 1. Go to bed only when sleepy. 2. Use the bed only to sleep or for sexual activity, so do not watch television or read in bed. 3. If unable to fall asleep after minutes, get up and go into another room. Stay up as long as needed to feel sleepy and relaxed. 4. Repeat step 3 as often as necessary. 5. Get out of bed at the same time each morning, irrespective of the amount of time slept. 6. Do not nap during the day. * Sleep restriction A variant of stimulus control is sleep restriction (Spielman 1987). Sleep restriction is designed to enhance the patient s nocturnal sleep while the patient temporarily accepts daytime fatigue as a side effect. If, for example, the sleep log shows five hours sleep when time in bed is eight hours, sleep efficiency is 63%. It is then suggested to the patient to reduce the time in bed to five hours (never below five hours!). After one week, total sleep time during one night per week may be one hour longer. If sleep efficiency increases to 85% or more for more than five nights, time in bed is gradually increased with 15 minutes each week. The first 2 3 weeks of treatment are the most difficult. For both stimulus control and sleep restriction it is necessary that the patient be motivated. During the first weeks of treatment daytime fatigue often increases. Relaxation The essential condition for sleep is that the patient be relaxed. Progressive relaxation techniques teach the patient to feel and use the difference between muscle tension and relaxation by stretching and relaxing muscular parts of the body, based on the idea that relaxing the body may also lead to a slowing of a racing mind (Jacobson, 1983). An alternative to progressive relaxation is autogenic training, which is a form of self-hypnosis. In section 1.5 (Basis of treatment) it is stated that relaxation procedures do not have much effect on sleep. However, relaxation procedures may be an effective coping mechanism for cognitive arousal (worrying). * Thought stopping The goal of thought stopping is to stop cognitive arousal like ruminant thoughts that interfere with sleep. During one of the treatment sessions thought stopping is practiced. The procedure is to let the patient think about ruminant thoughts with his/her eyes closed. Next, the therapist calls STOP and shows that the thoughts can be stopped. Then the patient says STOP during ruminant thoughts and visualizes an image that strengthens the word stop (red light, ravine, safe-deposit). The last step is to replace the ruminant thoughts by pleasant thoughts (holiday, 21

17 nature, etc.). Sleep disrupting cognitions may also be the focus of cognitive therapy. Cognitive therapy The goal of cognitive therapy in sleep disorders is to break through the so-called vicious circle of insomnia, in which dysfunctional cognitions and emotions lead to a further disturbance of sleep. The cognitive therapy component consists essentially of cognitive restructuring techniques. A three-step process is typically followed for achieving these goals: - identifying patient-specific dysfunctional cognitions - confronting and challenging their validity - replacing them with more adaptive and rational substitutes * Dysfunctional ideas about the cause of insomnia Some people have a very explicit conviction about the cause of their insomnia, for example, pain, allergy, age or depression. Although these factors may play a role in insomnia, they do not help to control the sleep problem. On the contrary, these ideas evoke a feeling of helplessness. My sleeplessness is caused by a biochemical disorder, implies the following underlying thought: If this disorder is not ameliorated, I cannot do anything about my sleep complaint. The mistake in thinking here is absolute thinking and incorrect argumentation. The re-attribution is: - insomnia cannot be explained solely by external factors - behavioral and psychological factors always play a role in the perpetuation of chronic sleeplessness, irrespective of the initial cause - sleep may be improved because these factors may be influenced. * Trying to control sleep Sleep may be different each night; this is especially true for insomniacs. This may lead to the idea that sleep cannot be controlled, which may lead to stress; thus the vicious circle is strengthened. Cognitive therapy tries to break through this process. The thought I am afraid that I will never sleep again may spring from the underlying idea that all things in life have to be controlled completely. Mistakes in thinking here are catastrophic and irrational thinking. A suggestion for an alternative thought may be What is the worst thing that might happen if you do not go to bed tonight? or The more you try, the less it will succeed. It is easier to try to stay awake than to try to fall asleep. * Non-realistic expectations about sleep and daytime consequences The most common misunderstanding about sleep is that everybody needs eight hours of sleep. This demand may lead to many sleepless nights, especially when this idea is accompanied with the idea that eight hours of sleep is necessary to function well during the day. The mistake in thinking is absolute thinking and generalizing. To help re-attribute this thinking, it may help to point out that also other factors influence mood and that worrying about sleeplessness may have a more harmful effect on health than poor sleep itself. People may worry seriously about the consequences of poor sleep on physical and mental health. Although the 22

18 burden one has because of sleep complaints may never be underestimated, research about the effects of sleep deprivation shows that effects are relatively small. People do feel tired, irritable and think they perform worse after a poor sleep, but objective tests show few symptoms. * False assumptions about sleep-inducing activities Assumptions like If I sleep poorly, I stay in bed longer the next day in the hope to sleep some more and I need a nap during the day have false starting points. With the help of a hypnogram (figure 1), one can explain that in the morning NREM1 and NREM2 predominate, a type of sleep with no function in energizing. A nap during the day often leads to a worse sleep during the night. Although psychoeducation and sleep hygiene guidelines can take away many misunderstandings, the tracing of dysfunctional cognitions is important. The main reason is that the patient tries to re-formulate alternative thoughts and to play an active role. Cognitive restructuring becomes a coping strategy that strengthens self-esteem, especially when it leads to better sleep. * Fear of sleep A different problem to treat is fear of sleep. The primary condition for sleep is to give up control. External stimuli (noise, sound, light) are dimmed, the eyes close, and temperature changes are absorbed by blankets. Still, much can happen during the night; burglaries, nightmares, or even death. For sick persons this is not unlikely; the end of the night is a critical phase for health. Falling asleep acquires the ambivalent meaning of passing away. In the Greek Antiquity the God of sleep (Hypnos) and the God of death (Thanatos) are half-brothers. This fear of loss of control will probably also manifest itself in other life areas. Treatment will require more that only behavioral treatment of the sleep disorder. Medication withdrawal Withdrawal from hypnotics is an essential part of treatment. Although it is generally desirable to begin decreasing medication intake early, a patient s readiness, anxiety level, and self-efficacy often determine the most appropriate timing for introducing this component. Apart from the many side effects, such as a hangover during the day, the long-term use of benzodiazepines (the most commonly-used hypnotics) can also induce sleep complaints (drug-induced insomnia). For many patients, it is surprising to know that the drugs they use to reduce their sleep complaints have an opposite effect in the long run because natural sleep architecture is affected (see also Pharmacological treatment). Although an occasional hypnotic may be helpful for some people, a significant proportion of patients seeking insomnia treatment are dependent on sleep medication. A structured withdrawal schedule for gradually discontinuing the usage of sleeping aids is provided. The design and timing of the schedule within the overall intervention are individualized and based on the type, dosage, and frequency of drug use; the patient s readiness to discontinue medication; and the presence of concomitant psychiatric or physical disorders. An explanation of the withdrawal effects (e.g. temporary worsening of sleep problems, nightmares and malaise 23

19 during the day) is necessary. Sometimes long-term intermittent use (maximum of two tablets per week) is advisable. Format of treatment In the United States of America and Canada, Hauri and Morin wrote excellent manuals on how to assess and manage insomnia (Hauri, 1991; Morin, 1993). The cognitive behavioral therapy as it is given in our Centre for Sleep and Wake Disorders today is based mainly on the content of these books. There are several possibilities for the setting in which CBT is carried out. In The Netherlands, one possibility is the sleep course offered by the National Association for Home Care ( Thuiszorg Vereniging ). In many cities, twice a year a course is given in small groups (8 10 people) on how to sleep better. Psycho-education, relaxation techniques and sleep behavioral guidelines are the main elements. Other possible settings in the Netherlands include a few psychologists who are specialized in sleep disturbances and a few sleep disorders centres that offer integrated insomnia treatment. The treatment in the sleep disorders centres can be implemented either individually or in a group format (5 8 people). The duration of treatment is short (mean of six sessions, exclusive follow-up). An overview of the treatment protocol is given chapter 5 (table 1) Pharmacological treatment * Benzodiazepines The most commonly-used treatment of insomnia is hypnotics. Benzodiazepines are still widely used as the first treatment for insomnia. In the Netherlands, temazepam is the first choice. Daily use of hypnotics has several disadvantages: dependency and tolerance may develop, the amount of NREM1 and NREM2 increases, slowwave sleep (NREM3 and NREM4) decreases and REM latency is delayed. In summary, natural sleep architecture is affected. For many physicians, hypnotics are still the first choice of treatment. Although the short-term efficacy is positive, there are concerns about the long-term treatment of chronic insomnia with hypnotics. There is a recognized need for long-term randomized, double-blind, controlled trials of hypnotics. The effects observed under acute administration of hypnotics may change with chronic use. As insomnia often is a chronic or recurrent condition, and current pharmacological treatments are symptomatic, as they do not cure insomnia, the clinician is left with an absurd therapeutic situation: prescribing effective short-term treatments for a long-term disorder. The problems of using hypnotics to treat insomnia are: residual daytime effects such as sedation; memory impairment; falling; respiratory depression; rebound insomnia; medication abuse; tolerance development; dose escalation; dependency and withdrawal difficulties; and increased risk of death. Before prescribing hypnotics, the physician should assess the following: - Thorough evaluation, including behavioral, psychiatric, medical and substances histories. 24

20 - Make sure that co-morbid conditions have been not only identified, but treated as well. - Educate the patient regarding healthy sleep practices ( sleep hygiene ) - Implement simple behavioral treatment. The guidelines of the NHG standards ( Nederlands Huisartsen Genootschap or Dutch College of General Practitioners ) regarding hypnotics are: - hypnotics are sometimes necessary (e.g. psychosocial problems, circadian sleep disorders, chronic somatic disorder) - always combine with sleep hygiene guidelines - give 10 tablets as a maximum - do not refill prescriptions via pharmacy assistant - prescribe short-acting benzodiazepines - halve dosage for elderly - hypnotics can have interactions with alcohol and psycho-pharmaceuticals. * New-generation hypnotics The new generation of hypnotics is characterized by a shorter duration of action, which leads to fewer hangover effects. Furthermore, these hypnotics have fewer negative effects on sleep structure. Stilnoct, an imidazopyridine, belongs to this new generation of hypnotics and is the first choice in the United States of America. Sonate is a new ultra-short hypnotic (the half-life is ± 2 hours). * Anti-depressants Pharmacological alternatives to hypnotics, such as anti-depressants, are often recommended. Anti-depressants have powerful REM-sleep suppressing effects. Some have sedative properties and may hasten sleep (e.g. mirtazapine), while others have more energizing effects (e.g. fluoxetine). The problems here are that anti-depressants have more frequent side effects than hypnotics and that little data is available regarding the short-term and long-term efficacies for these agents in insomnia. * Other drugs that affect sleep Several drugs prescribed for medical disorders may secondarily alter sleep. Most steroids produce insomnia and some bronchodilators prescribed in the treatment of asthma have a stimulating effect. Although antihypertensive medications usually cause daytime sleepiness, some of the beta blockers increase sleep-onset latency and wake after sleep onset. Almost any central nervous system stimulant interferes with sleep. Caffeine and nicotine are both central nervous system stimulants and they fragment sleep. Alcohol, which is a central nervous system depressant, may initially deepen sleep and decrease the percentage of REM sleep early in the night, but this is usually followed in the latter part of the night by a REM rebound, impairment of sleep continuity, and early morning awakening. 1.6 Sleep education Despite substantial evidence supporting the efficacy of behavioral therapy, this treatment is still relatively unknown to the public and underused by general 25