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Insomnia is a complaint of unsatisfactory sleep. Traditionally, insomnia is subdivided into 4 categories: difficulties falling asleep, mid-sleep awakenings, early morning awakenings, and nonrestorative sleep. However, there is vast overlap among these categories, most insomniacs fit into more than one (29). A better way to divide insomnia is into transient insomnia (lasting a few days), short-term insomnia (lasting weeks), and chronic insomnia (lasting months and years). Because sleep needs vary from about 4 hours per night to about 9 hours per night among healthy individuals, insomnia cannot be diagnosed by the amount of sleep a person receives. Insomnia is distinguished from healthy short sleep by daytime consequences such as feelings of restlessness, irritability, impaired social and occupational functioning (30). If you sleep poorly at night but feel well during the day, you are not an insomniac but a person with a low need to sleep.
The prevalence of insomnia varies with the definition of it. In the United States, about one-third of adults report occasional difficulties with sleeping, about 10 percent rate their sleep problems as chronic and serious (1,55). Similar data are reported from other parts of the world (e.g., 62). Insomnia complaints are about 1.3 times more likely in women than in men, and they increase with age. Patients over 65 complain about 1.5 times more about insomnia than those under 65 (37).
The consequences of insomnia are manyfold. Most insomniacs complain bitterly about their impairment of daytime functioning, ability to concentrate, memory, and mood (2). It is much harder to find objective, laboratory documented impairment: On psychomotor tests, insomniacs may be more variable and slower than good sleepers in some reaction time tests (23, 49), there may be some impairment in the Romberg test (39), and in the remembering of previously learned material (40). Although most insomniacs complain about increased daytime sleepiness and fatigue, they take longer to fall asleep during daytime naps than normal sleepers, i.e., they seem hyperalert (59).
Insomniacs are more likely to drop out of difficult jobs and they receive fewer promotions than good sleepers (32). Also, insomnia is clearly a risk factor for the reoccurrence of depression (13). Insomniacs seek out ineffective and potentially harmful treatments such as over-the-counter medications and alcohol (40 percent have tried OTC's and/or alcohol for their insomnia) (15). In the elderly, an inability to sleep or at least to remain in bed at night is among the most frequent reasons for admission to nursing homes.
Walsh et al (61), estimated the direct cost of insomnia in 1991 in the United States at about $11 billion. This includes costs of medical care, both for self treatment borne by the patient and the cost borne by organized health care providers, insurance companies, etc. Roth (55) estimated the overall economic costs of insomnia in the United States at about $30 to $35 billion. Besides Walsh's direct costs, this includes associated costs to society such as decreased work productivity.
There is considerable debate among sleep specialists about how much insomnia is a syndrome, with general traits that always are present, and how much it is a symptom of very different underlying dysfunctions that have to be treated differentially.
Reported here are mainly group differences between insomniacs and normals. These group differences do not mean that all insomniacs show all of these characteristics. Also, there is considerable overlap in these traits between insomniacs and normal sleepers.
On questionnaires such as the MMPI (8, 33), insomniacs consistently show more psychopathology than normals. Typically, there is increased depression and anxiety and, very often, increased somatization. Insomniacs frequently deny psychological or emotional factors, seeking a somatic explanation for their insomnia. They score high on scales measuring hyperarousal (51) and they are sensation avoiders (8).
The sleep of most insomniac patients is highly variable. Extremely poor nights may vary with nights of adequate or even good sleep in an unpredictable fashion (34).
There is considerable evidence that insomniacs may be generally hyperaroused. They commonly show an increased metabolic rate (3), increased body temperature, and increased fast activity on the EEG, both awake and in stages 1 and REM (14). This is directly contrary to the findings in sleep deprived normal patients who show decreased metabolism, decreased body temperature, and increased slow (theta) activity on the EEG. Recent research suggests that insomnia may be much more like caffeine intoxication than like sleep deprivation (2). Indeed, Bonnet even suggests that insomnia may be the organism's attempt of curing excessive hyperarousal by attempting to slow it down through sleep deprivation! However, there are opposing data. For example, when both insomniacs and good sleepers were kept awake lying in bed for 26 hours, their mean body temperature did not differ (36).
When comparing subjective estimates of total sleep with sleep assessed by polysomnography, most, but not all, insomniacs underestimate the amount of time they actually sleep. In some insomniacs, this underestimation may be extreme (e.g., "I have not slept for over a week," when the polysomnogram shows 6 hours of sleep per night). Such patients are said to suffer from a sleep state misperception syndrome (i.e., they may perceive that they are awake when they are actually asleep). However, on many dimensions, patients with sleep state misperception are very similar to those patients who have "bona fide" insomnia: They show the same deviations on the MMPI, they seem to have similar difficulties falling asleep when asked to take naps during the day, and they seem to have considerable hyperarousal (4). They respond to the same treatments (pharmacologic, behavioral) as do "bona fide" insomniacs. Therefore, some sleep specialists have begun to question the relevance of sleep parameters assessed by polysomnography when evaluating insomnia.
When interviewing a patient with insomnia for diagnostic purposes, one reviews the following 7 areas. (These areas have been established both by clinical judgment and by two cluster analyses) (11, 20).
Psychiatric/psychological factors are the prime problem in about half of all insomnia patients (56). Most frequent psychological factors are depression (often covert and denied), general anxiety, and stress. In addition, one considers post-traumatic stress disorder, obsessive-compulsive disorder, somatoform disorders, various adjustment disorders and personality disorders. However, in many patients, insomnia is not the result of some clear-cut DSM IV diagnosable psychopathology (9). Rather, insomnia may be caused by more subtle factors such as marital distress, unsatisfactory career choices, boredom following retirement.
Many medical disturbances cause insomnia, such as asthma and its treatment, pain, neurologic degenerative disorders, allergies. Also included here are the restless legs syndrome (RLS) and periodic limb movements. To evaluate RLS, ask whether a patient's legs are comfortable when trying to fall asleep. If the patient reports disagreeable but not painful paresthesias, "creepy-crawly" feelings in the legs (and occasionally in the arms), disappearance of these feelings when the legs are moved (e.g., walking), and a circadian rhythm to these paresthesias (worst at night), then restless legs is a likely diagnosis (43). Also included here are sleep onset central apneas, often associated with hyperventilation before sleep in anxious patients, then resulting in central apneas when the patient falls asleep and respiration becomes automatic. These sleep onset centrals often awaken the sleeper. There is then frequent alternating between wake with hyperventilation and sleep with central apneas causing arousal, until more solid sleep is established.
Insomnia may be associated with stimulating medications (theophylline, prednisone, some SSRI's) or with withdrawal from sedating medications (e.g., anxiolytics, antihistamines). There may also be highly idiosyncratic reactions to drugs that do not usually disturb sleep. Other insomnias may be induced by toxins (e.g., insomnia can be found long after CO poisoning or excess alcohol).
Typically, learned insomnia is acquired during a period when other factors such as stress cause insomnia. After a few days of sleeping very poorly, the patient becomes concerned about his inability to sleep, trying harder and harder to get to sleep. This causes arousal and aggravates insomnia (24). Also, the stimuli surrounding bedtime (such as the bed itself, the bedroom, the time of night) may become conditioned to arousal just as surely as the Pavlovian dogs salivate to the bell.
In some patients, insomnia is caused by their lifestyle (such as irregular times for sleeping and waking, lack of exercise). In others, poor sleep hygiene develops as a response to chronic insomnia. Patients might drink more coffee to remain awake, more alcohol to fall asleep, they might stay in bed longer in an attempt to get more sleep., etc.
There is an internal, circadian "clock" that regulates sleep/wake as well as many other bodily functions (e.g., some hormone secretions). If this internal "clock" is slow (longer than 24 hours), patients have difficulties falling asleep in the evening and difficulties getting up at the appropriate time in the morning. This is often seen in adolescents and young adults. In others, the circadian rhythm is fast, i.e., shorter than 24 hours. This causes the patient to go to bed and then awaken early. This is often seen in the elderly. Circadian factors are also involved in the insomnia of shift work, of jet lag, or in patients who have lost much of their circadian rhythm, e.g., because they are confined to the bed because of illness.
The neurologic sleep/wake balance is quite complex, with sleep inducing areas interacting with the reticular activating system on numerous levels. Just as there are various levels of intelligence without there being any CNS abnormalities, so there are various balances between sleeping and waking (25). Primary insomniacs may simply be at the extreme waking tail of the normal curve, or there may be some neurologic or neurochemical abnormality. Primary insomnia usually manifests in early childhood, but not all early childhood insomnias are primary. Childhood onset insomnia may also be associated with stress and abuse in early childhood.
In acute insomnia, a precipitating factor can usually be identified (such as a new medication or an overwhelming stress). The longer insomnia lasts, the more likely it is that learned factors perpetuate the problem. These factors need to be addressed in chronic insomnia, even if the cause of the original insomnia has been identified and dealt with (57).
There is considerable overlap between the different types of insomnia. For example, in primary insomnia, the main abnormality appears to lie in a deviant neurologic balance of sleep/wake. If this neurologic control is adequate but marginal, relatively mild psychological stressors may push a patient to develop insomnia. This happens in psychophysiologic insomnia. If the psychological factor is severe (e.g., a pathologic level of anxiety), then it alone may cause insomnia without any pre-existing problem in the neurological control. This would be insomnia associated with psychiatric disturbance. Where to draw the line between these categories is often arbitrary.
There are currently 3 viable classification systems for sleep disorders. The International Classification of Sleep Disorders (ICSD,30) is a detailed nosologic system designed for the professional sleep clinician. It contains over 80 individual entities, about 25 of them associated with insomnia. DSM IV, the psychiatric classification system (9) differentiates primary sleep disorders from those sleep disorders related to another mental condition, those due to a general medical condition, and those that are substance induced. Among the primary sleep disorders, it differentiates the dyssomnias (abnormalities in the amount, quality, or timing of sleep) and the parasomnias (characterized by abnormal events during sleep).
Four types of insomnia are recognized, one among the dyssomnias and one each for the three categories of sleep disorders associated with another condition. The International Classification of Disease (30) classifies all sleep disorders first into organic and nonorganic ones and then further separates these categories into insomnias, hypersomnias, parasomnias, and circadian sleep/wake disorders.
There are 4 distinct insomnia classifications in ICD 9-CM: Acute and persistent nonorganic insomnia, organic insomnia associated with sleep apnea and other organic insomnia (e.g., idiopathic, periodic limb movements, stimulant dependent). Although classification into organic versus nonorganic sleep disorder is often difficult and almost irrelevant, this is the classification used by most insurance carriers. Obviously, with the various nosologic systems still that widely discrepant, we have not yet formed a commonly acceptable way of understanding insomnia.
This is the main tool to assess insomnia. One first asks about the current state of the complaint, then its history. One then reviews organic issues (e.g., restless legs, pain, medications). Only then does one approach psychiatric issues, well knowing that insomniacs are prone to deny emotional problems. At the end of the interview, it is useful to discuss with the patient the probable etiology of the insomnia and the various contributing factors (22). This is necessary before starting treatment. For example, a patient is unlikely to be successful with a behavioral treatment of insomnia if he firmly believes that the insomnia is caused by a neurochemical imbalance within the brain which can only be treated pharmacologically.
If there is time before the evaluation, one typically requests a one to two week sleep log which asks for times going to bed, sleep latency, number and length of awakenings during the night, sleep quality etc. Usually some screening questionnaires for sleep problems and for psychopathology are also given, such as the MMPI, Beck depression and anxiety scales, HCL90. Many insomnia specialists require questionnaires focusing on specific aspects of insomnia, such as Regestein et al's (51) hyperarousal scale or Morin's (46) belief and attitude about sleep scale.
This is a wristwatch sized gadget patients usually wear on the nondominant wrist for a week at home. It measures and stores the number of wrist movements made per minute. Because humans move their wrists much less during sleep than during wakefulness, this allows an estimate of the patient's sleep and wake times, nap times, etc. However, the wrist actigraph is not a very accurate tool to assess total sleep time in insomniacs. About 45 minutes of discrepancy are commonly observed between total sleep time estimated by wrist actigraphy and by polysomnography (27, 28).
Only in rare cases of insomnia is a PSG indicated--for example, when one suspects periodic limb movements or central apneas or when one wants to document sleep state misperception or a mixing of alpha (waking) and sleeping waves (which is often called "nonrestorative" sleep) (42). A PSG is a poor method to assess average sleep length or sleep latency in insomnia because insomnia is very variable from night to night (34) and because the first night in the Sleep Disorders Center is usually quite atypical. Indeed, some patients, especially those with conditioned (psychophysiologic) insomnia, may sleep better in the laboratory than at home (26). A recent position paper by the American Sleep Disorders Association (52) does not recommend the routine use of polysomnography in insomnia.
Obviously, whenever a specific cause for insomnia is found, that cause is treated first: If restless legs are the culprit, Sinemet (25/100 h.s.) may be prescribed (43). If marital discord maintains insomnia, counseling may be the treatment of choice, etc. The comments in the rest of this paper assume that these disorder-specific treatments have already been carried out, but that a remainder of insomnia is left over.
If the insomnia has lasted only a few days or weeks, one determines its cause. Once that cause is dealt with, hypnotics are the treatment of choice. Acute insomniacs are expected to sleep well again within a few days or weeks, thus making questions of drug tolerance and withdrawal less salient. Also, behavioral techniques often take weeks to become effective, too slow for acute insomnia. It seems even reasonable to consider the prophylactic use of hypnotics, e.g., if a patient typically has insomnia before an important meeting or associated with jet lag.
The longer insomnia lasts, the more important behavioral therapies become, because the more chronic the insomnia, the more important are the various learned perpetuating factors. Also, issues of drug tolerance and rebound may become more important the longer hypnotics are prescribed, making sleeping pills less appropriate in chronic than in acute insomnia.
Although current FDA guidelines are that hypnotics be prescribed only for short-term use, in practice, they are often prescribed for many months or years. It appears that the fears of tolerance to hypnotics and rebound insomnia following withdrawal may have been exaggerated. There are now some research studies that show little decrease in the efficacy of hypnotics over many months in some patients (35). While there is still considerable debate, it appears that long-term use of hypnotics may be beneficial in many patients without doing harm. Many insomniacs seem satisfied with a relatively low, stable dose of a hypnotic. Caution is warranted mainly if the patient demands an escalation of the dose because tolerance has developed to a previously effective dose. Furthermore, caution is indicated in patients who have abused other substances such as alcohol or pain medication or are intensely drug seeking. In addition, one is careful when prescribing long half-life hypnotics in patients who may have to operate equipment or make crucial decisions before the hypnotic effects have dissipated or in patients, such as the elderly, where falls and confusion need to be avoided (38).
Until recently, benzodiazepines were the only hypnotics of choice for insomnia. They differ among each other mainly by the speed of absorption and by their elimination half life. The main worry when prescribing benzodiazepines is the development of tolerance and the possibility of rebound insomnia when the hypnotic is withdrawn. This involves not only physical dependence and laboratory documented withdrawal phenomena, but also psychological issues after having become habituated to taking a hypnotic at bedtime and trusting in its effectiveness, not taking the hypnotic has arousing, sleep-preventing effects even if the hypnotic had been a placebo.
Adverse reactions to benzodiazepines are rare (median frequency of reported adverse reactions is about one per 10,000 doses). Most can be viewed as extensions of the therapeutic effect beyond the desired time (41). Because the efficacy of benzodiazepines is usually tested in severe, chronic insomnia patients, the initially recommended doses are often too high. Many can derive benefits with lower doses, and this also cuts down significantly on the side effects.
Currently, the following benzodiazepines are approved as hypnotics:
Because of the concerns about habituation to benzodiazepines, there is now a new search for non-benzodiazepine hypnotics. The first of them on the U.S. market is Ambien (zolpidem), an imidazopyridine with a mean elimination half life of about 2.5 hours. This makes it an ideal drug for problems with sleep onset.
Another non-benzodiazepine hypnotic is Zaleplon, a pyrazolopyrimidine, with an elimination half life of about one hour. The short half-lives of either drug makes it possible to still take them during mid-sleep awakenings (as long as time to get up is at least 2 or 3 hours away), without much concern about daytime consequences. Other, similar drugs are in development or have been approved for use outside the United States. These newer hypnotics apparently show even less development of tolerance and less rebound insomnia on withdrawal. They appear to disturb sleep architecture less than the benzodiazepines do.
Because they appear to habituate much less than benzodiazepines, antidepressants with sedative side effects have increasingly been used as hypnotics. Typically, they are prescribed in very low doses. Unfortunately, very little research on their hypnotic efficacy is available.
Among the antidepressants, amitriptyline is often used because of its very strong sedating effects. Doses of 10 or 25 mg are often sufficient to help sleep. A recent study documents that doxepin in doses of 25 mg or less may also be quite effective (50). In about one-fifth of the 43 patients studied, doses of less than 3 mg even seemed effective!
However, especially with amitriptyline, daytime sedation during the first two or three days following nighttime administration may be quite severe. Also, tricyclics are known to aggravate periodic limb movements and restless legs, even in very low doses. Because of this, trazodone in doses of 25 or 50 mg is frequently prescribed. That medication seems to have similar sleep-inducing properties as many of the tricyclics without aggravating periodic limb movements and restless legs.
Antihistamines (e.g., Benadryl) are rarely indicated in the treatment of insomnia, mainly because their benefit-to-side-effect ratio is much worse than that of either benzodiazepines or antidepressants.
Melatonin is an indoleamine secreted by the pineal gland at night. It is clearly implicated in the regulation of the sleep/wake cycle and is therefore quite useful in treating jet lag. It is frequently suggested in the lay press as a hypnotic. Indeed, in one study (17), melatonin was effective in inducing sleep in elderly insomniacs who were presumed to be melatonin deficient. Its use in non-melatonin deficient insomniacs is controversial. It appears to help no more than 5 to 10 percent of the insomniacs seen in our Sleep Disorders Center.
The lay press suggests various minerals and vitamins to induce sleep, such as calcium and magnesium, herbal preparations, etc. These substances are rarely as effective as claimed, but they have shown remarkable efficacy in some isolated cases. It is rarely useful to simply discount the claims that are made. Rather, one might suggest an evaluation with sleep logs. The patients may take the suggested compound for one or two weeks and every morning report that night's sleep on a log. They then do not take the compound for two weeks and again fill out sleep logs. Averaging the logs from the two experimental periods will show whether the patient is one of the rare persons who can benefit.
No sleep hygiene advice works in all patients. For example, about 80 percent of insomniacs sleep better when they do not take afternoon naps, while about 20 percent sleep better with such naps. Therefore, one often uses the same "co-scientist" model that was just described above. Each sleep hygiene rule to be evaluated is used for a minimum of one week while reporting sleep every morning on a log. It is then not used for a week, with the same reporting on sleep logs. If results are equivocal, another week on and one off might be needed before the patient knows whether a certain sleep hygiene rule is applicable in his/her case (21).
Lifestyle issues are part of any discussion on good sleep hygiene. It is difficult to sleep soundly when a person is over-committed and stressed, working until shortly before bedtime. Such excessive stress may be externally imposed, but more often is internally driven by feelings of insecurity and inferiority. These feelings need to be addressed before admonishing a patient to relax and work less. Also, insomnia may be caused by excessive boredom, such as often experienced following retirement.
The following comments discuss some sleep hygiene issues one typically evaluates with sleep logs:
Many other sleep hygiene issues may be investigated. Excess caffeine intake disturbs sleep. Most need to avoid all caffeine after lunch. Alcohol in the evening helps with sleep onset but then arouses patients after a few hours. Nicotine is a stimulant, but nicotine withdrawal also disturbs sleep.
Regularity of the final awakening, somewhat before one has totally slept out, is important in the young, while regularity of going to bed somewhat later than comfortable is important in most elderly patients. A bedtime snack may help. If a patient complains about a racing mind, a 30-minute "worry time" in the early evening may help.
During this time, the insomniac tries to list all current concerns and then find one thing that could be done during the next day towards a solution of each concern. Other issues such as diet, placement of the evening meal, a warm bath before bedtime may be important for individual cases and should also be evaluated by the co-scientist model (22).
Behavioral therapy is the treatment of choice for psychophysiologic insomnia, idiopathic insomnia, and patients with inadequate sleep hygiene. It serves as adjunctive therapy in most other chronic insomnias such as those secondary to psychiatric or medical illness. Behavioral therapies work about equally well for difficulties falling asleep, mid-sleep awakenings, and early morning awakenings.
The issue is not why patients awaken (even normal sleepers awaken frequently during the night), but what happens to thoughts and behaviors once the insomniac is awake. It is crucial that both clinician and patient understand the rationale for a specific behavioral therapy before attempting it.
Some behavioral techniques such as exposure to bright light can be undertaken concomitantly with drug treatment for insomnia. In other cases, concomitant treatment using behavioral therapy and hypnotics may decrease the efficacy of behavioral therapy, in part because the newly learned behaviors are rarely put to the test and because the insomniac usually attributes all improvements in sleep to the hypnotics.
Two recent meta analyses have summarized the current evidence on nonpharmacologic therapies. Both of these analyses are based on self-reported data (45, 47). According to their findings, the average patient with sleep onset problems treated with behavioral therapy was better off than 81 percent of untreated controls. The average patient with sleep maintenance problems was better off after behavioral therapy than 74 percent of the untreated controls. Self-reported sleep latency typically decreased from about 60 minutes pre-treatment to 35 minutes post-treatment when averaging over all behavioral techniques. Morin, et al (45) found stimulus control therapy and sleep restriction therapy to be most effective, Murtagh, et al (47) found no differential efficacy among the various behavioral therapies.
Bright light changes the timing of the sleep/wake (circadian) rhythm. This is done through the retinohypothalamic tract, which connects the retina directly to the superchiasmatic nucleus, the location of the circadian clock (18).
Although even dim light has an effect on the timing of the circadian rhythm (60), to cause the marked changes in circadian cycling necessary to treat disordered sleep typically needs very bright light, at a minimum about 2,500 lux. Most clinicians prefer about 10,000 lux when trying to shift circadian cycling because that intensity allows shorter time exposure.
Traditionally, bright light has been used mainly to treat patients with delayed or advanced sleep phase syndrome (60). Thus, if a patient gets excessively somnolent during the evening but then awakens too early on the next morning, bright light is applied in the evening.
Patients who cannot fall asleep until 3 or 4 am but then typically sleep until noon are encouraged to be in the bright light in the morning. Usually a "nudging" procedure is used. For example, a patient unable to get up until noon is asked to get up at 11 am and immediately go outside for 30 to 60 minutes. After about a week, especially if the patient starts falling asleep earlier, he then gets up at 10 am, a week later at 9 am, etc.
Unfortunately, bright light only affects the timing of the circadian rhythm, not the inherent periodicity. Therefore, the light exposure needs to be incorporated permanently into the patient's lifestyle. For example, an elderly person with a tendency towards early morning awakening might be encouraged to develop a chronic habit of a 30 to 60 minute outdoor stroll after supper.
Outdoor light is usually bright enough from about 30 minutes after sunrise to 30 minutes before sunset. In northern latitudes, specialized bright light boxes are used in the winter to replace the natural light. A useful rule of thumb suggests that light is bright enough to clinically affect the circadian cycling if the automatic flash on a simple camera does not go off when taking a picture.
Recently, it has been shown that the same procedures used for advanced and delayed sleep phase syndrome can also be used for patients with difficulties falling asleep or for those with early morning awakenings, even if circadian issues seem not to be the primary reason for the insomnia (7, 54).
Concerning side effects, patients with eye problems (other than corrective glasses) should first check with their ophthalmologist. Occasionally, there are complaints of irritability, eye strain, or headaches. Bright light is discontinued if these complaints last for longer than a few minutes after light exposure. Hypomanic responses have occasionally been observed. Side effects can usually be managed by decreasing the amount of bright light exposure. Care is needed in patients who take photosensitizing drugs such as hydrochlorothiazide, diuretics, amiodarone, or long-term treatment with lithium (53).
If Bonnett's hyperarousal theory is correct, then relaxation techniques should be our best techniques. They are not, although they are useful. This may be because patients do relaxation only for a limited time during the day (e.g., 30 minutes), while hyperarousal goes on 24 hours per day.
There are different kids of tension: anxiety (psychological tension), muscular tension, and sympathetic arousal. Relaxation techniques need to be tailored to the specific type of tension the patient experiences. Because patients need to use their relaxation techniques at the time of near sleep onset (when conscious control is waning or absent), relaxation needs to be over-learned so that it can be used automatically (19).
Most patients hold various erroneous beliefs and attitudes about their sleep. Unless these erroneous beliefs are addressed, insomnia treatment is unlikely to be successful (44).
Common cognitive errors found in insomnia patients are:
Cognitive therapy attempts to restructure these faulty thoughts. One challenges them based on the patient's own experience (e.g., "in the past I have been able to function adequately during the day, even after very little sleep"). The goal is to decatastrophize insomnia, reattribute those problems that are not caused by insomnia, and replace the maladaptive thoughts with more functional ones.
For example, in a patient who used to think "My insomnia tonight will surely lead to a catastrophe tomorrow" - it is a great step forward if he can think "My insomnia is surely a miserable condition, but I know from past experience that tomorrow I can get by in spite of it."
Doing cognitive therapy is a complex skill. Simply telling the patient that his thoughts are wrong leads nowhere. The patient has to be intensely involved in reassessing and challenging his cognitions and replacing them with more adaptive thoughts (44).
This treatment is based on the fact that even in insomniacs, sleep becomes more "robust" as a result of sleep deprivation (63). This means that even insomniacs fall asleep faster, show fewer awakenings, more stage 3 and 4 sleep, and longer total sleep time after a night of no sleep at all. However, the improvement is short lived: one or two nights. Sleep restriction therapy was designed to exploit the consequences of sleep loss for enhancing natural sleep while temporarily accepting daytime sleepiness as a side effect (16).
Procedurally, one first examines a patient's sleep logs. One then restricts bedtime hours to the total hours of actual sleep reported on these logs, although never to less than 4.5 hours in bed. Typically, wake up time is held constant, time to bed is delayed (e.g., if a patient is allotted 5 hours bed time and typically gets up at 7 am, bedtime would be no earlier than 2 am). It is important to discuss with the patient how wakefulness can be maintained until that time. Usually, this needs stimulation from others (e.g., playing cards) or physical activity (e.g., walking). Watching television until 2 am is not sufficient because the patient may fall asleep.
Each morning, the patient reports to the therapist's answering machine the time to bed, sleep latency, time out of bed in the morning, total amount slept, and whether or not there has been napping. If, according to these telephone calls, sleep efficiency for the last five nights has been over 90 percent, an additional 15 or 30 minutes of time in bed is allowed. (Initially, 15 minutes less sleep was allowed if the five night moving average dropped below 85 percent, but this is now rarely done because it feels quite punitive to the patient.) In the elderly, sleep efficiency criteria are lowered by 5 percent and, where indicated, a short afternoon nap is allowed.
Patients need to be aware that the first two or three weeks on this program are most difficult but that insomnia is often totally eliminated in about eight weeks. Frequent therapist contacts are necessary to keep patients from dropping out during that time. There are considerable sleep improvements in a large number of those who are able to stay with the program (58).
This therapy is based on the finding that sleep is under partial control of the stimuli that surround it. In a good sleeper, these stimuli are associated with relaxation. They encourage sleep. In the poor sleeper, these same stimuli have become associated with arousal. Bootzin's stimulus control therapy (6) tries to change these associations.
The following six steps are explained to the patient:
Notice that the injunction to use the bed only for sleeping but not for reading or watching television is part of an overall set of rules. Patients get up if they cannot sleep. Simply forbidding reading or television in bed and having patients lie there frustrated for hours is not following the Bootzin technique.
Of all the behavioral techniques available today, the Bootzin technique is the best researched (5, 12). In all studies comparing this technique with any other behavioral treatment of insomnia, stimulus control has always been found either equal to the other technique or superior. However, there is more to it than simply giving a patient the above-described rules. The patient has to understand the reason for each of the rules and cognitive errors need to be dealt with. For example, a patient who feels that he absolutely needs eight hours of sleep to function will have difficulties following these rules unless that misperception is dealt with.
Follow-up evaluations (19, 22) suggest that the sleep inducing effects of behavioral therapy may even strengthen over time, as patients gain renewed confidence that they may be able to sleep adequately. Behavioral therapies of insomnia require considerable skill of the person administering them. They are time consuming and more expensive than hypnotics in the short run, but over a patient's life span, they may well be more cost effective than frequent physician visits and prescriptions.
Understanding and treating insomnia is clearly more complex than had initially been assumed. However, in the hands of a skilled clinician, many causes of insomnia can now be determined with confidence. Treatment is considerably more sophisticated now than it was twenty years ago and involves not only improved hypnotics but also a discussion of sleep hygiene and the use of specific behavioral therapies. By now these therapies have demonstrated clinically significant effects in a majority of insomniacs.
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