WEEK 8 - 12 Flashcards
(98 cards)
~WEEK 8~
What is Insomnia?
- There are actually many different ways to define insomnia, and we have many different diagnostic systems with differing diagnostic criteria for insomnia
- Of the main classification systems in North America, we most often use the Diagnostic and Statistical Manual for Axis I Disorders (DSM5; American Psychiatric Association, 2013)
- Research Diagnostic Criteria (RDC; Edinger et al., 2004) is not used in clinical practice; rather, RDC is used specifically in research studies
- Additionally, the International Classification of Sleep Disorders (ICSD-2; American Academy of Sleep Medicine, 2005) provides specific criteria for sleep disorders
- Generally, sleep disorder specialists use ICSD-2 criteria to communicate with each other, but DSM5 is used in a hospital setting for billing and communication with other professionals.
The DSM5 made several bold changes to the diagnostic criteria for insomnia:
- insomnia is no longer called a sleep disorder; it is called a sleep-wake disorder, to reflect that insomnia is a twenty-four-hour disorder with both daytime and nighttime problems
- we used to be concerned with whether insomnia was on its own (formerly called Primary Insomnia) or with a mental disorder (formerly called Insomnia Related to Another Axis I Disorder). Distinguishing between these two types of insomnias is not useful and there is little validity in Insomnia Related to Another Axis I Disorder = so this is no longer a category
- there are no quantitative criteria for insomnia; that is, you need not be awake for a particular amount of time before we diagnose insomnia
- One proposal has been to stipulate that the insomnia sufferer must take more than thirty minutes to fall asleep or be awake for more than thirty minutes in the middle of the night more than three nights per week, but there is mixed evidence for such a proposal
Sleep Regulation and Insomnia
Recall that sleep is regulated mainly by two systems:
- the homeostatic system (Process S)
- the circadian system (Process C)
- When you wake up and become active you build a drive for deep sleep; the longer you are awake and active, the greater the build-up of pressure for (deep) sleep
- Conversely, the less you are awake and active, the less the pressure for (deep) sleep
The two main things to consider for circadian system (Process C) are that:
- the clock keeps a rhythm that is unique to you
- The rhythm that is unique to you is genetically determined but there are developmental influences as well
- The degree to which we are a night owl or morning person has a genetic influence
- although there are tendencies towards morningness early and late in life, and there is a tendency towards eveningness during puberty and young adulthood
- Nonetheless, there is an ideal sleep window for every person at any given point in time
- There are other important considerations for the ideal window for sleep
- For example, remember that Process C generates alerting signals that increase in magnitude as the day progresses and fades in intensity in the hours after darkness
- If we have to sleep in the morning hours (e.g., staying up all night studying or working), although Process S will be strong because of the sleep deprivation, we may be attempting to sleep during a time when REMS is dominant (not a particularly physically restorative stage of sleep) or when the alerting signals are increasing
- an important consideration is environmental input into the clock
- There is always drift in the clock because the clock length at the cellular level is not exactly twenty-four hours
- For most people it is longer than twenty-four hours
- Thus, if we had no cues to reset the clock each day (for example, we lived in darkness in a cave), our clock would drift about an hour each day until twenty-three days later in which we would have gone completely around the clock to where we started
- Recall that jet lag is in fact the result of a mismatch between the clock in your body and the local time on the clock on the wall
- The lighting conditions, as well as the timing of eating and sleeping in local time, help to entrain the clock to local time
- If we do not have these activities, we are prone to jet lag symptoms of insomnia, fatigue, mood and gastrointestinal upset
What Factors Cause Insomnia?
- We have now reviewed the regulatory systems and before we explore how there are problems in these systems in insomnia, let us consider a more basic causal model for chronic insomnia
Diathesis Stress Model
- In psychopathology, the most common conceptualization is a diathesis stress model
- In such a model, individuals have a predisposition or vulnerability to a disorder, but in the absence of a significant stressor, there is no disorder
- Spielman and colleagues (1987) proposed a diathesis stress causal model of chronic insomnia called the three P model:
- Predisposing
- The predisposing factors in insomnia could include a biological and/or psychological vulnerability
- for example, increased anxiety, perfectionism, hyperarousal, and/or rumination
- if one has a weakened homeostatic mechanism or reduced photosensitivity (such that there is reduced potential input into the circadian system)—these are all possible predisposing risk factors for insomnia
- Precipitating
- There are probably as many precipitating causes for an insomnia symptom (e.g., having a poor night’s sleep) as there are people
- The causes of a poor night’s sleep need not be negative; for example, one cause of poor sleep could be excitement about something positive
- The cause could also include taking a medication that disrupts sleep
- All of these examples would be considered precipitating causes of insomnia; in other words, they are factors that could cause a poor night of sleep
- In some cases, precipitants can be longer term (e.g., working on a big project at work); thus sleep loss can go on for an extended period of time
- With a stress-related insomnia, the expectation is that once the stressor abates, normal sleep should resume
- Unfortunately in a chronic insomnia, this is not the case
- although a precipitating factor can be associated with a crossover into a diagnosis of insomnia, it is typically short-lived and directly related to the presence of the stressor
- Perpetuating
- The important point is that possessing these vulnerabilities in the absence of a stressor does not result in meeting insomnia diagnosis criteria
Common ways that people cope with sleep loss:
- Go to bed earlier?
- Try to sleep in later?
- Cut back on physically demanding tasks?
- Take a sleeping pill?
- Drink alcohol to help you relax?
- Listen to relaxation or meditation CDs?
- Try to nap?
- Unfortunately, many, if not all of these behaviours, can become perpetuating factors for insomnia, and take over from the predisposing and precipitating factors as the main (current) cause of the insomnia
- In other words, even if the excitement of buying a new car was the precipitating cause, the reaction of drinking alcohol before bed and becoming worried about the sleep problem, takes over and becomes the main cause
- ## The precipitant is no longer a factor—the excitement of the new purchase has abated, but the sleep problem remains
What Are Predisposing Factors That Adversely Affect Process S (i.e., Deep Sleep)?
- If we need to “build” adequate sleep drive to have continuous and quality sleep, behaviours that will have a negative impact on this build-up will include spending a greater amount of time in bed than the amount of sleep you can currently produce night after night
- In other words, if during a week you sleep four, five, five and a half, six, five, three and a half, and seven hours respectively, the mean amount of sleep you are producing on average is a little over five hours ([4 + 5 + 5.5 + 6 + 5 + 3.5 + 7]/7 = 5.14)
- This is how much sleep your body can reliably produce on average at this point in time
- Five hours of sleep is very low, but this is how much the body can produce currently
- If you attempt to produce more sleep by getting into bed earlier, staying in bed in the morning after you have woken up or napping, it will result in a decreased drive for deep sleep
- This is a common strategy in insomnia
- If a person is not an eight-hour sleeper on average, so this amount of time in bed would produce insomnia, because they are only capable of sleeping around five hours
- On Monday it took twenty-five minutes to fall asleep and they were awake twenty minutes in the night, so they were awake in bed for forty-five minutes; forty-five minutes on Tuesday and fifty-five minutes on Wednesday
- On Thursday, after several nights of insomnia, this person responds by going to bed early and they also stay in bed a little later (until 7:25 a.m.); this results in over nine hours in bed
- Most adults cannot produce nine hours of sleep, so they will have to experience some insomnia given the mismatch between their current sleep production and the exorbitant amount of time in bed
- Moreover, by spending over nine hours in bed, they cut short the amount of hours in a day in which they could build a drive for deep sleep
- Building less sleep drive means that this person will sleep less deeply
- Note that on Saturday they spend over eleven hours in bed and on Sunday they spend about twelve hours in bed attempting to sleep; this severely limits the drive for deep sleep and sends the message to the system that less sleep is needed
What Are Predisposing Factors That Adversely Affect Process C?
If optimal sleep is produced during a dynamic, idiosyncratic timing window, the following behaviours would have a negative impact on sleep:
- poor input to the clock (i.e., not engaging in behaviour that will set the clock and prevent drift)
- sleeping outside of your optimal window (i.e., keeping late hours if you are a lark or getting up early if you are an owl)
Poor input to the clock
- Remember that you need to reset the clock each day and the best way to do this is to engage in regular behaviour, particularly behaviour that provides sufficient light input to set the clock
- Such behaviour includes getting out of bed at the same time each morning
- Having a stable rise time permits an adequate build of Process S but it also sets light exposure for around the same time each day (because when we are awake and out of bed we tend to expose ourselves to light)
- We tend to have an impression that we are more regular than we actually are, so it is vital for someone with insomnia to keep a diary
- This person set an alarm for 6 a.m. during the week, but did not set an alarm on the weekend
- The result of these habits however is that there is almost five hours difference between the earliest rise time of 7 a.m. and the latest rise time during the week of 11:45 a.m
- This is nearly equivalent to the jet lag one would experience travelling from Toronto to the UK
- If you took such a trip, you would expect some jet lag symptoms, but because people don’t understand jet lag they don’t understand that varying rise times within the week by more than an hour has the same effect
- Likewise the difference between the earliest (10:15 p.m.) and latest bedtime (2:15 a.m.) is four hours which is greater than a trip from Toronto to Vancouver
- hus, some insomnias and the corollary daytime symptoms are perpetuated by variability in schedules
Sleeping outside of your optimal window
- The second Process C factor to consider is sleeping outside of your optimal window
- If a conventional window is 11 p.m. to 6 a.m., then those who become sleepy later and consequently wake up much later, are “delayed” in their sleep phase relative to normal or conventional sleepers
- Similarly, those who become sleepy earlier and consequently wake up much earlier than is conventional, are “advanced” in their sleep phase relative to normal or conventional sleepers
- Most adults tend to try and maintain a conventional bed and rise time, particularly if they have a bed partner
If a delayed sleep phase person (a night owl) maintains a conventional schedule (depicted with the dashed line) what will happen when they go to bed at 11 p.m.?
- They will have trouble sleeping
- Their body is not ready for sleep; in fact, they continue to receive alerting signals from the clock, and most night owls report that they have significant energy in the evening
What will happen when they try to rise at a conventional time, after laying awake in bed from 11 p.m. to 2 a.m.?
- They will have great difficulty getting up
- The same is true for an advanced phase person attempting to maintain a conventional schedule
- They will have great difficulty staying awake until the conventional time and will likely have mini-naps in the evening attempting to stay awake
- If they try to sleep in until the conventional time of 6 a.m., they will likely wake up several hours earlier and complain of difficulty re-initiating sleep
- Thus, sleeping outside of your optimal window will have a negative impact on your sleep and how you feel during the day
The Third Process: The Arousal System
- You can have both Process C and S operating optimally, and still have difficulty sleeping
- This is because the arousal system can trump the sleep promoting system
- It is adaptive that this system can override the other two; this allows us to adequately respond to dangerous threats
- For example, you would not want to decide to sleep through a break-in in your apartment just because you had built an adequate drive and you were sleeping at the right time in your sleep window
- You would want to inhibit the urge to sleep to deal with the intruder
- However, sometimes this system cannot discern real emergencies very well
- There are rarely pressing emergencies in our bedroom at night, but a future stressor such as a term paper due the following week can seem like an emergency and produce emergency sensations in the body
- Arousal is also a consequence of sleep loss; this process is both protective and sleep disruptive
- That is, people with insomnia are typically not impaired on cognitive tasks after sleep loss—one possibility is that their body becomes hyperaroused following sleep loss and this allows them to compensate
- There is plenty of evidence that the body is hyperaroused
- For example, on brain image studies we see that there is greater cortical arousal in those with insomnia
- Although this helps them to continue doing tasks the following day, the increased arousal is also expected to be a perpetuating factor for the insomnia; this is because we need deactivation to sleep
Increased arousal can come from a variety of different sources too, such as:
- taking a medication with increased arousal as a side effect,
- having a comorbid disorder characterized by increased arousal such as PTSD,
- or living with a partner when there is ongoing relationship conflict
Conditioned arousal:
- best explained using the most “classic” of classical conditioning examples—Pavlov’s dogs
- Dr. Pavlov is widely known for a series of experiments in which he exposed dogs to a pairing of a bell with meat; in response to the food, the dog drooled
- Food elicits drooling from a dog without any training
- But every time the meat was presented, the sound of the bell was paired with the meat, until finally, the bell was rang, the meat was not presented, but the dog drooled any way
- The drooling response became conditioned to the bell
- When someone develops insomnia, the typical experience is that the bed becomes paired night after night with wakefulness—the result is that simply presenting the bed can produce increased wakefulness/alertness
- Here is a typical scenario: the person with insomnia is exhausted and falling asleep on the couch so they go upstairs and get into bed—upon getting into the bed, it is like a switch goes off and they are instantaneously awake = conditioned arousal
- Although it is not a precipitating cause, it becomes an important perpetuating cause in the insomnia that will need to be addressed
- Another possible source of conditioned arousal occurs when wakeful activities are done in bed
Wakeful activities include:
- checking smartphones,
- using a computer,
- eating or drinking in bed,
- making mental to-do lists in bed,
- worrying in bed,
- or otherwise remaining in bed while awake for prolonged periods
- All of these habits increase the likelihood that your body will associate the bed with wakefulness and you may become increasingly alert when you get into bed
Summary Week 8
- There are many ways to define insomnia but common to most systems are a subjective complaint of difficulty initiating or maintaining sleep, daytime symptoms or complaints, and chronicity (greater than three to six months)
- Chronic insomnias are caused by perpetuating factors
- Even if initially caused by a precipitant interacting with a predisposing (vulnerability) factor, an insomnia is expected to abate coincidentally with the abatement of the stressor
- If sleep is controlled by a circadian system that determines optimal timing of sleep and alertness, problems arise when there is body clock instability (i.e., variable schedule or ill-timed given chronotype)
- If sleep is controlled by a homeostatic system that balances bouts of sleep with bouts of wakefulness, problems arise when there is homeostatic system diffusion (i.e., too much time in bed and/or reduced activity)
- Lastly, if we have an arousal system that can override sleep during “emergencies,” problems can arise if the arousal system is overactive (e.g., conditioned arousal)
Practice Test
Insomnia is mainly defined by:
- A complaint of difficulty sleeping accompanied by daytime complaints as well (e.g., fatigue).
- a subjective disorder with both daytime and nighttime complaints
Which of the following causes of insomnia are most likely to be biological in nature?
- Any or all can be biological in nature = Perpetuating, Precipitating, and Predisposing
Hyperarousal in insomnia refers to:
- A particular cortical activation pattern seen in neuroimaging studies
- Increased nervous system activity
- A protective factor in insomnia, allowing people to function even with sleep loss
Overcoming Insomnia Chapter 1
Overcoming Insomnia Intro
- Cognitive-behavioral therapy (CBT) for insomnia is reasonably easy to learn, simple to implement, and highly efficacious for the management of insomnia
- It has proven effective with patients who have both simple and complex forms of this type of sleep difficulty
- As such, it currently is recognized as a front-line and preferred therapy by the National Institutes of Health and the British Association of Psychopharmacology
- Despite this recognition, patients often have a difficult time accessing this treatment due to a lack of healthcare providers with expertise in this intervention
- In fact, the sheer volume of insomnia sufferers who would benefit by the techniques described in this manual will far outstrip the providers of such therapy for many years to come
- cognitive-behavioral insomnia therapy includes techniques designed to alter sleep-disruptive behaviors and cognitions that get in the way of normal sleep and that serve to perpetuate insomnia
- The primary purpose of this manual is to aid in the dissemination of cognitive-behavioral insomnia therapy to the cadre of healthcare providers who encounter insomnia patients
Nature and Significance of Insomnia
The sleep disorder insomnia is characterized by:
- difficulties initiating,
- sustaining,
- or obtaining qualitatively satisfying sleep that occur despite adequate sleep opportunities/ circumstances and result in notable waking deficits
- Over one-third of the adult population experiences insomnia at least intermittently
- 10% to 22% suffer chronic, unrelenting sleep difficulties
Insomnia may result from:
- various medical disorders,
- psychiatric conditions,
- substance abuse,
- and other primary sleep disorders (e.g., sleep apnea)
- between 1% and 2% of the general population suffers from an insomnia disorder that persists either in the absence or independent of any comorbid condition
- Whereas middle-aged and older adults are most prone to develop one of the many subtypes of comorbid insomnia
- an independent insomnia disorder is the most common diagnosis found in younger age groups
- the risk for developing this condition remains relatively stable across the life span
- Although many insomnia sufferers go undetected insomnia is common in primary care settings and accounts for over 20% of all insomnia sufferers who present to specialty sleep disorder centers
- insomnia appears sufficiently prevalent and disturbing so as to frequently come to the attention of both sleep specialists and general medical practitioners
- Since insomnia may present in the absence of secondary causes, isolated forms of insomnia traditionally have been viewed as less serious than those insomnias co-occurring with sleep disruptive medical psychiatric, substance abuse, or other sleep disorders (e.g., sleep apnea)
- epidemiologic evidence suggests that insomnia, uncomplicated by comorbid psychiatric, substance abuse, or medical disorders, substantially increases health care utilization/costs
- One recent national insomnia survey found that insomnia alone accounted for significantly more days out of role than did other serious conditions including diabetes, hypertension, major depression, and congestive heart failure
- Also, several studies have shown that insomnia dramatically increases subsequent risk for developing a depressive illness, serious anxiety disorder, or substance abuse problem, even after other significant risk factors are controlled
- When occurring comorbid to major depression, insomnia often remains as the most common residual symptom once other depressive symptoms resolve
- its presence in this setting dramatically enhances risk for both relapse and eventual suicide
Insomnia contributes to:
- reduced productivity,
- accidents at work,
- increased alcohol consumption,
- serious falls among older adults,
- and a sense of being in poor health
Diagnostic Criteria for Insomnia Disorder
- Insomnia disorder is a diagnosis listed in the American Psychiatric Association’s sleep/wake disorder classification system, outlined in the fifth edition of its Diagnostic and Statistical Manual (DSM-5)
Previous versions of the DSM and other diagnostic manuals conceptualized insomnia as either a:
- primary disorder
- or a symptom occurring secondary to other sleep-disruptive primary conditions (e.g., depression, chronic pain)
- However, over time it has been recognized that often, if not typically, insomnia develops partial or total independence from whatever comorbid condition is viewed as its original cause
- In such cases, the insomnia itself often warrants separate clinical attention to enhance patients’ overall treatment results
- there is evidence that simultaneous treatment of insomnia and depression produces better results in regard to both depressive and insomnia symptoms of patients with major depression than does treatment of merely the depression alone
- Given these considerations, the DSM-5 now provides the diagnostic term insomnia disorder, which may be assigned to patients who have either isolated or comorbid forms of this sleep difficulty
Patients meeting criteria for insomnia disorder report difficulties with:
- sleep onset,
- sleep maintenance,
- and/or early morning awakenings that cause clinically significant distress or impairment in:
- social,
- occupational,
- educational,
- academic,
- behavioral,
- or other important areas of functioning
- such patients have sleep difficulties at least three times per week for 3 or more months, and their sleep problems occur despite allotting sufficient time for sleep and having environmental circumstances that are permissive of sleep
- Of course, when patients present with the sort of sleep/wake difficulties described, alternate possible causes of sleep disturbance should be ruled out, including other sleep disorders, a sleep-disruptive medical condition, or substance use or abuse
- When these alternative causes can be ruled out, a diagnosis of insomnia disorder would apply
- Patients who meet criteria for this diagnosis can and should be considered as candidates for a trial of the treatment techniques outlined in this text
Development of This Treatment Program and Evidence Base
- It is intuitively obvious that practicing good sleep habits (i.e., following a routine sleep/wake schedule; avoiding daytime napping, etc.) and relaxing before bedtime facilitate nocturnal sleep
- As such, it seems reasonable to speculate that psychological and behavioral strategies designed to improve sleep habits and reduce bedtime arousal may be useful for treating insomnia
- However, not until the late 1950s did the usefulness of these forms of insomnia interventions receive attention in the scientific literature
- In 1959, Schultz and Luthe (1959) were the first to formally report their success in treating a patient with sleep-onset insomnia using the form of relaxation therapy (RT) known as autogenic training
- Several years later, Jacobson (1964) reported similar results in a case he treated with his progressive muscle relaxation
- However, not until the early 1970s were the first randomized clinical trials conducted to document the efficacy of RTs
- Although limited in number, these early reports were sufficient to spawn substantial research and clinical interest in the use of psychological and behavioral therapies for insomnia treatment during the past two decades
- Arguably one of the more monumental breakthroughs in behavioral insomnia research was Bootzin’s (1972) observation concerning the important role of behavioral conditioning in disrupting or promoting sleep
- Bootzin was the first to suggest that sleep, like other overt behaviors, should respond to behavioral conditioning
- Specifically, Bootzin surmised that insomnia patients developed conditional arousal to their beds and bedrooms from repeated associations of these cues with unsuccessful sleep attempts
- Therefore, a treatment paradigm designed to reverse this aberrant conditioning history and associate the bed and bedroom with successful sleep efforts should help patients overcome their insomnia
- Consistent with this speculation, Bootzin first presented his innovative stimulus control (SC) insomnia treatment in the early 1970s
In his early reports, he demonstrated that:
- a simple, straightforward counter-conditioning approach,
- involving standardization of the sleep/wake schedule,
- eliminating daytime napping,
- and discouraging sleep-incompatible behaviors in the bed and bedroom, was particularly effective for treating chronic primary insomnia
- Perhaps both due to its practical appeal and its general efficacy, SC quickly became one of the most widely used behavioral insomnia treatments
- In our early clinical work, we found stimulus control and relaxation therapies to be moderately effective for treating the sleep problems of many of the insomnia patients we encountered
- However, these treatments also appeared to have some limitations
- Most notably, neither of these treatments included specific strategies for addressing patients’ cognitive symptoms that contribute to their sleep difficulties
Specifically missing from these treatments were:
- strategies to address insomnia sufferers’ tendencies to take their worries to bed,
- ruminate about the negative consequences of their sleep difficulties
- and harbor many unhelpful beliefs that support their sleep-related anxiety and that promote many of their sleep disruptive habits
- many people with insomnia report that cognitive arousal is the most significant factor in the maintenance of their sleep difficulty
- however, these treatments did not employ specific strategies shown to be effective for decreasing pre-sleep arousal
- Finally, these treatments did not specifically address the practice of spending excessive time in bed displayed by many of the patients with sleep maintenance complaints whom we encountered
- Spielman et al. (1987) were the first to note the importance of addressing time in bed by showing that restricting time in bed led to sleep improvements in a small group of insomnia patients they treated
- Given this finding in conjunction with our own observations, we thought a truly omnibus insomnia therapy should include such a strategy
- Finally, we noted the need for specific strategies to enhance patients’ treatment adherence
- In this regard we found that patients seemed more likely to adhere to treatment recommendations if they were first provided some limited psycho-educational material designed to give them a basic understanding of what regulates the human sleep system and the types of habits that help and hinder the normal sleep process
The need for a multi-component cognitive behavior therapy for insomnia
We thus constructed a treatment that included a number of components, including:
- a cognitive module designed to provide psycho-education about factors that regulate the human sleep system and to address unhelpful beliefs about sleep
- standard stimulus control instructions to address patients’ conditioned arousal and to eliminate common sleep disruptive habits (daytime napping; maintaining an erratic sleep/wake schedule)
- a protocol for limiting each patient’s time in bed to an individually tailored time-in-bed prescription
To test this approach, we conducted two small case-series studies
using multiple baseline designs:
- Hoelscher and Edinger 1988:
- included four primary insomnia patients,
- provided initial support for our multi-component approach in that three of the four patients treated responded well once treatment was initiated
- Edinger, Hoelscher, et al. 1992:
- seven patients underwent baseline monitoring that varied from 2 to 4 weeks in length
- successively completed four weekly sessions of relaxation training
- followed by four sessions of our multi-component treatment
- Results of this latter trial again suggested that most patients showed marked improvements in key sleep measures
- such improvements occurred only after our multi-component cognitive behavior therapy (CBT) was initiated
Morin et al. (1993):
- published the first randomized clinical trial that showed that a multi-component CBT similar to our approach was effective (compared to a wait-list condition) for treating older adults with insomnia
- Since the time of these early works, a number of larger randomized clinical trials have demonstrated that multi-component CBT insomnia treatment is both efficacious and clinically effective for treating insomnia
In efficacy studies conducted with thoroughly screened insomnia sufferers without significant comorbidities, CBT has proven superior to:
- relaxation training,
- sham behavioral intervention,
- sleep medication (temazepam),
- a medication placebo,
- and a no-treatment wait-list for treating insomnia complaints
In larger effectiveness trials conducted with insomnia patients seen in primary care
clinics, CBT proved more effective than:
- usual medical management strategies (medication and sleep advice) for producing sleep improvements
- a recent critical literature review (Morin, Bootzin, et al. 2006) concluded that there have been a sufficient number of efficacy and effectiveness studies conducted to conclude that CBT for insomnia is a well-established and proven treatment approach particularly for those with insomnia uncomplicated by sleep-disruptive comorbidities
- the majority of patients whom clinicians encounter are those who do have sleep-disruptive comorbidities
- it is reasonable to question the utility of this sort of intervention with those types of insomnia patients
- Over the past decade there have been a growing number of studies to test the effectiveness of CBT for managing the insomnia complaints that accompany a wide array of comorbid disorders
Results of these studies indicate that CBT produces sleep improvements among insomnia patients with:
- chronic peripheral pain syndromes
- breast cancer
- fibromyalgia
- mixed medical disorders
- alcoholism
- and depression
A subset of these studies also suggest that an insomnia-targeted CBT leads to improvements in:
- mood status,
- enhanced likelihood of depression remission,
- and reductions in other disease-specific symptoms among patients with various comorbidities
- with reasonable confidence we can offer the treatment strategies outlined in this manual as a “treatment that works” for patients with chronic insomnia disorders
Theoretical Model for Cognitive-Behavioral Insomnia Therapy
Spielman’s theoretical model:
- provides a conceptual framework for understanding the evolution of chronic insomnia and the role of CBT for managing this condition
- According to this model, predisposing factors, precipitating events, and perpetuating mechanisms all contribute to the development of chronic primary sleep difficulties
Some individuals may be particularly vulnerable to sleep difficulties either by:
- virtue of having a “weak,” “highly sensitive,” biological sleep system
- or personality traits that dispose them to poor sleep when confronted with stress
- When such individuals are confronted with the proper precipitating circumstances (e.g. a stressful life event, sudden unexpected change in their sleep schedule), they tend to develop an acute sleep disturbance
- This sleep problem, in turn, may then be perpetuated by a host of psychological and behavioral factors that emerge in reaction to such sleep difficulty
- Thus, predisposing and precipitating factors contribute to the initial development of insomnia
- psychological and behavioral factors perpetuate it and serve as the treatment targets for cognitive-behavioral insomnia therapy
The cognitive-behavioral model:
- posits that an interplay of cognitive and behavioral mechanisms act as the key perpetuating mechanisms for insomnia patients
Setting the stage for sustained sleep difficulty is a thinking style that can include:
- misattributions about the causes of insomnia,
- attentional bias for sleep-related stimuli,
- worry and/ or rumination about the consequences of poor sleep,
- and unhelpful beliefs about sleep-promoting practices
- These cognitions, in turn, support and sustain sleep-disruptive habits and conditioned emotional responses that either interfere with normal sleep drive or timing mechanisms or serve as environmental/behavioural inhibitors to sleep
- For example, daytime napping or spending extra time in bed in pursuit of elusive, unpredictable sleep may only serve to interfere with the body’s homeostatic mechanisms that operate automatically to increase sleep drive in the face of increasing periods of wakefulness (i.e., sleep debt)
- Alternately, the habit of remaining in bed well beyond the normal rising time following a poor night’s sleep may disrupt the body’s circadian or “clock” mechanisms that control the timing of sleep and wakefulness in the 24-hour day
- Additionally, the repeated association of the bed and bedroom with unsuccessful sleep attempts may eventually result in sleep-disruptive conditioned arousal in the home sleeping environment
- An excessive worry about sleep, trying hard to sleep, or failure to discontinue mentally demanding work and to allot sufficient “wind-down” time before bed may all serve as significant sleep inhibitors that raise physiological or cognitive arousal levels to the point of making sleep difficult
- In sum, all of these factors may contribute to and perpetuate insomnia
- As a result, our CBT approach is designed to modify the range of cognitions and sleep-related behaviors that ostensibly sustain or add to patients’ sleep problems
In summary, good sleep is dependent upon:
- having adequate sleep drive (sleep debt),
- proper timing as a result of a consistent sleep/wake schedule,
- and low physiological and psychological arousal during the period when sleep is attempted
Conversely, insomnia arises when there is:
- insufficient sleep drive,
- improper timing,
- and/or excessive arousal present during the designated sleep period
- When managing a specific patient’s insomnia problem, it is important to ascertain and correct the cognitive and behavioral factors that adversely reduce sleep drive, result in improper sleep timing, or make the patient too aroused to sleep
Risks and Benefits of CBT for Insomnia
- Although systematic studies of CBT-related side effects have not been conducted, the experience base with CBT-based insomnia interventions suggests that this intervention is a safe and effective treatment modality
- This is not to say that side effects do not occur
- those that do occur are generally transient and are manageable with strategies outlined later in this manual
- Perhaps the most common side effect is enhanced daytime sleepiness during the initial stages of treatment, resulting from restricting patients’ times spent in bed
- In some patients the initial time-in-bed restriction results in mild partial sleep deprivation and, thus, elevated daytime sleepiness.
- This sleepiness is usually transient and is corrected by gradual increases in time in bed
- Some patients also show elevated anxiety about sleep when limits are placed on their times spent in bed and choices of rise times
- This side effect also is easily managed via some relaxation of the treatment protocol
- In contrast, there are many benefits to this treatment program
- CBT treatment is fashioned to address and eradicate the various cognitive and behavioral mechanisms that presumably sustain insomnia
- thus enhance chances for sustained improvements long after treatment ends
- this treatment differs from most pharmacological approaches (i.e. sleeping pills) that provide symptomatic relief but fail to address the cognitive and behavioral factors that sustain insomnia
- there are currently no data available to show that sleep improvements persist long after pharmacotherapy for insomnia is discontinued
- In addition to this benefit, it appears that many patients may prefer CBT over medicinal approaches
- For example, results of one study (Morin, Colecchi, et al. 1999) showed that patients were more satisfied with behavioral insomnia therapy and rated it as more effective than sleep medication
Findings from another study (Morin, Gaulier, et al. 1992) suggested that patients with chronic insomnia not only preferred CBT to pharmacotherapy, but also expected that CBT would produce:
- greater improvements in daytime functioning,
- better long-term effects,
- and fewer negative side effects
- Collectively, these data suggest that insomnia patients regard behavioral insomnia therapy as a viable and acceptable treatment for their sleep difficulties
Alternative Treatments
Various “stand-alone” behavioral strategies, including:
- relaxation therapies,
- stimulus control,
- sleep restriction,
- and paradoxical intention, have proven efficacy for management of insomnia and currently are regarded as “well-established” insomnia treatments
- Each of these therapies addresses a specific subset of insomnia-perpetuating mechanisms
- In addition to these therapies, cognitive therapy and sleep hygiene education are often employed in insomnia management
- Sleep hygiene education has generally proven ineffective as a stand-alone intervention, whereas there is very limited evidence suggesting that cognitive therapy can be used in isolation to treat insomnia
- Other non-medicinal approaches for insomnia management have included forms of yoga and acupuncture
- Both of these treatments have shown some efficacy, but neither treatment enjoys the sizable research support that the behavioral insomnia therapies have acquired
- Moreover, access to these interventions as applied to insomnia may be much more limited than current access to the behavioral therapies
- There are also a number of devices marketed for insomnia treatment
- Generally such devices are designed to address the sleep-disruptive arousal manifested by insomnia patients
- Currently such devices have either limited or no data supporting their effectiveness, and they are not yet regarded as first-line insomnia treatments
- Nonetheless, since it is likely an increasing number of such devices may be available in the future, their efficacy relative to current insomnia therapies will need to be evaluated
Role of Medications
- The most commonly prescribed FDA-approved sleep medications are benzodiazepine receptor agonists (BzRA)
- These include several benzodiazepines (e.g., temazepam) and newer non-benzodiazepine agents (e.g., zolpidem, eszopiclone, zaleplon)
- they act at the same site on the GABAA receptor complex melatonin receptor agonists (e.g., remelteon and the tricyclic antidepressant doxepin)
- More recently, the orexin/ hypocretin receptor antagonist suvoxen has been developed and should receive Food and Drug Administration (FDA) approval for insomnia management
- In addition, the sedating antidepressant medication trazodone (TRZ) and the atypical antipsychotic quetiapine have been widely used “off-label” for insomnia management
- The benefit of the medications used for insomnia is that they can have immediate effects on sleep
- As such, sleep medications have their greatest advantage over CBT for managing acute and brief forms of insomnia
- For example, sleep medications are well suited for treatment of insomnia arising from an abrupt sleep/wake schedule change (e.g., jet lag) or as a stress reaction (e.g., bereavement) to unfortunate life circumstances
- In contrast, the role of medications in the management of chronic insomnia has been debated
- Some studies (Krystal, Walsh, et al. 2003; Roth, Walsh, et al. 2005) have shown continued efficacy of some sleep medications when taken continuously for periods up to 12 months in duration
- However, tolerance and consequent reduction of efficacy may emerge with continued use of some of the sleep-inducing agents, and all sleep medications hold the risk of psychological dependence when used over time
- Whereas medications may reduce sleep-related anxiety for some patients, pharmacologic treatment, in general, is not designed to address the range of cognitive and behavioral insomnia-perpetuating mechanisms mentioned previously
- Of course, the relative value of BzRA and CBT therapies largely depends upon their comparative efficacies for short- and long-term insomnia management of patients with and without sleep-disruptive comorbidities
- Unfortunately, there are currently limited data that speak to the relative efficacy of these two treatment modalities
- One study (Sivertsen, Omvik, et al. 2006) compared CBT with the sleep medication zopiclone and showed that CBT produced significantly better short- and longer-term improvements on objective indices taken from electronic sleep recordings but not on subjective measures taken from sleep logs
- Some other studies (e.g., Morin, Colecchi, et al. 1999; Jacobs, Pace-Schott, et al. 2004) that compared treatments consist - ing of a sleep medication alone, CBT alone, and a combined CBT/ sleep medication therapy showed little difference in short-term outcomes
- but superior longer-term outcomes with CBT alone compared to medication and combined treatment
- Hence, it does seem possible that a short-term combined treatment followed by CBT alone may be an optimal treatment approach
- However, this study focused on patients with insolated insomnia disorder and did not include patients with sleep disruptive comorbidities
- Furthermore, there has yet to be a follow-up study to replicate this study’s dramatic outcomes for those patients receiving the sort of treatment regimen described
- Thus, additional studies of the relative values of CBT and sleep medications would be useful
Treatment Program Outline
- The treatment described in the manual should be preceded by a thorough insomnia assessment
- This assessment session should be conducted to assure that the patient is suitable for CBT and to instruct the patient in collecting the baseline sleep diary data needed in the initial stages of treatment
- The subsequent treatment sessions are then employed to address a range of behavioral and cognitive treatment targets (perpetuating mechanisms)
The following outline shows the organization and flow of the overall assessment and CBT insomnia intervention:
I. Insomnia Assessment—Session 1
a. Assess nature of insomnia and appropriateness for CBT
b. Assign baseline (pre-therapy) sleep diary monitoring
II. Presenting Primary Behavioral Treatment Components—Session 2
a. Presenting treatment rationale and sleep education module
b. Presenting sleep rules—behavioral insomnia regimen
c. Calculating initial time in bed prescription
d. Homework
III. Presenting Cognitive Therapy Strategies—Session 3
a. Review and comment on sleep diary findings showing progress and adherence
b. Provide cognitive rationale to patient
c. Discuss Constructive Worry technique
d. Discuss use of Thought Records
e. Assign homework
IV. Follow-up/Troubleshooting—Sessions 4 onward
a. Adjusting time-in-bed recommendations
b. Reviewing and reinforcing treatment adherence
c. Troubleshooting—Behavioral Component
d. Troubleshooting—Cognitive Component
e. Consideration of therapy termination
~WEEK 9~
Stimulus Control explanation video
Stimulus control:
If wakefulness and the bed have become associated, re-associate bed with sleep by:
- increase the stimulus value of the bed
- you want the bed and this time period to be under strict control
- only sleep can occur = only be in bed when asleep/sleepy
- sleepy = being able to fall asleep quickly, finding yourself falling alseep - getting out of bed when unable to sleep
- do something enjoyable, doesn’t have to be boring
- don’t let the bed be paried with wakefulness
- bed = sleep - Getting out of bed at a consistent time each morning (ireespective of how you slept)
- sleepiness = falling asleep in under 10 mins
- if it’s taking longer than 10 mins, can get up, but don’t want to be fixated on the clock
- therefore, as soon as you realize you’re not sleepy, get up and do anything else
- when you get out of bed at consistant time = builds up sleep for the next night - Using the bed and bedroom only for sleep (and sex)
- Refrain from daytime naps
- naps take away from the homeostatic system
Sleep restriction explanation video
- to improve sleep qaulity you must increase your sleep drive
- a strong sleep drive will reduce wakefulness and lead to better qality sleep
- overtime, as your sleep quality improves, the time in bed prescription will slowly be extended
Sleep Restriction Therapy (SRT) or Time-in-Bed Restriction
To restore homeostatic sleep drive:
- match time in bed with current average sleep production (add 30 mins for normal sleep onset latency)
- if you’re a 6 hour sleeper and you spend 10 hours in bed = you actually get less sleep
- 6 hours are the lowest end of normal
Window
- important to set a sleep opportunity window because relying on our clocks for when to wake up and sleep can cause social jet lag
The Components of CBT-I
The most common components of cognitive behaviour therapy for insomnia (CBT-I) (Edinger & Carney, 2014) are:
- Stimulus Control (Bootzin, 1972): a set of sleep rules to address conditioned arousal.
- Sleep Restriction (Spielman et al., 1987): a technique to increase sleep drive by matching the time spent in bed with current sleep production time
- Sleep Hygiene: a set of rules designed to address sleep-interfering habits or substances
- Cognitive Therapy: a set of techniques to modify beliefs about sleep and fatigue that cause or exacerbate insomnia
- The business of the first session of CBT-I is really about assessment
- this first session is really about establishing this diagnosis,
- clarifying the patient’s goals for treatment,
- and assessing for any contraindications or conditions that could complicate treatment
- As in all cognitive behavioural treatments (CBT), we also orient the patient to what to expect in CBT-I
- For those patients who have participated in insight or support-oriented therapies, the didactic nature of CBT sessions as well as the intense between-session work can be surprising to some people, and may not be a good fit
- Although CBT-I is a highly efficacious treatment, it does not mean that all patients are ready or well-suited for the rigours of the treatment recommendations
- As you will see, it requires commitment, and hard, sustained effort for a number of weeks, in order to see treatment benefits
- Additionally, engaging in the core strategies of stimulus control and sleep restriction, exposes patients to what they fear: spending less time in bed and thus, potentially getting less sleep
- Not everyone is ready for this exposure to an anxiety provoking experience
- Being highly distressed and knowing that CBT-I is the treatment of choice for insomnia does not necessarily mean that a patient is ready to make the changes needed to address the insomnia
- The initial session may reveal that the patient is not ready for the treatment
- If the patient is ready to engage in the treatment, towards the end of the session the patient is taught how to monitor their sleep and provided with sleep diaries to complete over the next two weeks