WEEK 8 - 12 Flashcards

(98 cards)

1
Q

~WEEK 8~

A
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2
Q

What is Insomnia?

A
  • 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:

  1. 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
  2. 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
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3
Q

Sleep Regulation and Insomnia

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Recall that sleep is regulated mainly by two systems:

  1. the homeostatic system (Process S)
  2. 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:

  1. 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
  1. 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
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4
Q

What Factors Cause Insomnia?

A
  • 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:
  1. 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
  1. 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
  1. 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
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5
Q

What Are Predisposing Factors That Adversely Affect Process S (i.e., Deep Sleep)?

A
  • 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
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6
Q

What Are Predisposing Factors That Adversely Affect Process C?

A

If optimal sleep is produced during a dynamic, idiosyncratic timing window, the following behaviours would have a negative impact on sleep:

  1. poor input to the clock (i.e., not engaging in behaviour that will set the clock and prevent drift)
  2. 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
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7
Q

The Third Process: The Arousal System

A
  • 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
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8
Q

Summary Week 8

A
  • 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)
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9
Q

Practice Test

A

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
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10
Q

Overcoming Insomnia Chapter 1

A
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11
Q

Overcoming Insomnia Intro

A
  • 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
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12
Q

Nature and Significance of Insomnia

A

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
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13
Q

Diagnostic Criteria for Insomnia Disorder

A
  • 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:

  1. primary disorder
  2. 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
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14
Q

Development of This Treatment Program and Evidence Base

A
  • 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
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15
Q

The need for a multi-component cognitive behavior therapy for insomnia

A

We thus constructed a treatment that included a number of components, including:

  1. a cognitive module designed to provide psycho-education about factors that regulate the human sleep system and to address unhelpful beliefs about sleep
  2. standard stimulus control instructions to address patients’ conditioned arousal and to eliminate common sleep disruptive habits (daytime napping; maintaining an erratic sleep/wake schedule)
  3. 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:

  1. 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
  1. 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
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16
Q

Theoretical Model for Cognitive-Behavioral Insomnia Therapy

A

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
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17
Q

Risks and Benefits of CBT for Insomnia

A
  • 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
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18
Q

Alternative Treatments

A

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
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19
Q

Role of Medications

A
  • 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
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20
Q

Treatment Program Outline

A
  • 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

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21
Q

~WEEK 9~

A
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22
Q

Stimulus Control explanation video

A

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
  1. only sleep can occur = only be in bed when asleep/sleepy
    - sleepy = being able to fall asleep quickly, finding yourself falling alseep
  2. 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
  3. 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
  4. Using the bed and bedroom only for sleep (and sex)
  5. Refrain from daytime naps
    - naps take away from the homeostatic system
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23
Q

Sleep restriction explanation video

A
  • 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
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24
Q

The Components of CBT-I

A

The most common components of cognitive behaviour therapy for insomnia (CBT-I) (Edinger & Carney, 2014) are:

  1. Stimulus Control (Bootzin, 1972): a set of sleep rules to address conditioned arousal.
  2. Sleep Restriction (Spielman et al., 1987): a technique to increase sleep drive by matching the time spent in bed with current sleep production time
  3. Sleep Hygiene: a set of rules designed to address sleep-interfering habits or substances
  4. 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
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25
Stimulus Control
- Stimulus Control is a treatment for insomnia that can be delivered on its own - however it is most commonly delivered in the context of a cognitive-behavioural package - Stimulus control addresses one of the most common problems in insomnia: conditioned arousal Conditioned arousal: - a situation in which a patient has learned (often outside of their awareness) to associate the bed or sleep situation with increased alertness - To counteract this very common problem they can unlearn the association by being in bed only when sleepy, or very close to it There are five rules: 1. Go to bed only when sleepy (i.e., about to fall asleep if given the chance to sleep) - Sleepiness is a sensation we experience as we are about to transition into sleep - Sleep naturally unfolds when we feel sleepy and give ourselves a sleep opportunity - Getting into bed because it is a particular, habitual time rather than because we are sleepy, can result in increased wakefulness while in bed - Your bedtime may be 11 pm routinely but if you just received a distressing phone call 15 minutes earlier, what are the chances you would be able to fall asleep quickly if you were to get into bed? - Implicit in this instruction is the idea of acceptance when sleep is not forthcoming - Patients who practice this rule unlearn conditioned arousal, but they also covertly challenge the idea that one must sleep simply because one wants to or because it is a particular time - They face the fear: “What if I never get sleepy…?” = immpossible, but this is a common distortion in insomnia - Many patients are unaware that they are challenging the belief but if a patient is adhering to this rule, they are inadvertently building their confidence as someone who can cope with sleep loss - and someone who need not exert effort to sleep because they trust their body to produce sleep when it is truly needed - Additionally, by limiting time in bed to times at which you are most likely to sleep, you are inadvertently building some sleep deprivation and increasing the drive for deep sleep - Systematic sleep deprivation has benefits for someone with insomnia because an increased sleep drive, increases the likelihood of a good night sleep the following night 2. Get out of bed when unable to sleep - Conditioned arousal occurs because there are repeated pairings of the bed with wakefulness in bed - It is a common experience for people with insomnia to lie in bed awake for long periods of time feeling frustrated with their inability to sleep - Most people do not leave the bed because they are exhausted and believe that staying in bed gives them their best odds for eventually falling asleep - However, conditioned arousal prolongs the time that it takes to fall asleep, so this strategy does not work - Getting out of bed when unable to sleep, prevents the pairing of wakefulness and the bed - Moreover, giving up the effort to sleep makes it more likely that arousal will decrease and that the patient will be more likely to be mentally, emotionally, and physically ready to return to the bed - One additional consideration is that when people lie in bed attempting to sleep, they unknowingly go in and out of N1 sleep - Many people have little awareness of this transition and believe they were awake the entire time—missing minutes here and there of sleep - The reason this is significant is that this would impact cognitive-emotional processing - We are more primitive and have less control when we are asleep - Ever heard the saying, “things will look better in the morning”? This is because information processing, problem solving and emotion regulation are less than optimal while in a light stage of sleep - Getting out of bed shakes off this light stage of sleep and increased lucidity improves information processing, problem solving and emotion regulation so that the patient can be more calm and ready to return to bed 3. Get out of bed at a consistent time each morning - Ideally, we would set the sleep opportunity every night but because of the first rule (i.e., only go to bed when sleepy) we cannot control the bedtime - However, we can control when we get out of bed because we can set an alarm - Setting an alarm sets the end of a window of opportunity so that the body can learn that this window is the only chance it has to sleep - Stimulus control is a technique in which we increase the stimulus value of the bed at night for sleep - That is, we learn, this is the only opportunity I have and the only place in which I can sleep 4. Use the bed and bedroom only for sleep (and sex) - If we are trying to increase the stimulus value of the bed for sleep only, then we want to avoid doing anything in the bed that we do when awake - If you do anything in the bed that you normally do while awake, you will train your body to be awake in the bed - During our assessment we ask whether people eat, read, watch TV, do work or homework, use the computer, phone or other devices in the bed - These are activities we do when awake, so pairing a wakeful activity with the bed over and over, we automatically elicit alertness when getting into the bed - We say that sex is an exception because for many people, sex is relaxing and is most often done in a bed - However, for some, sex can be alerting or they may not be able to predict whether it will be alerting, so we ask people whether they can predict if sex will be alerting or relaxing and they can choose if it will be an exception to this rule 5. Do not take daytime naps - If we are trying to strengthen the stimulus value of the bed, during a particular window at night, to be associated with sleep only, then sleeping outside of this opportunity will undermine our efforts - This is one of the reasons why naps are prohibited - Each of these rules increase the probability of sleep (and sleep only) occurring in the bed at night There are other reasons to object to naps. Try and pick the reasons why naps in the context of insomnia are ill-advised in the list below (select all that apply): - Naps can reinforce the idea that one cannot sleep during the night, so to cope with the sleep problem, one must produce sleep whenever possible, even if it is during the day (e.g., Feinberg et al., 1985). - Napping also reinforces the idea that one cannot cope with fatigue, or that one cannot sleep during the night so sleep has to occur whenever possible. - Naps reduce the drive for deep sleep at night by reducing Process S - Naps are sleep effort and sleep should be effortless - Naps reinforce beliefs about low sleep self-efficacy - Naps are not relevant for the circadian system - By following all of these rules, we un-pair the paired association of the bed with wakefulness - Eliminating conditioned arousal is a key target for addressing insomnia - Following these rules also challenges some key beliefs implicated in insomnia - For example, if a patient is fixated on needing a particular number of hours of sleep each night, following stimulus control will typically vary the amount of sleep one obtains - By accepting that sleep duration will vary a bit initially, it helps the patient face their fears about needing particular magical numbers of sleep - Challenging these fears will reduce anxiety about sleep
26
Sleep Restriction
- To increase sleep drive, we create systematic sleep deprivation by restricting the time spent in bed to match the amount of average sleep produced - Then, once sleep deprivation increases and we see sleepiness and improved sleep, we can start to spend more time in bed - This may seem counterintuitive Many people think that people with insomnia are already sleep deprived; however there are a few things to consider: 1. people with insomnia have very horrible nights but then they typically have a few recovery nights; thus their overall average total sleep time may be within normal adult limits (i.e., between 6 to 9 hours) 2. when people with insomnia have a bad night, they increase their time in bed, thus reducing their sleep drive - We need to find a way to send a message to Process S to produce more deep sleep, not less - Consider this: when someone has a stomach virus that causes them to vomit, as soon as people start to feel hungry, the natural tendency is to eat - There is nothing pathological about eating when hungry, but while ill, this behaviour will have a negative effect—it will feed the virus and the virus will continue - A different behaviour is needed in response to this illness, and the different response is “gut-rest” - Gut-rest is a 12-hour fast to starve out the virus; once the virus is gone, normal eating can be slowly reintroduced - It is important that patients understand the rationale for this technique because it is counterintuitive - If you have poor sleep, resting or increasing your sleep attempts with increased time in bed makes good sense, limiting time in bed further does not make intuitive sense - However, since we know this is a homeostatic system that automatically recovers deep sleep, we can understand that the system needs less time in bed to trigger compensation; that is, more deep sleep - The technique of sleep restriction requires sleep diary monitoring - CBT-I sessions are scheduled every other week to accrue two weeks of monitoring, so sleep restriction occurs after gathering a picture of average sleep - The first step is to calculate the average sleep time, which is best accomplished by working backwards - Start by calculating time-in-bed each night - The time-in-bed is the difference between getting into bed and getting out of bed in the morning - ex. On Monday, the intervening time between 11 pm and 7:15 am is 8 hours and 15 minutes
27
Calculations for time in and and time awake while in bed
Monday 1. Bedtime: 11:00 pm 2. Time to fall asleep: 25 3. Time awake during night: 20 4. Wake time: 7 am 5. Rise time: 7:15 am Tuesday 1. Bedtime: 11:30 pm 2. Time to fall asleep: 20 3. Time awake during night: 25 4. Wake time: 7 am 5. Rise time: 7:20 am Wednesday 1. Bedtime: 11:05 pm 2. Time to fall asleep: 40 3. Time awake during night: 15 4. Wake time: 7 am 5. Rise time: 7 am Thursday 1. Bedtime: 10:35 pm 2. Time to fall asleep: 60 3. Time awake during night: 35 4. Wake time: 7 am 5. Rise time: 7:25 am Friday 1. Bedtime: 10:55 pm 2. Time to fall asleep: 35 3. Time awake during night: 20 4. Wake time: 7 am 5. Rise time: 7:15 am Saturday 1. Bedtime: 12:15 am 2. Time to fall asleep: 15 3. Time awake during night: 45 4. Wake time: 8:40 am 5. Rise time: 10:50 am Sunday 1. Bedtime: 10:15 pm 2. Time to fall asleep: 95 3. Time awake during night: 60 4. Wake time: 7:50 am 5. Rise time: 11:45 am CALCULATIONS Time in bed: ``` Tuesday: 7 hours 50 minutes Wednesday: 7 hours 55 minutes Thursday: 8 hours 50 minutes Friday: 8 hours 10 minutes Saturday: 10 hours 40 minutes Sunday: 13 hours 30 minutes ``` - If you add all of these time-in-bed values together and divide them by the number of days, you will get approximately 8 hours and 50 minutes (it’s a little more, but we just need an approximate amount) - Now we need to calculate the total time spent awake while in bed - To do this, we need to add item 2 and 3 together, as well as calculate the amount of time the patient was awake from the time they woke up (item 4) and the time they got out of bed for the day (item 5) - Let’s do Monday together: the time to fall asleep is 25 + the time awake during the night is 20 + the time between final awakening and rise time is 15 minutes = 25 + 20 + 15 = 60 minutes or one hour CALCULATIONS: Time awake while in bed: Mon Time to fall asleep: 25 + Time awake during night: 20 + Time between final awakening and rise time: 15 = 60 Tues Time to fall asleep: 20 + Time awake during night: 25 + Time between final awakening and rise time: 20 = 65 Wed Time to fall asleep: 40 + Time awake during night: 15 + Time between final awakening and rise time: 0 = 55 Thurs Time to fall asleep: 60 + Time awake during night: 35 + Time between final awakening and rise time: 25 = 120 Fri Time to fall asleep: 35 + Time awake during night: 20 + Time between final awakening and rise time: 15 = 70 Sat Time to fall asleep: 15 + Time awake during night: 45 + Time between final awakening and rise time: 130 = 190 Sun Time to fall asleep: 95 + Time awake during night: 60 + Time between final awakening and rise time: 235 = 390 Total wake time= 60 + 65 + 55 + 120 + 70 + 190 + 390/7 = about 135 minutes or 2 hours and 15 minutes - Now that we have the total time in bed and the total time awake during the night, if we subtract them, we are left with the total amount of time they slept - If the average time in bed is 8 hours and 50 minutes and the average time awake is 2 hours and 15 minutes, then the average time asleep is approximately 6 hours and 35 minutes - Now that we have this amount, we want to match their time in bed with this amount - However, we add 30 minutes to allow for a normal amount of time to fall asleep, so we will ask this patient to spend a maximum of about 7 hours and 5 minutes in bed during the initial restriction phase - Once their sleep improves and they show signs of sleepiness, we will increase the time in bed 15 minutes per week until the sleepiness resolves or their sleep worsens - Alternatively, we can increase their time in bed by 30 minutes every two weeks - We leave it up to the patient to decide - This technique sends a message to Process S to increase the depth of sleep, because systematic nightly deprivation is occurring - If the patient does not increase their time-in-bed following a poor night’s sleep, there will be an increased pressure to sleep deeply, and this system can naturally compensate for lost sleep - You may be wondering how the patient knows when to get into and out of bed for their time-in-bed prescription - This is done collaboratively - The window must be the same every night in order to optimize Process C (that is, the clock) - In the example above, the prescription is to spend no more than 7 hours and 5 minutes in bed, and currently, it appears as though they have to be awake around 7 am 5 days a week, thus the patient may want to keep 7 am as their standard rise time - Keeping the rise time at 7 am every morning, that is, 7 days per week, will optimize the clock’s functioning and follows Stimulus Control’s rule of setting a standard rise time - If we count back 7 hours and 5 minutes, this is approximately midnight; however, we add 30 minutes to allow for normal time to fall asleep, so it would be about 11:30 pm - This is called the “earliest possible bedtime” because remember that Stimulus Control has a rule that stipulates that you are not to go to bed until you are sleepy. - So this patient can go to bed at 11:30 pm only if they are sleepy at this time - If they find themselves anxious or not sleepy at 11:30 pm, they stay up until they become sleepy - This minimizes the amount of time they spend awake while in bed and simultaneously increases the drive for deep sleep If this patient is sleepy at 10 pm, what do you think they should do? - We have established an earliest bedtime so they are not to go to bed earlier just because they are sleepy - Find some activities to keep them awake until at least 11:30 pm - By keeping the bedtime and rise time the same every day, this is positive for the clock but also generates a strong drive for deep sleep
28
Sleep Hygiene
- Sleep Hygiene is the treatment that most people in the general public know about and the least effective treatment we have - Sleep Hygiene is categorized as not empirically supported according to APA criteria - In fact, it is often a control group (i.e., an effective treatment group) when testing CBT-I in a clinical trial - It is not that these practices are not healthy; however following these rules will not eliminate insomnia - In other words, they are necessary, but rarely sufficient to treat insomnia Sleep Hygiene Rules (in no particular order) 1. Caffeine: - Reduce your intake of caffeine, preferably one cup (200 mg) per day early in the day - If you consume more than this, be sure to cut off consumption in the afternoon so that it is not too close to bedtime - Caffeine blocks adenosine build-up so theoretically it could limit the drive for deep sleep - It is also a stimulant that can increase arousal - Thus there are likely multiple reasons to manage caffeine use - There are likely individual differences in the sensitivity to caffeine and the efficiency with which one eliminates caffeine for the body, so a one-size-fits-all recommendation may be impractical 2. Nicotine: - Eliminate or reduce consumption of tobacco products - Tobacco has stimulant properties and thus interferes with the depth of sleep - Moreover, once the nicotine is eliminated, withdrawal symptoms are produced and patients can wake up with a craving needing a cigarette 3. Prescribed exercise: - Be sure to be active and exercise if possible - Exercise and increased activity should have a positive impact on Process S - The original recommendations also recommend refraining from nighttime exercise for fear that it is alerting 4. Bedtime snack: - Consume a light bedtime snack, preferably one that contains tryptophan (e.g., milk, peanut butter) - Tryptophan is a building block for producing serotonin (a neurotransmitter implicated in sleep) so the thought is that tryptophan-rich foods would help you to sleep - There is no real evidence for this in insomnia 5. Avoid middle of the night eating: - There are a few reasons for avoiding eating in the middle of the night - First, gastrointestinal upset can interfere with sleep - Second, if you eat upon awakening, you can become conditioned to rouse and eat at the same time each night 6. Reduce alcohol and other substances: - Alcohol and substances such as marijuana lighten sleep - Both substances can decrease arousal and may even help with sleep onset; however the body must work to break them down and eliminate them from the body - While the body works to eliminate these toxins, REMS is displaced - When most of the substances are broken down, REMS rebounds and lightens sleep - Thus the net result from a sleep perspective is negative 7. Environment: - Optimize environment to minimize light, noise, or extremes in temperature - In some ways this is common sense - It is difficult to sleep if you are too hot or too cold or if there is excessive noise in your environment - However, merely producing an ideal environment will not help someone with insomnia sleep What all treatment providers should know about Sleep Hygiene: - In a Ryerson University study, 106 non-sleep specialty health care providers were asked about how they treat insomnia - Of all of the interventions listed for insomnia the most commonly used intervention for insomnia was Sleep Hygiene (88% reported using Sleep Hygiene in their practice) - A similarly high number believed that it was an effective treatment for insomnia (80%) - When quizzed about efficacious treatments such as Stimulus Control, they mistakenly thought that SC included: caffeine, alcohol, bedtime snack and temperature/light recommendations (these recommendations are actually Sleep Hygiene) - This study tells us that treatment providers have a poor understanding of the evidence base in insomnia treatment
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Cognitive Therapy
- Cognitive therapy is a therapy based on the idea that solutions to difficulties can be found by changing the way you think - In this model, there is an emphasis on the idea that how you think affects what you do and how you feel, so making changes in thinking can affect powerful change - There are a number of beliefs that are associated with insomnia - People with insomnia often believe that there is a particular amount of sleep needed in order to “function” adequately - In particular, most people believe that 8 hours is needed, however there is no magic number of hours needed to function - Sleep is highly variable from night to night and functioning is not tied to the amount of sleep you obtain - The one exception is when dealing with sleep deprivation, but people with insomnia tend to obtain normal amounts of sleep on average - The consequence of this belief is that when one obtains less than the magical number of sleep, one becomes anxious about the ability to cope, and it can become a self-fulfilling prophesy - Moreover, functioning is not an all-or-none entity - Even if you are functioning poorly, you are functioning - Thinking in dichotomous or all-or-none terms creates anxiety because things seem more dire than they are - In Cognitive Therapy the therapist encourages the patient to examine whether these beliefs are unhelpful, and encourages them to challenge the belief - In some ways the behavioural strategies of stimulus control and sleep restriction are ways to challenge beliefs about sleep - For example, if someone with insomnia believes that they cannot cope without a particular number of hours of sleep, encouraging them to stay out of bed except for certain hours of the night (stimulus control and sleep restriction) forces them to face their fear - Another key belief in insomnia is that effort is required to sleep - Sleep is like falling in love, you cannot make it happen, you can only set the stage to make it more likely - Sleep effort beliefs are generally behind any perpetuating factor - For example, perpetuating factors include going to bed early, napping, drinking alcohol to relax, or sleeping-in; - if you did not believe that you had to “do” something to produce sleep, you would not engage in these perpetuating factors - A cognitive therapist helps patients make these connections and helps them to engage in the behavioural strategies that will fix their sleep problem
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Pharmacological Treatments for Insomnia
- Sleep medications, approved by Health Canada (Canada) or the Food and Drug Administration (FDA in the United States), are an effective treatment option for insomnia - Generally, medications have been in the benzodiazepine or non-benzodiazepine categories - Benzodiazepines are a class of medications that facilitate GABA, which is important in the onset of sleep - Benzodiazepines are benzodiazepine receptor agonists that target GABA alpha receptors - An agonist is a drug that potentiates or increases the action of that receptor; in other words it facilitates GABA—an important chemical for the production of sleep Examples of benzodiazepines include: - estazolam, - flurazepam, - temazepam, - triazolam - There are also non-benzodiazepine medications, called z-drugs, that do not have a benzodiazepine structure but are GABA agonists that target very specific alpha receptors - For example, zolpidem or eszoplicone - the binding for the first five drugs is to GABA receptors generally, that is, there is not binding to a specific type of GABA receptor - But for the next four drugs, the drug binds to very specific GABA receptors in the brain - For example, zolpidem binds to GABA A alpha 1 receptors only - The half-life refers to the time it takes for the drug to lose half of its action (half of the drug is used up) - A very long half-life would be most effective for people with problems staying asleep throughout the night (e.g., dalmane) - A long half-life is also associated with increased sedation throughout the day because the drug remains in the system during the day - A short half-life is most commonly used for those with sleep onset insomnia only - The short half-life would limit the leftover effects of the medication the next day but such drugs would not help the patient if they woke up in the middle of the night - The medications in the table have established efficacy for treating insomnia - However, sleep medications have a variety of negative side effects that limit their attractiveness to all people with insomnia - Moreover, CBT-I has a greater durability of effectiveness which is why it is the frontline recommended treatment for a chronic insomnia - There are a number of medications used for insomnia that are not approved—this is called “off-label” use - Additionally, there are a number of over-the-counter (OTC) medications designed for insomnia or medications with sedation as a side effect, that are used off-label for insomnia - A good example is the allergy medication Benadryl or Diphenhydramine - Benadryl is an antihistamine and histamines are important in maintaining wakefulness - Thus, blocking histamines can produce a sensation of sleepiness, so some use it for insomnia - Side effects include: sedation, dizziness, blurred vision, constipation, and urinary retention - Antihistamines are not recommended in the treatment of chronic insomnia due to the relative lack of efficacy and safety data The Z-drugs: - ex. zolpidem and zopliclone - were developed to have a better side effect profile than the benzodiazepines - The thought was that a more specific binding would lead to fewer side effects - This is generally true, that is, the side effects are less severe for Z-drugs but there are plenty of problems associated with these medications - For example, epidemiological studies show that road accidents are increased in people taking benzodiazepines or zopiclone - It is important to note that risk for auto accidents are not increased for those with insomnia not on medications - There are also issues with a sensation of daytime sedation and cognitive issues, e.g., difficulty concentrating, remembering - As a result, there are now regulations abut warnings on the medications about driving and the lowest recommended doses have been reduced - Additionally, the FDA issued a ruling mandating manufacturers to place warnings about parasomnias developing and to notify patients about the changes - A small proportion of those taking these medications are at risk for parasomnias such as sleepwalking and sexsomnia (engaging in sexual activity while asleep) - Patients also complain that they become psychologically dependent and that the efficacy reduces over time Remelteon: - Perhaps because patients became wary of sleeping pills, lots of research and development activity occurred in the pharmaceutical industry to produce medications that were different from the benzodiazepine agonists on the market - One new drug that emerged was a melatonin agonist called ramelteon - Please see the section on melatonin below about how melatonin is not a problem in insomnia - To gain approval for the labeling as a sleep aid, remelteon had to demonstrate efficacy for insomnia - There is published evidence for this drug for sleep onset insomnia, but not maintenance insomnia - he side effects include sedation (when taken during the day), slowing in performance and a risk for sleep walking and sexsomnia - There is also a mild increase in prolactin for women taking it for 6 months Doxepin (Silenor): - is a prescription medication that is a histamine (H1) receptor antagonist, or antihistamine - There is some evidence for maintenance insomnia although this drug doesn’t appear to be consistently effective by patients’ appraisal - Side effects include rebound insomnia (a worsening of insomnia upon discontinuation related to withdrawal), sedation, nausea, upper respiratory tract infection, weight gain, constipation, urinary retention, dry mouth, blurred vision, and this drug is highly toxic in an overdose attempt Melatonin: - a hormone excreted in the evening that sets the stage for sleep many hours later - Melatonin is subject to environmental input such that exposure to evening light will delay the release of onset and this is associated with taking a longer time to fall asleep - There is no evidence of any melatonin problems in insomnia - One old study reported that circulating levels of melatonin decreased with advancing age but these results may be meaningless; that is, the clinical significance of “decreased” melatonin is unclear - Oral melatonin is effective in a disorder called Delayed Phase Syndrome - This is because melatonin release occurs much later and thus, sleep onset is delayed - Melatonin is not delayed in insomnia which explains why there is no efficacy for insomnia - Curiously, melatonin is taken by people before bed; a time at which melatonin would already have been present in the brain and would therefore exert no effect - Taking melatonin before bed does not improve sleep at night because when endogenous melatonin is already present in the brain, there is no effect of introducing exogenous melatonin (i.e., a pill) - If you give oral melatonin during the day, the brain responds by increasing sleepiness several hours later because there was no melatonin present in the brain when the pill was taken - But taking melatonin at night makes no sense since the brain will not respond because it already knows it is night, i.e., melatonin was released by the brain several hours earlier - Studies reporting positive effects for melatonin are so small that they lack any clinical utility - For example, Brzezinski and colleagues’ (2005) meta-analysis found an increase of sleep efficiency of only 2% and an increase in total sleep time across the entire night of only 12 minutes, and a decrease in sleep onset latency of only 4 minutes - Although there may be some statistical significance for some of these findings, we would not consider these findings to be particularly meaningful - Especially in light of some studies reporting negative findings for melatonin (i.e., that sleep worsens) - For example, in Buscemi and colleagues’ (2007) meta-analysis, melatonin’s hypnotic effects were negative when given before bed - Thus, melatonin is not used for insomnia in sleep settings despite the belief by many that it is helpful for insomnia Valerian root: - is thought to improve anxiety and promote sedation - It appears to work by facilitating adenosine and amino acids such as GABA - Valerian root has shown some positive effects for sleep outside of the realm of insomnia, so it makes sense that people would think it useful in treating insomnia - According to the National Center for Complementary and Alternative Medicine (NCCAM), “there is not enough evidence from well-designed studies to confirm [efficacy]. No information is available about the long-term safety of valerian. Valerian can cause mild side effects, such as tiredness the morning after its use, headaches, dizziness, and upset stomach” - There is wide variability in how valerian, and other non-regulated substances are prepared, and the extraction process and form, e.g., whether it is dry or aqueous and whether alcohol is used or not, affects the active ingredients - The average consumer is not well-educated enough to understand and make informed decisions about such products - In addition, many types of valerian involve valepotriates which have been linked to cytotoxicity (cell death) and carcinogenic (i.e., cancer) potential 5-Hydroxytryptophan (5-HTP): - is an amino acid that is the intermediate step between tryptophan and 5-HT - Because of the role of 5-HT (serotonin) in sleep, it makes sense that one would investigate ways to boost serotonin to help sleep - However, there is no scientific evidence for the use of 5-HTP in insomnia - In sum, there is a lack of efficacy evidence for any alternative or complementary medicine approach for insomnia Aromatherapy: - specifically lavender, has been associated with improved sleep onset latency but the effects are very small and there is “little scientific evidence of lavender's effectiveness for most health uses” - Fact sheets on herbal remedies (no evidence) are published by the NCCAM, National Institutes of Health Table 9.2: FDA-approved Sleep Medications, as reviewed in Walsh & Roth (2011) and Krystal (2011) Generic: Estazolam (prosom) Binding: nonspecific LRD: 1 mg Half-life: 10 to 24 hours Generic: Triazolam (halcyon) Binding: nonspecific LRD: 0.125 mg Half-life: 2 to 6 hours Generic: Temazepam (restoril) Binding: nonspecific LRD: 15 mg Half-life: 8 to 20 hours Generic: Flurazepam (dalmane) Binding: nonspecific LRD: 15 mg Half-life: 48 to 120 hours Generic: Quazepam (doral) Binding: nonspecific LRD: 7.5 mg Half-life: 39 to 73 hours Generic: Eszopliclone (lunesta in US) Binding: GABAAα1, 2, 3 LRD: 1 mg Half-life: 6 hours Generic: Zaleplon (sonata in US) Binding: GABAAα1 LRD: 5 mg Half-life: 1 hour Generic: Zolpidem (ambien in US; sublinox in Canada) Binding: GABAAα1 LRD: 5 mg Half-life: 1.5 to 2.4 hours Generic: Zolpidem-ER* Binding: GABAAα1 LRD: 6.25 mg Half-life: 1.6 to 4.5 hours Generic: Ramelteon Binding: MT1,MT2 LRD: 8 mg Half-life: 0.8 to 2 hours Generic: Silenor (doxepin)* Binding: H1 LRD: 3 mg Half-life: 15 to 31 hours
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Cognitive Behaviour Therapy for Insomnia versus Sleep Medications
- CBT-I and approved sleeping medications have comparable efficacy - That is, they both typically produce medium to large effect sizes across a variety of sleep indices - There is no evidence that one is better than the other in the short-term - There are, however, a few ways in which they diverge - For example, unlike pharmacotherapy, the treatment gains achieved with CBT-I endure for years after the end of active therapy - CBT-I is also rated as more “acceptable” to patients than hypnotic medications - There is also greater satisfaction with CBT-I than hypnotic medications - CBT-I also avoids issues like medication interactions or physiologic side effects - This is why CBT-I is regarded as the frontline recommended treatment for chronic insomnia
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Summary
We have two main efficacious treatments for insomnia: 1. Hypnotic medications 2. Cognitive behaviour therapy for insomnia (CBT-I) - Hypnotic medications are less effective than CBT-I long-term and have a number of side effects that can make them undesirable CBT-I is comprised of: Stimulus Control, Sleep Restriction, Sleep Hygiene and Cognitive Therapy: - Stimulus Control helps to disassociate the bed with wakefulness (i.e., conditioned arousal) - Sleep Restriction increases the drive for deep sleep - Sleep Hygiene is sometimes necessary but rarely sufficient to address insomnia - Cognitive Therapy modifies sleep-interfering beliefs
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Overcoming Insomnia (pp. 35-80)
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Treatment Rationale
- predisposing factors (e.g., biological or personality traits) - precipitating events (events or circumstances that are stressful or otherwise disruptive to normal sleep/wake routines) - predisposing and precipitating events can lead to the development of sleep problems - These problems arethen made worse by various perpetuating mechanisms, including unhelpful misconceptions about sleep, anxiety about sleeping poorly, conditioned arousal to the bed and bedroom, and various sleep disruptive habits (e.g., daytime napping, spending excessive time in bed) - Explain that this treatment program is designed to correct those unhelpful sleep-related beliefs and anxiety as well as common sleep-disruptive habits that maintain or contribute to insomnia You may use the following sample dialogue: "We have conducted a thorough evaluation of your sleep problem and, based on our findings, we believe that you will benefit from some information about sleep and some recommendations designed to help you change your sleep habits. When sleep problems linger on, as they have in your case, usually unhelpful sleep-related beliefs and habits develop and add to the sleep problem. The treatment you receive will educate you about your sleep problem and help you correct those unhelpful beliefs and habits you have so that you can again develop a more normal sleep pattern." - Then, move on to providing the patient information about sleep.
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Sleep Education
- The sleep education provided to patients during CBT has two primary functions - First, it helps patients overcome their misconceptions and anxiety-provoking beliefs about sleep so that they may develop realistic sleep expectations - Also, it enables patients to better understand how the human biological sleep system functions - Since much of the behavioral portion of CBT is fashioned to re-establish normal functioning of the patient’s sleep system, the education helps the patient to understand the rationale for the behavioral regimen used in this treatment - This understanding, in turn, increases the likelihood that patients will adhere to treatment recommendations - During this first session of treatment, provide the patient with information on sleep norms, circadian rhythms, the effects of aging on sleep, and sleep deprivation You may use the following sample dialogue: "This treatment will require you to make some major changes in your sleep habits so you can improve your sleep. However, before you learn these new habits, it is important that you have a better understanding of your sleep needs and what controls the amount and quality of sleep you obtain. The information I’m about to give you will help you understand how your body’s sleep system works and will prepare you for the specific treatment suggestions you will be given." "Before you make any changes in your sleep habits, it is important that you ask the question, “How much sleep do I need each night?” Generally speaking, there is no one amount of sleep that “fits” everyone. Most normal adults sleep 6 to 8 hours per night. However, some people need only 3 or 4 hours of sleep each night, whereas others require 10 to 12 hours of sleep on a nightly basis. At this point, it is important to set aside any previous notions or beliefs you might have about your sleep needs. These beliefs may be wrong and may hinder your progress. The treatment you are about to receive will help you discover the amount of sleep that satisfies your needs and lets you feel alert and energetic during the day." "In addition to getting rid of any old ideas you have about your sleep needs, it is important that you learn some facts about how your body’s sleep system works. People, like many animals, have powerful internal “clocks” that affect their behavior and bodily functioning. The “body clock” works in roughly a 24-hour period and produces 24-hour cycles in such things as digestion, body temperature, and the sleep/wake pattern. For example, if we record a person’s body temperature for several days in a row, we will see a consistent up-and-down pattern or rhythm in temperature across each 24-hour day. The temperature will be at its lowest point around 3 or 4 A.M, will rise through the morning and early afternoon, and will hit its peak around 3 or 4 P.M. Then, once again the temperature will begin to fall until it hits its low point in the early morning hours." "The influence of the internal circadian clock on the sleep/wake cycle is apparent if one studies the relationship between the body’s 24-hour temperature rhythm and the timing of the sleep period. Suppose a person is placed in a place like a cave, away from daylight, external clocks, and all other time of day indicators. In this situation, the person will continue to show a consistent temperature rhythm and sleep/wake pattern that complete a full cycle about every 24 hours. In most people, there is a close relationship between the temperature cycle and the sleep/wake pattern they show. This relationship is shown in the Circadian Temperature Rhythm Graph included in your workbook. [Direct patient to the graph in the workbook or show him the copy provided in Figure 3.1.] As shown by this graph, the main sleep period begins when body temperature is falling and later ends after the body temperature begins rising again. Hence, although the 24-hour temperature cycle shown does not control the human sleep/wake pattern, the temperature rhythm reflects the working of the body clock and can be used to predict when sleep is likely to occur in the 24-hour day" "In the real world, exposure to daylight, work schedules, mealtimes, and other activities work together with our body clocks to help us keep a stable sleep/wake pattern. However, significant changes in our sleep/wake schedule can interfere with our ability to sleep normally. This may be caused by what is often called “ jet lag.” If, for example, a man who lives in New York flies to Los Angeles, he initially is likely to have some difficulty with his sleep and to experience some daytime fatigue once he arrives in California. This occurs because the 3-hour time-zone change places his new desired sleep/wake schedule at odds with his “body clock” that is “stuck” in his old time zone. This situation is shown in the second graph included in your workbook. [Direct patient to the graph in the workbook or show him the copy provided in Figure 3.2.] The man’s body clock remains on New York time and initially lags behind the real world clock time in California." "This traveler is likely to become sleepy 3 hours earlier than he wishes and to wake up 3 hours before he prefers on the initial days of his trip. Fortunately, with repeated exposure to the light-dark pattern in the new time zone, the body clock resets and allows the traveler to “get in sync” with the new time zone. However, this traveler is again likely to experience temporary problems with his sleep and daytime fatigue when he first returns to New York." MORE ON PG 41 TO 42
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Behavioral Treatment Regimen
- The behavioral treatment regimen uses stimulus control and sleep restriction strategies to standardize the patient’s sleep/wake schedule, eliminate sleep incompatible behaviors that occur in the bed and bedroom, and restrict time in bed (TIB) in an effort to force the development of an efficient, consolidated sleep pattern. - The majority of behavioral recommendations included in this regimen are standard for all patients - However, the TIB prescriptions provided are based on a pre-treatment estimate (derived from sleep diaries) of each patient’s sleep requirement - Since TIB prescriptions may vary from patient to patient, these prescriptions allow for the tailoring of this regimen to fit each patient’s specific sleep needs - Refer the patient to the Sleep Improvement Guidelines sheet in the workbook and provide a brief justification for each behavioral recom - mendation included in the regimen - This worksheet provides a list of “recommendations” to follow and also includes spaces for noting the patient’s standard wake-up time and suggested earliest bedtime You may use the following sample dialogues as you review each sleep rule with the patient: Guideline # 1: Select a Standard Wake-Up Time: - Emphasize the importance of choosing a standard wake-up time and sticking to it every day, regardless of how much sleep the patient actually gets on any given night - This practice will help the patient develop a more stable sleep pattern "As discussed earlier in the session, changes in your sleep/wake schedule can disturb your sleep. In fact, you can create the type of sleep problem that occurs in jet lag by varying your wake-up time from day to day. To maintain a reliable and predictable sleep pattern, it important that your body clock becomes trained into one specific sleep/wake schedule. By sticking to a standard wake-up and rising time, you will accomplish this task and establish a more consistent and satisfying sleep pattern. By adhering to this recommendation you should soon notice that you usually will become sleepy at about the right time each evening to allow you to get the sleep you need." Guideline # 2: Use the Bed Only for Sleeping: - Explain to the patient why it is critical that the bed only be used for sleeping and sexual activity "While in bed, you should avoid doing things that you do when you are awake. Do not read, watch TV, eat, study, use the phone, work on your computer, engage in social media with a smartphone or other electronic device, or do other things that require you to be awake while you are in bed. If you frequently use your bed for activities other than sleep, you are unintentionally training yourself to stay awake in bed. If you avoid these activities while in bed, your bed will eventually become a place where it is easy to go to sleep and stay asleep" "Sexual activity is the only exception to this recommendation. However, if you are someone who often feels more alert after sex or you cannot predict if you will feel alert or relaxed afterward, you may want to consider moving sexual activity to earlier in the evening and/or consider places other than the bed in which you sleep. If this is of concern to you, talk to your partner and find an arrangement that works well for both of you" Guideline # 3: Get up When You Can’t Sleep: - Many people linger in bed for minutes, or even hours, when they can’t fall asleep - Lying in bed awake and trying harder and harder to go to sleep only increases anxiety and frustration, which usually delay the onset or return of sleep "Never stay in bed, either at the beginning of the night or during the middle of the night, for extended periods without being asleep. Long periods of being awake in bed usually lead to tossing and turning, becoming frustrated, or worrying about not sleeping. These reactions, in turn, make it more difficult to fall asleep. Also, if you lie in bed awake for long periods, you are training yourself to be awake in bed." "Remember that we are all passive recipients of sleep. There is nothing one can do to bring on sleep, in the moment on demand. Therefore lying in bed for extended periods hoping for sleep or engaging in activities to bring sleep on simply don’t work. When sleep does not come on or return quickly, it is best to get up, go to another room, and only return to bed when you feel sleepy enough to fall asleep quickly. Generally speaking, you should get up if you find yourself awake for 20 minutes or so and you do not feel as though you are about to go to sleep." Guideline # 4: Don’t Worry or Plan in Bed: - Bedtime is not the time to attempt problem-solving, or to engage in thinking or worrying - Engaging in these sorts of activities only serves to keep the mind awake, making it extremely difficult to fall asleep "Do not worry, mull over your problems, plan future events, or do other thinking while in bed. These activities are bad mental habits. If your mind seems to be racing or you can’t seem to shut off your thoughts, get up and go to another room until you can return to bed without this thinking interrupting your sleep. If this disruptive thinking occurs frequently, you may find it helpful to routinely set aside a time early each evening to do the thinking, problem-solving, and planning you need to do. If you start this practice you probably will have fewer intrusive thoughts while you are in bed." Guideline # 5: Avoid Daytime Napping - Strongly recommend to the patient that he or she refrain from taking daytime naps. - If the patient absolutely must take a daytime nap, instruct him or her to keep it to less than an hour and to complete it before 3 P.M - However, the patient should do all that he or she can to avoid or limit taking naps, even if strongly tempted to do so "You should avoid all daytime napping. Sleeping during the day partially satisfies your sleep needs and thus will weaken your sleep drive at night. Let’s suppose for the moment that you require 7 hours of sleep per night to function at your best in the daytime. If on a particular occasion you decide to take a 2-hour daytime nap, in doing so you would be “spending” 2 hours of your 7-hour sleep requirement and therefore have only 5 hours left to “spend” the subsequent night. Hence, refraining from daytime napping allows you to build your sleep drive through the day so you can spend your entire daily compliment of sleep through the night" Guideline # 6: Go to Bed When You Are Sleepy, but Not Too Early: - Advise the patient to attempt sleep only when he or she is feeling sleepy "In general, you should go to bed when you feel sleepy. However, you should not go to bed so early that you find yourself spending far more time in bed each night than you need for sleep. Spending too much time in bed results in a very broken night’s sleep. If you spend too much time in bed, you may actually make your sleep problem worse. I will help you to decide the amount of time to spend in bed and what times you should go to bed at night and get out of bed in the morning."
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Determining Time-in-Bed Prescriptions
- As briefly discussed in Chapter 2, you will use the patient’s pre-treatment sleep diaries to determine how much time he or she should stay in bed - First, calculate the average total sleep time (ATST) displayed by the patient as shown on his or her completed sleep diaries Once this value is calculated, we recommend that the patient’s time-in-bed prescription be derived using the following formula: Time in Bed (TIB) = Average Total Sleep Time ( ) ATST + 30 minutes - Traditional applications of this treatment protocol advocate the use of ATST as the amount of time the patient should initially allot in bed for sleep - However, ATST as a TIB prescription does not allow for normal sleep onset time and normal middle of the night awakenings that occur spontaneously or to use the restroom - Moreover, insomnia sufferers, as a group, tend to underestimate their sleep times - Hence, use of ATST as the TIB prescription may result in an actual reduction of the patient’s usual sleep time - In our experience, use of the prescription, ATST + 30 minutes, which accounts for the time it takes to fall asleep as well as a few normal, brief nocturnal arousals, is a more reasonable starting point for most of the patients we encounter - Note in this example, the patient slept 375 minutes per night, on average, but had an average time in bed of 505 minutes (i.e. almost 8.5 hours) per night - The ATST falls between 6 and 6.5 hours and, as such, does not seem at all abnormal - However, there is a marked discrepancy between the average time slept and the average time in bed - Given the data shown, the TIB prescription derived using the above formula would be 405 minutes or 6.75 hours - Hence, that TIB prescription would be used as the initial time allotment for the nocturnal sleep period - Of course, patient preferences should be considered when establishing the initial TIB allotment, and it is perfectly acceptable to round the TIB prescription identified in this example to either 6.5 hours or 7 hours if this helps with the patient’s sleep scheduling and initial acceptance of the protocol - It should be noted that in practice it is preferable to derive the initial TIB prescription from sleep diary data collected for 2 or more weeks so that a more stable estimate of ATST can be made - Once the initial TIB prescription is determined, it is important to help the patient choose a standard wake-up time and earliest bedtime so that the prescription can be followed - In doing so, it is important to have the patient consider both “ends” of the night - A patient may initially decide that 7:00 A.M. is a desirable wake-up time - That choice may seem reasonable to the patient with the TIB prescription derived in the preceding example - However, if the initial TIB prescription is much shorter, say 6 hours, this wake-up time would result in an earliest bedtime of 1:00 A.M - Upon discovering this fact, the patient may wish to select an earlier wake-up time so that bedtime can be earlier during the night - Whatever bedtimes and wake-up times are chosen, it is important to involve the patient in this decision-making process - Adherence to the TIB prescription will usually be best when the patient takes an active role in selecting his or her own bedtimes and wake-up times
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Managing Patients’ Expectations and Treatment Adherence
- Once the treatment regimen has been explained and an agreed-upon sleep schedule has been established, it is helpful to provide the patient some additional information about the likely course of treatment and the importance of treatment adherence - Most treatment-seeking insomnia patients are notably distressed by their sleep/wake disturbances and desire rapid relief from such symptoms - However, as is the case with most psychological and behavioral interventions, the current treatment produces improvements gradually and requires consistent treatment adherence on the patient’s part to achieve optimal results - In our experience, most patients who show consistent adherence to the behavioral regimen described earlier show marked reductions in their wake time during the night within the first 2 to 3 weeks of treatment implementation - Improvements (increases) in average sleep time at night are less dramatic and occur much more gradually during treatment - However, many patients continue to appreciate some sleep time improvements even after formal treatment (therapist contact) ends - Of course, patients who do not adhere well to the treatment recommendations may improve more slowly or not at all - Thus, encouraging consis - tent treatment adherence is highly important to the treatment process and outcome overall You may wish to use the following sort of dialogue to emphasize these points to the patient: "Now that we have discussed what you are to do to improve your sleep, you should understand that it is important to follow all of the recommendations we have discussed consistently each and every day of the week. If you are able to do that, you likely will start to see some improvements in your sleep within the next 2 to 3 weeks. What you are likely to notice first is that the time you take to get to sleep and the amount of time you spend awake during the night will decrease significantly. Although you may not see large changes in the amount of time you sleep each night during this time period, your sleep should start to become more solid and restorative. However, if you do not follow the recommendations we have discussed consistently, your progress will likely be much slower or you may not see any significant changes in your sleep. Thus, it is important that you follow the treatment recommendations we discussed consistently so that you obtain the types of results you are seeking" "As you begin this treatment at home, it is also important for you to understand that the sleep schedule we agreed upon for you today may leave you feeling a little sleepy in the daytime, particularly during the first week as you get adjusted to this new schedule. If you notice an increase in sleepiness, avoid activities wherein your sleepiness might be dangerous to you, such as driving long distances or operating hazardous machinery. If you continue to feel sleepy in the daytime beyond the first week, that usually means we have limited your time in bed at night too much and you would benefit by increasing this time somewhat. If this is the case, when you return for your next session we will review your sleep diaries and make the needed adjustments in your nightly sleep schedule to address this problem. If needed, we can consult by phone prior to your next visit to determine what adjustments may be required. Moreover, we can continue to make such adjustments from session to session until we arrive at the schedule that works best for you. It is important that you follow the treatment recommendations consistently from week to week and chart your progress on the sleep diaries in your workbook. This will allow us to assess your progress and determine what, if any, changes in your schedule might be needed."
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Managing Patients Unable to Attend Routine Follow-Up Sessions
- It is desirable to provide patients with one or more return visits to encourage and reinforce treatment adherence, resolve difficulties they are having with treatment enactment, and assist them in making TIB adjustments - However, we encounter some patients who live a great distance from our clinic or for other reasons are not able to return for follow-up sessions - Both our clinicalexperiences and our recent research findings suggest that some patients are able to achieve significant sleep improvements over time following only one session wherein the information covered in this chapter is presented - However, in such cases, it is useful to give the patient instructions that will enable him or her to make needed TIB alterations to establish an optimal sleep/wake pattern For such individuals, you may use the following sample dialogue: "You should try this sleep/wake schedule for at least 2 weeks and determine how well you sleep at night and how tired or alert you feel in the daytime. If you sleep well most nights and are as alert as you would like to be in the daytime, then you probably should make no changes in your time in bed each night. If, however, you find you are sleeping well at night, but you feel tired most days, you should try increasing your time in bed at night by 15 minutes. If, for example, you begin with 7 hours in bed per night the first week and find that you are tired in the daytime despite sleeping soundly at night, you should try spending 7 hours and 15 minutes in bed each night during the second week. If, with this amount of time in bed, you continue to sleep soundly at night but still feel sleepy in the daytime, you can add another 15 minutes to the time in bed during the third week, and so on. However, when you notice an increase in the amount of time you are awake in bed each night, you will know that you are spending too much time in bed at night. If this occurs, you should decrease your time in bed by 15 minutes per night each week until you find the amount of time that enables you to sleep soundly through the night and feel reasonably alert in the daytime. You should also decrease your time in bed after the first 2 weeks if the initial amount of time in bed we choose together today does not reduce your time awake in bed each night." "To help you make decisions about changing your time in bed, it may be helpful to consider some simple guidelines. If you routinely take more than 30 minutes to fall asleep or you are routinely awake for more than 30 minutes during the night, you probably should reduce the amount of time you spend in bed each night. You also should consider decreasing your time in bed if you find that you routinely awaken more than 30 minutes before you plan each morning. Of course, the key word here is “routinely.” Occasional nights during which you have a somewhat delayed start to your sleep or you have more wakefulness than usual once you get to sleep should not be viewed as reasons for changing your sleep schedule. Only when such occurrences are frequent or routine should you try a somewhat shorter time in bed. In the end, the best guideline to use is how you feel each day. If you are satisfied with how you generally feel in the daytime, you can assume that the sleep you are obtaining at night is sufficient."
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Providing Basic Sleep Hygiene Education
- In addition to providing the Sleep Improvement Guidelines mentioned earlier, the patient should be given some standard sleep hygiene education and instructions so as to encourage lifestyle practices that promote sleep quality and daytime alertness - These recommendations are a common component of behavioral insomnia therapy, have good “face validity,” and are easily understood by the majority of patients These recommendations are a common component of behavioral insomnia therapy, have good “face validity,” and are easily understood by the majority of patients "The sorts of daytime activities in which you engage, the foods and beverages you consume, and the surroundings in which you sleep may all influence how well you sleep at night and how you feel in the daytime. Thus, in addition to making the specific changes to your sleep habits that we have discussed, you also may benefit from making some changes to your lifestyle and bedroom to promote a more normal sleep/wake pattern." Once this general rationale has been presented, the patient should be given the specific sleep hygiene recommendations described in the following instructions: "Recommendation 1: Limit your use of caffeinated foods and beverages such as coffee, tea, soft drinks with added caffeine, or chocolates. Caffeine is a stimulant that may make it harder for you to sleep well at night. You should also know that caffeine stays in your system for several hours after you consume it. Therefore we recommend that you limit your caffeine to the equivalent of no more than 3 cups of coffee per day and that you not consume caffeine in the late afternoon or evening hours." "Recommendation 2: Limit your use of alcohol. Alcoholic beverages may make you drowsy and fall asleep more easily. However, alcohol also usually causes sleep to be much more broken and far less refreshing than normal. Therefore, we recommend against using much alcohol in the evening or using alcohol as a sleep aid." "Recommendation 3: Try some regular moderate exercise such as walking, swimming, or bike riding. Generally, such exercise performed in the late afternoon or early evening leads to deeper sleep at night. Also improving your fitness level, no matter when you choose to exercise, will likely improve the quality of your sleep. However, avoid rigorous exercise right before bed because that activity may make it harder to get to sleep quickly." "Recommendation 4: Try a light bedtime snack that includes such items as cheese, milk, or peanut butter. These foods contain chemicals that your body uses to produce sleep. As a result, this type of bedtime snack may actually bring on drowsiness." "Recommendation 5: Make sure that your bedroom is quiet and dark. Noise and even dim light may interrupt or shorten your sleep. You can block out unwanted noise by wearing earplugs, running a fan, or using a so-called “white noise” machine that is specifically designed to screen sleep-disruptive noise. Also, if possible, eliminate the use of nightlights and consider using dark shades in your bedroom so that unwanted light does not awaken you too early in the morning." "Recommendation 6: Make sure the temperature in your bedroom is comfortable. Generally speaking, temperatures much above 75 degrees Fahrenheit cause unwanted wake-ups from sleep. Thus, during hot weather, we suggest you use an air conditioner to control the temperature in your bedroom." - Before closing the session and assigning homework, review the patient’s expectations for treatment and encourage consistent treatment adherence. - Also ask the patient if he or she has any questions about today’s session
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Homework
- The following summarizes the homework to be assigned to the patient at the close of this first treatment session. - Instruct patient to review sleep education material in the workbook (or listen to the audiotape recording if one was made), as well as the behavioral sleep improvement guidelines and sleep hygiene recommendations outlined. - Instruct patient to continue recording his or her sleep habits using the sleep diaries provided in the workbook - Review treatment expectations and encourage consistent treatment adherence - For patients who cannot return for routine follow-up, review methods for adjusting TIB prescriptions if necessary, based on the information provided in today’s session
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~WEEK 10~
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What is Sleep Disordered Breathing?
- There are many ways to define sleep disordered breathing (SDB) - In simple terms, SDB refers to breathing abnormalities during sleep - We have several different types of diagnostic systems establishing criteria relevant to SDB, among the most relevant in North America are the American Psychiatric Association’s (APA) Diagnostic and Statistical Manual - There are several different SDB diagnoses but we will primarily focus on the most prevalent: obstructive sleep apnea
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Obstructive Sleep Apnea
- Obstructive Sleep Apnea (OSA) is the most common type of treatment-meritorious sleep disordered breathing - The word “apnea” is from the Greek word for “no breathing.” Essentially, in OSA we see stopped or greatly reduced airflow during sleep of 10 seconds or more - The airflow problem relates to an obstruction - There is also a disorder called central sleep apnea which refers to a stoppage in airflow but the pathology is generated from the brain, not obstruction in the airway - OSA is comprised of apneic events but can also be characterized by hypopnea events - Hypopneas are similar to apneas in that airflow is disrupted, but in the case of apneas, airflow is completely stopped whereas hypopneas are characterized by at least a 50% reduction in airflow (i.e., air flow does not cease entirely) - The only way for us to know if you have apnea is to do an overnight study so that we can see if there is reduced airway flow and accompanying arousals; however we have several suggestive signs that tell us when we should do an overnight study
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Detecting Apnea
- One system we use to identify possible sleep apnea is STOP - The STOP acronym refers to 4 signs with high sensitivity for detecting apnea - Having 2 or more of these signs is suggestive of sleep apnea and in such cases, we typically order an overnight study to rule out OSA The four signs are: 1. Snoring: - We want to know if you have loud and/or persistent snoring - Snoring alone does not suggest you have apnea, but loud snoring (e.g., the snoring can be heard through a closed door or it is as loud as a conversation) and/or persistent snoring (i.e., most nights per week) in combination with one other sign from the STOP is suggestive of OSA 2. Tired: - To qualify the term “tired,” what is actually meant is “sleepiness.” - Sleep apnea produces many arousals across the night leading to impaired depth of sleep - This causes sleep deprivation and excessive daytime sleepiness (EDS), so we want to know if the person is struggling to stay awake during the day - If it is unclear whether this sign is present, we will often use another measure called the Epworth Sleepiness Scale to determine if they are having significant sleepiness - It is possible to have EDS without OSA - For example, those with Periodic Limb Movement Disorder (discussed in Module 12) have EDS but do not necessarily have OSA 3. Observed apneas: - This refers to someone observing an event - This could be the patient (i.e., they were awoken by the sound of them snorting or gasping for air) or it could be someone who lives with the patient who witnesses them stopping breathing or resuscitating themselves with snorts, gasps or choking sounds 4. High blood pressure: - One of the first signs of OSA is increased blood pressure - There is a disrupted flow of oxygen, and increased work in the heart - As a result, there is cardiovascular stress on the system - In sleep apnea blood pressure does not exhibit the normal rise and fall observed in sleep—it remains high - There is also a link between sleep deprivation and increased blood pressure - High blood pressure is linked to many medical disorders so this is one of the ways in which OSA has earned the name as a silent killer There are a few other correlates of OSA that increase the risk of OSA. These include: Obesity: - The link with obesity relates to the added weight that sits on the airway, particularly when lying supine (i.e., on the back) - Imagine a fabric sleeve that becomes a tube when air is passing through it (like a promotional air puppet outside a car dealership or gas station) - When air is blowing through the sleeve it makes a tube, however when the air supply is disrupted the fabric sleeve collapses flat and the air puppet goes limp to the floor - Now imagine placing a large weight on top of our fabric sleeve and how it would affect air flow—it would cut it off almost entirely - OSA also increases risk for obesity because many people with OSA develop a metabolic syndrome that makes it almost impossible to lose weight - In such cases, the sleep loss creates increased hunger-producing chemicals (grehlin), decreased sensations of feeling full because of a drop in leptin, an impaired ability to process/use insulin and a very slow metabolism; this is a recipe for obesity Increasing age: - Weight gain accounts for some of the increased risk associated with increasing age; however another reason for the increased prevalence with age may be due to changes in the anatomy of the airway - The aging airway and soft palate become longer, pharyngeal fat pads increase in size, the shape of bony structures in your pharynx changes and the response of the back of your tongue to negative pressure stimulation diminishes Large neck size: - The increased neck size simply means that more mass is pressing onto the airway which increases the risk of obstruction Male: - Men have a larger neck size than most women and tend to have greater body mass which increases their risk - There may also be a link with hormones, as lower levels of testosterone is associated with greater rates of OSA - As age increases, the risk for females increases, particularly in menopause, and presumably due to decreased estrogen Structural abnormalities in the airway: - Deviated Septum, overbites, chronic allergies, and recurrent tonsil infections, to name a few, are conditions that can occlude the airway - Part of the examination for sleep apnea involves looking into the patients’ nose and throat - All of these conditions can create intrusions into the airway and thus can cause OSA Nocturia (a condition in which you wake up during the night because you have to urinate): - If you pee more than twice per night in conjunction with other signs, it may be suggestive of sleep apnea - When there is a disruption in breathing, the heart falsely perceives an overload and responds with diuretic hormones; that is, increased atrial natriuretic peptide and decreased vasopressin - Vasopressin is the hormone that slows urine production so if you decrease it, you will get urine production and the patient will wake up having to void - This is important from an OSA point of view but it is also of note because as someone ages, nocturia is associated with an increased risk for falls in older adults and a fall is associated with a loss of independence and a cascade of other medical problems - thus, OSA is important to detect and treat Modifiable risk factors include: Alcohol consumption - Alcohol is a depressant that causes narrowing of the air passageways during sleep - Alcohol also leads to a lightening of sleep so this compounds the EDS already produced by the OSA Smoking - Have you ever seen a smoker spitting and expectorating? It is not pleasant - This is because smoking causes inflammation in the airways, fluid retention in the upper airway and congestion - The created pathology in the airways makes the airway smaller and can result in obstruction - Smokers are three to six times more likely to develop OSA so smoking cessation is an important goal in treating OSA
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Assessing Excessive Daytime Sleepiness in OSA
- Excessive daytime sleepiness occurs when there is a disruption in the depth and continuity of sleep - If someone’s brain has to continuously rouse to reinitiate breathing, this is likely to result in poor objective sleep and thus increased sleepiness - When analyzing data from the overnight study, one of the things we examine is whether there is daytime sleepiness - Generally speaking if one has an apnea/hypopnea index (AHI) of 15 or greater (i.e., they have an apnea/hypopnea with an arousal 15 or more times per hour across the night) they will receive an OSA diagnosis - However, they can have an OSA diagnosis if the AHI is as low as 5-14 if they also have excessive daytime sleepiness - This is because daytime sleepiness is clinically significant and requires treatment - One way to assess sleepiness is with a questionnaire such as the Epworth Sleepiness Scale - The Epworth Sleepiness Scale (ESS) asks patients to rate the likelihood of them falling asleep (dozing) while doing a range of activities such as being a passenger in a car, watching television, having a conversation, etc - A score of 10 or greater on this scale is suggestive of self-reported excessive daytime sleepiness, although the data to support the predictive value of the ESS for objective measures of sleepiness is somewhat poor - Thus, if you are interested in the patients’ perception of their sleepiness, the ESS is valid but if you are interested in whether they would actually doze from an objective perspective, the ESS is a poor substitute for something objective like the multiple sleep latency test (MSLT)
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Self-assessment of Pizza, Contardi, Mondini, Trentin & Cirignotta (2009) article
I assigned a complex methodology paper on assessment of excessive daytime sleepiness in OSA (see Course Readings link in Learning Management System). I would like you to get practice reading scientific articles for your paper. I don’t expect you to get every nuance in the paper, but want you to be able to pick out the dependent variables (i.e., what is measured in the study), be able to summarize the main points of the paper, and critically appraise whether it is a good study. Below is a quiz to test your comprehension of this article: 1. The best way to evaluate sleepiness is - Maintenance of Wakefulness Test, this is a gold-standard test of sleepiness 2. In Dr. Pizza’s study, what was the dependent variable(s)? - Latency to fall asleep during MWT - Latency to fall asleep on MSLT - Crashes in driving simulator 3. MWT evaluates sleepiness via: - The length of time it takes to fall asleep when sitting, this is a gold-standard test of sleepiness
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OSA and Comorbidity
In addition to causing excessive daytime sleepiness, OSA causes many severe medical conditions, including: - increased mortality, - headaches, stroke, - major depressive disorder, - glaucoma, - cardiac disease, - high blood pressure, - Type II Diabetes, - obesity, - erectile dysfunction, - and feet edema as a result of heart failure - Those with apnea and accompanying daytime sleepiness are as dangerous as a drunk driver on the road and their risk for car accidents double that of someone without apnea - The cost of untreated OSA is in the billions annually (think of the costs associated with the many comorbid conditions it causes, the costs relating to auto accidents and the amount of decreased productivity at work) - OSA decreases people’s functional capacity and their quality of life
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Effective Treatments for Obstructive Sleep Apnea
There are several approaches available for those with OSA which include: 1. surgical: - Surgical options involve removing tissue from the airway - For example an uvulopalatopharyngoplasty (UPPP) procedure scrapes back the uvula (the hanging structure in the back of your mouth that people typically mistake for tonsils) - Some have their tonsils removed or scrape back any tissue that impinges on the airway - Such procedures can lead to scar tissue and rely on the assumption that because a structural abnormality exists, then it must be responsible for the obstruction - This is not always the case and the reason why surgery is often not successful - Surgery is not the gold standard of treatment Below are the published guidelines surrounding surgical interventions for OSA: - The presence and severity of obstructive sleep apnea must be determined before initiating surgical therapy (Standard) - The patient should be advised about potential surgical success rates and complications, the availability of alternative treatment options such as nasal positive airway pressure and oral appliances, and the levels of effectiveness and success rates of these alternative treatments (Standard) - The desired outcomes of treatment include resolution of the clinical signs and symptoms of obstructive sleep apnea and the normalization of sleep quality, the apnea-hypopnea index, and oxyhemoglobin saturation levels (Standard) - Tracheostomy has been shown to be an effective single intervention to treat obstructive sleep apnea - This operation should be considered only when other options do not exist, have failed, are refused, or when this operation is deemed necessary by clinical urgency (Option) - [Maxillomandibular Advancement (MMA) - a surgery in which the bottom jaw is extended forward to open the airway] is indicated for surgical treatment of severe OSA in patients who cannot tolerate or who are unwilling to adhere to positive airway pressure therapy, or in whom oral appliances, which are more often appropriate in mild and moderate OSA patients, have been considered and found ineffective or undesirable (Option) - [Uvulopalatopharyngoplasty (UPPP) is a surgery in which tissues in the throat are removed] - UPPP as a sole procedure, with or without tonsillectomy, does not reliably normalize the AHI when treating moderate to severe obstructive sleep apnea syndrome - Therefore, patients with severe OSA should initially be offered positive airway pressure therapy, while those with moderate OSA should initially be offered either PAP therapy or oral appliances (Option) 2. prosthetic and behavioural: - Prosthetic approaches involve devices, the most common of which are positive airway pressure devices and dental appliances - There is one gold standard treatment for OSA and it is positive airway pressure (PAP) because it keeps the airway inflated - The patient wears a mask over the nose and/or mouth and air blows throughout the night to keep the airway open - It is a highly effective treatment - The main issue with it is that many people do not like it and refuse to use it - Dental devices involve a retainer type device worn overnight to advance the lower jaw forward to create more space in the airway - Take a breath in through your mouth normally - Now advance your bottom jaw like a bulldog and take a breath through your mouth - Notice how much more air can come in? - It opens the airway considerably - Dental devices can be effective for some people but comfort can be an issue and not all obstructions would resolve with this type of approach Behavioural approaches: - The final approaches are behavioural and typically accompany other treatments like PAP rather than replace them - Behavioural approaches include weight loss and position training - Because OSA can be associated with obesity and increased weight puts pressure on the airway, weight loss may be recommended - For some people the weight loss may result in a resolution of the apnea, as evidenced by a re-testing with an overnight study - However, because OSA can result in a metabolic syndrome that makes it difficult to lose weight, this recommendation may be very difficult - The presence of OSA typically excludes someone from being considered for bariatric surgery so traditional diet and exercise may be the only option - Thus, this is often a poorly implemented recommendation that may, or may not resolve the OSA Positional training may be used if: 1. the sleep study reveals that the events occur almost exclusively when the person is on their back 2. OSA is mild (e.g., AHI<15) 3. the patient is not obese 4. there is no excessive daytime sleepiness - Positional training is most often accomplished by wearing something in the shirt or a belt that protrudes, so that if the patient rolls onto their back, the bump causes them to roll back onto their sides or stomach - A patient can be restudied wearing their device to see if the OSA is eliminated by preventing them from going onto their backs
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Positive Airway Pressure Treatment Adherence Problems
- The gold standard, most effective treatment is to keep the airway open by blowing air continuously throughout the night, but two thirds of people who are prescribed a positive airway pressure (PAP) device report having problems with it - The most common problems include: mask problems (i.e., doesn’t fit so air blows in face or it falls off), creates nasal congestion and/or dry throat, the noise causes frequent awakenings, the mask creates sensations associated with claustrophobia, and it is inconvenient (e.g., having to bring a device when travelling, having to clean all the parts each night, etc.) - The mask problems can typically be resolved with persistence with the sales company for the mask - There are several different types of mask that can be tried - The noise is typically something that people can get used to over time and devices are not particularly noisy any longer - One common problem that may require treatment is having a claustrophobic reaction to the mask - Claustrophobia related to the mask affects about 30% of apnea patients and it can occur in patients without histories of claustrophobia - Wearing anything over our airway is unnatural and we have a natural tendency to take away anything from our face during sleep - Thus, wearing a mask is challenging and something that one has to become accustomed to over time in order to use it - One of the problems is that the anxiety can become a conditioned anxiety response - Think about Pavlov’s dogs again and how pairing meat with a bell over and over can eventually result in the bell alone eliciting a drooling response - If you pair the mask with anxiety over and over again, even seeing the mask, let alone putting it on could result in anxiety - Once someone feels anxious, the next tendency is to avoid - In this case, the mask is removed and the response is decreased anxiety - So mask=anxiety and removal of mask=decreased anxiety - The fear-mask response is now conditioned - The treatment for this is re-exposure and anxiety extinction - We begin the exposure process by explaining what apnea is and how it will likely lead to early mortality - People often do not understand that apnea is a deadly disease and are often unaware that they have the disorder because they are unaware of awakenings during the night - They may have beliefs such as: “But I don’t snore (that much)”; “I am not overweight”; “I sleep great. I can sleep anywhere, anytime, even during the day. I don’t have a sleeping problem.” - These beliefs are understandable. Apnea’s effects are often silent. - No one perceives their heart enlarging, oxygen deprivation or insulin changes - It may be a shock, so ambivalence is understandable - It is important to work with such beliefs in order for the person to become motivated to use this life-saving device - Once motivation is increased, we teach them that the device is worn to save their life and improve their daytime functioning, not to sleep better - We explain this because it is not uncommon for someone to develop insomnia symptoms because of the anxiety associated with wearing the device and the noise associated with it - Thus, they may say, “This device doesn’t work. I slept better before. I am not wearing it anymore.” - The first step is to ask the patient to hold the mask over their mouth (without wearing it so they have a sense of control) while awake in the therapy session - They continue to do this until they signal that their anxiety has decreased - They do this a number of times until the next session wherein they wear the mask while awake in the therapy session - They continue to wear the mask until they signal that their anxiety has decreased - Again they practice between sessions increasing the exposures to longer and longer durations - They then progress to taking a nap with the device on and eventually wearing it at night - This protocol is successful in increasing the number of nights in which the patient uses this very important health device and also increases the number of hours per night that the patient uses the device
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Summary WEEK 10
- OSA occurs when the airway is blocked and breathing ceases for at least 10 seconds at a time or at least 15 or more times per hour of sleep - These events are associated with arousals in the brain of which the patient may or may not be aware There are a few other correlates or risk factors for OSA: - Snoring - Excessive daytime sleepiness (EDS) - High blood pressure - Obesity - Age - Increased neck size - Males - Structural abnormalities in the airway (e.g., deviated septum) - Nocturia - Alcohol - Smoking - OSA causes many severe medical conditions, including increased mortality, and greatly increases the risk of automobile accidents Effective treatments for Obstructive Sleep Apnea include: - Surgery (e.g., UPPP) which is sometimes effective, but should be a last resort after patient does not accept PAP - Prosthetic devices such as positive airway pressure (PAP) devices and dental appliances - Behavioural approaches include positional training, PAP-related claustrophobia treatment, and weight loss Positional training may be used if: 1. events occur exclusively on their back 2. OSA is mild 3. the person is not obese 4. there is no excessive daytime sleepiness Positive Airway Pressure adherence problems include: - mask fit, - nasal congestion, - dry throat, - noise, - claustrophobia, - and inconvenience - PAP-related claustrophobia is treated successfully with exposure therapy
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Activities | Sleep Disordered Breathing
1. Obstructive sleep apnea (OSA) is characterized by (please check all that apply): - Brief stoppages in breathing caused by structures in the airway - Brief reductions in the flow of air (i.e., at least a 50% reduction in airflow) caused by structures in the airway 2. Modifiable factors for SDB include all but the following: - Nocturia, frequent urination, in some cases, can be treated, but it is not necessarily a modifiable factor and is frequently caused by SDB 3. The gold standard treatment for OSA is: - Positive airway pressure masks 4. OSA causes many severe medical conditions, including (please select all that apply): - Type II Diabetes - High blood pressure - Erectile dysfunction 5. Common reasons for failing to use PAP therapy include (please select all that apply): - A belief that the PAP should help with sleep, and a rejection of PAP when it does not operate as a sleep aid - The mask creates a stuffy nose - Claustrophobia related to the mask
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Moorcroft Chapter 13 (pp. 324–328)
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13.1 Sleep Apnea
- R.P.2 is a 43-year-old high school math teacher who came to the sleep disorders center— or rather was pushed here by his wife, his third—because of excessive snoring - During the interview he indicated that he had ‘‘always been a snorer.’ - His snoring got worse in his late twenties, coinciding with a 40-pound weight gain - He says that he is never aware of snoring, because he is a very, very deep sleeper who awakens slowly and in a ‘‘fog.’’ - His wife reported that he sometimes snores so loudly that, even when she goes to another part of the house in a desperate attempt to get her own sleep, she can still hear him ‘‘through closed doors and with a pillow over my head.’ - She said his snoring has a gagging, choking quality separated by a minute or so of silence - His wife also mentioned that he ‘‘flails around a bit’’ in his sleep, and he related that even in a cool room, he will wake up with sweaty pajamas - While teaching he always has to be moving or standing at the blackboard in order to stay alert - Even during tests, he paces around - During teachers’ meetings, he often has to fight off the urge to sleep by sitting in uncomfortable positions - When grading papers, he drinks a lot of coffee, gets up frequently, and sometimes splashes cold water on his face - He does not nap because naps have never been refreshing for him - He says that he does not attend movies, watch TV, or play cards, claiming to be bored by them ‘‘They must be boring because I always fall asleep!’ - He avoids long drives because of accidents he has had from sleeping behind the wheel - He used to coach basketball but had to give it up - Some screening for sleep disorders can be done in the patient’s own bed at their home - It is thought as technology improves there will be even more home screening for sleep disorders - ‘‘The practices were O.K.—I could keep moving around, but during the bus trips, in the locker room, and even during the games, I would drift off to sleep!’’ - R.P. is overweight by about 50 pounds - He appears to have no neck; rather his head continues straight down to his shoulders - He has a history of high blood pressure and heart problems - Otherwise, he appears to be in good health - R.P. reported trying several methods to stop snoring, including a special thick neck collar he purchased through the mail - Nothing helped - He also related that he had tried hypnosis - When asked if that had helped, he hesitated, showing a wry smile and replied, ‘‘Well, yes.’’ When asked to elaborate, he continued, ‘‘The hypnotist gave me a post hypnotic suggestion—every time I would start snoring, I would turn over.’’ - ‘‘And did it work?’’ - ‘‘Well, I spent the next three nights spinning!’’ - ‘‘Well, I spent the next three nights spinning!’’ but awakened 62 s later with a gasping, snoring sound - This cycle continued throughout much of the rest of the night; as soon as he was in N1 or N2 sleep, his breathing ceased, and then he would awaken a minute or so later, gasping and snoring loudly - He woke 424 times in 433 min of the sleep period - The profile of his sleep was very abnormal - In addition to the frequent arousals, he never reached N3 and had very little REMS - Most of his sleep was N1 with the rest N2 - Time awake totaled about 1/5 of the sleep period - Sleep efficiency was low - Considerable body movements accompanied most of his arousals - Additional data were included on the polysomnogram about his breathing by electronically measuring the air going into or out of his mouth and breathing movements of the chest, the amount of oxygen in the blood, and his sleep position - These measurements confirmed that, although the chest was making breathing movements, no air was entering or leaving his body between the bouts of snoring - This condition is called obstructive sleep apnea ( i.e., absence of breathing while sleeping) due to his upper air passages collapsing shut while he is asleep - At other times the air passages were only partially blocked, allowing some air to move in and out of his body but at well below normal levels - This condition is called sleep hypopnea ( i.e., partial breathing while sleeping) - The average number of apneas plus hypopneas per hour was 57 - His blood oxygen level was significantly low for a total duration of 108 of the 433 min of the sleep period - The next morning R.P. stated that he had a typical night of sleep for him and thought he had awakened maybe 8–10 times - He did not feel refreshed, and he had a headache - He asked if we could help him - Treatment consisted of placing Mr. R.P. on a CPAP (i.e., continuous positive air pressure) machine - Each night, he placed a small, soft plastic breathing mask over his nose - This mask was connected to a specially designed air pump placed close to the bed that was carefully adjusted so that air pressure would keep the throat open to allow normal breathing - A check with Mr. R.P. a few days later revealed a dramatic change - He said he felt alert and rested during the day - Although sleeping with the mask on was a bit uncomfortable, he loved it because of the rest he was now getting - And his wife said he was no longer keeping her awake with his snoring - And his wife said he was no longer keeping her awake with his snoring - This time his sleep was essentially normal for his age - He showed only few apneas and almost no oxygen desaturations - He stated his sleepiness during the day had almost disappeared. - His blood pressure was also much improved. - Because of obstructive sleep apnea, people like R.P. wake up regularly throughout some or much of the night in order to breathe - Waking frequently results in very poor sleep with little, if any, N3 and reduced REMS and excessive daytime sleepiness- The breaths are frequently accompanied by loud snoring - Usually there is little awareness of the snoring and no awareness of the frequent awakenings during the night - Those who do complain of the awakenings tell of the choking or suffocating sensations at such times that may be accompanied by anxiety - Some patients show sleep apnea for only a part of the night or only in some sleep positions, such as on the back - One out of four adult males have obstructive sleep apnea but only one out of ten premenopausal females - Post-menopausal women have as frequent incidence of obstructive sleep apnea as men - Two to three percent of children suffer from obstructive sleep apnea with the incidence of obstructive sleep apnea increasing with age - It tends to run in families - Many, but not all, sufferers are overweight and have thick necks - Sleep apnea is frequently accompanied in middle-aged patients by high blood pressure and various heart problems, especially arrhythmias - Sleep apnea gets progressively worse with time - The hypertension and heart problems may be caused, at least in part, by a fall in blood oxygen and a dramatic increase in blood pressure during the apneic episodes - Some people with years of obstructive sleep apnea are in danger of dying in their sleep from heart failure - On the other hand, following successful treatment, some people with obstructive sleep apnea show dramatic reductions of high blood pressure and heart problems - People with untreated sleep apnea may complain of other problems such as blackouts, automatic behaviors, night sweats, and morning headaches - They frequently maintain that they sleep deeply and are hard to arouse, yet they often awaken disoriented and ‘‘foggy headed.’ - They may complain that they gag easily and that naps are not refreshing - Almost half complain of insomnia - Alcohol, antihistamines, tranquilizers, and sleeping pills make their symptoms worse - Some individuals may show symptoms only after having several alcoholic drinks prior to going to sleep - Because of the excessive sleepiness, they frequently have a history of divorce, multiple car accidents, and employment problems - It is not unusual for them to become depressed and irritable and have diminished sexual desires - Many also complain of concentration, judgment, and memory problems, as well as changes in personality marked by irritability and hostility - Obstructive sleep apnea occurs because the throat is constricted shut during sleep in patients with this disorder - The chest is moving, trying to inflate the lungs, but air cannot get through the throat - Snoring occurs because the throat does not completely open up during the brief awakenings causing the air and throat tissue to vibrate as the air is forced through the narrow passage - CPAP, or one of its more recent variations, has become the most commonly prescribed treatment for obstructive sleep apnea - In some cases, other treatments are often tried first including avoidance of alcohol, certain sleeping pills, opioids, and muscle relaxants - Weight loss may be prescribed, especially in those patients who showed a dramatic gain in weight prior to the onset of the apnea - People who only have obstructive apnea when sleeping on their backs may be advised that sewing a tennis ball into the upper rear of their pajamas prevents them from sleeping in that position - Increasingly an oral appliance is used instead of CPAP - Some of these oral appliances resemble mouth guards worn by athletes when competing; others are more metallic and mechanical looking - The appliance holds the lower jaw or tongue forward, thereby opening the throat - A qualified dentist must fit them - If these treatments are not successful, surgery such as enlargement of the throat can be considered - Abnormal constrictions of the respiratory passages are frequently found in children complaining of excessive daytime sleepiness or who show attention deficit/hyperactivity problems - Most often surgically removing the tonsils and adenoids corrects obstructive sleep apnea in children - Obstructive sleep apnea is the most common of a group of sleep disordered breathing problems Others include: (1) hypopneas and upper airway resistance when the throat is partially constricted during sleep allowing insufficient air through; (2) central sleep apnea when the brain does not send out breathing commands during sleep; (3) a pattern of a one-half to two-minute cycle of increasingly deeper and occasionally faster breathing, followed by a gradual decrease in breathing depth and rate, sometimes up to the point of breathing cessation
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Box 13.1 Sudden Infant Death Syndrome (SIDS)
- The sudden death of an infant that is not explained by medical history, autopsy, or death scene investigation is labeled sudden infant death syndrome - One possibility is that it is a version of sleep apnea - However, SIDS may also be caused by cardiovascular failures, viral infections, over wrapping/overheating, and genetic sources - It may be that SIDS in any individual is caused by multiple, interacting factors - ‘‘Back to sleep’’ and avoiding soft sleeping surfaces and loose bedding or other soft items has reduced the incidence of SIDS - Additionally, use of a pacifier during sleep has been identified with reduced risk of SIDS, but such use has been criticized because of associated side effects
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13.2 Narcolepsy
- L.I. is a 35-year-old female who said her symptoms first appeared as a teenager when she noticed a weakness in the knees especially when she laughed at something funny - Eventually she began to drop things she was holding, and her eyelids would often droop - Gradually the symptoms became more frequent and more intense - About the time she started college she noticed that she was increasingly sleepy during the day - Even after a long night of sleep, she would fall asleep in class, at movies, after dinner, and at other quiet times - These behaviors began to affect her functioning, especially in social situations - Her symptoms became worse if she became emotionally aroused; the example she gave was that a number of times she had ‘‘passed out’’ while kissing her date - She was obliged to take frequent naps, after which she felt refreshed - If she tried to ‘‘fight off’’ the need to nap, she would subsequently fall asleep in inappropriate places, such as the dinner table - She had tried ‘‘sleeping-in’’ in the morning but was unable to do so - About once a week, usually when going to sleep, she experienced hallucinations that were strong and frightening such as someone in the room holding a knife about to stab her - The same thing also sometimes happened when awakening from sleep - Usually at these times she was unable to move for 1–2 min, even after awakening - In the past, she experienced blackouts - She reported having periods of time when she had no memory of what she was doing - For example, she noted several instances of driving home, then suddenly becoming aware of having driven many miles past her home - L.I.’s sleep was assessed in the lab for one night followed by an MSLT the next day - First, she reported a vague awareness of someone ‘‘lurking in the shadows’’ of the room and feeling very frightened but being unable to call out or move - Second, she fell asleep quickly after the second time the lights were turned out and went into REMS almost immediately, followed by a relatively normal cycle of REMS - Third, her sleep was fragmented with more N1 and less N2 and N3, as well as a high number of awakenings - This entire pattern resulted in low sleep efficiency for her age
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Daytime Sleepiness and Driving Performance in Patients with Obstructive Sleep Apnea: Comparison of the MSLT, the MWT, and a Simulated Driving Task Fabio Pizza, MD1,2; Sara Contardi, MD1,2; Susanna Mondini, MD1; Lino Trentin, RPSGT1; Fabio Cirignotta, MD
- We measured the daytime sleepiness of 30 patients with se- vere OSAS with concurrent (objective and subjective) meth- odologies to test the reliability of our simulated driving test to detect EDS Our key findings are: (1) the reproducibility of the driving test across time; (2) the stronger correlations between simulated driving performance and the ability to maintain wakefulness (MWT), compared with the propensity to fall asleep (MSLT); (3) the suitability of our simulated driving test to predict MWT results indicative of full alertness or impaired vigilance; and (4) the association of subjective EDS (ESS score > 11) and reported history of traffic crashes, with significantly lower performances on the driving simulator - The current medicolegal problem concerning the fitness to drive of sleepy subjects, together with the ascertained relevance of sleepiness-related crashes, has led to an urgent need to iden- tify objective tools suitable for detecting patients’ ability to drive - To our knowledge, 6 studies have analyzed the correla- tions between simulated driving performance of patients with OSAS and MSLT or MWT results, and our study was the first to consider both MSLT and MWT simultaneously with driving simulation - Reports of subjective sleepiness have obvi- ously been disregarded because most subjects could bias their report fearing that their driving license would be revoked, ir- respective of the real danger to themselves and others - The MSLT showed a high sleep propensity (mean sleep la- tency < 8 min) in 71% of the population, according to interna- tional diagnostic criteria, whereas the MWT was indicative of an inability to stay awake (mean sleep latency < 8 min) in 29% of the patients, according to current practice parameters for its clinical use - In parallel, our simulated driving test proved to be reproducible on several occasions over time without suffer- ing from learning effect for the primary vehicle-control task (crashes, lane-position variability) - Interestingly, our simula- tion measured, in parallel, different aspects of drivers’ condi- tions: driving performance was stable over time for the primary The stability of the driving test (together with subjective sleepiness measures) proved that patients were in a comparable alertness condition on the 2 days of the study and that the discrepancy between MSLT and MWT results reflected complementary aspects of daytime sleepiness measured by the 2 tests themselves.vehicle-control task (number and time to crash, lane-position variability), probably reflecting intrinsic drivers’ features, whereas it showed a significant learning effect on secondary tasks (speed limits, DADT) that were clearly influenced by the cognition of the driving test itself - Interestingly, our simulation measured, in parallel, different aspects of drivers’ conditions: driving performance was stable over time for the primary vehicle-control task (number and time to crash, lane-position variability), probably reflecting intrinsic drivers’ features, whereas it showed a significant learning effect on secondary tasks (speed limits, DADT) that were clearly influenced by the cognition of the driving test itself - Driving is a complex task that necessarily requires alertness as a sine qua non for efficient sensorimotor interaction with the simulated environment - The significant correlations of simulated driving parameters with objective daytime sleep latencies on the MSLT and MWT confirmed the relationship between simulated driving abil- ity and vigilance, as has already been suggested in previous studies - In particular, the stronger relationship between driving performance and the MWT results, compared with the MSLT results, suggests that the real condition permitting driv- ing was closer to the ability to maintain alertness than to the proneness to fall asleep - This finding was in line with the cur- rent clinical use of MWT that is highly recommended to “assess an individual’s ability to remain awake when his or her inability to remain awake constitutes a public or personal safety issue - The efficacy of the MWT as a good predictor of alertness was also confirmed in a paradigmatic example of 2 aviators safely returned to flying duty despite pathologic MSLT results - https://courses.ryerson.ca/d2l/le/content/617825/viewContent/4336880/View
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Abbott, A. (2005). Neuroscience: While you were sleeping. Nature, 437(7063), 1220–1222
- Alison Abbott finds out, this sleep disorder is shedding fresh light on the development of neurodegenerative disorders - Sleep neurologist Brad Boeve recalls one couple who described a particularly horrendous night-time event - While they slept in their bed, the husband suddenly grabbed his wife's head, shook it around roughly, then slammed it down hard and threw up his arms - Far from being intentional, this distressing episode was the result of a disorder that sees sleeping people physically act out their dreams - In this instance, when the husband woke up he revealed that he had been playing rugby in his dream, had scored a try and then raised his arms in victory - The case is just one of many that Boeve has investigated at the Mayo Clinic in Rochester, Minnesota - Beyond the obvious immediate trauma, Boeve believes that the sleep problem could hint at something more sinister - A large proportion of those affected by it go on to develop Parkinson's disease or a closely related neurodegenerative condition - “I get weekly e-mails from people who have had these episodes and are afraid,” says Boeve. - The idea that the sleeping problem, known as REM sleep behaviour disorder, or RBD, and Parkinson's could be linked poses difficult ethical questions for doctors - But it could also overturn current theories on how Parkinson's disease works and how it could be treated - There are many sleep disorders, from insomnia to sleep-walking (see Sleep Insight), but few are more bizarre and disturbing than RBD in its chronic form - About a quarter of a healthy night's sleep is occupied by rapid eye movement (REM) sleep, snatched in ever lengthening stretches as the night progresses - REM sleep is the time of dreaming, and voluntary muscles — apart from those of the eyes, which flicker continuously — become temporarily paralysed - Described as REM atonia, this paralysis stops us from physically acting out our dreams - RBD sufferers lose this atonia - Instead, they flail their limbs and carry out coordinated movements — like the head-grabbing — following the course of their dreams - These dreams are always vivid and frequently involve fighting or being chased - Experts believe that the subjects of the dreams are, in turn, influenced by the mobilized limbs whose movements get woven into the stories - Episodes of RBD may occur only once a year, or as often as four or five times a night - So far, there seems to be no link between the frequency of the episodes and the likelihood of developing a neurodegenerative disease — or how soon such a disorder might appear - Of the 26 RBD patients studied by neurologists Carlos Schenck and Mark Mahowald at the University of Minnesota in Minneapolis, 18 have developed Parkinson's disease or closely related conditions - The degenerative diseases that have been linked to RBD have a common underlying feature - A protein in the brain called α-synuclein becomes misfolded and clumps together to form aggregates - Collectively, these diseases are called synucleinopathies, although it remains unclear exactly what role the α-synuclein protein plays in the conditions - RBD patients develop diseases involving misfolded α-synuclein disturbingly often - Schenck, for example, notes that about 70% of his RBD patients go on to develop a synucleinopathy - In his patients, it took an average of 13 years from the onset of RBD until the patient began to show symptoms of synucleinopathy — although the range was between 3 and 29 years - In unpublished work, Boeve, for example, has studied more than 250 RBD patients, many of whom had Parkinson's disease or another synucleinopathy when they arrived at his sleep clinic - About half of those who showed up with just RBD developed a synucleinopathy an average of eight years later - Tell-tale α-synuclein aggregates called Lewy bodies were found in the brains of 26 of the 27 patients who died during the study - By the mid-1990s, it was clear that there was probably a connection between RBD and synucleinopathies - But researchers had no idea what might lie behind the link — anatomically it just didn't add up - A muscle's readiness to contract, or its tone, during REM sleep seems to be controlled by the brain stem, a complex structure that shuttles information between the body and higher areas of the brain - This was demonstrated in the 1960s by sleep researcher Michel Jouvet at the University of Lyon, France - He damaged the pons, part of the brain stem, in cats and found that the animals no longer slept peacefully but would, for example, stalk imaginary prey during REM sleep - But according to scientific dogma, Parkinson's disease results from the death of nerve cells in the substantia nigra, a different region that sits above the brain stem in an area called the midbrain - These nerve cells release a chemical called dopamine, which transmits signals to other parts of the brain and so helps to control movement - The link between Parkinson's and the loss of these cells in the substantia nigra is reasonably well established - Treating Parkinson's patients with dopamine, for example, can dramatically improve their movement control, at least for a while - And autopsies of people with the disease have shown that they had lost at least 80% of their dopamine-producing cells in the substantia nigra - So how can this be reconciled with the apparent correlation between RBD and Parkinson's disease? - The small community of scientists researching this field are now wondering whether the dogma needs a rethink - They suspect that RBD is the first sign of a degenerative process that begins in or near the brain stem and then creeps up the brain to other areas - According to this idea, first put forward by Boeve, RBD results from damage to a brain area affected early in the course of a more extensive condition - This disease really cripples only when it hits, and strips, the substantia nigra = However plausible it seems, this idea leaves many questions unanswered - Why, for example, do only two-thirds of Parkinson's patients seem to suffer from RBD — shouldn't they all? - But there is also some compelling support for the concept, particularly from the work of Heiko Braak, a neuroanatomist at the University of Frankfurt in Germany - Braak performed detailed anatomical investigations of 41 autopsy brains from people who had Parkinson's disease - He also looked at 69 brains from people who had no clinical record of neurodegenerative disease but whose autopsies revealed that parts of their brains contained Lewy bodies - Braak showed that the emergence of Lewy bodies seemed to follow a defined and fairly predictable path, which he graded into six distinct steps - In the least affected brains, the Lewy bodies are confined to distinct areas of the lower brain stem - In stages 3 and 4, damage extends into the upper brain stem - And in stages 5 and 6, the damage reaches the substantia nigra and, ultimately, the cortex, impinging on areas involved in emotional and intellectual activities - The Lewy bodies seem to multiply and spread through the brain, never appearing at higher levels unless they are also present lower in the brain stem. - “By the time you see the distressing motor symptoms of Parkinson's, the damage is well advanced,” says Braak - But because the early stages of this condition don't seem to have any obvious symptoms, it is very difficult for clinicians to correlate Braak's stages with signs of disease - So it is impossible categorically to conclude that the progression of the Lewy bodies has anything to do with Parkinson's - “It is only a hypothesis, although a plausible one” Braak says. “We'll have to see if any symptoms are eventually associated with early stages.” - clinician-researcher William Langston, heads the Parkinson's Institute in Sunnyvale, California - Langston is keenly aware that his patients report all manner of weird symptoms that at the moment are not classified as part of classical Parkinson's - “There is a ringing association on the clinical side,” he says. “I have a feeling that in Parkinson's disease we may have trouble seeing the forest for the tree — the tree being the devastating motor effects.” - What would it mean if the early stages identified by Braak were indeed relevant to the disease? - And what if the march of the Lewy bodies could be tracked in the living brain, for example through unexpected clinical manifestations such as RBD?" - Then we could give people advance warning that they were at very high risk for Parkinson's,” says Ilonka Eisensehr, a neurologist now in private practice whose research at the University of Munich has added to the body of evidence linking RBD with synucleinopathies - Eisensehr found that some patients who came to her sleep clinic for reasons unrelated to RBD had some muscle tone during REM sleep - In other words, they no longer had complete sleep paralysis, although they had not yet begun acting out their dreams - She carried out brain imaging studies on a group of these ‘subclinical’ RBD patients, comparing them with RBD patients, those with Parkinson's disease and healthy controls - She measured levels of proteins called dopamine transporters in the upper brain stem - These proteins are found only on dopamine-producing neurons, giving Eisensehr a way of monitoring the fate of these cells in patients. - She saw a clear pattern: the greatest loss of dopamine transporters was in patients with Parkinson's disease, although RBD patients also showed fairly low levels - In the subclinical RBD patients, the transporter level was better but was still lower than than in the healthy controls, and the loss correlated directly with how much muscle tone they had during REM sleep - “Loss of REM atonia could indeed be a measurable, very early indicator for Parkinson's disease,” Eisensehr says. - Karin Stiasny-Kolster at the University of Marburg in Germany has taken this further by showing that nearly all of her 30 patients with clinical or subclinical RBD had a badly disturbed sense of smell, a very common complaint among Parkinson's patients - These observations fit well with Braak's hypothesis that Parkinson's progresses up through the brain in distinct stages, says Stiasny-Kolster - Smell signals enter the brain directly in the olfactory bulb, one of the areas, along with the brain stem, that Braak categorizes as stage 1 - Despite this evidence, some sleep neurologists have yet to be convinced - One of them is Alex Iranzo at the University of Barcelona in Spain - He says that over the past nine years, 40% of his RBD patients have developed a neurological disease, but in many cases that disorder was not a synucleinopathy - “RBD is certainly an anatomical disease, but I'm not sure there is a simple molecular explanation for it,” Iranzo says - Clearly the phenomenon requires a lot more research to unravel exactly what is going wrong in the brains of those who suffer from RBD - But whatever the outcome, the statistics are stark: these patients have a highly increased risk of developing Parkinson's disease, or another irreversible degenerative disorder - At the moment there are no drugs to protect neurons against the disease, raising the ethical dilemma of whether or not patients should be warned when they are diagnosed with RBD - Like Eisensehr, Schenck thinks they should be - “Then they will stay in touch with clinics and may eventually be able to be recruited into studies testing potential neuroprotective agents,” Schenck says - Many drug companies are trying to develop such drugs, and enrolling people at high risk of developing Parkinson's, but who have no symptoms, into clinical trials could help bring products to the market faster - Recruiting those who already have Parkinson's disease is not ideal as they have already lost a high proportion of their dopamine-producing cells, leaving few neurons to protect - “Most trials have failed because we are not getting in early enough,” says Langston - Jacques Montplaisir, a neurologist at the University of Montreal in Canada, prefers not to bring the issue up with his patients unless one of them specifically asks - He is concerned about needlessly alarming the subgroup of RBD patients who are not suffering from a neurodegenerative disease - Montplaisir tests his RBD patients' sense of smell as well as their ability to discriminate colours, which is also frequently lost in Parkinson's disease, hoping that this will help to identify those who are at high risk - Only at such a point, or when a neuroprotective agent is available, would it be ethically justified to inform patients, he says - “The best approach is to make clinicians aware of the possible correlation between RBD and Parkinson's, so they will be alert to danger signals such as RBD, and also disturbances to the sense of smell,” says Kieran Breen, director of research at the Parkinson's Disease Society in London “Clinicians could then monitor the patients closely.” - But Breen adds that patients should be told they have Parkinson's only when the first motor symptoms start - “It would not be fair on the patient otherwise,” he says, “given the uncertainty of the link and the long time-lag that can sometimes occur between onset of RBD and onset of Parkinson's.” - Neurologists currently prescribe clonazepam, a drug used to treat epilepsy, to RBD patients to suppress their dream enactment - But no prescription can help patients live with the fear that a diagnosis of RBD brings - In the future, those with early warning signs may turn out to be the lucky ones if effective neuroprotective agents are developed - “We are facing a revolution in Parkinson's disease,” says Langston. “We've been fixated on movement disorder linked to cell death in the substantia nigra, but we may now have to think more broadly.” - He believes that early warning signs such as RBD may turn out to be exactly what is needed to understand this terrible disease and learn how to stop it in its tracks
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What Are Parasomnias?
- Parasomnias are unusual behaviours and experiences during sleep - We frequently categorize them according to what stage of sleep in which they occur - There are some parasomnias that can occur more frequently in REM or NREM, however, they can also occur in the other type; we will categorize them as “other” parasomnias NREM parasomnias: - Confusional arousals - Sleepwalking (somnambulism) - Sleep terrors (night terrors) REM parasomnias: - REM sleep behaviour disorder - Isolated sleep paralysis - Nightmare disorder Other parasomnias: - Catathrenia (groaning) - Sleep sex (sexsomnia) - Sleep related eating disorder (SRED) - Sleep Starts (hypnic jerks) - Teeth grinding (bruxism)
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Non-REM Parasomnias
- Non-REM parasomnias are disorders that occur predominantly during NREM stages of sleep. Confusional Arousals: - Confusional arousals are much like the name implies - The person awakens in a semiconscious state and is confused - It should be noted that it is most prevalent in children - Patients can be unresponsive, staring, crying, and/or flailing about - Bouts typically last about 5 minutes, but in severe cases, it can last hours - The patient does not remember the event - It most typically occurs in the first third of the night, and occurs during awakenings from N3 or delta sleep - Generally, it is harmless, although it is distressing for parents and partners to have a loved one unresponsive - The main treatment is to manage sleep deprivation, because sleep deprivation makes it worse - When we are sleep-deprived, our drive for deep sleep increases; with more deep sleep comes an increased risk for a confusional arousal - In addition to counseling about sleep deprivation, bed partners and parents are encouraged to keep the environment safe for the sufferer (because they are unaware of their surroundings) and refrain from waking the patient up Sleepwalking: - Sleepwalking includes walking as well as other behaviours that are initiated in someone who has not fully awakened from NREMs - Sleepwalking can include mumbling or talking, simple behaviours like tugging at sheets, complex behaviours that involve unlocking the door and leaving the house and of course, walking around - Complex behaviours are somewhat rare and are of concern for safety reasons - Behavioural treatments include practical strategies to prevent injury, including getting complex locks that would be difficult for the patient - Sleepwalking has been used as a defense in criminal cases - It is clear that those engaged in sleepwalking have no awareness of what they are doing and are capable of doing even complex activities Sleep Terrors: - Sleep terrors involve an awakening in the first third of the night characterized by a reaction of utter terror, including screaming, sweating, and sometimes flailing about - There is some overlap with confusional arousals in that: both occur in the beginning of the night; both occur out of NREM sleep; there is amnesia over the event; and the patient is difficult to console (or rouse) - The obvious difference is the terror piece - In the case of confusional arousals, the patient is confused, but with sleep terrors, it looks like the person is absolutely terrified and it takes several minutes for the reaction to dissipate - Treatment most often involves reassurance, prevention of sleep deprivation, stress management (it is more common during times of stress), and in some cases, medication, most notably clonazepam
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REM Parasomnias
- Unlike non-REM parasomnias, REM parasomnias occur predominantly during REMS and thus are more likely in the second half of the night REM Behaviour Disorder (RBD) - Remember that when we are in REM sleep we are paralyzed and unable to act out our dreams - Thus, even if we are doing something active in our dream such as playing baseball, we lay still in bed; our muscles in repose - In RBD, the paralysis does not occur and the patient engages in movements which can involve talking, shouting, or even hitting - Imagine if someone was chasing or attacking you in your dream, you would try to physically ward off the attacker; in someone with RBD, you may observe them actively fighting and if you were nearby, you might be attacked as well - Someone with RBD is not clued into the reality in the bedroom; they remain in the dream in a state in between REMS and wakefulness - This can look somewhat like night terrors but RBD is more common in the second half of the night because of its association with REMS - Differential diagnosis includes an overnight study, in which the absence of muscle atonia during REMS is a key feature for a RBD diagnosis - Treatment of RBD most often involves clonazepam but it is also often necessary to make the patient’s sleeping environment safe Isolated Sleep Paralysis - Sleep paralysis is a benign but distressing condition in which the patient is paralyzed briefly while awake - It is essentially an intrusion of REMS into wakefulness (i.e., in REMS, there is paralysis) - It is highly common—about 50% of the population have at least one experience in their lifetime - It is a characteristic of narcolepsy, so a report of this symptom must be evaluated further to determine if there are other symptoms of narcolepsy such as sleep attacks or cataplexy - The singer-songwriter Sheryl Crow has been open about having this problem - There can be an accompanying hallucination experience in which the patient imagines a demon or an old witch, sometimes called an “old hag”, sitting on their chest - Differing cultures have differing names for this common hallucination - After ruling out narcolepsy, sleep paralysis is treated mainly with psychoeducation, reassurance that it is normal and an instruction to engage the muscles in the eyes to bring about alertness - During REMS, although most major muscle groups are paralyzed, the eyes have full muscle tone so patients are instructed to dart their eyes back and forth to shorten the length of the episode and bring about a full awakening Nightmare Disorder - Nightmares are very common but nightmare disorders affect less than 5% of the adult population - Nightmare disorder in preschoolers is as high as one third, but most kids outgrow the disorder - A nightmare disorder is characterized by recurrent frightening dreams (i.e., nightmares) that cause awakenings - There is a memory of at least some of the nightmare content upon awakening - Nightmares most frequently occur in the second half of the night, a time at which REMS is most common - Nightmare disorder must be distinguished from several other disorders - Night terrors are similar in the sense that there is a frightening awakening, however, in contrast to night terrors, those with nightmare disorder can typically recall parts of the bad dream immediately upon awakening and in the morning - Those with night terrors often don’t remember the episode in the morning and although they know something terrifying happened in the dream, they don’t recall what happened - Likewise a confusional arousal involves an awakening in which the sufferer is very distressed but they are not aware of dream content and are unresponsive - Nocturnal panic disorder involves an arousal with heightened anxiety, but the arousal is in response to physical sensations, not a nightmare - Nightmare disorder is common in the context of Post-Traumatic Stress Disorder - Nightmares may or may not relate directly to the narrative of the trauma - Nightmares are most commonly treated with Imagery Rescripting and Rehearsal Therapy or the medication prazosin - In IRT, patients write down their bad dreams and write down an alternative, non-distressing dream. - Often the patient merely changes the ending of the dream - They then rehearse the new dream several times per day and the new content often intrudes into their dreams in place of the nightmare content - IRT has been shown to decrease the number of nights with a nightmare, the number of nightmares per night and self-reported sleep quality disturbance Night terrors: - Screaming/crying fearfulness - Fear associated with a scary situation but no elaborate story - Morning amnesia to event Nocturnal panic: - Reports panic symptoms - Not tied to a bad dream Confusional arousals: - Confusion awakening; appears awake - Disoriented - Slow mentation and/or speech
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The Link of RBD with Parkinson's | In the article “While You Were Sleeping,” you read about RBD and neurologic disorders. Test your knowledge here.
1. All the following are characteristic of REMS except: Tissue restoration: primarily associated with deep or delta stages of sleep (e.g., N2 and N3). 2. Acting out one’s dreams is only possible if: You do not have atonia 3. The best predictor of the development of Parkinson’s is: The presence of RBD. The severity or frequency of RBD is not a robust predictor of PD. 4. Which of the following statements is most accurate? The disease process for Parkinson’s Disease (PD) develops over years undetected. Symptoms typically develop in a mild form and then progressively worsen, and the actual process starts many years earlier. It may develop from the formation of Lewy bodies in the brain stem that make their way up to midbrain structures like the substantia nigra—wiping out the dopaminergic cells in the area 5. Correlates of PD include: Tactile problems Colour vision problems Near-sightedness
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Other Parasomnias
Catathrenia (groaning) - Catathrenia is a parasomnia which can occur in REMS or NREM - the person groans very loudly - If you Google some videos you may notice that it sounds like loud snoring - Snoring involves an obstruction in the airway that creates a sound on inhalation, but the noise associated with catathrenia occurs on the exhalation - Unlike a breathing disorder associated with an obstruction, catathrenia does not have any negative effects on sleep and typically does not rouse the sleeper - Perhaps the most significant adverse effects for the sufferer is for the bed partner because the groaning can be loud and in some cases persistent - Because the sufferer is not aware of the groaning and not roused by it, it is not uncommon for them to deny or not believe the bed partner about the groaning - This is probably why, if you search for videos of catathrenia, most of them start off with: “My brother didn’t believe me that he groaned, so here is the proof….” - If someone seeks treatment it is most often because their bed partner is bothered by it - There are no known treatments and no established etiologic factors - Some believe it is a type of sleep disordered breathing rather than a parasomnia, and small studies have suggested it may be treated using positive airway pressure devices - Assessment procedures entail an overnight study to rule out other conditions such as SDB or sleep talking - The most common recommendation is for the bed partner to sleep with ear plugs Sleep Sex (Sexsomnia) - Sexsomnia is a disorder in which the sufferer engages in sex acts while asleep - This can cause many serious problems around consent as the person is unable to consent while asleep nor are they apt to get consent from the person they may be attempting to have sex with - It is a disorder that can have serious problems associated with it - Sexsomnia appears in the news when it is used as a legal defense - Sexsomnia was also in the news because of its apparent association with taking particular insomnia (e.g., zolpidem) drugs Sleep Related Eating Disorder (SRED) - Sleep related eating disorder is characterized by eating, sometimes large amounts, typically without awareness at night - The patient is not fully awake and therefore may eat non-food or uncooked food, e.g., raw bacon - They may injure themselves because they may attempt to cook or use utensils like knives and they can cut themselves - It is also possible that they may be totally unaware of the eating (because they are asleep) and thus may present with unexplained weight gain and sleepiness - This is to be distinguished from impulse control problems in which eating occurs at night with full awareness - Treatment includes safety measures to protect the patient during sleepwalking, decreasing the calorie value of the available foods in the house as well as pharmacotherapy The three most common medications include: 1) dopaminergic drugs, 2) an anti-epiletic drug, used off-label for obesity, called topiramate, 3) opiates Sleep Starts (Hypnic Jerks) - This is not actually a parasomnia; it is associated with normal sleep but for some, their reaction to it becomes excessive and they seek treatment - Sleep starts are a normal experience between the transition of wake and sleep - It may relate to a reflex - As you lose tone in your body, it can trigger a reflex that causes your body to flex - Have you ever seen a baby being laid down in its crib and how they jerk their arms and legs in response to the sensation of “falling”? - Some suggest it may relate to an ancient reflex needed because we slept in trees - Some experience it along with a sensation of falling and they “jerk” awake; thus there is distress accompanying it - Some also have unusual accompanying sensations like a loud noise, somatosensory experiences like seeing things or feeling as if you are floating - Most people have had some sort of variant, but for chronic sufferers, these sensations are experienced with high distress and the greater the anxiety and distress associated with the experience, the greater the likelihood of recurrence - Hypnic jerks can precipitate and even perpetuate insomnia, because the experience will increase arousal and then prolong sleep onset latency - Treatment is typically psychological in nature, psychoeducation to explain it is benign, distress tolerance training, and treating sleep habits and insomnia to minimize sleep deprivation. - Some patients are prescribed benzodiazepines to manage the contribution of anxiety as a maintaining factor Teeth Grinding (Bruxism) - This is exactly as it sounds—the patient grinds their teeth during sleep - It is relatively benign but it can cause damage to the teeth and jaw pain - It is not uncommon for a dentist to notice the damage and bring it to the attention of the patient - It is most often treated with a dental device that guards the teeth against being ground down any further - It may cause problems with the bed partner because it is an objectionable noise - There is some suggestion that it worsens during periods of stress so anxiety and/or stress management may augment dental appliances
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Summary WEEK 11
- Parasomnias are a range of unusual behaviours that occur during sleep - We typically separate them into REMS and non-REM parasomnias, but there are some that don’t fall neatly into these categories Non-REM parasomnias include: 1. Confusional arousals 2. Sleepwalking 3. Sleep terrors REM Parasomnias include: 1. REM Behaviour Disorder (RBD) 2. Isolated sleep paralysis 3. Nightmare disorder Other Parasomnia-like conditions include: 1. Catathrenia (groaning) 2. Sleep sex (sexsomnia) 3. Sleep related eating disorder (SRED) 4. Sleep Starts (hypnic jerks) 5. Teeth grinding (bruxism)
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Moorcroft Chapter 12 (pp. 308-322) WEEK 11
12.4.2 Parasomnias - Parasomnias are undesirable and usually unpleasant experiential or behavioral occurrences primarily or exclusively during sleep - Common examples are sleep walking, sleep terrors, and bed wetting - Many are exclusive to NREMS, others to REMS, and a few to either stage of sleep - Most are much more common than generally thought but are treatable - Parasomnias occur because waking, NREMS, and REMS are not all-or-none unitary states - Rather each is a condition in which various components in the brain usually function together and operate in a coordinated fashion - However, in some people one or more of these components can break away at times and operate independently of the rest - Put another way, components of one state can intrude into another state - A common example is sleepiness where elements of sleep are occurring during wakefulness - The mechanisms of parasomnias are not always clear, but both genetic and environmental factors are thought to play a role - It is important to emphasize that, contrary to popular belief, parasomnias are not often related to psychopathology 12.4.2.1 NREMS Parasomnias - The NREM parasomnias occur when the brain is in NREMS but also partly awake - That is, the brain is sufficiently awake to carry out very complex, and often lengthy motor or verbal behaviors while still being primarily asleep - There is no conscious awareness while performing these behaviors The most common NREM parasomnias include: - confusional arousals, - sleep walking, - sleep terrors, - sleep-related eating, - sleep sex, - and sleep starts or hypnic jerks
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Confusional Arousals
- Confusional arousals occur when waking up - They are more common in children (16 %) but also occur in adults (around 4 %) Typically there may be: - confusion, - lack of responsiveness, - inconsolable crying, - and/or unacceptable behavior in bed that may range from flailing to violence lasting 5–15 min - There is no subsequent memory of what happened - Sleep inertia may be a variant if there is greater waking but with lingering elements of sleep - Relatives of people with confusional arousals may also have them - Treatments involve avoiding sleep deprivation and even obtaining more sleep, scheduled awakenings, and medication
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Sleepwalking
- Sleepwalking is not what most people think it is - At one time many parasomnias, including sleepwalking, were thought to be due to demons or other supernatural phenomena - Subsequently sleepwalkers were thought to have a mental disorder - Today many people assume that sleepwalkers are acting out their dreams - This is not true - However, people with REM Behavior Disorder do act out their dreams - Sleepwalking begins during NREMS, not REMS, typically occurs in the first half of the night, results in little if any dream recall, and can be induced in people who are predisposed to sleepwalking by forced arousal - It occurs when the brain does not fully awaken from a deep sleep - Sleepwalking begins with the person moving about in bed and then suddenly sitting up with a glazed look on their face and in their eyes - Next, they may repeatedly engage in stereotyped behaviors such as picking at their covers, undressing, and dressing - Simultaneously, they may mumble or make other sounds - The event may end at this point as they lie down and resume normal sleeping - Or the next step may be for them to get out of bed and walk around the room - Sometimes, they may walk to nearby rooms, the yard, around the neighborhood, or even further. - The frequency of these components diminishes the greater the distance from the bed - A person who is sleepwalking may be anywhere between calm and agitated - Most instances last from less than a minute up to 15 min but sometimes last an hour or more - Movements during sleepwalking appear purposeless and tend to be clumsy - The person may trip, bump into things, or knock things over - Injuries can occur, but violent acts are rare - Yet, at other times, they may do something very complex like prepare a meal, play a musical instrument, or even drive a car - They may vocalize or even have conversations, yet screaming is highly unusual - However, full mental abilities such as memory, planning, and interacting with others are greatly or entirely lacking - Responsiveness to the environment, including to their own name, may be greatly reduced - Because a person who is sleepwalking does not have conscious awareness, they are not held responsible for their actions, even criminal ones - Several things contribute to the occurrence of sleepwalking - About 33 % of sleepwalkers have an immediate family member who also sleepwalks or has sleep terrors - Studies of twins show a pattern of genetic inheritance - People who sleepwalk are more likely to talk in their sleep, wet their beds, and have confusional arousals or sleep terrors - Sleepwalking is most common in children, with up to 30 % having done it at least once, and 3–4 % frequently - The onset of sleepwalking is typically from 4–6 years of age, with the peak occurrence at 11–12 years of age - It most often abates by 15 years of age, but 10 % continue through adolescence - By adulthood, 3.6 % report sleepwalking once a year and 1 % report it happens two or more times per month - Eight out of every 10 adults who reported sleepwalking say it has been going on for years - It usually continues from adolescence but is rare in the elderly - Sleepwalking is not associated with any psychological pathology in children but tends to occur more in children who sleep very deeply Most sleepwalking in adults is not a sign of psychiatric or psychological conditions, yet it is more likely in people with: - obsessive–compulsive, mood, or anxiety disorders - those taking certain medications, including over-the-counter sleeping compounds, - and those abusing alcohol - It is also more common in people with other sleep disorders - Sleep deprivation is the most common precipitating factor; - others include an irregular sleep–wake schedule, - fever, - stress, - a full bladder, - or noise - There are several things that can be done for people who sleepwalk - Awakening a person who is sleepwalking is difficult and may be met with resistance or even violence - It is sometimes possible and more successful to gently lead them back to bed without awakening them - By all means, the sleepwalker should be kept out of harm’s way - Since most children outgrow sleepwalking, the best thing for parents to do is simply to wait for the child to grow out of it - While waiting, they can try to reduce the things that trigger sleepwalking events, such as sleep deprivation and stress - Encouraging good sleep hygiene is important - Making the bedroom and the rest of the house safer is also advisable - Scheduled awakenings— waking the person briefly about 15–30 min before the time of the typical occurrence—may be helpful However, if the sleepwalking is intense, frequent, potentially dangerous, or occurs in adulthood, then one of the following might also be tried: - relaxation therapy, - stress management skills, - hypnosis, - medications, - or treatment of any causal psychological problems
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Sleep-Related Violence
- Mr. Parks was a young married man in Canada who had fallen asleep on the couch, then in the early morning hours got up from the couch, put on his shoes and jacket, and drove his car for about 20 min along 14.5 miles of a well-traveled road with turns and traffic lights - Upon arriving at the home of his in-laws, he carried the tire iron in from the car and retrieved a knife from the kitchen, killed his mother-in-law, and attempted to kill his father-in-law - After testimony by sleep disorder specialists based on their examination of Mr. Parks and the circumstances of the incident, the court acquitted him of responsibility for the murder on the basis that he was sleepwalking - There are other well-documented cases of other sleep-related violence and aberrant behaviors including attempted suicides, self-injury, damage to objects, and indecent exposure - These cases have been found to be due to sleepwalking, sleep inertia, REMS behavior disorder jet lag, or sleep disorders such as narcolepsy and sleep apnea - Elements common in such cases include sleep deprivation, chronic stress, and, occasionally, use or overuse of sleep medications and caffeine - In many cases violent sleepers got shortened, fragmented sleep - Such incidences are more common than might be expected and generally thought to involve 2 % of adults - However, individuals rarely repeat these behaviors - Such cases are examples of automatisms—complex behaviors that occur without conscious awareness or voluntary intention, and therefore the person is not held responsible and punished, because in some countries such as the United States a person must ‘‘knowingly intend to commit the crime’’. - Instead, they may be required to get treatment for their sleep problems - Yet, many skeptical people have asked how a person who is asleep can perform behaviors complex enough to commit a crime - Disbelief occurs because of the assumption that sleep is an all-or-none phenomenon - A person can be asleep but have elements of wakefulness occurring - These elements of wakefulness can be sufficient to perform automatic complex behaviors - A number of people accused of crimes have tried to use sleep walking and other sleep disorders as their defense - Some were genuine but many were faking - Since 2000, there have been well-established criteria and sleep lab methods to determine if a person is a sleepwalker or has other sleep disorders that may have been active during the criminal incident - When the lab evidence is negative, the person is not able to use the sleep behavior defense - But while some people have been acquitted because they were sleeping when they committed the crime, many more who should have been acquitted have been convicted because the evidence from the sleep lab has not yet been authorized as a legally valid diagnostic tool
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Sleep Terrors
- Sleep terrors differ from nightmares and bad dreams in several significant ways and are associated with children - Typically, the child partially arouses suddenly from N3 in the first third of the night and emits a piercing scream that awakens parents who rush into the room to see the child sitting up with a terrified facial expression and maybe thrashing about - This may be followed by getting out of bed and running around, sometimes even out of the house - Injury or property damage may result - The child may be sweating, have a racing heart, and be breathing rapidly with wide open eyes - Although not apparent, the child may also have an elevation in blood pressure and a decrease in skin resistance - The attempts of the parents to soothe the child are unsuccessful and the child may become physically hostile toward the comforter, for the child is in a dazed state and not readily responsive to them - After about 1–5 min, the child usually does calm down a bit and returns to sleep, but other times may frantically run around with what can only be described as a glassy-eyed expression - The next morning, the child has very little or no recall of the incident and little or no dream recall - If there is recall, it is only of an image of something like a monster or a wall closing in - Sleep terrors are generally considered to be benign and are usually outgrown, much to the relief of the parents - They occur in about 3 % of children, peaking at 3–5 years of age with most ceasing by adolescence - Their occurrence in adults at 4–5 %, especially males, is more common than generally thought - They tend to be found in others in the family and may overlap with sleepwalking - Sleep deprivation, emotional stress, and fever may increase their frequency, but there is no relationship with psychopathology - Treatment consists of scheduled awakenings, stress reduction, hypnosis, or avoidance of precipitating factors - Severe cases that do not remit over time may be successfully treated with prescribed medications
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Sleep-related Eating Disorder
- Frequent eating or drinking while asleep occurs in some people with their fully realizing it the next morning until they discover the remains of their meal - They may consume food, often highly caloric, or inappropriate even inedible substances, such as buttered cigarettes, often in bizarre quantities - The result can be negative consequences for health such as poor sleep and weight increase. - Sleep-related eating disorder is not associated with real hunger or waking eating disorders but can occur in people with restless legs syndrome, periodic limb movements during sleep, or obstructive sleep apnea - Sleep-related eating disorder has been reported to occur in a small but noteworthy percent of people using the sleeping medication Ambien - It is more frequent in females - Treating any underlying sleep disorder can help, as well as taking steps such as reducing poor sleep hygiene, stress, and mood disorders - Sometimes medication is necessary
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Sleep Sex
- Although not common, sleep sex describes a variety of sexual behaviors, often inappropriate, that repeatedly are performed during sleep without conscious awareness - It can range from masturbation to intercourse - An episode may occur in the sleeper’s bed or may begin with sleepwalking to another bedroom in the house or even a different house - It occurs in both genders, although it seems more common in males than in females - It can happen anytime during the night - Treatment consists of reassurance that this is usually benign, does not have psychological implications, and tends to fade over time - Advice is also given to avoid recreational drugs and sleep deprivation - Additional treatment is usually not necessary unless there is a history of disturbing or injuring others - In such cases psychotherapy, teaching relaxation methods, hypnosis, or medication treatment may be necessary - Additionally, sleeping in separate beds or different bedrooms or even in a sleeping bag that is fully zippered-up has been found to be useful
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Sleep Starts (Hypnic Jerks)
- Most people, probably including you, have experienced a sudden jerk of a leg or arm when falling asleep - This is called a sleep start or hypnic jerk and may awaken you or your bed partner - In some people it may instead be a flash of light or other brief hallucination, a loud bang or snapping noise that is also called exploding head syndrome, or a sensation in the body such as tingling, pain, or floating - Sleep starts are considered benign and are treated with explanation and reassurance
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REMS Parasomnias
The major REMS parasomnias include: - sleep paralysis, - hypnagogic and - hypnopompic hallucinations, and nightmares - They all tend to occur during the second half of the sleep period because REM sleep is relatively more common - related sleep problems, REM behavior disorder and narcolepsy
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Isolated Sleep Paralysis
- You, like most other people, have probably experienced waking up but unable to move, maybe accompanied by a hallucination - This experience, typically lasting about a minute, is called sleep paralysis - Although it is a component of narcolepsy it is also very frequent, especially during adolescence, as an independent occurrence - It is the continuance into wakefulness of the paralysis that is a part of REMS - Sleep deprivation, an irregular sleep schedule, and lying on the back can make it more likely to occur - It is benign and no treatment is necessary - Coming out of it can be speeded by moving the eyes back and forth, then extending these movements to the face and the rest of the body
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Hypnagogic and Hypnopompic Hallucinations
- Sometimes upon awakening or when just falling asleep people have a vague experience such as an indistinct person or creature in the room - These are called hypnopompic and hypnagogic hallucination respectfully and are quite common - They may be accompanied by sleep paralysis - They are benign and no treatment is necessary
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Nightmare Disorder
- The term nightmare comes from night ? maere (Old English for goblin or demon) - It originally referred to a specific kind of occurrence when persons would awaken with what seemed like a demon, also called an incubus, sitting on their chest causing a feeling of suffocation - In the last century, nightmares came to include other negative, upsetting sleep experiences including all sorts of bad dreams While there are similarities between the experiences we commonly group together as nightmares, there are important differences among: - true nightmares and bad dreams, - post-traumatic stress disorder nightmares, - and sleep terrors - The official definition of nightmares is ‘‘coherent dream sequences that seem real and become increasingly disturbing as they unfold - Emotions usually involve anxiety, fear, or terror … or other negative feelings’’ - The person having a nightmare often abruptly awakes - Upon awakening there is full alertness frequently with a moderate increase in heart rate and breathing rate and immediate, good recall of the content of the nightmare - They usually occur after at least 10 min into a REMS episode during the last half of the sleep period
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Nightmares and Bad Dreams
- Bad dreams, also known as anxiety dreams, are sometimes distinguished from nightmares by the fact that the person does not awaken during the dream but recalls the disturbing content upon awakening later - However, this distinction does not matter - More important is how distressing they are to the person when awake and if they result in functional impairments and sleep disturbance - Some people are greatly distressed by them, but an equal number are very little, if at all, distressed - Some people look upon their nightmares and bad dreams as creative, interesting, and fascinating and even enjoy them much as they would enjoy a horror film - Others simple dismiss and ignore them - Some experts believe that the important factor is whether the nightmare or bad dream has a negative effect on waking life, not whether the person has nightmares or bad dreams - Almost everyone can recall at least one nightmare or bad dream during their lifetime, but recalls are more frequent among those who are generally better at recalling their dreams - Many children experience nightmares and bad dreams with a peak occurrence between 3 and 10 years of age - As many as one out of every four college students report having one nightmare or bad dream per month with 5 % reporting them once per week - This number declines to 1–2 % in adults and the elderly - They usually become less frequent in adults but with a greater number of females experiencing them - From another perspective, 4–8 % of all people report that nightmares and bad dreams are a ‘‘current problem’’, and another 6 % say they were a past problem - Yet, retrospective self-reports underestimate nightmare and bad dream frequency when compared to daily logs by a factor of at least 2 in young adults and by a factor of 10 in the elderly - Bad dreams are often spontaneous but can be triggered by other sleep disorders, fevers, ingestion of or withdrawal from drugs and alcohol, and trauma - Nightmares and bad dreams are more frequently reported during times of personal crisis, loss, and trauma - Persistent nightmares and bad dreams can cause insomnia, daytime sleepiness, and anxiety - According to some, bad dreams and nightmares are a failure of the dream function - while others see them as a normal response to psychological trauma and can help us recover from it - When they help, nightmares or bad dreams change over time and then seem to gradually fade away - But they may return in the future when some new experience revives memory of the trauma that originally precipitated the nightmare or bad dream - Sometimes the content of the nightmare literally reflects the precipitating event, but the terror and vulnerability triggered by the event can also be metaphorically represented by nightmares and bad dreams of tidal waves and big whirlwinds, for example - The nightmares and bad dreams occurring soon after the trauma may result in a lot of terror and fear, sometimes accompanied by feelings of great vulnerability - Survivor guilt, and sometimes grief and anger, may follow - Nightmares and bad dreams can also be caused by general stress, normal childhood fears and problems, illness and fever, and be a side effect of some medications - Contrary to widespread belief, nightmares and bad dreams are not necessarily a sign of mental disorder, although there may be psychiatric, personality, and biological links - Nightmares are also more frequent in people who have suffered trauma or abuse - If anything, it is the concern about them that contributes to anxiety, depression, and other psychological problems - Those who suffer from nightmares and bad dreams often share the psychological trait of what psychiatrist Ernest Hartmann calls ‘‘thin boundaries’’ - People with thin boundaries are more open, sensitive, and responsive to their internal and external environments, and as a result, view more events as more personally traumatic than do most people - Nightmare and bad dream distress has also been found to be more likely in those who are creative and absorbed in fantasy and esthetic experiences - But there are also people who have nightmares who fit none of these categories Often reassurance is the best therapy for most people and children who have nightmares, but for more serious cases cognitive behavior therapy such as: - relaxation techniques, - systematic desensitization, - or a drug that suppresses REMS may be necessary - In contrast, traditional psychotherapy has not been shown to be effective for treating nightmares and bad dreams - The most effective treatment has been the use of imagery rehearsal (IRT) - sufferers write, talk, paint, or draw about their nightmares and bad dreams; then to change one or several of their components in some way when awake; and followed by frequently rehearsing the new scenario - In the context of a safe and supportive relationship with a psychotherapist, sufferers may also be encouraged to adopt a more playful attitude toward such dreams and to be aware that the content of the dream cannot really hurt them - Sometimes persons are encouraged, when awake, to converse with the characters in their nightmares and bad dreams - Other approaches encourage sufferers to become lucid during the nightmare or bad dream and change it then - For some people, hypnosis has proven to be effective - Parents can help their child who is particularly distressed by their nightmare by taking the child to a soothing location and having the child describe it - If the child becomes distressed during the relating, try to calm them down, yet not reinforce this upset by giving the child too much comfort or cuddling - The key is to disconnect the emotion of the nightmare from the images - Handle the emotion in a more ‘matter-of-fact’ manner - Repeat this later as much as necessary until the fear of the dream is gone
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Post-traumatic Stress Disorder (PTSD) Nightmares
- Following a harshly menacing traumatic experience, a small but noteworthy number of people will develop PTSD - Ninety percent of them will have nightmares that are a repetitive re-experiencing of the traumatic event, although not always an exact depiction of trauma - This kind of nightmare is intense, emotional, distressing, beyond present waking experience, and easily recalled - People with a history of nightmares prior to the trauma are more likely to have more severe PTSD - They can start at any age and may persist - PTSD nightmares can occur during any stage of sleep, although they are more likely to occur during REMS early in the night, and are more emotionally intrusive and anxiety causing than most nightmares - It is as if the normal, beneficial dream process gets stuck and the normal function of dreams is not occurring - They also are a cause of sleep disruption including more awakenings, fear of sleep, and various changes in REMS - Gross body movements and activation of the autonomic nervous system accompany the nightmare and subsequent awakening - When aroused from the nightmare, the person will be confused and anxious but not always remember the entire nightmare - Treatment for PTSD nightmares can be complex and difficult, but recent new approaches are showing much promise - The treatment has to be individualized because of related psychological and medical conditions Some common repetitive metaphorical elements reported in dreams: - Being chased - Being trapped - Appearing naked in public - Large-scale disasters such as floods and tornadoes - Falling - Being paralyzed and unable to move - Ghosts returning from the dead - Being kidnapped - Being endangered - Rejection, humiliation - A violent attack - Losing teeth - An out-of-control vehicle - The cognitive-behavioral techniques used with other nightmares and bad dreams, especially IRT, can also be helpful with PTSD nightmares, but additional psychotherapy, psychosocial therapy, and medications are also often helpfu
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Recurrent Dreams and Repetitive Nightmares
- Recurrent dreams and repetitive nightmares range from virtual duplication of the entire dream or nightmare to the recurrence of themes or components in various dreams - They have a negative quality and often involve only the dreamer - Also typical are recurrences of metaphorical depictions of conflicts or stress such as tidal waves, tornados, and hurricanes - They are more frequent in childhood - Their occurrence correlates with increases of waking anxiety, depression, stress, or personal adjustments - Resolution of a waking situation usually is accompanied by less frequent repetitive elements in dreams or their compete disappearance
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Miscellaneous Problems That Occur During Sleep
Teeth Grinding (Sleep Bruxism): - Ten to twenty percent of people may grind or click their teeth frequently during sleep, but it is most prevalent in adolescents - For the vast majority of these people, bruxism is not serious, but it can cause damage to the teeth or cause sore jaw muscles for some - While bruxism has not been shown to be associated with any psychological problems, it may be more prevalent during times of stress - Bruxism occurs most frequently during N2 sleep and REMS but has also been observed during other stages of sleep - It may be accompanied by a partial arousal, yet the sleeper has no awareness of it and seldom awakens - Other body movements and an increase in heart rate frequently accompany it - Dentists can treat bruxism by fitting the sleeper with a guard worn over the teeth during sleep Bedwetting: - Bedwetting (enuresis) is considered an annoying but otherwise typically benign problem - It is much more common than generally realized but is usually outgrown - It can occur during NREM or REM sleep, usually earlier in the night, but the sleep is otherwise normal - Thirty percent of 4 year-olds wet the bed, more so in males than females, but the percent decreases with age after that - For some children, neurological control of the bladder sphincter can even come as late as 12–15 years of age - Yet up to 2 % of 18 year-olds still wet the bed as do 0.5 % of adults, more so in females than males - It is better not to make a big issue out of bedwetting that occurs in children under 6 or 7 years of age if they have never been dry for more than a few successive nights The reemergence of wetting the bed after a number of dry months or years can indicate: - urinary tract problems, - psychological problems, - or even neurological problems such as epileptic seizures and should be brought to the attention of a medical doctor - Bedwetting tends to run in families but seems unrelated to behavioral or psychological problems - The most effective treatment (70 %) involves placing a pad that is sensitive to wetness under the child - The wet pad causes a bell to ring awakening the child - Eventually, the child learns to associate the pre-urination sensations with self-awakening in time to get up and go to the toilet to urinate - Drug therapy is an alternative, especially when control is needed on specific nights such as sleepovers - Psychotherapy is usually ineffective Rhythmic Movement Disorder: - Some young children have stereotyped movements such as rhythmic head-banging - It is usually self-limiting and not considered serious unless it is severe enough to cause injury - It rarely persists into adulthood - It can run in families - It can occur when falling asleep or in any stage of sleep - The only known treatment is medicinal Somniloquy (Sleep Talking): - Sleep talking is often related to sleepwalking and is most common in children, but also occurs in adults - Estimates of people who have sleep-talked one time or another range from 20 % to nearly 100 % - Most often, sleep talking consists of a few mumbles to, occasionally, a few understandable words to, more rarely, a hundred or so intelligible words - People have been known to sing, laugh, and make other kinds or utterances - Most often sleep talking lasts for only a few seconds - Although you may have heard accounts of two-way conversations with a sleeptalker, verification of this occurrence in the sleep lab has only been partially successful - Although occasionally used in literature, such as Othello being convinced by Iago’s relaying the supposed sleep talking of Cassio, secrets are seldom spoken - While sleep talking can occur during any stage of sleep at any time during the night, most of it occurs during N2 sleep and only 10–20 % during REMS - Although sleep talking during REMS tends to be more grammatically correct and more emotional, it usually is without reference to the person’s surroundings - Rarely has it been shown to be related to the content of the ongoing dream, and attempts to use it as a play-by-play narration of the dream have failed because the speech is too frequently garbled or nonsensical - Sleep talking tends to occur more frequently in related family members but is considered benign and therefore not treated - There is only one reported case of serious consequences resulting from sleep talking; a firefighter who frequently talked in his sleep in the fire station dormitory was in danger of losing his job because he was keeping other firefighters awake! - There are several other parasomnias, most of which are quite rare, that are not covered here other than mentioning two with noteworthy names — nocturnal groaning (catathrenia) and painful nocturnal erections
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Conclusion
- Many people would find improvement in their quality of life if they regularly got the amount of sleep that they truly needed - It begins with realizing that sleep is important and necessary and then making adequate time for it - But sometimes sleep is not easily achieved because of problems involving the circadian clock For others it is the unusual things that happen during their sleep that cause problems for them such as: - bedwetting, - snoring, - sleepwalking, - and nightmares - In most cases there are solutions available for these people
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~WEEK 12~
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Narcolepsy
- Narcolepsy is a neurological disorder characterized by an intrusion of REMS into wakefulness - The classic tetrad of this disorder includes: cataplexy, hallucinations, sleep paralysis and excessive daytime sleepiness (EDS) - However, not all have to be present so differing narcolepsy presentations can appear quite differently
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Cataplexy
- Cataplexy is a loss of muscle tone in response to increased emotional arousal - It is a feature of narcolepsy seen in around two thirds of those with the diagnosis - The loss of tone may result in total collapse onto the floor or mild buckling of the legs such that the patient can continue to stand - The head and jaw often slump forward and the arms often collapse to their sides Common emotional triggers include: - laughing, - being frightened, - or being angered - The person remains aware throughout the attack which can frighten them and leave them vulnerable to prolonged symptoms - Imagine someone with this condition going to the beach and becoming excited while jumping waves in the ocean - In response to the excitement, their legs would buckle which would frighten them and trigger more cataplexy - This can be a life-threatening condition - Cataplexy appears to have a genetic basis - More specifically it appears that there is a gene that turns on an autoimmune response that attacks hypocretin cells - The most famous experiments on cataplexy involve a colony of hypocretin-knockout Doberman Pinschers raised at Stanford - An interesting study by Oishi and colleagues (2013) used hypocretin knock-out mice and studied their cataplectic reaction to chocolate - Chocolate is a highly palatable food that excites mice - In mice whose hypocretins are knocked-out, the introduction of chocolate was associated with increased activity in the medial prefrontal cortex (mPFC) and resultant cataplexy - During the cataplexy, there was also increased activity in parts of the limbic system, namely the hypothalamus and amygdala - Blocking mPFC activity in these mice resulted in a reversal of the chocolate-induced cataplexy; thus, emotional areas and the mPFC are likely critical for cataplexy The most common treatment approaches are to: 1) use gamma hydroxybutyrate (GHB) to consolidate REMS; and/or 2) facilitate adrenergic activity with selective reuptake inhibitor (SSRIs) antidepressant medications such as fluoxetine or fluvoxamine
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Taking gabba hydroxybutyrate (GHB)
- GHB is colloquially known in the media as the “date-rape” drug - It is a liquid drug that has been poured into unsuspecting victims’ drinks so that they become incapacitated and prone to sexual assault - It is a controlled substance that must be ordered from a handful of pharmacies across the country - It is also abused by some, including athletes to enhance growth hormone production, and substance users in clubs - It is a potentially highly lethal drug because it suppresses respiration and produces heavy sedation and when taken with alcohol there can be vomiting and the person could choke to death - Because of the potency of this drug, narcoleptic patients most typically ingest the dose when already in bed to avoid accidents, e.g., falls - The patient measures out the two doses and leaves them on the night stand next to their bed - They drink the first dose and then set an alarm to take the second dose on their night stand - Two doses are necessary because the drug has a very short half-life - Can you imagine the difficulties that someone with narcolepsy on this regimen would face? - Nonetheless, the patient can consolidate sleep by taking this medication and it has been shown to help with other narcolepsy symptoms too - The mechanisms of this drug are poorly understood - One mechanism appears to be through the consolidation of nocturnal REMS
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Hallucination
- Those with narcolepsy can experience hypnopompic or hypnagogic hallucinations - Hypnopompic hallucinations occur upon awakening - hypnagogic hallucinations occur while falling asleep - They are most often visual hallucinations involving shapes and colours on the wall but it can also include sounds or music or perception of someone touching the body - Like sleep paralysis, hypnopompic or hypnagogic hallucinations can occur in the normal population - There are no hallucination-specific interventions except for psychoeducation to reassure the patient of the normalcy of this experience
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Sleep Paralysis
- We learned about this phenomenon in the parasomnia section - Sleep paralysis is when you wake up and are unable to move - Paralysis of most major muscle groups occurs in REMS and narcolepsy is essentially an intrusion of REMS into wakefulness so the person awakens but has no control over their major muscle groups - Additionally, using GHB to consolidate REMS helps with sleep paralysis and hallucinations
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Excessive Daytime Sleepiness
- Narcolepsy is characterized by many symptoms but most associate it with falling asleep throughout the day in sleep attacks - This was depicted in the movie My Own Private Idaho - Narcolepsy fragments sleep across a 24-hour period and results in sleep deprivation - Although GHB can consolidate REMS and may help somewhat with EDS, another treatment approach that can help with daytime sleepiness is to use stimulants - Traditional stimulants can be used however there are more modern stimulants - An important adjunct to pharmacological approaches is the behavioural approach to schedule multiple naps to address the sleepiness and to ensure that the person allocates a large enough time for a sleep opportunity at night Narcolepsy: the clinical tetrad 1. sleepiness 2. cataplexy 3. sleep onset (hypnagogic) hallucinations 4. sleep paralysis + disrupted, non-restorative sleep
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Periodic Limb Movement Disorder
- When people hear about Periodic Limb Movement Disorder (PLMD) they often think that it is merely restless sleep; that is, moving around a lot and stealing the covers from their partner - This is not PLMD - PLMD is a neurologically-based sleep disorder in which there are tiny leg twitches terminating in the big toe - Most often the patient is unaware of the twitches - The bed partner may or may not be aware of the movements because they can be rather subtle - So why is it important? - With each twitch, there is an accompanying brain arousal seen in the EEG channels - This is similar to what we see in apnea, in which there is an event (i.e., in apnea it is breathing related and in PLMD the source is captured on the EMG as a leg movement) and an associated brain arousal which lightens and fragments sleep, leading to sleep deprivation - Sleep deprivation often results in excessive daytime sleepiness so patients with PLMD are at risk for all of the disorders we learned about in Module 3 - To diagnose this disorder, we need to obtain an overnight study so that we can examine whether leg muscle activity on the EMG and brain activity on the EEG are correlated and count the number of times per hour in which twitches on the EMG relate to arousals on the EEG - Because patients are often unaware of these events, the most common reasons for assessment of PLMD occur because the patient is complaining of EDS or the partner has witnessed twitches - Thus, in an interview we ask: “Has a bed partner ever complained about your leg twitching?” and we enquire about the propensity to fall asleep, particularly involuntarily - If there is EDS and the presence of a highly comorbid condition called Restless Leg Syndrome, this would be highly suggestive that an overnight study is necessary - Additionally, if the patient is suddenly feeling sleepy and they recently started an antidepressant medication such asvenlafaxine, mianserin or mirtazapine, we would consider an overnight study because such medications increases the risk of periodic limb movements in sleep - PLMD is treated pharmacologically and the most effective approaches are ones that target dopamine - Remember, dopamine is involved in movements so it makes sense that a dopaminergic drug would be most helpful - Although the etiology is not fully understood, dopamine is the major suspect; that is, low dopamine is presumed in those with PLMD - Gabapentin (i.e., anticonvulsant medication) or opiates are also strategies that are used if the dopaminergic agents are ineffective or contraindicated - Stimulants are sometimes used during the day to counteract the daytime sleepiness - PLMD and sleep disordered breathing (SDB) are highly comorbid and sometimes treating the apnea successfully with positive airway pressure devices can resolve the PLMD or bring the events to a subclinical level
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Restless Leg Syndrome
- Restless Leg Syndrome (RLS) is also called Willis-Ekbom disease (WED) named after Willis, who first discovered the disease and Ekbom, who expanded on the condition some years later - RLS is somewhat difficult to describe - Those who have this disorder complain of a creepy feeling in the evening when at rest, particularly in the calves, and the only thing that provides relief is to move the legs - In mild cases it is annoying and in severe cases it interferes with sleep because of the need to constantly move the legs - Some sufferers have to continuously get out of bed and pace to ease the irritation - An overnight study is not needed to diagnose RLS because it is a subjective disorder with no known EEG correlates - RLS is highly comorbid with PLMD so many people with RLS are referred for an overnight study to assess whether there is also PLMD - In clinical interviews we ask: “Do you get a strange, irritating sensation in your legs in the evening?” - “Do you have any sensations deep in your legs (calves) when at rest in the evening?” - “What do you do to manage it?” Does it interfere with sleep?” - We want to know if it is the strange creepy crawly sensation characteristic of RLS, rather than the cramps or “pins and needles/parathesia” feeling that anyone can get - We want to know if it occurs mainly in the evening rather than all through the day or with no discernible diurnal pattern - We want to know whether the person is compelled to move the legs to alleviate the sensation - In RLS assessment, it is the irritating compulsion to move the legs in the evening that is the pattern of prime nosological interest - Sleep onset can become highly delayed because the need to move the legs can interfere with lying restfully in bed There are a number of risk factors for RLS including: - family history of RLS (i.e., genetics), - anemia (iron/ferritin deficiency), - pregnancy (because it is associated with decreased iron levels), - certain medications (e.g., antidepressants, antihistamines), - and certain medical conditions (e.g., kidney failure, polyneuropathy, diabetes mellitus, OSA) Treatments are the same as PLMD, i.e., - mainly a dopaminergic agent, - gabapentin (an anticonvulsant to address the increased sensorimotor excitability) - or an opiate - In cases in which there is a deficiency of iron, the anemia is treated and in some cases this will resolve the RLS - There is some suggestion that those with RLS may have a magnesium deficit and there is evidence to suggest that magnesium supplementation may be helpful; however the level of evidence for magnesium remains low
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Summary Week 12
Narcolepsy can include: - cataplexy (muscle weakness in response to emotional stimuli) - hallucinations, - sleep paralysis - and excessive daytime sleepiness Treatment for narcolepsy includes: - GHB and/or SSRI medications, - as well as behavioural treatments that include: - nap and sleep opportunity scheduling - and providing psychoeducation about narcolepsy (e.g., hallucinations are a normal part of the disorder) - PLMD is characterized by repeated muscle twitches mainly in the lower limbs accompanied by brief arousals in the brain (diagnosed by an overnight study), and daytime sleepiness - PLMD and RLS are highly comorbid - RLS is characterized by a self-reported strong urge to move the legs in the evening RLS and PLMD are most often treated with: - dopaminergic drugs, - opiates - or gabapentin
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Test how well you understand the neurological disorders: narcolepsy, RLS, and PLMD.
1. The putative etiology of narcolepsy includes (please check all that apply): Dopamine, Hypocretins, and Autoimmune processes 2. The tetrad of narcolepsy includes all but: Leg twitching -- characteristic of PLMD 3. All the following are true regarding RLS except: An overnight study is required 4. Treatment approaches for narcolepsy include: GHB, Sleep scheduling, and Antidepressant medications 5. All of the following have strong evidence for treating PLMD except: magnesium
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Moorcroft Chapter 13 (pp. 328–334) | Disorders of Sleep
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Narcolepsy ch 13
- The most common complaints are those of excessive, seemingly perpetual, sleepiness - Less commonly, people with narcolepsy experience sleep attacks that are irresistible and occur without warning, even in arousing situations - The resulting nap may last up to an hour and be refreshing - The next most common complaint (60–90 %) is that of cataplexy, ranging anywhere from weakness in the limbs, face, or speech muscles to total, wilting collapse - Cataplexy is often triggered by emotions - During brief catapletic attacks a person is conscious, but if prolonged to over 2 min REM sleep may occur - Hallucinations at the beginning or end of sleep and sleep paralysis occur together, or singly, in almost one-half of people with narcolepsy - These hallucinations are vivid, brief, dream-like occurrences at entry to and from sleep, respectively, that sometimes leave the person with a sense of fear or dread but may also be reenactments of a part of the past few hours - They may be visual, auditory, tactile, or involve movement - Sleep paralysis is the inability to move that occurs on awakening or when attempting to fall asleep - Hallucinations and paralysis can also occur in individuals without narcolepsy, especially children and sleepdeprived adults without narcolepsy - About half of people with narcolepsy report sometimes acting out their dreams while still asleep (REM behavior disorder) - About one-third of all people suffering from narcolepsy report experiencing automatic behavior or blackouts - Blackouts are probably similar to sleepwalking - During these episodes, persons may continue behavior typical of wakefulness but later have no memory of what they did - These episodes can last minutes or even hours - Naps, although inconvenient, are often refreshing to people with narcolepsy - Narcolepsy appears to be a problem of components of REMS intruding on waking but also poor NREMS at night - Cataplexy and sleep paralysis are the muscle paralysis of REMS, while hypnogogic hallucinations are the dreams ** - REMS occurring soon after sleep onset that occurs in people with narcolepsy is not typical of normal adult sleep - Another factor is poor night sleep with frequent arousals and awakenings contributing to excessive sleepiness - Poor sleep may result from overactive REMS-on mechanisms in the brain or from frequent awakenings, less N3, and fragmented REMS - People with narcolepsy, in contrast to those with normal sleep, fall asleep quickly during the MSLT and usually have two or more REMS onsets - Typically, narcolepsy begins to appear in the teens or early twenties, although onsets in younger and older people do occur - Sleep attacks are usually the first symptoms - Gradually the sleep attacks worsen, then cataplexy and other symptoms begin to appear and become more frequent - However, 10–50 % have narcolepsy without cataplexy - Overall, narcolepsy impairs a person’s life, including their social life, as they cannot go to movies, concerts, dinner parties, play cards, or participate in other ‘‘quiet’’ activities - The sleepiness of persons with narcolepsy even affects their participation in more active events such as sports - Since catapletic attacks are likely to be triggered by strong emotions, people with narcolepsy tend to guard their emotions, thus appearing dull and emotionally flat - Many have a history of being fired for falling asleep on the job, and people with narcolepsy frequently have had a number of accidents, both while driving automobiles and on the job - They also complain of problems with their memories, which may really be a problem of paying attention - As a result of these problems, they often are somewhat depressed, anxious, and frustrated - Others describe them as being unmotivated, withdrawn, and aggressive or believe they are lazy, bored, slothful, or depressed - Divorce is frequent, reflecting interpersonal complications caused by the symptoms - Narcolepsy occurs in over 5 out of every 10,000 persons - There is evidence of predisposing genetic factors, but narcolepsy may also be caused by damage to the brain or from other medical conditions - People with narcolepsy plus cataplexy typically have reduced levels of orexin/hypocretin resulting from a gradual die-off of cells that produce it and show other brain chemical defects Treatment includes: - improvement of sleep with good sleep hygiene and sleeping pills; - control of waketime symptoms with scheduled naps and drugs such as a stimulant for the sleepiness and other drugs for the cataplexy; - and avoiding potentially dangerous activities - Also important are psychological support and family therapy
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Idiopathic Hypersomnia
- Some people are always excessively sleepy - They are classified as having idiopathic (meaning not caused by something else) hypersomnia There are two types: (1) when nocturnal sleep time plus nap time are not unusually long, or (2) when nocturnal sleep time plus nap time is unusually long and followed by lengthy sleep inertia - Both types of individuals with idiopathic hypersomnia sleep deeply and normally at night - Neither variation is common but striking when it occurs - It often begins for no apparent reason in adolescence or early adulthood - In both variants daytime naps can be resisted but when taken are only refreshing in the first variant - Those with the second variant may also experience automatic behavior, blackouts, and microsleeps - Family members typically show a similar condition - The only treatment is emphasis on good sleep hygiene and use of simulant medications - Idiopathic hypersomnia needs to be distinguished from the long sleeper syndrome as well as behaviorally induced insufficient sleep syndrome and recurrent hypersomnia - Long sleepers may arrive at the sleep disorders clinic complaining about many of the same things as people with idiopathic hypersomnia, but careful history taking and polysomnographic testing reveal differences - Long sleepers need 10 or more hours of sleep per night If they try to get along on less, they show the effects of continuous partial sleep deprivation , including excessive daytime sleepiness, shown both by their own subjective reports of: - a constant struggle to stay awake, - multiple napping, - blackouts, - and automatic behavior, - and by a low average MSLT sleep latency - They usually report having difficulty arousing and often experience ‘‘sleep inertia’ = the transitional state between sleep and wake, marked by impaired performance, reduced vigilance, and a desire to return to sleep - They are hard to awaken and can be abusive and aggressive if awakened, even when they themselves have requested it - If they do get the 10 or more hours of sleep per night they require, the daytime sleepiness and accompanying symptoms remit to normal levels - Behaviorally induced insufficient sleep syndrome occurs in those people who voluntarily sleep deprive themselves - They typically sleep more on weekends and holidays but otherwise suffer the consequences of lack of enough sleep - People with recurrent hypersomnia experience weeks of excessive daytime sleepiness, often around 10 times per year - Sleep, alertness, and cognitive functioning are normal during the intervening periods
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Restless Legs
- R.S. is a 59-year-old male Postal Service employee who came to the clinic complaining of a problem falling asleep - He said it has been getting worse - He said that he cannot be still in the evening because of feelings in his legs - The feelings go away while moving his legs but this makes it difficult to fall asleep - He said that he had tried ‘‘everything’’ including natural herbal sleep aids, hypnosis, and acupuncture, but none of them helped very much - He said that his inability to get to sleep easily was ‘‘getting to him.’’ - Even when he is just sitting still, he feels the discomfort inside his calves and must get up every 15 min to ‘‘walk it off.’’ - These sensations become more noticeable during the evening as bedtime approaches and are getting worse as he gets older - They are also worse when he is tired - His father may have had a similar problem because he couldn’t stand deskwork and would rather have a job that kept him moving around - One of his brothers complains of problems similar to his - Restless legs syndrome (RLS) is characterized by unpleasant, ‘‘creepy-crawly’’ sensations from deep in the legs, or in some people also in the arms, when stationary that may be relieved by movement temporarily or for up to an hour. - Up to half describe the sensations as painful - It begins or worsens during times of rest or inactivity becoming especially worse at night - As a result, people with restless legs complain that they have trouble getting to sleep - Many also report experiencing excessive daytime fatigue or sleepiness but others do not report fatigue and maintain that they are completely alert during the day - It is thought that 5–15 % of the general population have restless legs with occurrence twice as often in females - RLS can begin at any age including children, often misdiagnosed as growing pains or attention-deficit/hyperactivity, but the highest incidence is in middle-aged and older people - The evidence is strong for a genetic basis for RLS - Up to a third of cases may be caused by iron deficiency - A total of 15–40 % of people undergoing dialysis complain of RLS - Twenty percent of pregnant women temporarily experience RLS - Sometimes it is a side effect of medications - For some, RLS seems to be related to irregularities in the brain - However, in many cases no direct cause is apparent - Caffeine, warm rooms, and exposure to cold can intensify restless legs symptoms - Strangely, RLS has been reported to disappear with fever - Treatment begins with encouraging good sleep hygiene and improving exacerbating circumstances such as stress or fatigue - If blood tests show that iron levels are low then iron supplementation can be helpful For some people: - stretching, - massage, - or heat or cold will help as will moderate exercise, - relaxation procedures, - and avoiding alcohol in the evening - If none of these are sufficient, one of several different types of medication may be prescribed
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Periodic Limb Movement Disorder
- E.C. is a 51-year-old woman who came to the clinic complaining of insomnia and serious sleepiness during the day - She reports that although she sleeps very deeply, she awakens not feeling refreshed or rejuvenated - Her husband reports that she often ‘‘shakes the bed’’ during sleep and kicks off the bedcovers - E.C. reported trying many remedies for her ‘‘insomnia’’ including many drugs, both prescribed and over-the-counter, but to no avail. - Likewise, 6 weeks off caffeine was of no help - She exercises on an Exercycle or plays tennis daily - She occasionally takes voluntary naps, but they are not refreshing - Her sleepiness has caused her to have a car accident and several near misses - The polysomnogram showed that E.C.’s sleep was punctuated with many, usually brief, awakenings - Most of these awakenings were caused by leg kicks measured by placing a pair of sensors on the front of each leg half way between the knee and ankle - The kicks were very stereotyped, that is, identical to one another, abrupt contractions of certain lower leg muscles each lasting a few second that occurred every 42 s - The kicks tended to come in sets of 30 or more - Typically the early kicks in a series disturbed and lightened her sleep, with only the later jerks actually awakening her - The quality and characteristics of her overall sleep pattern was not good - Both the time to get to sleep and the REMS latency were very long - Note the high percentage of wake time and N1 accompanied by lowered amounts of N2 and N3 - The number of awakenings is very high as are the number of movements and stage shifts - Sleep efficiency was a very poor 70 % - During the 425 min of the sleep period, she had 353 kicks with slightly more of them during REMS - The next morning she reported that her sleep was typical and that she felt tired and unrefreshed as usual - She had no awareness of the many awakenings or leg kicks during the night - People with periodic limb movements (PLMs) go through spurts of jerking their legs or arms during their sleep - The movements are of short duration, 0.5–10 s and come at remarkably regular intervals in an individual ranging from 5 to 90 s - The movements come in clusters lasting several minutes to hours - They are more likely to occur during the first half of the night - When there is an accompanying complaint of insomnia or excessive daytime sleepiness it is considered periodic limb movement disorder, yet many who have periodic leg movements have no sleep complaints of difficulties with daytime sleepiness or fatigue - About 5 % of the general population is thought to have PLMs, but it is much more common in middle-aged people and in up to one-half of older adults - Three-fourths or more of people with restless legs have PLMs and one-third of persons with PLMs have restless legs - PLMs also accompany many other sleep disorders such as narcolepsy, obstructive sleep apnea, and REM behavior disorder - There is usually no awareness of the movements during sleep and awareness of only a few of the multiple awakenings caused by them - However, the bed partner is very aware of them because of the bed shaking or being repeatedly kicked - PLMD tends to run in families, where it is frequently associated with leg cramps - It tends to get worse with insufficient sleep, stress, or emotional upheaval - A person may have PLMD every night or only occasionally - Although often occurring spontaneously, PLMD may be precipitated or caused by other medical conditions or drugs - Therapy for periodic limb movement disorder is similar to that for restless legs, but no treatment is required unless it causes daytime sleepiness or disturbs the bed partner
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Circadian Rhythm Sleep Disorders
- W.N. is a 20-year-old student living in the dorm at a nearby college - During the initial appointment, he was reasonably alert and energetic, yet looked tired - He was 20 min late for his 11 a.m. appointment - He described his problem as insomnia - ‘‘I just can’t get to sleep.’’ - The problem started midway through the first semester of his junior year, when he had to take a required course only offered at 8 a.m - He said he was lucky when he started college to have no earlymorning classes - He could ‘‘take advantage of college dorm life’’ at night without having to worry about getting up early - As a result, he typically went to sleep between 3 and 4 a.m.—even later on weekends - After that he carefully selected his courses in order to avoid those that met early in the morning - This schedule worked well for him and he felt that he was getting sufficient sleep - All this changed this semester - Because he could not get to sleep early enough at night, he had missed many of his 8 a.m. classes this semester, since he ‘‘just could not wake up.’ - He had repeatedly tried going to bed at midnight, but just lay awake for several hours - He had tried ‘‘everything’’ including: warm milk and graham crackers, sleeping pills, herbal teas, exhaustive exercise, alcohol, a dull textbook, and, on the advice of a friend, facing his bed due north to get the ‘‘proper magnetic pull’’ on his brain - Nothing worked - He was desperate, because when he did get up after only a few hours of sleep, he was so ‘‘wiped out’’ that he got little out of the 8 a.m. lecture - He actually fell asleep in the class several times - He missed so many classes that his professor threatened to drop him from the course - Upon questioning, he related how weekends and breaks were his salvation, because he slept in until mid-afternoon - When asked when he felt most alert, he immediately and emphatically stated ‘‘in the evening—once I make it past supper, I’m O.K.’’ - He also related that he is more moody in the morning and daytime than in the evening - He scored 15 on the morning type/evening type questionnaire which classified him as a strong evening type - His psychological tests were within normal limits - Circadian rhythm sleep disorders occur when there is a misalignment between the desired or necessary sleep schedule and the circadian sleep-wake rhythm - the rhythm can be delayed, such as in this case, or advanced - Other types include non-24-hour sleep/wake rhythm, irregular sleep/wake rhythm, and the effects of shift work and jet lag - Circadian rhythm sleep disorders can be chronic as in the case of W.N. or temporary as with jet lag or shift work - The most common is phase delay syndrome