Slide Lecture with Audio
This activity is based on a 45-minute slide lecture presented by Dr. Milton K. Erman and Dr. Shari Fine. This program is available as read only and with accompanying audio.
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Slide 1: Welcome to the teleconference, “Evaluating the Impact of Novel Approaches to the Management of Insomnia.” This activity is jointly sponsored by the American Academy of CME, Incorporated and Princeton CME, and is supported by an educational grant from Takeda Pharmaceuticals North America, Incorporated.
I'm Dr. Milton Erman, Clinical Professor of Psychiatry at the University of California, San Diego School of Medicine. I will be your presenter, along with Dr. Shari Fine, Director of Medical Education at Christ Hospital. Please note that all faculty disclosures for this activity are included in the front of your activity booklet.
Slide 2: My goal in speaking to you today is to review the different types of insomnia and their prevalence in US adult populations; to define the causes and comorbidities of insomnia, including specific sleep disorders, such as restless legs syndrome, periodic limb movement disorder, sleep apnea, and circadian rhythm sleep disorders; summarize the impact of insomnia and comorbidities on quality of life and healthcare costs; and to discuss the benefits and limitations of nonpharmacologic and traditional pharmacologic approaches to the management of insomnia; and to assist you in applying the evidence for recent insomnia treatment advances in your clinical decision-making to maximize outcomes.
Please remember that to receive education credit following the conclusion of this activity, each participant must successfully complete the post test and the evaluation form located in the back of your activity booklet. These forms can be easily completed online for immediate receipt of credit at www.princetonme.com. Thank you again for joining us.
Dr. Fine will now introduce the case study.
Slide 3: Thank you, Dr. Erman. I’m going to present the case presentation.
Slide 4: The chief complaint is fatigue, difficulty concentrating, especially at work, and difficulty sleeping. This is a 53-year-old white female who complains of fatigue for the past 3 months. She states that she is most tired in the afternoon. She has difficulty focusing on her work because she is so tired. The patient states that she has difficulty falling asleep at night. She is busy all evening with chores or work that she brought home to finish because she couldn’t focus while at work. The patient requires 2 hours to fall asleep almost all nights, and she wakes up in the morning feeling tired. She has no symptoms of sleep-disordered breathing or restless leg syndrome, and she is otherwise well. Her past medical history is negative for significant medical problems and she has no psychiatric problems. Her social history—she’s married with 2 teenagers. She works full-time as a corporate executive. She works long hours and has a high-pressure job. She is a nonsmoker and occasionally drinks alcohol. Medications: none.
Slide 5: Her physical exam includes a blood pressure of 120/74; heart rate of 72. Her heart is a regular rate and rhythm, her lungs were clear, abdomen was benign, and her neurologic exam was within normal limits. Her lab tests included a CBC (complete blood count), a basic metabolic panel, and a TSH (thyroid-secreting hormone), all of which were normal.
Slide 6: The diagnosis of chronic insomnia was made based on the patient’s history. She has a stressful job and is active late into the evening with family errands or work-related duties. She doesn’t allow any down time before going to sleep. Her physical exam and lab studies were within normal limits, excluding other causes for her insomnia.
Based on this patient’s issues, a trial of cognitive behavioral therapy was the initial approach to treatment. Cognitive behavioral therapy has been well established as effective in chronic primary insomnia. Cognitive behavioral therapy comprises a group of techniques that address the factors that help perpetuate chronic insomnia, regardless of the cause.
This patient’s cognitive behavioral therapy focused on stimulus-control therapy, which assumes that insomnia is a maladaptive response to factors, such as bedtime and the bedroom environment (for example, regularly reading or watching television in bed rather than sleeping), and requires a learning process to reassociate the bed with sleep.
In addition, the patient was instructed in sleep hygiene. Sleep-hygiene education addresses extrinsic factors that can perpetuate insomnia, such as noise in the bedroom and the use of caffeine. The patient was also instructed to keep a sleep diary documenting time to sleep, and she was asked to return to the office in 2 weeks for reevaluation.
Slide 7: At the 2-week follow-up visit, the patient continues to have difficulty falling asleep despite her best efforts at stimulus control and sleep hygiene. At this point we might consider pharmacologic intervention. I will now turn the program back to Dr. Erman for his presentation. While you are listening to the presentation, I encourage you to consider this patient’s situation and the treatment options that could be most appropriate.
Slide 8: Thank you, Dr. Fine.
Slide 9: Today we're going to be starting our program, Evaluating the Impact of Novel Approaches to the Management of Insomnia, with a slide that takes a brief look at the electrophysiology of sleep. This is a fascinating topic usually for practitioners because it goes into sleep stages, and we're looking in the slide here at the EEG (electrocardiogram) recording that we would typically obtain from a sleep record. The left-hand side of our slide here shows the traces going from very nondreaming sleep stages to traces with high altitude slow waves all the way up to traces from waking and rapid eye movement (REM) that really look quite similar in many ways where we're seeing very fast activity.
We use this information to help to generate a sleep hipnogram, this is what we have on the right-hand side here, a picture of the progression of sleep over the course of the night. And in a healthy normal individual we would expect to see a short sleep-latency, falling asleep quickly, we're going to see some deep nondreaming sleep stages 3 and 4 in the early part of the night, and some REM occurring 90 minutes to 2 hours into the night. Sleep is dynamic; it progresses over the night, and we're going to see much more REM sleep later in the night. We see a few arousals in the night as we would typically expect to see in any normal individual.
Slide 10: The situation is very different for insomniacs, so we can define insomnia using some terminology that's pretty widely accepted, now included also in a recent NIH consensus and State-of-the-Science conference on insomnia is that there are 4 different conceptual models for how insomnia may present problems falling asleep, staying asleep, waking too early, or poor quality sleep. See the consequences of these listed. Any of these or all of these may be present at one time and more than 1 disturbance is present; and they also can change over time. What's important to appreciate is that there are next-day consequences. This is a symptomatic complaint that we assume is going to be linked with next-day complaints.
Slide 11: So, in classifying insomnia, we can think of this as really a primary insomnia; this is the type of insomnia that we study in research studies used to generate work on developing new medications. The patient who says “I have no reason for my insomnia, it's always been bad,” is very different from what we see in most of our patients, which is comorbid insomnia. This used to be called secondary insomnia. The terminology has changed a bit here, and it has changed because the insomnia isn't necessarily secondary, it's not caused by another condition, but rather it is often associated with it; examples would be depression, pain, et cetera.
Conceptually we can talk about acute insomnia, which is lasting up to several weeks, specific causes often are apparent, it can progress into a more chronic state; and chronic insomnia, which is present for those individuals who have complaints that are persistent for more than 30 days.
Slide 12: Well, we have a slide here that is a bit provocative, intended to be, and that is why treat insomnia? And it's a source of discussion, because some physicians might say “well, you know, nobody would die from lack of sleep.” Rationale here is that like many other conditions, we have reasonable reasons to think it causes distress, it impairs functioning, increases healthcare costs, we'll go into this in a moment, associated with increased risk of comorbid disease; these other diseases, like depression, can be made worse by persistence of insomnia, and it is indeed responsive to treatments.
Slide 13: So, as we go into our slide labeled annual cost of insomnia, this is some recent data that was published in the Journal of Sleep, and it tried to look at both direct and indirect costs of insomnia.
The direct costs are primarily these healthcare costs that we're talking about, and looking at these numbers, the authors were able to document very highly significant increased costs associated with these direct-care expenses. Certainly some of this we would not be surprised if people were taking medications. But other elements play a role as well. These people are fatigued, they're being worked up for other conditions, they have headache, they have worsening of pain.
We also see that there are indirect costs, and part of these relate to issues like absenteeism from work and short-term disability, and in the population that was of relevance here in terms of the primary working-age population, the authors were also able to show that there were significant increases in these indirect costs as well. We see from these numbers, by the way, a very large sample of patients in healthcare plans compared with insomnia patients and control.
Slide 14: Insomnia is a prevalent condition. There are various ways of defining the prevalence, and if we look at complaints of sleep disruption we see something like 30% of the general population. If we look at chronicity, those people who have a chronic problem and functional impairment, we’re looking at 10%, and as we've seen already, very significant increases in costs that can be associated with these conditions.
Slide 15: It does increase in prevalence in association with increased age. We don't sleep as well as we age, but the primary contributing factor it turns out as we find from meta-analyses is that these comorbid medical conditions—things like pain, like arthritities, like nocturia, like psychiatric problems—these increase also with age, and these are the primary determinants of this increase in insomnia prevalence associated with increased age.
Slide 16: Going forward, we can look at the notion of functional impairments. This is data that was generated from a Gallup Poll survey that was sponsored by the National Sleep Foundation. They do these polls every year in relation to National Sleep Awareness Week. And I have always liked this data because of its linearity. What we see is that across the board as we look at these various tasks that are being assessed hoping mood, relationships, the more chronic the problem, the worse the performance. We're looking here on the Y axis at the percentage of patients who say that their functional abilities in these areas are poor, and we can, I think, understand this. As we think about our own lives with a poor night of sleep, we don't do as well in our empathy; we're more irritable, we don't handle tasks as well. If this becomes a chronic problem, this is going to become worse.
Slide 17: This has been looked at as well. Gary Zammit, in a study that was published in Journal of Sleep in 1999, looked at this and showed across the board that the quality of life for insomniacs was worse relative to age- and sex-matched controls who did not have insomnia complaints.
Slide 18: Looking at the issue of risk factors and associated features, first of all let's try to understand how it is that insomnia develops.
Slide 19: You've got a slide here that is titled determining factors of insomnia. This is a model that was developed by Dr. Art Spielman, who is on the faculty of SUNY University of New York. And what it says is that we have this arbitrary theoretical insomnia threshold. We are all closer to or further away from this threshold, and that's the baseline level. This is the predisposing contributions to insomnia—these are various traits, biologic, genetic, et cetera, that can predispose. We can imagine a stressor for all of us that would be enough of a precipitating factor to take us over this threshold—a personal injury or illness, illness in the family, life stress. What we want to recognize, though, is that many individuals will develop perpetuating factors that make it more likely that their insomnia is going to remain present over long-term periods of time. And these include things like conditioning factors, and we'll talk about this as we talk a bit more about some of the behavioral therapies we can use, conditioning factors, poor sleep hygiene, excessive anxiety, worry about sleep, all of these can lead to chronic insomnia. Our goal is to try to minimize the probability that chronicity will occur to make interventions to prevent this from occurring.
Slide 20: We've addressed this issue of risk factors somewhat already. There is a risk factor as well of female gender. We don't fully understand this; certainly some contribution from this relates to another component of comorbidity. Hormonal status in women is a factor. Women, perimenopausally and menopausally, have increased rates of insomnia. We've dealt with this advancing age, and high percentages of individuals over the age of 65 are likely to have problems. Occupational status, shift work, variable work schedules play a major role, as do these comorbid, medical, and psychiatric disorders. Substance use, certainly substance use, other agents like alcohol and caffeine, and a family history of insomnia—if people have a family history, this is a contributing component, and this may be one of these predisposing factors we were talking about as a genetic component; it may be that certain individuals have predispositions. These are more likely to be our primary insomnia subjects.
Slide 21: When you look at associated features, and all of these come through in many surveys that have been done, increased risk of depression, increase of absenteeism. We see our list, including these reductions in performance. So once again, we're talking about why it is that we would think about treating this condition and why we're motivated to treat it; beyond symptom relief, it's also to try to reduce the impact that insomnia may be having in all these areas of function.
Slide 22: The absenteeism was looked at in this study that we had mentioned before from Dr. Zammit, and what we're seeing here is an almost 10-fold increased risk of absenteeism in this insomnia group. This is the number of days of work per year that people were absent. Lots of factors may play a role—people just not feeling that they're capable of working, including issues like use of over-the-counter agents that might predispose to residual sedation the next morning and perhaps interfere with the capacity for people to get to work the next day.
Slide 23: Accidents have also been shown to be associated with patients with chronic insomnia. There certainly is a psychic distress factor that's looked at here. Is this just a component of patients who have psychiatric illness, which is why they have insomnia? The answer is no. It is higher in those with chronic insomnia than it is in those without chronic insomnia. Yes, it is higher in those with high psychic distress. We should not be surprised that the impact of chronic sleep loss may be impairment of function, poor capacity to attend to details, and therefore consequences in terms of safety.
Slide 24: We've mentioned some of these precipitating factors. We'll say a little bit more about some of the specific issues here, they include circadian rhythm disorders, specific sleep disorders, and we'll talk more about psychiatric disorders, and very briefly about medication.
Slide 25: As we can see from our slide here on the relationship of circadian sleep-phase sleep disorders, most of us we hope are going to be here in the middle: bed time, 11 pm, midnight, and we're getting up in the morning when we'd like to get up, and our body clock is in sync. There are people who have alterations in 1 of 2 directions; there are people who have an advanced sleep phase, and these are individuals who get sleepy early in the evening and wake up in the early morning, and then we have people with a delayed sleep phase, something we often see in adolescents, young adults, where there is a tendency to not feel sleepy until the early morning hours, 2, 3 in the morning, and then they have trouble getting up in the morning to get to work, or school; this is an obvious concern.
Slide 26: We may see problems in association with restless legs, which is associated as well with periodic leg movements. This is a sensory motor disturbance that is characterized by this sense of the need to move the legs. Relatively high prevalence, we see a broad range here, but most studies we're going to see in the 5%, 6%, 7% range in the general population. It is underdiagnosed and it does have impact on sleep, on cognitive function, on capacity to function throughout the day in general.
Slide 27: Finally from our issues of these primary disorders, we have our prevalence of sleep apnea in the general population. This is taken from work by Terry Young. It shows that the numbers are high and go up with age—they're up, in general we're going to talk maybe 8% to 12% of the population, we're seeing a range in age here from the 6% to 7% range, up to about the 20% range in older populations.
Slide 28: And, as we mentioned previously, the restless legs syndrome may be associated with actual leg movements. When we study people in the lab with restless leg complaints, there is a very high probability that this syndrome will be present. These complaints are associated with disruption of sleep with these actual leg movements, and this is diagnosed on the basis of sleep studies that show that sleep is being disrupted by this leg movement activity.
Slide 29: We've also mentioned this issue of comorbidity, and this goes back to the specific language from this State-of-the-Science Conference that was organized by the NIH in 2005.
Slide 30: Their point is that most cases of insomnia are comorbid, and that it's a more appropriate term than primary. But the notion of secondary insomnia really gives the notion “gosh, if we just treat this primary condition, the insomnia will go away”—doesn't happen. Great example here; excellent data showing that even with effective treatment of depression, insomnia persists.
Slide 31: And there is this model again that all insomnia or a vast majority is really depression, this is what's causing it. Our slide here showing the circular relationship between these disorders shows that there is this relationship, that yes, psychiatric disorders cause insomnia, but that there is also excellent evidence from many, many studies that show that the persistence of insomnia will lead to a greater risk of psychiatric disorders.
Slide 32: We have data we're going to show from 2 studies here. The first is from Breslau et al; this is a group that works out of Henry Ford Hospital in Detroit. And showing that there is this increased risk if you follow individuals over 3-and-a-half years who do not have problems at baseline with psychiatric illness. We look at those who have insomnia versus those that don't, we see what the numbers are like 3-and-a-half years later. What is the incidence rate that has developed? We see these very highly significant differences between those with insomnia in relation to development of anxiety, of depression, and of drug abuse.
Slide 33: And another study that should ring very close to home is data that Chang generated from survey work. This is a survey that is filled out by Johns Hopkins medical graduates. This is looking at people as we see over many years, the data of the mean period of time for analysis is about 13 years. And what we see is that those individuals who had problems with insomnia or whose sleep was disrupted by stress in med school as they were followed over the years, there's a point of divergence. And the longer that they are followed, the greater the probability that depression will develop, and the sole determining factor here was insomnia versus no insomnia.
Slide 34: Evaluating and Treating Insomnia
Slide 35: Well, in the evaluation we see that we want to get a good history here. This is what really allows us to be able to recognize that a problem is present. There are some tools that we may consider, and we see these listed: sleep diaries, sleep studies may be help with some of these. Insomnia typically is multifactorial. It is a consequence for most of these patients of predispositions to insomnia complaints associated with stressors and other factors that make things worse.
Slide 36: And so, we have a broad range here of nonpharmacologic therapies that can be used. We have our listing of the strategies, we have our listing of the goals. Some of these are practical and some of these are not practical for primary care physicians. But the point here is to recognize that we can look at these goals and say “gosh, I can help patients using some of these nonpharmacologic techniques.” The one that is most widely studied and that has been shown really to be quite effective is this approach of cognitive behavioral therapy. This has been used for other conditions, used for depression as well. It's a multi-component approach. It uses sleep education and sleep hygiene, but also helps with various cognitive therapeutic approaches.
Slide 37: So, if we look at our slide that says cognitive therapy on it, one of the goals: challenge patients' dysfunctional belief perceptions. The patient that says, “If I don't sleep tonight, I will just not be able to function tomorrow.” We can look at that patient's history and say “gosh, last Wednesday you didn't sleep at all; did your boss get on you at work? Did you function okay?” Try to help change some of these attitudes.
Slide 38: So, let's say a word about general sleep-hygiene measures. These are some techniques that I have modified from approaches that we're likely to see published elsewhere. My recommendations are to try to get up at the same time every day and to get morning light exposure. I worry less about when do you go to bed—don't go to bed by the clock, go to bed when you feel sleepy, restrict napping. If we nap, we're going to reduce sleep drive that night; we want to certainly avoid caffeine in the hours before bedtime, and also to try to avoid alcohol and heavy meals close to bedtime. Exercise is good. It alone will not cure insomnia, but if we can do it in the morning or afternoon it's better. If it's done close to bedtime, it may wake the individual up and really interfere with capacity to sleep; and we want to have the bedroom as dark, quiet, and comfortable as possible. We also want to try to recognize that the bed is a place where relaxation should occur.
Slide 39: If reading is helpful, great, use a low-light level, read things that are not stimulating. Don't read a new action adventure novel or something that you get to the end to find out what happens. Journals may be helpful for people to fall asleep. We want to minimize work and stress in the bedroom: no computers, television. And patients say “well it puts me to sleep,” but you know what, people work very hard to keep you involved in that program until the end of the show or the commercial. Really, we should try to avoid this. We want to help people relax before bedtime, use relaxation techniques, meditation, a warm bath. We want the bedroom to be associated with capacity to sleep, and so we want relaxing activities. So, sexual activity for most people probably okay. And, we don't want them using the alarm clock to look at during the night; this just wakes them up. It's very hard for insomniacs to give up on this. Instead, let them set an alarm for as late as they could sleep in the morning. If the alarm hasn't gone off, it's irrelevant what time it is. Again, it’s very hard to break insomniacs of these habits.
Slide 40: We're going to talk now about some of the agents that are approved—there are 2 general classes of agents. What we have listed here is BZRAs, benzodiazepine receptor agonists. These are compounds that work through the benzodiazepine receptor site in the gaba A complex in the brain. Two subgroups, the actual benzodiazepine and the agents that are nonbenzodiazepines, also work through these receptor sites, and 1 agent, which is a melatonin receptor agonist.
Slide 41: So, we have our drugs here, which are indicated for short-term use. Going from the older benzodiazepine drugs we've got flurazepam to temazepam, triazolam, these are some of the older drugs. These are actual benzodiazepines. The newer compounds that are benzodiazepine receptor agonists included zolpidem and zaleplon, and we see the half lives in these.
Slide 42: We now have 3 agents that are indicated for use without a restriction on duration. It does not have the statement in their packaged labeling for the short-term treatment of insomnia, eszopiclone, zolpidem ER. These are both the BZRA—benzodiazepine receptor agonist type. And we have ramelteon, which is a melatonin 1, MT1, MT2 receptor agonist.
Slide 43: We'll see some data from some of these that help us to understand why the approval has been generated for longer-term use. The first is data with the extended-release formulation of zolpidem and what we're seeing is a 6-month study compared to placebo. This actually was a study that allowed individuals medication as needed 3-to-7 times per week, and we see that there is a significant improvement in the active treatment group looking at sleep-onset latency as well as wake times showing at the end of 1 month, sustaining itself over a 6-month period of time.
Slide 44: And this is data in the next slide that looked at the efficacy. The side-effect patterns here showed that headache was the most prevalent complaint. There was impression on the basis of the clinicians involved showing that yes, there was a significant improvement in performance for these individuals as well.
Slide 45: We also have data on ramelteon looking at patients with chronic insomnia. This is data that has recently been presented, all of this that we're showing, at the American Psychiatric Association meeting recently held in San Diego. The data for ramelteon, our first slide on this is from work that was done, Lewis Mini first author, looking at safety in females with chronic insomnia, looking at the 8-mg dose, which is the recommended dose, looking at latency to persistent sleep, and looking at both short-term 2-night studies. And this is data that was sleep-laboratory data looking at polysomnographic findings and showing that this 8-mg dose led to significant reductions in latency to persistent sleep compared to placebo.
And a 5-week study; this is looking at subjective reports over a 5-week period of time that compared to placebo the ramelteon 8 mg significantly reduced the reported latency to persistent sleep. At all the time points you see very robust P values throughout the duration of the study.
Slide 46: Another study was done looking at the potential impact of ramelteon on balance. This was a comparison study looking at comparison with zolpidem with a middle-of-the-night awakening. This I guess was intended to try to look at safety issues if people have to get up in the middle of the night. There is very good data from multiple sources showing that ramelteon does not have a lot of impact on balance, on memory cognition, et cetera, in this situation of awakening in the middle of the night. There was a very clear difference between these 2 agents with regard to their functional impact, the sensory organization testing, which included a balance measure, turning speed, stability, memory showed significant impairment with zolpidem compared to placebo. And a memory task as well showed significant decline with zolpidem compared to placebo; no impact of ramelteon compared to placebo.
Slide 47: We have some data here that has been presented at a number of settings and is published now on eszopiclone. This is also part of some of these changes in recommendations about duration of use. Six-month data showing in a double-blind format that the eszopiclone 3 mg showed superiority to placebo with regard to sleep latency—the following 6 months was an open-label phase when those who had been on placebo were shifted over to active treatment. And they moved into the same general range as those who had been on the active drug in the first 6 months, showing that there was not a sense of loss of effect, of tolerance developing over the 6-month period, something we've seen as well in the studies with ramelteon and the data that we saw earlier with regard to the extended-release zolpidem.
Slide 48: Over-the-counter agents (OTC). There are some statements about these compounds mentioned in the NIH consensus conference study report basically saying that there are adverse effects in cognitive impairment and that there is no data on their safety with regard to the herbal agents not FDA approved. So, there are significant concerns about hangover effect with the general OTC agent.
Slide 49: Well, we've got our slide here about over-the counter agents, going on to some new data that has been generated regarding drugs and development.
Slide 50: This is all data recently presented at the ADA. Just very briefly, we have a compound that is working as a partial agonist. This is NG2-73. It has a preference for the alpha 3 receptor subunit, slightly different from the agents that are currently available. The data showed that it was generally well tolerated. The adverse effects that were seen were seen as the primary extension of drugs that is in fact, in essence, talking about some residual sedation beyond the period of time desired for the therapeutic actions.
Slide 51: A sublingual-zolpidem preparation. Also, this is an agent that's being developed for middle-of-the-night use with low doses of zolpidem. Its 3.5 and 1.75 were tested, both of these goad efficacy with regard to the latency, the return to sleep. Looking at the risk/benefit analyses they were able to identify the 3.5 mg dose as what appeared to be their optimal dose going forward.
Slide 52: And data as well on an agent, really an old agent looking at it in a new formulation, doxepin now available as a generic and looking at a low-dose strategy with this agent for longer-term administration. The notion here: up to 35 days of treatment for patients with chronic insomnia complaints. Both doses were effective; the 3- and the 6-mg doses, quite low relative to the therapeutic doses for depression, were effective when measured on nights 1 and 29 of administration; so, not a sensation here of any tolerance developing either.
Slide 53: Well, why not treat insomnia? This is really a companion to our earlier slide. Why do physicians have hesitancy? They don't understand that they may not appreciate that it has impact, they're busy; we like to hope that by education we can help them to be more aware and more understanding of this. There are fears of the complications associated with the extended use. Are people going to become dependent? There are certainly concerns about scheduled agents. We have 1 agent now that is not a scheduled agent available. That is the melatonin receptor agonist ramelteon, and concerns about abuse tolerance and dependence.
Slide 54: Among the other barriers that are present to effective management are the lack of training and this type of experience we hope will help with, to ameliorate that. It's very tough. Time constraints certainly play a role. If you're busy seeing 20, 30 patients a day, it’s tough to fit this in. There are some screeners that can be used. But, simply asking a few questions in the office may be one way to address this. I think lack of appreciation that there is all of this impact that is present on sleep, and I think it'd be educational help. And, I think a perception that the risks outweigh the benefits. Again, we have newer agents that have fewer limitations, some of which are nonscheduled, and certainly I think we can make a very strong argument that the benefits appear to outweigh the risks.
Slide 55: Guidelines for practice—we'd like to encourage asking questions about sleep: what is going on, how are you sleeping, what's interfering? Trying to recognize that there is this issue of comorbidity that when insomnia persists it makes these other conditions worse. We would certainly like to work on sleep hygiene. These elements really should be incorporated as part of our routine with all patients, CBT, and options primarily for specialists. We want to be aware of the options we have available and of the suitability of these various agents for individual patients, and to try to recognize that patient materials are available that may help us to assess therapy, to see how effective it is, and to help us to evaluate outcomes.
Slide 56: For our summary slide, chronic insomnia is a major health problem. It affects millions of individuals. It has impact on their families, has impact on their work settings, it can be the cause of or it can be a result of associated problems. This is our comorbidity model. We like to have appropriate and accurate diagnoses in order to have effective treatment, and we have a number of approaches that really show promise. We saw some drugs in development, and we have 3 agents that are now approved for use without limitations in terms of duration of treatment. We can certainly help to feel much less concerned about the issue of chronicity of treatment on the basis of this data. Well, I want to thank you now for your participation. We're now going to turn back to Dr. Fine for a discussion of the case study that was presented at the beginning of this activity. Thank you very much.
Slide 57: Thank you, Dr. Erman. Now we’re going to continue with the case presentation. I will remind you, we have a 53-year-old patient with a family and a full-time career who complains of daytime fatigue, trouble concentrating, and difficulty sleeping. Her diagnosis is chronic insomnia. She has attempted cognitive behavioral therapy with stimulus control and sleep hygiene, which have been inadequate. The classes of prescription medications that are used to treat insomnia include benzodiazepines, select benzodiazepine-receptor agonists, and melatonin-receptor agonist. Benzodiazepines tend to have more adverse effects, such as a hangover effect. Given this patient’s busy lifestyle, the select benzodiazepine-receptor agonists or the melatonin-receptor agonist is a more optimal choice for this patient because of their improved adverse-effect profile. This patient has problems with sleep onset, so the 3 agents most appropriate would be zolpidem, zaleplon or ramelteon, based on their indications. Ramelteon also has no limitation on duration of use, which could be especially helpful to this patient’s chronic insomnia. Other agents that have no limitation on duration of use include eszopiclone and zolpidem ER. All these agents show efficacy with regard to sleep onset, so it is up to the individual clinician as to what may best suit the patient’s needs.
Slide 58: At the patient’s 2-week follow-up appointment, the patient was started on a pharmacologic agent approved for sleep induction to address this patient’s needs. The patient reports improvement: she falls asleep quickly and wakes up feeling well rested.
Slide 59: Insomnia increases healthcare costs both directly and indirectly. The direct costs include office visits, lab studies to rule out other conditions, the cost of the medication to treat her insomnia. The indirect costs include decreased productivity at work secondary to the inability to concentrate as well as absenteeism because of doctor visits. For this patient, daytime fatigue negatively affected her quality of life. A combination of CBT as well as pharmacologic treatment addressed her sleep needs. Thank you for your attention.
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