Cognitive Behavior Therapy for Insomnia in Those with Depression: A Guide for Clinicians 1st

Cognitive Behavior Therapy for Insomnia in Those with Depression Cognitive Behavior Therapy for Insomnia in Those with Depression is the book for clinicians who recognize that insomnia is more often a comorbid condition that merits separate treatment attention. These clinicians know that two thirds of those who present for depression treatment also complain of significant insomnia and that one third of such patients are already taking sleep medication, and they may be familiar with the research showing that treating insomnia is often important in the management of depression. But what strategies should clinicians use for treating insomnia? How can motivation be enhanced? What about medications? Students and professionals alike will find the pages of Cognitive Behavior Therapy for Insomnia in Those with Depression replete with advanced tools to address the adherence problems often encountered in this group, and they’ll come away from the book with a wealth of techniques for improving both sleep and overall symptom management as well as for treating the insomnia that occurs in comorbid disorders. Colleen E. Carney, PhD, is an associate professor in the department of psychology at Ryerson University and the director of the Sleep and Depression Laboratory in Toronto, Canada. She was previously on faculty at Duke University Medical Center, where she was awarded the prestigious National Sleep Foundation Pickwick Fellowship and where she also established the Comorbid Insomnia Clinic. She is the president of the Behavioral Sleep Medicine Special Interest Group of the Association for Behavioral and Cognitive Therapies and a fellow of the Canadian Psychological Association. She is also certified in cognitive behavior therapy by the Canadian Association for Cognitive and Behavioral Therapies, and is an active writer, presenter, and workshop trainer. Donn Posner, PhD, is currently working at the Palo Alto VA on clinical research in insomnia. Before this he served as a clinical associate professor of psychiatry at the Warren Alpert Medical School at Brown University and as director of behavioral sleep medicine for the Sleep Disorders Center of Lifespan Hospitals. Dr. Posner is a member of the American Academy of Sleep Medicine and is one of the first certified behavioral sleep medicine specialists recognized by that group. He is also a founding member of the Society of Behavioral Sleep Medicine and was recently awarded the society’s Peter Hauri Career Distinguished Achievement Award.

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Cognitive Behavior Therapy for Insomnia in Those with Depression A Guide for Clinicians Colleen E. Carney and Donn Posner

First published 2016 by Routledge 711 Third Avenue, New York, NY 10017 and by Routledge 2 Park Square, Milton Park, Abingdon, Oxon OX14 4RN Routledge is an imprint of the Taylor & Francis Group, an informa business © 2016 Colleen E. Carney and Donn Posner The right of Colleen E. Carney and Donn Posner to be identified as authors of this work has been asserted by them in accordance with sections 77 and 78 of the Copyright, Designs and Patents Act 1988. All rights reserved. No part of this book may be reprinted or reproduced or utilized in any form or by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying and recording, or in any information storage or retrieval system, without permission in writing from the publishers. Trademark notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. Library of Congress Cataloging in Publication Data Carney, Colleen. Cognitive behavior therapy for insomnia in those with depression: a guide for clinicians/Colleen E. Carney, PhD and Donn Posner, PhD. pages cm Includes bibliographical references and index. 1. Insomnia—Treatment—Popular works. 2. Depression, Mental— Complications—Popular works. 3. Cognitive therapy—Popular works. I. Posner, Donn. II. Title. RC548.C363 2015 616.8′49820651—dc23 2015016125 ISBN: 978-0-415-73837-8 (hbk) ISBN: 978-0-415-73838-5 (pbk) ISBN: 978-1-315-81740-8 (ebk) Typeset in Minion by Florence Production Ltd, Stoodleigh, Devon, UK

I dedicate this book to my family, Shannon, Sydney, and Theo. Their love, support and understanding, allows me to pursue my passion. Colleen E. Carney, PhD I dedicate this book to my wife Karen and son Max who definitely put the drive into my life each and every day. Thank you for your bottomless reservoir of support. I would also like to thank my co-author Colleen for giving me the opportunity to be part of this thought provoking project. Donn Posner, PhD

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Contents Acknowledgment ix 1 Depression and Insomnia: An Overview 1 2 Non-psychological Treatments for Those with Insomnia and Depression 14 3 Cognitive Behavior Therapy for Insomnia (CBT-I): Treatment Considerations 26 4 Assessment of Insomnia in Those with Depression 37 5 Behavioral Strategies for Insomnia 60 6 Cognitive Factors and Treatment 79 7 Encouraging Adherence and Troubleshooting Potential Barriers 96 8 Rumination Strategies for Insomnia 120 9 Combining Depression and Insomnia Therapies 134 10 Case Study 157 Appendices A Core Sleep Diary 185 B Expanded Sleep Diary 188 C Daytime Insomnia Symptom Response Scale 194

D TRAP or TRAC Worksheet 195 E Daily Activity Monitoring Form 196 F Goal Tracking Form 197 G Blank Pro-Depression and Anti-Depressant Worksheet 198 H Blank Pro-Sleep versus Pro-Insomnia Worksheet 199 I Blank Pro-Energy versus Pro-Fatigue Worksheet 200 J BABIT Continuum Exercise 201 K Behavioral Experiment Monitoring 202 References 203 Index 225 viii Contents

Acknowledgment We thank Dr. Rachel Manber for her intellectual contributions to this book and her contributions to the field in the area of sleep and depression.

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1 Depression and Insomnia An Overview Insomnia is Important Sleep is a significant issue for those with major depressive disorder (MDD). Up to 90 percent of those with MDD complain of insomnia (Kupfer, Reynolds, Ulrich, Shaw, & Coble, 1982; Reynolds & Kupfer, 1987). In community samples, just under half of people with MDD meet criteria for an insomnia diagnosis (Breslau, Roth, Rosenthal, & Andreski, 1996; Stewart et al., 2006). In sleep clinics, the most common insomnia patient seen is one with comorbid MDD (Buysse et al., 1994; Coleman et al., 1982; Edinger et al., 1989; Jacobs, Reynolds, Kupfer, Lovin, & Ehrenpreis, 1988). Additionally, there can be complaints of hypersomnia and sometimes an alternation between hypersomnia and insomnia. Despite the high prevalence, the importance of sleep is under-recognized and as a result undertreated. There are several studies showing that a separate insomnia diagnosis is not considered when MDD is suspected. For example, the best predictor of a MDD diagnosis is the presence of an insomnia complaint (Haponik, Frye, Richards, Wymer, & Hinds, 1996). However, insomnia is not one of the two cardinal symptoms (i.e., depressed mood and/or anhedonia) needed for a MDD diagnosis (American Psychiatric Association, 2013) and thus should not be predictive of this diagnosis. Another potential issue in the underdiagnosis of insomnia is being presumptuous about etiology. Some problems in this area include the presumption that it is important to establish temporal precedence of the insomnia—even in such cases, some presume that the insomnia is merely the first MDD symptom to appear. There are several problems with this view. One is that patients may not be able to remember which symptoms came first, especially given that those with MDD have autobiographical deficits (Lyubormirsky, Caldwell, & NolenHoeksema, 1998). Second, even in sleep specialists, clinicians exhibit poor reliability in determining whether an insomnia diagnosis is present when there are mood symptoms present (Edinger et al., 2011). There are also assumptions that MDD is more serious and therefore clinical attention should be exclusively focused on the MDD. Although MDD is a very serious disorder, on some quality of life indices, chronic insomnia produces greater impairment than MDD (Foley et al., 1995). Insomnia is associated with large societal costs (Carney et al., 2008; Daley, Morin, LeBlanc, Gregoire, & Savard, 2009; Ozminkowski, Wang, & Walsh, 2007). Indeed, the costs associated with MDD increase by an additional $1K annually in those with untreated insomnia and MDD (Asche, Joish, Camacho, & Drake, 2010). Additionally, insomnia is predictive of developing alcohol and substance abuse (Ford & Kamerow, 1989). Lastly, chronic insomnia is associated with

increased suicidal ideation (Agargun, Kara, & Solmaz, 1997; Li, Lam, Yu, Zhang, & Wing, 2010; Woznica, Carney, Kuo, & Moss, 2014), and insomnia is an independent predictor of suicide (Bernert, Joiner, Cukrowicz, Schmidt, & Krakow, 2005); that is, even after controlling for depression, there is an increased risk for suicidality. In those with MDD, suicidal ideation is increased when there is insomnia present and insomnia is a significant predictor of suicide completion (Fawcett et al., 1990). Inherent in the assumption that MDD is always more serious is perhaps an implicit assumption that treatment of the MDD will likely resolve the (less serious) insomnia problem. There are many studies to confirm that this is a faulty assumption. Across studies using sleep items from depression inventories, the rate of residual insomnia problems after depressive recovery following antidepressant therapy or psychotherapy is a little less than half (Carney, Segal, Edinger, & Krystal, 2007b; Manber et al., 2003; Nierenberg et al., 1999). It is possible that the rate exceeds 50 percent, as a study that utilized a validated sleep questionnaire in lieu of sleep items from a depression measure found a much higher rate (Carney, Harris, Friedman, & Segal, 2011). Additionally, in the same study, although depression cognitions significantly decreased and were in the nonclinical range after depressive recovery, insomniagenic beliefs did not significantly improve with depression recovery and remained in the pathological range (Carney et al., 2011). Insomnia is also a complicating factor for depression treatment because insomnia predicts poorer response to evidence-based psychotherapy or pharma cotherapy depression treatments (Buysse, 1999; Thase, 1996, 1997). Collectively, the data above confirms what was con - cluded at the National Institutes of Health (NIH) Consensus Conference on Insomnia: Insomnia should be considered a comorbid condition and treated in the presence of MDD. Moreover, after a review of the evidence, the DSM5 Sleep-Wake Disorders Work group concluded that there should be no diagnostic distinction between comorbid insomnia and insomnia alone; the disorder in the fifth edition of the DSM is simply insomnia disorder (American Psychiatric Association, 2013). Etiological Factors in Insomnia In considering the relationship between insomnia and depression, it may be helpful to first consider causal factors for insomnia. There are many causes of sleep disturbance and there may be as many precipitating or initial causes as there are clients. Although sleep problems initially can be caused by just about anything, there are three main causes or factors that perpetuate a chronic insomnia: problems with the homeostatic, circadian and/or arousal systems. This idea was first presented in Spielman’s Three P Model (Spielman, Caruso, & Glovinsky, 1987a). The model postulates that there are pre - disposing factors that increase vulnerability to insomnia (e.g., a tendency towards rumination), but having a vulnerability factor does not mean that insomnia is inevitable; it simply provides fertile ground for an insomnia disorder in the presence of a stressor. The stressor is the precipitant in the model. As stated above, there are many precipitants, even positive stressors such as having a baby can precipitate sleep disturbance. MDD can be a stressor in this model. Although insomnia is often a precursor to MDD, in some cases, MDD could lead to more protracted insomnia. Sleep disturbances that are associated with a stressor are expected to resolve with the resolution of the precipitant. Thus in the case of MDD precipitating sleep disruption, we would expect insomnia to 2 Depression and Insomnia

resolve when the MDD resolves. Unfortunately we know that insomnia frequently does not remit with the resolution of the depressive episode (Carney, Edinger, Meyer, Lindman, & Istre, 2006). Why? Sleep disturbance becomes a chronic insomnia when there are perpetuating factors present. Perpetuating factors are those factors that often arise from coping with the precipitating factor and initial sleep disturbance. The consequence of these coping behaviors can create disturbances in the homeostatic, circadian and/or arousal systems. Below we discuss each of these factors and then return to the situation of MDD and insomnia. Perpetuating Factor: Homeostatic System Problems Sleep is regulated by two systems: a homeostatic and a circadian system. We will discuss the circadian system and its role in chronic insomnia in the next section. First, the homeostatic system is a system that balances between wakefulness and sleep. From the moment we are awake and active, we accumulate a chemical in the basal forebrain called adenosine. The build-up of this chemical is associated with increasing sleepiness and pressure for deep sleep; the greater the duration of wakefulness, the greater the buildup of a drive for deep sleep. The greater the amount of time since rising, the greater is the pressure to sleep. This system ensures that we neither sleep too much nor too little. It compensates for sleep loss and lightens sleep if the person was attempting to produce copious, unnecessary amounts of sleep. This means that people needn’t do anything during periods of sleep loss except maintain their schedule, because the body will make up for lost sleep with subsequent deep, restorative sleep. However, attempting to make up for lost sleep by spending increased time in bed or at rest, sends a message to the body that less deep sleep is needed; thus the compensatory mechanism is thwarted. Below we include a sample script for CBT-I psychoeducation. Such an explanation is included in the first treatment session of CBT-I. There are other examples of psychoeducation delivery throughout the book, including in Chapter 5 wherein we describe the behavioral components of CBT-I delivered in the first treatment session. Therapist: From the moment you get up and are active, you begin to build a drive for deep sleep. You build it all day and into the evening until so much has built up that when you go to sleep, you produce some deep sleep and it keeps you asleep throughout the night. Client: Well, that never happens to me anymore. Therapist: It may well be that you have a problem with this system. Let’s continue and you can tell me what you think. This system determines how much deep sleep you get and it is based on how many hours you have been awake and active. So if you get up later, go to bed earlier, attempt to nap or rest throughout the day or you are less active, less deep sleep drive is accumulated and the result is light, broken sleep and maybe difficulty in falling asleep too. Client: I definitely don’t get deep sleep anymore but it’s not like I am totally inactive . . . Therapist: Let me ask you this, when you feel tired, or you’ve had a poor night’s sleep, or your mood is really low, how much do you feel like keeping up with your regular activities? Depression and Insomnia 3

Client: I’m not sure what you mean. I feel really tired so I try to do my normal activities but I can’t always do what I want. Therapist: Can you tell me more about that? Are you able to get right out of bed when your alarm sounds? Are you always able to go to work? Do you keep up with all your social engagements? Client: Sort of. Not everything. Like I said, I feel exhausted so it’s not always possible. Therapist: This is very common. Most people do an excellent job trying to do all the things they used to but when the fatigue sets in, they find it more and more difficult and they find themselves spending a little more time in bed and a little more time inactive than before they had their sleeping problems . . . Client: I wouldn’t say I spend more time in bed. Therapist: Ok. I was making that assumption based on what you told me was your routine two years ago, before all this trouble started. You had said that you went to bed around 11 PM and got up at 6 AM each morning, you never took naps, you had a weekly card game with friends, lunch on Fridays with coworkers, and you worked out 4 days per week. Client: Well it’s true that I don’t work out anymore, and guess I don’t go to lunch or the card game. I don’t really take naps now because I often can’t sleep. I just try to sleep. I still go to bed at 11 and get up at 6 AM. Therapist: I see. So some of your activities have decreased and you spend more time resting but not always napping? Client: Right. Therapist: Can we take a look at your sleep diary? [See Figure 10.2 in Chapter 10] Client: Sure. See how I go to bed around 11 PM most nights? Except for Tuesday and Wednesday. Therapist: Yes, I see. Most nights were around 11 PM and Tuesday you went to bed an hour earlier and Wednesday you went to bed about 2 hours earlier, around 9ish, right? Client: That’s right. Therapist: And I see that your final awakening during the work week was 6:30 AM and on the weekend it was closer to 8 AM correct? Client: That’s right. Therapist: The item below your final awakening is the time that you actually got out of bed, what do you notice about the time at which you physically get out of bed? Client: It’s later than 6:30 AM. It’s because I am tired. Therapist: Right. Because you are tired, you have difficulty getting up at the time you used to and it is even later on weekends. You used to spend 7 hours in bed each night. How many hours were you in bed on Wednesday? Client: Almost 10 hours. Wow. I never knew that. But I am not sleeping during this time. Therapist: Right, you are not sleeping, but you are also not building a drive for deep sleep. You also told me that you attempted to nap for 90 minutes that afternoon. If you spent 11.5 hours inactive in bed that day, how much time were you building sleep drive? Client: I don’t know [pauses] I think, 12.5 hours? 4 Depression and Insomnia

Therapist: Yes. So if there were two people and one spent 7 hours in bed so they had 17 hours of deep sleep drive build-up, and the other had 12.5 hours of build-up, who is more likely to have deep, continuous sleep? Client: Ok, I get it. The person who builds 17 hours has a better chance at better sleep. Therapist: And don’t forget that the person with 17 hours of build-up also has much more activity to add to the build-up. The person with only 12.5 hours also has a lower amount of physical activity to contribute to the build-up. Client: Ok, I get it. Therapist: So we will discuss ways to work with this system to produce more deep sleep for you. But first, I had said there is another system that works with your homeostatic system. I think it’s important to talk about this system too. Perpetuating Factor: Circadian System Considerations In addition to the homeostatic system that balances sleep and wakefulness, there is a body clock that regulates many systems in the body, including the timing of the sleep and alerting systems. The circadian system is slightly longer than a 24 hour day and thus is highly responsive to cues in the environment, such as the light, for entrainment purposes. The light provides input via the eye into the brain about what time it is. When blue spectrum light is present (i.e., in sunlight) it signals that it is day and this situation is associated with alertness. When red spectrum light is present (i.e., following sunset) it signals night and is associated with melatonin release; a sedative hormone. Improperly timed cues can create sleepiness or alertness at undesirable times. Thus decreased exposure to light can be associated with drift in the circadian system, and ill-timed light (blue light exposure at night) can be associated with ill-timed alertness. Although light is the most powerful cue for the clock, keeping a regular schedule of activities including rise and bedtimes, and perhaps meal times and other activities can help set the clock. Each of these activities is typically associated with light too, i.e., we typically eat under lighted conditions, when we travel to work we are often exposed to daylight etc. In those with insomnia, the regularity of daily activities is diminished relative to good sleepers even when overall levels of activity are the same between those with insomnia and good sleepers (Moss, Carney, Haynes, & Harris, 2014). When there is irregular environmental input (e.g., light or activities) to the clock, the system drifts, because it is more than 24 hours, and symptoms such as difficulty in sleeping, cognitive difficulties, fatigue, and mood disturbance can occur. These are the symptoms experi - enced during jetlag. That’s because jetlag is the result of the mismatch between the internal time and the time in the environment. Even one hour is enough to produce these symptoms; most people can relate to this because daylight savings is only one hour and it typically produces at least mild symptoms. The reason this is important is that if the rise time is varied by an hour or more then the client will experience jetlag symptoms. When people suffer from sleep or mood disturbance they often struggle at getting up at their regular time. They may continue to set the alarm but will remain in bed longer because they feel tired. The circadian system regulates a variety of systems in the body including sleep, alertness, and mood. There are regular predictable patterns for the rise and fall of these activities across a 24 hour period but this system is also largely responsive to Depression and Insomnia 5

environmental output. One way to envisage this system is to visualize a curve that rises in the morning, continues to rise all day, and then begins to fall in the evening and throughout the night (see Figure 1.1). The peak is in the evening and the trough or lowest point is in the early morning. This curve would correspond to the core body temperature curve as this exhibits circadian periodicity. This curve would also help us to understand alertness in a 24 hour period as the clock emits an alerting signal when the curve is ascending; thus increasing as the day goes on and competing with the buildup of sleepiness to keep us awake. Alertness diminishes when the curve is falling (ideally an hour or so before bed) which sets the stage for sleep. Prior to the fall in alerting signals is the release of melatonin in the early evening, coincident with the offset of light (i.e., sunset), which also sets the stage for sleep. Attempting to make up for lost sleep during times at which alertness signals are being sent from the clock, or when melatonin is not present or is present in only small amounts, makes sleep less likely. Thus, trying to sleep during the day is ill-timed given that alertness signals will intrude. For example, those working a night shift will have a strong sleep drive because they stayed up all night building pressure. However, when they attempt to sleep in the morning, they are sleeping in competition with alerting signals from the clock. This is partly why those working night shifts also complain of less restorative sleep or shortened sleep duration. Another consideration is maintaining a schedule that is a poor match for biology, or chronotype. Chronotype refers to the placement of a sleep wake cycle within a 24 hour period. Thus someone who typically becomes sleepy very early (e.g., 9 PM) and typically starts to wake up around 4 AM exhibits morningness or an advance in phase, and someone who typically becomes sleepy very late (e.g., 2 AM) and typically starts to wake up later (e.g., 10 AM) exhibits eveningness or a phase delay. There is some evidence that there is a significant genetic contribution, and there is a developmental pattern (e.g., morningness at the early and late years of life). There is some ability to make shifts using bright light therapy, melatonin, or maintaining a strict schedule but there are individual differences in the ability to maintain the shift. The important consideration is whether someone is keeping a schedule discrepant from their chronotype. 6 Depression and Insomnia Alerting signal from the clock Low High Time of day Morning Afternoon Evening Night Morning Sleep opportunity Figure 1.1 Strength of alerting signals from the clock

For example, if a client has a lifelong pattern of going to bed late and rising late, and they are suddenly obliged to rise at 7 AM for work, they will not be able to go to bed early just because they have to wake up early. Also important is that people can have particular beliefs about what it means to be a morning person or a night person. Night owls are associated with a stereotype of laziness so clients can be ambivalent about maintaining a schedule consistent with their chronotype because there is something “wrong” with going to bed late. Likewise, there may be a negative stereotype of being “boring” associated with keeping an early schedule. Below is an example of how to deliver psychoeducation about the clock in an interactive way, using the client’s data and Socratic questioning. Therapist: We have a clock inside our body that is not quite 24 hours in length. To keep this clock running optimally, we have to set the clock every day with regular habits. Client: What happens if it is not running properly? Therapist: A variety of things can happen. The clock is responsible for mood, alertness, sleep, in addition to other processes, so you could experience insomnia, fatigue, and low or irritable mood and difficulty with performance, for example, it might require more effort to concentrate. Client: Sounds like me. What do you have to do to make it run better? Therapist: We need to set our internal clock with regular habits such as regulating the time at which we get out of bed. Client: What about the time I go to bed? Therapist: It would be ideal if we could regulate bedtime however we are not always sufficiently sleepy at bedtime and we shouldn’t get into bed without feeling sleepy or it will increase the likelihood of lying awake while in bed. Setting the time at which you get out of bed at the same time every morning will regulate your clock and make it more likely that you will begin feeling sleepy around the same time each night. All things being equal, your bedtime would become more regular by getting out of bed at the same time each morning. Client: I already get up at the same time most mornings, so this probably doesn’t apply to me. Therapist: Have you ever taken a flight where you travelled and the time zone changed? Client: Yes. Recently I flew from Colorado to Boston. Why? Therapist: What were the symptoms you had a result of the jetlag? Client: I was tired, I had a headache and I found it hard to eat when everyone else was and couldn’t fall asleep when everyone else was asleep. Therapist: So you essentially had insomnia and other unpleasant related symptoms? Client: Yes, I guess so. Therapist: And how long did it last? Client: Maybe two days? I think I felt tired for longer than that though. Therapist: So there was an immediate effect and then it took a few days before things completely improved? Client: That’s right. What does this have to do with travel? Therapist: Jetlag symptoms are really about this mismatch between the clock in your body and the clock showing local time. The difference between Boston and Denver Depression and Insomnia 7

is only 2 hours but it produced immediate negative effects that lasted a few days. Can you take a look at your sleep log and tell me the difference between the earliest and latest time at which you got out of bed last week? [See Chapter 10 to review specifics of this case, including the Figure 10.2 sleep log] Client: A little over 2 hours. Do you really think it would make that much of a difference? Therapist: Don’t take my word for it. What was your experience when your body expected it to be a particular time and suddenly everything was shifted 2 hours later? How did your body respond? Client: Wow, ok, I get it. The problem is that I am tired so I have to make-up for lost sleep. Therapist: Given what you just learned about building sleep drive, do you think you are making up for the lost sleep? Client: I forgot. No, I guess not. And it looks like I am giving myself jetlag, which sucks. Ok, I get it. Therapist: There is one last consideration for the clock system and that is that there is a window of opportunity for people, specific to them, at which time the best sleep will be produced. Some of this relates to genetics. That is, would you consider yourself to be a night owl or an early bird, or somewhere in between? Client: I used to be a night owl in my early twenties but then I got insomnia and it went away. I would say I am somewhere in between but maybe more of a morning person than not. Therapist: Developmentally, people tend to shift towards being night owls in their teens and early teens and then gradually shift to somewhere in between a morning and night person throughout adulthood. Late in life and also very early in life, older adults and small children tend to be on the earlier side. Even though there are developmental changes, genetics play some role so if you are born with a genetic loading for being a night owl, it means that you will be shifted earlier as a young child but will still be much later than all of your peers. Does that make sense? Client: Yes. My Dad was a night owl and my Mom was an early bird or maybe somewhere in the middle. Therapist: What this all means is that it is important to keep a schedule that makes sense for your body. Since you are somewhere in the middle, we wouldn’t want you to keep a very late bedtime and rise time because that wouldn’t suit you, nor would an extremely early bedtime and rise time. Make sense? Client: Yes. Perpetuating Factor: Arousal System Considerations In sum, two regulatory systems interact to produce quality sleep: the circadian system and the homeostatic system (Borbély, 1982). Even when these two systems are operating optimally; that is, the sleep-wake schedule is regular and well-matched to the person’s chronotype and there is close correspondence to the amount of sleep currently produced and the time spent in bed, these systems can be overridden by the arousal system. This is important, because even when homeostatic pressure is high and the timing of a sleep opportunity is ideal, in emergency situations it is most advantageous to be able to 8 Depression and Insomnia

postpone sleep to be able to respond to the emergency. However, sometimes the body becomes more alert in situations that are not emergencies. There is ample evidence of hyperarousal in insomnia across multiple physiological indices (Bonnet & Arand, 1995, 1998; Nofzinger et al., 2004; Vgontzas et al., 2001). Thus, arousal is an important consideration in insomnia and two types of arousal (e.g., conditioned arousal and cognitive arousal) tend to figure prominently as treatment targets. There is evidence of conditioned arousal in many people with insomnia. Conditioned arousal refers to the repeated pairing of wakefulness with the sleep situation (e.g., bed), such that the bed itself begins to acquire alertness-promoting properties. Many people with insomnia report that they are able to feel sleepy and even produce sleep elsewhere (e.g., on the couch) but when they get into bed, they become instantly alert. Such a report is consistent with conditioned arousal. Conditioned arousal is explained to clients during the psychoeducation component of the first treatment session and is easily explained as the body has learned that the bed is no longer associated with sleeping; this has occurred (unintentionally) via repeated pairings of the bed with wakefulness. People with insomnia typically respond to wakefulness in bed by staying in the bed, further pairing the bed with wakefulness and perhaps negative emotions such as anxiety or frustration. Moreover, in an effort to fall asleep or to produce greater amounts of sleep, people with insomnia do activities associated with wakefulness in the bed, such as reading, watching television, gaming, or working on the computer. Performing activities done while awake can create an association with the bed and wakefulness. Thinking about sleep, worries, or anything distressing is predictive of difficulties sleeping (Harvey, 2000; Wicklow & Espie, 2000) and cognitive arousal is seen by insomnia patients as accounting for their insomnia (Lichstein & Rosenthal, 1980). Worrying about sleep and fatigue is characteristic of those with insomnia (Carney & Edinger, 2006) and when in bed and faced with wakefulness, it can perpetuate worries about insomnia and further delay sleep onset. Thus arousal can be a major factor in insomnia that is targeted with CBT-I. For more on how these associations are addressed in CBT-I, see Chapters 5 and 7. The Sleep of Those With Depression and Insomnia There are several interesting sleep characteristics of those with MDD-I. There are many assumptions, some true and some not, about the sleep of those with MDD. One of the most common assumptions is that MDD-I is characterized by early morning awaken - ings (EMAs). Although EMAs can occur in depression, when considering all of the insomnia complaints, including increased sleep onset latency and increased wakeful - ness throughout the night, EMAs have the lowest rate of occurrence (Carney et al., 2007b). Moreover, EMAs may reflect an advancing circadian phase that occurs naturally in aging and can be misdiagnosed as a depression in those with a circadian change only. Because of the sleep changes seen in MDD, there have been many attempts to identify sleep markers that could reliably identify depression. Some of the sleep-related markers include: decreased total sleep time, decreased sleep efficiency (i.e., the proportion of time asleep while in bed), decreased slow wave sleep (SWS), increased REM sleep, and increased wakefulness, including increased sleep onset latency and wakefulness after sleep onset (Benca, Obermeyer, Thisted, & Gillin, 1992). Depression and Insomnia 9

Slow wave sleep is also called delta sleep or N3 because it is stage 3 of non-rapid eye movement sleep (NREM). There may be abnormal proportions of SWS in those with MDD. The number of slow waves in the first NREM period is lower than the waves counted in other NREM periods (Kupfer, Frank, McEachran, & Grochocinski, 1990). This is unusual because normally increased slow waves are seen in the first NREM period and reflect a release of homeostatic pressure. It is possible that people with MDD have decreased homeostatic pressure, given that they tend to have decreased activity and increased time in bed in a 24 hour period, but this can also be seen in insomnia. Another possibility is that rapid eye movement (REM) initially displaces slow waves until later in the sleep period. A decreased slow wave count predicts MDD recurrence and also predicts suboptimal MDD treatment outcomes (Jindal et al., 2002; Kupfer et al., 1990) and one could expect that the consequence of this marker would be less deep sleep, resulting in sleep continuity (e.g., difficulty staying asleep) and sleep quality complaints. Another frequently explored biomarker is rapid eye movement sleep (REMS) related phenomena. There are a collection of findings in MDD of REMS abnormalities including: decreased REMS onset latency (i.e., it appears earlier in the night), as well as increased REMS density. This has been thoroughly reviewed elsewhere (see Benca et al., 1992; Buysse & Kupfer, 1993) so we will review only briefly. Interestingly, markers such as REMS density appear in nondepressed first-degree probands of those with depression and may predict vulnerability to depression (Giles, Biggs, Rush, & Roffwarg, 1988; Giles et al., 1989; Giles, Roffwarg, & Rush, 1987). Increased REMS density is also predictive of negative depression treatment outcomes irrespective of treatment approach (Clark et al., 2000). The fact that several (although not all) antidepressants suppress REMS, as well as the effectiveness of sleep deprivation in the second half of the night where REMS is most pronounced, has been taken by some to mean that REMS must be depressogenic (e.g., Vogel, 1983). REMS deprivation produces immediate antidepres - sant effects although they are reversed on the subsequent recovery night (Vogel, 1975; Vogel, Traub, Ben-Horin, & Meyers, 1968; Vogel, Vogel, McAbee, & Thurmond, 1980). One possible explanation for these phenomena is the internal coincidence model (Wehr & Wirz-Justice, 1980); a model that posits that sleep occurs at a time coincident with circadian vulnerability for mood disturbance. This theory might explain the occurrence of EMAs for some as well as increased REMS. An alternative perspective for the REMS findings, and one that accounts for the finding that insomnia is often prodromal in depression (Baglioni et al., 2011), is the suggestion that the chronic instability of REMS seen in insomnia (Feige et al., 2008) may eventually result in REMS rebound (i.e., a subsequent increase in density) and resultant depression (Riemann et al., 2012). There are also a number of other circadian-related explanations for these phenomena including: 1) The regularity of activities erodes and provides less regular non-photic input into the circadian system (e.g., the social zeitgeber hypothesis (Ehlers, Frank, & Kupfer, 1988)), 2) The sleep phase of those with depression has advanced (Wehr, WirzJustice, Goodwin, Duncan, & Gillin, 1979), and 3) There is a problem with the restactivity ratio (Fulton, Armitage, & Rush, 2000). In humans, with decreasing light, total sleep time and melatonin secretion increases, and activity decreases (Goodwin, WirzJustice, & Wehr, 1982), thus the ratio of rest to activity increases. There is some evidence that in teens these effects are mediated by gender (Armitage et al., 2004). If a client is unaware of a phase advance, their bedtime would not change even though sleepiness 10 Depression and Insomnia

should occur earlier, there may also be dozing during this period of sleepiness, thus activity would both be increased in this scenario and may actually be less. Most clients with EMAs do not respond to the awakening by getting out of bed for the day, so in this scenario, the rest period is extended, and again, this would increase the ratio of rest to activity. An increase in rest to activity might have a negative impact on interpersonal contact, as people are less likely to socialize when exhausted, and they would be unlikely to have significant social contact in the evening while dozing. Other lines of research have focused on analyzing the EEG data of sleeping patients with MDD with spectral analytic techniques. One line of research has focused on coherence, or the similarity of activity in two areas (Fulton et al., 2000). There is evidence that decreased coherence is associated with MDD and also predicts MDD recurrence (Fulton et al., 2000). One caveat to this finding is that findings are moderated by age and sex (Armitage, Hoffmann, Emslie, Rintelmann, & Robert, 2006). Many of these socalled markers can be characteristic of insomnia with perhaps the exception of REMS abnormalities; thus the specificity of these indices can be somewhat poor. There is a longstanding tradition to view psychiatric disorders as emanating from an imbalance in neurochemicals, and there are purported chemical abnormalities (e.g., cholinergic hypersensitivity (Gillin, Sitaram, & Duncan, 1979) and/or serotonergic or noradrenergic sensitivity (McCarley, 1982)) as key in the sleep disturbances in those with MDD-I. It is unclear which of these can be considered traits versus state-like markers (Berger, Riemann, Höchli, & Spiegel, 1989) moreover some predictions about medications with particular properties (e.g., see Riemann, Berger, & Voderholzer, 2001; Sitaram, 1982) do not always yield data consistent with such theories. Of course, in each of these models, one could posit more depression-specific models as accounting for some of the sleep problems in MDD-I. For example, interpersonal theories could suggest that engaging in less interpersonal activity could decrease stimulation and reinforcers and lead to decreased overall activity, thus increasing the rest to activity ratio. With fewer people around to constrain a schedule towards conventional regularity, there would also be less social zeitgeber input into the clock. Lastly, cognitive etiological models focus on the importance of depressogenic thought leading to avoidance behaviors including less social behaviors. Avoidance would have a negative impact on the circadian system as there would be less exposure to light (perhaps increasing the rest to activity ratio) and less exposure to regular non-photic zeitgebers that provide input into the clock. All theories of depression and MDD-I have mixed evidence or competing explanations; likewise, the failure to discover a universal marker with high sensitivity and specificity is perhaps not surprising given that MDD is a polythetic disorder (for discussion, see Carney & Moss, 2014). A polythetic disorder is a disorder in which there are numerous variations of clinical presentations within the diagnostic criteria. Whereas everyone with Bulimia Nervosa meets the same symptom criteria for the disorder, someone with MDD could have insomnia, hypersomnia, or no sleep complaint at all. Additionally, appetites can be increased, decreased, or unchanged. There may or may not be a disturbance in mood, there may be anhedonia or this may be absent, or one could have both anhedonia and depressed mood. Psychomotor activity may appear significantly sped-up or remarkably slowed down and there may or may not be fatigue. The permutations of presentations become quite large and it is difficult to imagine that all would have the same biological substrates and sleep characteristics. Depression and Insomnia 11

Perhaps a more parsimonious way of conceptualizing etiology in MDD-I clients who present for treatment is to understand that it is not always possible to identify the precipitant cause of the MDD-I so focusing on current perpetuators may be more important. Etiology in MDD-I As stated previously, Spielman (Spielman et al., 1987a) suggests that there are pre - disposing, precipitating, and perpetuating factors for insomnia, and perpetuating factors are key targets for chronic insomnia treatment. Applying Spielman’s ideas to MDD-I, predisposing factors are factors that increase vulnerability but, in the absence of a stressor, are not associated with an insomnia diagnosis. For example, particular genes, a tendency towards rumination or a particular endogenous chemical environ ment, may increase the risk for MDD-I, but without a stressor, whether endogenous or environmental, sleep disturbance may be expected to remain at a subclinical level. Broadly speaking, a precipitant is a stressor, which interacts with the predisposing factors to increase sleep disturbance. A strong enough stressor (e.g., a life event) may cause a sleep disturbance severe enough to warrant an insomnia diagnosis, however, the expectation is that when the stressor resolves, so should the insomnia. However, in the clinical histories of clients with MDD-I it is common to hear about the stressor resolving and to the client’s surprise and disappointment, the insomnia does not remit. The answer to why the insomnia does not remit, is that perpetuating factors arise that take over as the main cause of insomnia, and the insomnia becomes chronic. This is often explained to clients during the psychoeducation component of the first CBT-I session because the fact that the insomnia has persisted beyond the resolution of the initial stressor is often taken to mean that the sleep system is broken and the client believes they are powerless to fix it. Explaining that making behavioral corrections to perpetuating behaviors will fix the problem is empowering for clients. Perpetuating factors often originate from coping with the sleep and/or mood symptoms first created by the stressor. For example, when feeling fatigued, people tend to engage in fewer activities in response. When feeling tired, whether it is related to mood or sleep symptoms, people may spend more time at rest and in bed in the 24 hour period. For some, this may relate to how poorly they feel, for others this may relate to a belief that producing more sleep may help to improve their situation, and being in bed for longer periods gives them the best chance to produce more sleep. Some may take sleep aides, whether in the form of alcohol, marijuana, or sedating medications such as diphenhydramine, or sleep medications. A protracted sleep problem can result in a preoccupation about symptoms (Harvey, 2002) and why they are occurring (e.g., symptom-focused rumination) (Carney, Harris, Falco, & Edinger, 2013b; Carney, Harris, Moss, & Edinger, 2010b), and rumination can become a prominent factor in the case. A common perpetuating factor that develops is a belief about sleep effort. Understandably, to “solve” the sleep problem, people with insomnia increase their efforts to sleep and become cognitively inflexible in their belief that one must exert effort to produce and compensate for sleep (Espie, Broomfield, MacMahon, Macphee, & Taylor, 2006). In sum, although insomnia could develop from endogenous factors described above, insomnia may also develop as an acute stress reaction to the onset of 12 Depression and Insomnia

depression—additionally, depression could arise from endogenous factors relating to the sleep problem or other sources, or the depression could develop as a stress reaction to chronic insomnia. Now we turn to the three perpetuating factors of chronic insomnia and ask whether those with MDD-I have the same factors—the answer is yes. Those with MDD-I report comparable levels of unhelpful related thinking about sleep (Carney, Edinger, Manber, Garson, & Segal, 2007a), including the belief that sleep requires effort (Kohn & Espie, 2005) as those with insomnia only. Similar to those with insomnia, those with MDD-I also exhibit increased variability in the timing of the sleep period (Kohn & Espie, 2005), as well as other zeitgebers (Szuba, Yager, Guze, Allen, & Baxter, 1992). Again, similar to those with insomnia, those with MDD-I show decreased activity as well as increased time-in-bed (Kohn & Espie, 2005). Lastly, those with insomnia and those with MDDI similarly show increased arousal (Kohn & Espie, 2005) and symptom-focused rumination (Carney et al., 2013b). Given that: 1) Insomnia is such a prominent, debilitating part of MDD-I, with implications for quality of life and depression outcomes, and 2) MDD-I shares the same perpetuating factors effectively targeted by CBT-I, CBT-I seems particularly well suited for the task of dissemination in this group. Thus the remainder of this book focuses on CBT-I in this group, including, issues related to medication (Chapter 2), treatment delivery issues (Chapter 3), assessment in nonsleep specialty settings (Chapter 4), behavioral and cognitive components of CBT-I (Chapters 5 and 7), as well as how to troubleshoot common CBT-I delivery problems in MDD-I (Chapter 6), rumination strategies (Chapter 8), and combined approaches to MDD-I (Chapter 9). The last chapter follows a case through CBT-I treatment (Chapter 10). Summary • Insomnia is costly and important to treat in those with MDD-I. • Although there are innumerous possible precipitants for MDD-I, there are three main causes of chronic insomnia: issues with the circadian or homeostatic systems and/or problems with arousal. – Circadian system problems include schedule variability (e.g., varying rise time) or attempting to sleep during times that conflict with the biological clock. – Homeostatic problems include too little accumulation of sleep drive to sustain deep sleep (e.g., decreased activity or too much time at rest in a 24 hour period). – Arousal problems include conditioned arousal and cognitive and/or physio - logical hyperarousal. • There are a number of sleep abnormalities in those with MDD-I (e.g., REMS abnormalities) and theories to account for them. Such abnormalities are not characteristic of all clients with MDD-I. • Those with MDD-I share the same perpetuating factors for their insomnia as those with insomnia only, and are thus, good candidates for CBT-I. Depression and Insomnia 13

2 Non-psychological Treatments for Those with Insomnia and Depression Pharmacological Treatments for Depression There are a variety of effective pharmacological and other medical treatments for depression; some induce sedation and improve sleep, some increase arousal and interfere with sleep, and others are neutral with respect to sleep. In most cases the effects on sleep are variable, with some individuals experiencing benefits and others experiencing worsening or no effect on their sleep. The American Academy of Sleep Medicine (AASM) has published consensus guidelines for treating insomnia (SchutteRodin, Broch, Buysse, Dorsey, & Sateia, 2008). The algorithm from the AASM (see Figure 2.1) suggests to first evaluate cost, and then preference and availability options for Cognitive Behavior Therapy for Insomnia (CBT-I), pharmacologic, and combined treatments. It is of note that NIH consensus guidelines (National Institutes of Health State, 2005) and British Association of Pharmacotherapy guidelines (Wilson et al., 2010) are that CBT-I should be the frontline treatment, and CBT-I is at the top of the AASM algorithm. Once a decision is made to proceed with pharmacotherapy, the algorithm presents a sequence in which the physician begins with a full dose antidepressant and a Food and Drug Administration (FDA)-approved hypnotic such as benzodiazepine receptor agonist (BzRA) or ramelteon. Following a poor sleep response, the second step in the algorithm is to reconsider the diagnosis and consider switching therapy to CBTI or a combined approach. If there is non-response following this new approach, a different BzRA or ramelteon trial begins. Following a poor response to these approaches, a sedating antidepressant is suggested. Thus, all things considered, the suggestion of a sedating antidepressant is one of the last recommended options because other approaches have better efficacy and safety data available (Riemann et al., 2002; Wilson et al., 2010). One myth about antidepressant therapies is that they improve objective sleep, but patients are unaware of the improvements (Clark, Smith, & Jamieson, 2011). In other words, there are objective improvements but not subjective improvements. There are several problems with this idea. One problem is that it may be unrealistic to expect that clients will continue to adhere to a treatment regimen if they cannot perceive any improvements. Although sedating antidepressants can improve some polysomno - graphic sleep indices, the results are mixed both in terms of the specific medication and the specific indices of sleep fragmentation and sleep quality. There is also evidence that some antidepressants can worsen or create sleep problems. That said, of greater interest is that the use of objective indices as primary dependent variables in insomnia trials

ignores the essential fact that insomnia is a subjective, not an objective disorder. Diagnosis is based on a subjective patient complaint and there are no quantitative criteria for the disorder, so to emphasize objective indices in insomnia is not appropriate. The goal of therapy is to treat the insomnia complaint, and not a particular index on the PSG. Indeed, ordering PSGs in those with insomnia is not considered within practice parameters for the disorder (Littner et al., 2003). That is, overnight studies are not recommended for routine use in the assessment of insomnia unless there is a suspicion of another disorder such as apnea or periodic limb movements. Incidentally, there is evidence that some of these occult sleep disorders can in fact be caused or made worse by some antidepressants (Rottach et al., 2008). Objective measures of insomnia represent a different, but not a superior construct to prospective subjective ratings. Indeed, this is why sleep diaries are essential in the field of insomnia treatment (Buysse, AncoliIsrael, Edinger, Lichstein, & Morin, 2006). For more detail on why prospective self-report measures (i.e., the Consensus Sleep Diary) are preferred over objective indices, see Chapter 4. These issues above notwithstanding, below we will briefly review the antidepressant and sleep literature. There are several pharmacologic agents with established efficacy for depression, including monoamine oxidase inhibitors (MAOIs), tricyclics, selective serotonin reuptake inhibitors (SSRIs), Selective Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs), and atypical antidepressant medications. MAOIs are infrequently used because they are difficult medications to utilize given that the patient has to follow particular strict dietary restrictions lest they risk significant and potentially dangerous side effects. Given the uncommon use of MAOIs, we will focus on the other four classes. Non-psychological Treatments 15 Cognitive Behavioral Insomnia Therapy (CBT-I) possible? Weigh clinical factors. All things considered, sequencing is: Short-intermediate acting benzodiazepine receptor agonist or ramelteon Switch to other short-intermediate acting benzodiazepine receptor agonist or ramelteon Sedating antidepressant (e.g., TCA, doxepin) Atypical antipsychotic or anti-epilepsy (e.g., gabapentin, olanzepine) Cognitive Behavior Therapy for Insomnia (CBT-I) •symptom pattern •treatment goals •past treatment responses •patient preference •cost •availability of other treatments •comorbid conditions •contraindications •medication interactions •side effects nonresponse nonresponse nonresponse No. Yes. Figure 2.1 American Academy of Sleep Medicine pharmacotherapy treatment algorithm

Tricyclic antidepressants: Although there is good evidence for the use of tricyclic medications in the treatment of depression (Arroll et al., 2005), there are concerns with safety, so the use of these medications requires a cost-benefit analysis. Although tricyclic medications are primarily used to treat depression, they are sometimes used “off-label” for sleep. Off-label is the term applied when a medication is used for a problem for which there is no specific indication. There is one randomized controlled trial (RCT) for tricyclics (i.e., trimipramine) and insomnia (Riemann et al., 2002). In the Riemann and colleagues’ trial (2002) there was evidence for increased sleep efficiency only, as well as some indices of improvement in subjective appraisal of sleep. Whereas some believe that antidepressant effects may be mediated by REM suppression, trimipramine is one of the few drugs not known to suppress REMs. Based on the one RCT, the British Association for Psychopharmacology Consensus Guidelines on Insomnia concluded that evidence for tricyclics for insomnia was “limited” and that there may be safety issues and carry-over effects of concern for daytime driving and safety (Wilson et al., 2010). An additional reason tricyclics are seldom used is the lethality potential in an overdose. Both insomnia and depression are independent predictors of suicide (see Woznica et al., 2014) so overdose must be a heavily weighted clinical factor. Selective Serotonin Reuptake Inhibitors (SSRIs): SSRIs are efficacious, commonly prescribed antidepressant medications that inhibit the reuptake of the neurotransmitter serotonin. Commonly prescribed SSRIs for depression are: fluoxetine, citalopram, escitalopram, and sertraline. SSRIs are widely used because of their favorable side effect profiles relative to older medication classes. The effects of SSRIs on sleep are variable. About one third of those treated with SSRIs experience polysomnographic (PSG) verified worsening of sleep, including decreased slow wave sleep and reduced efficiency of sleep (Armitage, 2000). Disruptions in sleep have been reported as long as 30 weeks after SSRI discontinuation (Armitage, Yonkers, Cole, & Rush, 1997; Keck, Hudson, Dorsey, & Campbell, 1991; Minot, Luthringer, & Macher, 1993; Trivedi et al., 1999). Subjective assessment of insomnia using sleep items on depression inventories have revealed modest improvement for some (Asnis et al., 1999; Fava et al., 2006) and worsening in others (Zajecka et al., 1999). Although SSRIs are effective for depression, they are generally not helpful for insomnia, as insomnia is a residual problem after depressive recovery with SSRIs (Carney et al., 2007a; Nierenberg et al., 1999). Thus, because insomnia is sometimes caused by and often unresolved after SSRI treatment, the use of SSRIs alone cannot be considered a sufficient strategy for those with comorbid insomnia and depression. Instead, the independent targeting of both de pressed mood and insomnia is a more efficient, comprehensive alternative. A few trials have examined pairing SSRIs with another medication for enhancing overall treatment response. For example, combining a SSRI with trazodone improves insomnia to a greater degree relative to using an SSRI alone, although there is no advantage with respect to depression outcomes (Kaynak, Kaynak, Gözükırmızı, & Guilleminault, 2004; Nierenberg, Adler, Peselow, Zornberg, & Rosenthal, 1994). Despite improvement in insomnia, given the lack of additional antidepressant benefit and the presence of several safety issues (for more see atypical antidepressants below), there are reasons to pause in considering trazodone as an adjunct medication. An alternative is to com bine SSRIs with a U.S. FDA approved sleep medication. There are two studies com - bin ing SSRIs with approved hypnotic medications with promising results for both 16 Non-psychological Treatments

depression and sleep (Asnis et al., 1999; Fava et al., 2006). Of note, combining fluoxetine and eszopiclone improved sleep to a greater degree than fluoxetine alone, but more importantly, the combined group had greater depression outcomes (Fava et al., 2006). Likewise depression and sleep were improved in the Asnis et al. (1999) study, although there was a worsening of sleep after discontinuation of the hypnotic. In both trials, there were short treatment periods so it is unclear whether this approach is effective in the long run. One additional note is that antidepressant medications can cause or worsen restless leg syndrome (RLS) or periodic limb movement disorder (PLMD) (Hoque & Chesson, 2010) as well as bruxism (Ellison & Stanziani, 1993). Selective Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs): SNRIs are efficacious antidepressant medications that inhibit the reuptake of both serotonin and norepinephrine. Like SSRIs, they are preferentially used because of their relatively safe profile. The three most common SNRIs are: duloxetine, venlafaxine, and desvenlafaxine. SNRIs are comparable to SSRIs with respect to depression efficacy. However, there is some evidence that SNRIs have less of an impact than SSRIs on self-reported sleep improvement in those with depression (Pigott et al., 2007). However, in Pigott et al. (2007) sleep was evaluated using only single item questions from depression question - naires, not insomnia-specific questionnaires, and the differences did not reach statistical significance; so it is unknown as to whether SNRIs yield poorer sleep outcomes than SSRIs. As with SSRIs, insomnia can be a side effect of SNRIs and there is no reason to think that residual insomnia wouldn’t be a significant problem as well. Nonetheless, SNRIs are relatively well tolerated, efficacious, and their impact may be increased by adding an effective hypnotic medication. As with SSRIs, SNRIs can cause or exacerbate RLS and periodic limb movements in sleep (PLMS) (Hoque & Chesson, 2010). Atypical antidepressants: Atypical antidepressants have different pharmacokinetics than the commonly used SSRI and SNRIs. Below we will discuss two atypical anti - depressants: trazodone and mirtazapine and their use in those with MDD-I. At low doses, trazodone will not have much of an antidepressant effect, but can have sedation as a side effect, and thus was tested as a sleep aide for antidepressant-induced insomnia. Indeed, pairing low dose trazodone with a SSRI improves sleep to a greater degree than SSRI only (e.g., Kaynak et al., 2004; Nierenberg et al., 1994; Nierenberg & Keck, 1989; Zornberg & Rosenthal, 1994). Presumably because of its effectiveness as a treatment for the sleep-iatrogenic effects of antidepressant medications, trazodone has been used off-label use as a hypnotic despite the paucity of effectiveness and safety data in insomnia (e.g., Walsh & Uestuen, 1999). Mendelsohn (2005) reviewed the literature and concluded that the risk benefit ratio for selecting trazodone was uncertain. This was because the evidence is limited (e.g., studies available are small and with poor method - ology) and there are safety issues (e.g., sedation, psychomotor changes, and cardiac issues). These sentiments have been echoed by the leaders in sleep psychiatry in many other reviews and in guidelines, sedating antidepressants are low on the options list (Schutte-Rodin et al., 2008). Although there have been no new compelling trazodone studies, this drug frequently continues to be used off-label in those without depression. The British Association for Psychopharmacology Consensus Guidelines on Insomnia concluded that evidence for trazodone was “limited” and there is cause for concern about carry-over effects and safety (Wilson et al., 2010). Non-psychological Treatments 17

18 Non-psychological Treatments Mirtazapine has good efficacy in treating depression and one of its side effects is sedation. There are no studies of mirtazapine in insomnia without depression; therefore the somewhat common practice to treat only insomnia is considered off-label. There are however a number of studies evaluating sleep improvements in depression (Aslan, Isik, & Cosar, 2002; Winokur et al., 2000, 2003). Although total sleep time and sleep efficiency appear to be improved with this medication, these studies are limited by measurement issues (e.g., using only sleep items from depression measures or sleep measures with dubious psychometrics in comorbid groups) (Aslan et al., 2002; Hartmann, Carney, Lachowski, & Edinger, 2015; Winokur et al., 2000, 2003). Of greater concern is that the sedation can be severe enough to be associated with functional and psychomotor impairments, as well as impaired driving (Radhakishun, van den Bos, van der Heijden, Roes, & O’Hanlon, 2000; Wingen, Bothmer, Langer, & Ramaekers, 2005). Another concern with mirtazapine is that, as with many antipsychotic medications, there is risk for significant weight gain, increase in body fat mass, and leptin concentration (Laimer et al., 2006). Weight gain of this sort might be of particular concern in those prone to or with comorbid sleep apnea. Finally as with SSRIs and SNRIs, mirtazapine can cause or exacerbate RLS and PLMS (Hoque & Chesson, 2010). Many antidepressants may also produce daytime sedation and this common side effect has been linked to study participant withdrawals from sedating antidepressant trials (e.g., Metz & Shader, 1990). An additional unfortunate consequence of this side effect is that the increase in daytime sedation may interact with the sleepiness generated by the sleep restriction recommendations in CBT-I, and thus, may create the potential for a dangerous situation. In other words, delivering CBT-I to patients on sedating antidepressants warrants extra caution because of concerns of falling asleep during dangerous situations, such as driving. There may be other reasons (i.e., other than safety) to be concerned with using medication solely because it produces sedation as a side effect. The most common complaint in insomnia is daytime fatigue, and feeling fatigued can trigger rumination in those with insomnia (Carney et al., 2006, 2010b; Carney, Moss, Lachowski, & Atwood, 2013c). Figure 2.2 shows how medication with a side effect of daytime sluggishness can trigger preservative thinking about their sleep problem (i.e., symptom focused rumination). Symptom-focused rumination in insomnia, as well as MDD-I, is characterized by thinking about how badly it feels to be exhausted as well as thinking about the cause of the symptoms. In both insomnia and MDD-I, patients tend to presume that the sole cause of feeling tired or sluggish is the insomnia (Harris & Carney, 2009), so sleep worry, effort, and preoccupation become increased. Indeed, thinking repeatedly about sleep is the best predictor of sleep onset latency problems (Wicklow & Espie, 2000). Thinking repeatedly about exhaustion during the day further increases the tendency towards selective monitoring for feelings of sluggishness, and narrows attention on confirmatory examples that functioning is impaired (Harvey, 2002). Thus, daytime sedation from medication can inadvertently perpetuate insomnia in some, even when sleep itself may look objectively better with CBT-I. In other words, when delivering CBT-I, if daytime sedation remains (i.e., because of the sedating antidepressant), the patient may not appreciate improvements in sleep, even when sleep is verified with objective or self-reported indices such as the sleep diary. It can be difficult for patients to appreciate an improvement in their sleep because the number one complaint in insomnia is often daytime fatigue; thus, daytime sedation can be distressing

to insomnia sufferers (Harris & Carney, 2009). Thus, there are many reasons sedating antidepressants are one of the last options in the sequence in the list of treatment options presented in insomnia treatment algorithms (see Figure 2.1). St. John’s Wort: St. John’s Wort is not an approved, regulated medication for MDD, but is taken by many patients. The active ingredient in St. John’s Wort is hypericum perforatum. Large, controlled studies in those with moderate to severe MDD do not support hypericum as more effective than placebo (Hypericum Depression Trial Study Group, 2002; Montgomery, Hübner, & Grigoleit, 2000; Shelton et al., 2001). However some studies with mild depression report that hypericum produces comparable effects to standard antidepressant medications, but with a more favorable side effect profile (Linde, Berner, Egger, & Mulrow, 2005). In addition to questionable efficacy in clinically significant depressions, an additional concern with St John’s Wort, is that it may increase photosensitivity (Brockmöller et al., 1997; Lane-Brown, 2000). Photosensitivity may be of concern for sleep in St. John’s Wort users because it could delay melatonin release as well as sleep onset. Other Non-Psychological Treatments for Depression Electroconvulsive Therapy (ECT): ECT is an effective treatment for depression in which electricity is transmitted through electrodes on the scalp to the brain to induce cortical seizure activity. Effect sizes for ECT are large (The UK ECT Review Group, 2003). Although it is more effective than pharmacotherapy, it is less frequently used because Non-psychological Treatments 19 Sluggishness Thoughts about mental cloudiness Rumination about cause of sluggishness Presume cause is insomnia Increased anxiety about insomnia Medication Figure 2.2 Putative relationship between sedating medications and rumination

of the side effects (mainly memory impairments) and because of low patient preference. There are no studies specifically investigating the effects of ECT on sleep, but there appear to be no specific effects, disruptive or restorative, on sleep per se. Some studies on ECT have reported outcome data for various indices of sleep. One study reported that ECT increased core body temperature and increased circadian amplitude, which was taken to mean that circadian rhythm functioning improved (Szuba, Guze, & Baxter, 1997); however this finding has not been replicated. Additionally, in rats ECT did not exert an effect on the circadian pacemaker (Anglès-Pujolràs et al., 2009). There are no studies that have looked at the combination of ECT with hypnotics or CBT-I, or whether this has any advantage over CBT-I alone or combination therapy with medication for MDD-I. Transcranial Magnetic Stimulation (TMS): TMS involves placing a coil on the scalp so that magnetic pulses (similar to those produced in MRI) can change the magnetic field in the prefrontal cortex of the brain and stimulate activity. Meta-analyses suggest this is an effective treatment and that effect sizes are comparable to that of antidepressant medication (e.g., Berlim, Van den Eynde, & Daskalakis, 2013). There appear to be very few side effects; the most common is scalp discomfort, but there are rare reports of seizure or mania. There are no differences in sleep between TMS-treated and sham-treated patients so there does not appear to be a TMS-mediated sleep change (improvement or worsening) (Rosenquist, Krystal, Heart, Demitrack, & McCall, 2013). Vagus Nerve Stimulation (VNS): VNS is a treatment for depression in which a subcutaneous stimulation device is implanted in the chest, and the generator produces intermittent pulses into the vagal nerve. The stimulation of the vagal nerve has mood improving properties. Although it has Federal Drug Administration (FDA) approval for chronic, recurrent depressions (George et al., 2005), it is a costly procedure, with all the risks associated with surgery. Any study evaluating insomnia after VNS has been limited by assessing an insomnia symptom with a single item on an invalidated sleep tool (i.e., an adverse event inventory). One exception is a study of sleep architecture after VNS (Armitage, Husain, Hoffmann, & Rush, 2003). One paper cited this study as showing that VNS improves sleep architecture (Eitan & Lerer, 2006) however, it is important to note that the report of decreased N1 and time awake was not statistically significant and there was an increase in light transition stage of sleep (e.g., N2) (Armitage et al., 2003). One important negative consequence of VNS is a worsening of OSA (Ebben, Sethi, Conte, Pollak, & Labar, 2008); thus, an evaluation of OSA and con - current treatment with positive airway pressure (PAP) devices is needed if considering this treatment. Pharmacological Treatments for Insomnia Hypnotics Sleep medications approved by Health Canada or the Federal Drug Administration (FDA) are considered an effective treatment option for insomnia. A list of approved medications is contained in Table 2.1 that follows later. Generally, approved medications fall under benzodiazepine or non-benzodiazepine categories. Benzodiazepines are a class of medications that facilitate gamma aminobutyric acid (GABA). GABA is thought to 20 Non-psychological Treatments

have a calming effect on the brain and therefore may be important in the onset of sleep. Benzodiazepines work as benzodiazepine receptor agonists that target GABA alpha receptors. Examples include the first five in Table 2.1 (e.g., estazolam, flurazepam, temazepam, triazolam and quazepam). There are also non-benzodiazepine medications that do not have a benzodiazepine structure but operate in similar fashion to benzo - diazepines, in that they are GABA agonists that target very specific alpha receptors. Examples include zolpidem or eszoplicone (Z-drugs). Note in Table 2.1 that the binding for traditional benzodiazepines (the first five) is for GABA receptors generally, but this represents nonspecific binding to a receptor. In contrast, the Z-drugs (the next four on the list) bind to very specific GABA receptors in the brain. For example, zolpidem binds to GABA A alpha 1 receptors only. Z-drugs 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 in that the side effects are less severe for Z-drugs (Buscemi et al., 2007) but there are a variety of potential negative side effects with these medications that limit their attractiveness as an optimal solution for all people with insomnia. These include carry-over daytime sedation, tolerance, rebound insomnia upon discontinuation, or in rare cases, the emergence of parasomnia like behaviors during the night while asleep including sleepwalking, or sleep sex. Further, epidemio - logical studies show that road accidents are increased in people taking benzodiazepines or zopiclone (Barbone et al., 1998; Neutel, 1995). In contrast, it is important to note that there is no increased risk for auto accidents in those with unmedicated insomnia. There are also issues with a sensation of daytime sedation and cognitive issues, e.g., difficulty in concentrating, remembering, etc. As a result, there are now regulations requiring warnings on these medications about driving and the lowest recommended doses were reduced, especially for woman (United States Food and Drug Admin istra - tion, 2013, 2014). Additionally, the FDA (e.g., United States Food and Drug Admin - istration, 2007) issued a ruling mandating manu facturers to place warnings about parasomnias and to notify patients about the changes. Remelteon Perhaps because patients became wary of sleeping pills, there has been increased research and development in the pharmaceutical industry to produce medications different from the benzodiazepine agonists on the market. One new drug that emerged was a melatonin agonist called ramelteon. To gain approval for the labeling as a sleep aid, remelteon had to demonstrate efficacy. There is published evidence for this drug for sleep onset insomnia, but not maintenance insomnia. The side effects include sedation (when taken during the day), and slowing in performance (Mets et al., 2011). There is also a mild increase in prolactin for women taking it for six months (Richardson & Wang-Weigand, 2009). Doxepin Doxepin is a prescription medication that is a histamine (H1) receptor antagonist, or antihistamine. There is some evidence of improvement in maintenance insomnia although this drug doesn’t appear to be consistently effective by patients’ appraisal (Hajak Non-psychological Treatments 21

et al., 2001) and there is evidence of rebound insomnia. Side effects of doxepin include: sedation, nausea, upper respiratory tract infection, weight gain, constipation, urinary retention, dry mouth, and blurred vision. Doxepin is highly toxic in an overdose attempt (e.g., (Hawton et al., 2010)) and both MDD (Bertolote, Fleischmann, De Leo, & Wasserman, 2004) and Insomnia Disorder confer risk independently for suicide (Woznica et al., 2014), so this can be a dangerous drug in these populations. Table 2.1 also lists the half-life of each of the medications. The half-life of a medication refers to the time it takes for the concentration of the drug in the body to be metabolized by half and therefore to lose half of its effectiveness (i.e., 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 during the day as the drug remains in the system. 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 would be less effective if the patient woke up in the middle of the night. In summary, it should be noted that the hypnotic medications specifically designed to target insomnia have established efficacy for its treatment (Schutte-Rodin et al., 2008), but they also confer some degree of risk with regard to side effects. Moreover, CBT-I has demonstrated effectiveness equal to that of hypnotics in the short run, but a greater durability of effectiveness over time, which is why it is considered the frontline recommended treatment for a chronic insomnia (National Institutes of Health, 2005). Off-label and Over the Counter Medications 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. The most common example of this is the allergy medication diphenhydramine. Diphenhydramine is an antihistamine and histamines are important in maintaining wakefulness. Thus, blocking histamines can produce a side effect of sleepiness or sedation, so it seems intuitive that some people use it for insomnia. However, such medications can also 22 Non-psychological Treatments Table 2.1 FDA-approved sleep medications Generic name Binding Lowest therapeutic Half-life (hours) dose (mg) Estazolam Nonspecific 1 10–24 Tiazolam Nonspecific 0.125 2–6 Temazepam Nonspecific 15 8–20 Flurazepam Nonspecific 15 48–120 Quazepam Nonspecific 7.5 39–73 Eszopliclone GABA Aα1,2,3 1 6 Zaleplon GABA Aα1 5 1 Zolpidem GABA Aα1 5 1.5–2.4 Zolpidem-ER GABA Aα1 6.25 1.6–4.5 Ramelteon MT1, MT2 8 0.8–2 Silenor H1 3 15–31 Source: Adapted from Walsh and Roth (2011); Krystal (2011)

produce a paradoxical side effect of anxiety and restlessness which would clearly worsen or even precipitate insomnia. Other side effects include dizziness, blurred vision, constipation, and urinary retention. Ultimately antihistamines are not recommended in the treatment of chronic insomnia due to the relative lack of efficacy and safety data (National Institutes of Health, 2005). Melatonin Melatonin is a hormone excreted in the evening after the sunlight goes down that sets the stage for sleep several 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. That said, there is no evidence to date of any melatonin problems in insomnia. There is a report that circulating levels of melatonin decrease with advancing age (e.g., Iguchi, Kato, & Ibayashi, 1982) but it is unclear if these results are clinically meaningful (i.e., the significance of “decreased” melatonin is unclear). Oral melatonin supplementation has been demonstrated to be effective in a Circadian Rhythm disorder called Delayed Phase Syndrome. In those with a delayed sleep phase, their entire rhythm is shifted many hours later than most (i.e., they become sleepier many hours later than is conventional and they rise many hours later than is conventional, for more see Chapter 3). For those with this disorder, melatonin release occurs much later and thus, sleep onset is delayed. To correct this problem, melatonin properly timed in the evening can help to shift or advance their cycle earlier. Despite not suffering from a circadian rhythm disorder, some people with insomnia take melatonin before bed as a sleep aide. There are several problems with this practice. First, melatonin takes up to 2 hours to become effective. Second, when taken immediately before getting into bed, endogenous melatonin would have already been present in the brain for several hours 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 additive benefit of introducing exogenous melatonin (i.e., a pill) (Wyatt, Dijk, Cecco, Ronda, & Czeisler, 2006). In contrast, consuming oral melatonin in the early evening, results in sleepiness several hours later (because there was no melatonin present in the brain when the pill was taken) (Wyatt et al., 2006). Thus, it can be said that melatonin is a decent chronobiotic, but not a very good hypnotic. In other words, it can be useful in shifting circadian phase but not so useful in putting people to sleep. In the few supporting studies for melatonin, the effects are so small that it is questionable that the benefits are of any real clinical utility. For example, one meta-analysis examined positive studies and reported a mean increase of sleep efficiency of 2 percent, 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 (Brzezinski et al., 2005). Although there may be some statistical significance for some of these findings, these may not be particularly meaningful to the patient. Moreover there are studies reporting negative findings for melatonin (i.e., that sleep worsens). In Buscemi and colleagues’ (2006) meta-analysis, melatonin’s hypnotic effects were negative when given before bed (Buscemi et al., 2007). Therefore although the public at large may be increasingly using melatonin to help with insomnia, there is no real supporting evidence for its efficacy as a hypnotic. Non-psychological Treatments 23

Valerian Root Valerian root purportedly improves anxiety and promotes sedation. It appears to work by facilitating adenosine and amino acids such as GABA. Valerian root has shown some positive effects for sleep in healthy sleepers but not in those with insomnia. NIH’s Complementary Medicine branch has concluded that there is not enough evidence from well-designed studies to confirm efficacy and there is a lack of information about the long-term safety of valerian (National Center for Complementary and Integrative Health, 2012). Valerian can cause mild side effects, such as tiredness the morning after its use, headaches, dizziness, and gastrointestinal symptoms. Additionally there is wide variability in how valerian, and other non-regulated substances are prepared, and the variability in the extraction process and form. This is an important consid eration because whether it is dry or aqueous and whether alcohol is used in the process affects the active ingredients. Moreover, some types of valerian involve valepotriates which have been linked to cytotoxicity (cell death) and carcinogenic (i.e., cancer) poten - tial (Houghton, 1999). The bottom line is that because such preparations are not regulated, patients may not know what they are ingesting. 5-Hydroxytryptophan (5-HTP) 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 might consider boosting serotonin to help sleep. There is a paucity of rigorous studies testing 5-HTP thus, there is no scientific evidence for the use of 5-HTP in insomnia (Meolie et al., 2005). Cognitive Behavior Therapy for Insomnia (CBT-I) 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 (Smith et al., 2002). 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 (Edinger et al., 1996; Edinger, Hoelscher, Marsh, Lipper, & IonescuPioggia, 1992; Edinger & Sampson, 2003; Edinger, Wohlgemuth, Radtke, Marsh, & Quillian, 2001; Espie, Inglis, Tessier, & Harvey, 2001; Morin, Colecchi, Stone, Sood, & Brink, 1999a). CBT-I is also rated as more “acceptable” to patients than hypnotic medications (Morin, Gaulier, Barry, & Kowatch, 1992; Vincent & Lionberg, 2001). There is also greater satisfaction with CBT-I than hypnotic medications (Morin et al., 1999a). 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 (National Institutes of Health, 2005). For more on medication issues (i.e., whether hypnotic discontinuation is necessary for CBT-I), see Chapter 3. 24 Non-psychological Treatments

Summary • There are several efficacious pharmacological or other medical treatments for depression, and these treatments can have positive, negative, variable or no effects on sleep. • All antidepressant medications can have insomnia as a potential side effect. • Some antidepressants, antihistaminic agents, antipsychotics, and vagal nerve stimulation can cause or worsen other sleep problems such as periodic limb move - ments, restless leg syndrome, or bruxism. • St. John’s Wort may increase photosensitivity which can create a delay in the circadian phase and cause or worsen sleep onset problems. • CBT-I has comparable efficacy to sleep medications with several advantages over sleep medications for chronic insomnia. • The American Academy of Sleep Medicine recommends 1) CBT-I for chronic insomnia, however, if it is unavailable, 2) consider a short-intermediate benzo - diazepine receptor agonist or remelteon, 3) when this agent is ineffective, switch to another intermediate benzodiazepine receptor agonist or remelteon, and if these are ineffective, consider 4) an agent with sedating side effects (e.g., a sedating antidepressant). • Sedating agents warrant caution in combination with the Sleep Restriction portion of CBT-I as there are pre-existing safety concerns with these medications. Sedating agents may have a negative effect on the ability of the patient to appreciate treat - ment improvements, and they could potentially increase rumination. Non-psychological Treatments 25

3 Cognitive Behavior Therapy for Insomnia (CBT-I) Treatment Considerations Cognitive Behavior Therapy for Insomnia is an empirically based treatment focused on addressing research-identified maintaining factors for insomnia. It is a multicomponent treatment made up of techniques that have been empirically validated. One advantage of the CBT model is that it is applicable across a wide array of diagnostic categories. This is because the model is based on the concept, that despite the variety of precipitating events that might have initially caused the insomnia, the factors that tend to maintain the chronicity of the disorder are similar from case to case and are responsive to behavioral and cognitive change strategies. The idea is that in any case, if the maladaptive perpetuating factors are present, then alterations of these factors will lead to reductions in symptoms. Therefore, the debate about biological versus psycho - logical etiologies determining treatment modality is somewhat of a moot point since we know that there are many pathways to disorder and recovery. Even for biological sleep regulatory systems such as the circadian and homeostatic systems, we know that behavioral and environmental input can have profound corrective or disruptive influence. The evidence for CBT-I is strong and the effect sizes are similarly large when compared with pharmacotherapy. CBT-I is the frontline recommended treatment in those with chronic insomnia (Howell et al., 2012; National Institutes of Health, 2005; Wilson et al., 2010) because of the impressive short-term effects and because it is so brief, durable, without polypharmacy risks, patient-preferred (Morin et al., 1992; Vincent & Lionberg, 2001), and an excellent economical choice. Despite criticisms that it is not widely available, there have been excellent gains made in the past few years with respect to training (e.g., Manber et al., 2012), owing in part to an increase in workshop and training opportunities, and a CBT-I training program in the Veteran’s Affairs Administration. Moreover, there are online and telehealth treatment programs with support (Espie et al., 2012; Ritterband et al., 2009; Vincent & Walsh, 2013). Lastly, we have a large number of effectiveness trials demonstrating that non-sleep specialists can effectively deliver this treatment (Buysse et al., 2011; Espie et al., 2007; Jungquist et al., 2010). There has been discussion of utilizing stepped care modes of delivery for CBT-I in which large numbers of patients could be introduced into early steps such as self-help strategies and online programs, and, as needed, funnel through to steps that might include groups run by paraprofessionals, and eventually treatment by a therapist certified in behavioral sleep medicine for the more complex cases (Espie, 2009). Despite the success of CBT-I there are those who do not respond to this treatment. There is a paucity of moderator research investigating the variables that might be

influencing suboptimal response—a necessary step in refining the treatment. Addition - ally, there are currently a number of contraindications for CBT-I. For instance, sleep disorders characterized by excessive sleepiness are a contraindication for CBT-I because in the early stages of treatment the therapy tends to create sleepiness, which potentially makes sleepy clients vulnerable to accidents (e.g., falls, motor vehicle, or occupational accidents). Thus, untreated or suboptimally treated sleep-disordered breathing, narco - lepsy, or periodic limb movement disorder with accompanying excessive daytime sleepiness presents a challenge for CBT-I. Therapists should proceed with extreme caution to plan for daytime sleepiness (i.e. disallow driving until stable) or rule out the treatment entirely. In those with sleep apnea, it is important to determine the level of adherence with their PAP device. Ideally, one would want clients to use their device no greater than 75 percent of nights for a minimum of 4 hours per night at the prescribed pressure in order to consider the apnea as treated. Such devices typically have a feature that allows them to print out their usage, so adherence is easily verified. Another contraindication relates to when there are more important factors worthy of treatment. For example, when a client is in medical or psychiatric crisis, it is not appropriate to begin a highly demanding sleep-focused therapy. Attending to and resolving the crisis is necessary before proceeding with this treatment. For example, in clients who present as actively suicidal, it would be essential to first assure the client’s safety and wait for stability in mood before carrying out CBT-I. In addition to crisis, stability of treatment for the co-occurring psychiatric or medical condition is recom - mended. If the client has poorly controlled diabetes or thyroid issues, it is recommended to wait until the client is on a stable dose or treatment plan before proceeding with CBT-I. The same could be said for clients with poorly controlled depression. It may be sensible to hold off on CBT-I until a depression medication regimen is established that will allow for more stable mood and a better assessment of the client’s sleep and daytime symptoms on the medication. Similarly, active substance abuse or withdrawal are contraindications for CBT-I. Active substances greatly impact sleep, as does withdrawal. Once stability is established, CBT-I can be initiated, although this is one area where the effect sizes for CBT-I may be diminished in those with extensive abuse histories. Finally, conditions sensitive to sleep deprivation may be a contraindication or an indication to scale back on any part of the treatment associated with sleep deprivation (e.g., sleep restriction). Panic attacks, seizures, mania, and parasomnias can all become exacerbated with increased sleep deprivation so a cost-benefit analysis is necessary to determine if CBT-I is advisable or if the focus of treatment should be on stimulus control and counter arousal rather than sleep restriction therapy. That said, it should be noted that even in the good practice of stimulus control, there may be some sleep deprivation early in treatment as the client remains out of bed for longer periods of time, waiting to become sleepy and not compensating for any lost sleep by sleeping in, napping, or going to bed early. The bottom line is that whenever practicing CBT-I, especially with the disorders discussed above, it is always recommended to monitor for client sleepiness, take necessary precautions, and make adjustments to therapy as needed. In Chapter 2 we reviewed some of the costs and benefits to pharmacotherapy for insomnia. Given these considerations, CBT-I appears to be a particularly viable treat - ment for MDD-I since there is no risk of polypharmacy, it is as effective as hypnotic medication, and it produces superior, durable long-term improvements (Edinger et al., Cognitive Behavior Therapy for Insomnia 27

1992, 1996; Edinger & Sampson, 2003; Edinger, Wohlgemuth, Radtke, & Marsh, 2004b; Morin et al., 1999; Morin, Kowatch, Barry, & Walton, 1993; Morin, Kowatch, & Wade, 1989; Morin, Stone, McDonald, & Jones 1994b; Perlis et al., 2000). Although there are some variations, at the core of CBT-I treatment are Stimulus Control (Bootzin, 1972) and Sleep Restriction Therapy (Spielman, Saskin, & Thorpy, 1987b), which are empirically validated approaches designed to eliminate conditioned bedtime arousal, increase sleep drive and correct circadian abnormalities. CBT-I also targets the belief that one must engage in compensatory sleep behaviors (i.e., behaviors linked to chron - ically poor sleep; Edinger et al., 1992, 1996, 2001, 2004b; Edinger & Sampson, 2003). Thus far, research has suggested that CBT-I is highly safe and effective with various insomnia patients including those with Primary Insomnia (Edinger et al., 1992, 1996, 2001, 2004b; Edinger & Sampson, 2003; Morin et al., 1994b, 1999a), MDD (Edinger et al., 2009a; Kuo, Manber, & Loewy, 2001; Manber et al., 2008; Morawetz, 2001; Vallieres, Bastien, Ouellet, & Morin, 2000), Periodic Limb Movement Disorder (Edinger et al., 1996), mixed psychiatric or medical disorders (Edinger et al., 2009a; Morin et al., 1994b), cancer (Berger et al., 2002, 2009; Fiorentino et al., 2009; Quesnel, Savard, Simard, Ivers, & Morin 2003; Ritterband et al., 2012; Savard, Simard, Ivers, & Morin, 2005; Spiegelhalder, Espie, Nissen, & Riemann, 2008), and pain-related syndromes (Currie, Wilson, Pontefract, & deLaplante, 2000; Edinger, Wohlgemuth, Krystal, & Rice, 2005; Jungquist et al., 2010; Rybarczyk, Lopez, Benson, Alsten, & Stepanski, 2002; Vitiello et al., 2013). CBT-I also appears to affect the neurophysiology implicated in insomnia, as it results in decreased high frequency activity and increased slow wave activity in the EEG (Cervena et al., 2004). Moreover, contrary to the above-noted findings with hypnotic treatment, the gains achieved during CBT-I appear to endure long after the end of active therapy. CBT-I in Those with Depression Those with MDD-I manifest the type of treatment targets for which CBT-I has been specifically designed (Kohn & Espie, 2005). For example, those with MDD-I have comparable levels of unhelpful beliefs about sleep, schedule variability, increased timein-bed, pre-sleep hyperarousal, and sleep effort behaviors to those with insomnia only (Carney et al., 2007a, 2010; Kohn & Espie, 2005). Thus, those with MDD-I would appear to be excellent candidates for CBT-I. Indeed, there are some promising early findings for use of CBT-I in MDD-I patients. Morawetz (2001) found that by treating sleep alone in MDD-I, the vast majority of patients (N = 86) treated with a self-help form of CBT-I reported marked depression improvement in addition to the sleep improvement (Morawetz, 2001). Morin and colleagues (2000) showed CBT-I resulted in an improvement for sleep, and an associated mood improvement among a series of cases with comorbid insomnia and MDD (Vallieres et al., 2000). Several studies have documented the efficacy of CBT-I in patients with complex, multiple comorbidities including MDD and PTSD (Edinger et al., 2009a). A randomized clinical trial combining SSRI medication with CBT-I showed that in comparison to a SSRI alone, there were greater insomnia symptom improvements, and greater depression symptom improve - ments (Carney, Edinger, Krystal, & Shapiro, 2014; Manber et al., 2008). In fact, the addition of CBT-I to an antidepressant medication resulted in greater rates of depression 28 Cognitive Behavior Therapy for Insomnia

remission than antidepressant medication alone (Manber et al., 2008). Thus, there is growing support for superior depression symptom outcomes by combining depression treatments with sleep treatments, both pharmacologic and cognitive or behavioral, over depression-only focused treatments. Brief Delivery for Medical Settings CBT-I is already a brief treatment but it has been adapted to very brief versions for delivery in settings with limited patient contact, such as primary care settings. Because there is evidence for SC and SRT as monotherapies, CBT-I is easily delivered in a session or two. One study used abbreviated behavioral and cognitive therapy (ABCT), which was delivered in two 25-minute sessions two weeks apart with take-home reading materials (Edinger & Sampson, 2003). ABCT was tested using a novice therapist supervised by a behavioral sleep medicine expert. The content of the first therapy session focused on SC, SRT, SH, and psychoeducation. The content closely mirrors the material presented in Chapter 5 including the patient handouts. The psychoeducation is delivered briefly with a more in-depth explanation provided in written materials assigned as homework. The second session is devoted to troubleshooting and making adjustments to the schedule. Another version, brief behavioral insomnia therapy (BBIT) (Buysse et al., 2011) consists of one treatment session and a 30 minute booster two weeks later administered by a nurse practitioner. This treatment has been tested with older adults (Buysse et al., 2011; Germain, Shear, Hall, & Buysse, 2007). The content for this one session treatment was selected rules from SC and SRT: (1) match time in bed to the current average number of hours of sleep (minimum sleep opportunity was set at 6 hours); (2) get up at the same time every day of the week; (3) do not go to bed unless sleepy; and (4) get out of bed when unable to sleep. The second booster session was allocated to troubleshooting and making adjustments, if needed, to the schedule. The results of this study indicated that BBIT fared better than Information Control on both Sleep Diary and actigraph indices of SOL, WASO and SE. Additionally, BBIT-treated participants continued to improve after treatment; at the 6 month follow-up, they were sleeping about 45 minutes more than they were at post-treatment (Buysse et al., 2011). BBIT has also been used to successfully treat treatment-refractory insomnia after depression treatment (Watanabe et al., 2011). A variety of CBT-I effectiveness studies have shown that common disciplines in medical settings including nurses, primary care counselors, physicians assistants, social work, nurse practitioners, can effectively deliver CBT-I to patients (Espie, 2009; Espie et al., 2001, 2007). Given that both insomnia and depression, and certainly MDD-I commonly report to primary care first, implementing CBT-I into these settings is an important frontline priority. Medication Issues: Is Discontinuation Necessary? Clinicians are often faced with the apparent dilemma of what to do about medications taken for sleep during treatment. Only treatment providers with prescription privileges should provide advice related to medication. Some medications taken for sleep, depending on dose, frequency of use, and duration of use, require a supervised taper and Cognitive Behavior Therapy for Insomnia 29

stopping them abruptly could result in serious consequences. Not all clients who want to sleep better necessarily want to stop taking their sleeping medications. It is important to have an open conversation about the client’s treatment goals as this may or may not include the need for cessation of sleep medication. CBT-I has been found to work with or without sleep medications. In some trials, there are no differences between those with CBT-I alone versus CBT-I plus sleep medications (Jacobs, Pace-Schott, Stickgold, & Otto, 2004); so sleep medications may not hamper the response except in those who are hypnotic dependent. The best long-term benefits appear to be related to withdrawing the sleep medication after the acute treatment phase of CBT-I, and before treatment has ended. During the medication withdrawal period, clients should continue with extra CBT-I sessions to manage the sleep disruptive process of withdrawal (Morin et al., 2009). It is not uncommon in CBT-I treatment that clients often simply stop taking their medications during treatment once they see that they can improve their sleep on their own. These clients should always be made aware that they should make no changes on their own before consulting with their physician. Others remain skeptical that CBT-I would work without their medication and remain on the medications. Ultimately the pros and cons of such a decision should be discussed between the therapist and client, and if there is a decision to discontinue medication, a collaboration should take place between the client, therapist, and the prescribing physician. There is some evidence that those who are hypnotic dependent have somewhat diminished CBT-I treatment outcomes relative to non-hypnotic dependent clients (Verbeek, Schreuder, & Declerck, 1999). This may be due to the decreased self-efficacy and increased unhelpful beliefs about sleep of those who are hypnotic dependent (Carney et al., 2010a). Thus, it is not imperative that clients select hypnotic discon - tinuation as a goal, however when a client decides to remain on medication, the following goals are meritorious of discussion with the client: 1) establish usage within the recommended dose range (ideally the lowest recommended therapeutic dose) and 2) eliminate using the medication as a rescue (i.e., take the medication at the same dose and time each night to eliminate contingent use). Most approved hypnotic medications have tolerance properties (diminishing effectiveness over time), which often prompts an escalation of dose. When increasing doses are used, it is often because the medication is not as effective as the client desires, and the belief is that a higher dose will have the same effect as the previously effective lower dose. This may be true at first, but when the higher dose also loses effectiveness, other medications or substances such as alcohol are often added, or another increase in dose occurs. In many cases, the client may not share these changes with the prescribing treatment provider. This is not only a very dangerous practice, but there is no increased efficacy, and further, it erodes the client’s self-efficacy and increases sleep anxiety. It is important to work with the client so that they understand both the physical dangers of such habits but also the role in perpetuating the insomnia. It is often important to encourage the client to discuss the issues openly with the treating physician. Many clients worry that the prescribing treatment provider will not renew prescriptions if they are made aware of the ways in which the client is using the medication and/or adding other substances. Collaborating with the treating treatment provider on a plan toward safer medication use or a medication discontinuation can help the client to feel more confident about how best to reach their goals. In other words, it is important for the client to understand that 30 Cognitive Behavior Therapy for Insomnia

unlike possible past failed attempts to deal with medication dosing they may have attempted on their own, this time they are not alone and that with your help they can learn strategies that will make success much more likely. There is good evidence for the use of CBT-I as part of the discontinuation process (Morin et al., 2004, 2009; Morin, Colecchi, Ling, & Sood, 1995). Below is a description, adapted from Morin’s (Baillargeon et al., 2003) discontinuation protocol, for hypnotic discontinuation. The first step is an assessment of treatment goals. Proceeding with action phase interventions (i.e., a taper) makes little sense if the client is in a stage of contemplating change rather than preparedness for change (Prochaska & Velicer, 1997). If discontinuation is a goal and the prescribing treatment provider (if applicable) has provided a safe taper schedule, CBT-I can begin. As stated, in those with or without a discontinuation goal, it is important for the client to set a goal of taking the same, safe amount of medication every night at the same time. Although it is a common practice to prescribe such medications “prn” or as needed, long-term prn use sets up medication use as contingent on a poor (previous night’s) sleep. We would expect the body to produce some compensatory sleep following very poor nights and if the medication is taken under these conditions, the medication is paired with recovery sleep; however, the improved sleep is attributed to the medication, rather than the body’s natural compensation for poor sleep. Additionally, in those taking sleep medications long-term, there are inevitable but unsuccessful attempts to stop the medication. The typical scenario is that the client decides not to take the medication on a given night and they experience withdrawal from the medication. The withdrawal symptoms include increased insomnia. Clients typically do not know that this is a side effect and they attribute the severe insomnia symptoms as evidence that the medication must have been working more than they thought, and they quickly resume taking the medication either later that night or the next night, and their confidence in their sleep system is further compromised. Moreover, if noncontingent sleep medication use is not established, the sleep improvements associated with CBT-I will be attributed to the medication. By making the dose and timing of medication stable every night, then any changes to the baseline sleep after that will be attributable to the behavioral changes associated with CBT-I, which will be the only variables that were allowed to change. Thus, clients starting CBT-I on sleep medication need not have a discontinuation goal, but ideally, their use is kept predictable and safe throughout treatment. Likewise if the client has just switched or begun an antidepressant medication, it is best to wait until the drug is at steady-state so that CBT-I related improvements are not attributed to the antidepressant medication. Those with chronic hypnotic use have greater levels of unhelpful beliefs about sleep than those who are not on medication or not dependent on medication (Carney et al., 2010a); so it may be important to spend more time modifying beliefs that may get in the way. For example, it is helpful for clients to explore the consequences of thinking that their body can no longer produce sleep without medication. If clients attribute improvements to the medication, the client is encouraged to look at the evidence (e.g., the medication was associated with poor sleep at pre-treatment and the medication remained unchanged throughout treatment, thus the only change was in sleep habits). These techniques are covered in Chapter 6. They are also part of the cognitive therapy component of CBT for depression so unhelpful thoughts about medication and selfefficacy can be explicitly targeted within the context of comorbid treatment. Cognitive Behavior Therapy for Insomnia 31

Once non-contingent sleep medication use is established, and there is only one steady medication used (e.g., rather than a benzodiazepine one night, melatonin a second night, and diphenhydramine on another night) at a stable dose, CBT-I can be initiated. As CBT-I is delivered with an emphasis on increasing sleep self-efficacy and observing how the body compensates for sleep loss naturally when sleep effort is removed, the clients who initially felt they would not attempt medication discontinuation, may now be more amenable to such a goal. At that point, it can be desirable for the treatment team to proceed with the discontinuation component. The first step is to provide psycho - education regarding rebound insomnia and psychological dependence. This was detailed above (i.e., that contingent use of sleep medications creates a situation in which the medication appears to be a rescue from a faulty sleep system). Instead, by providing education regarding normal sleep regulation, the therapist can focus on the idea that the body would be expected to compensate for poor sleep anyway (with or without the medication) and that stopping the medication creates a worsening of insomnia symptoms. It is important that clients understand that the worsening is a side effect of the medication withdrawal and not indicative of an underlying insomnia that the medication was successfully treating. This will be true even for clients that are dependent on nightly medication. They can be made aware that, as with any withdrawal symptoms, they are expected to fade with time, and if properly harnessed, the processes of sleep regulation can then help them back to more normal sleep if they stay the course. After psychoeducation, a taper schedule is constructed in consultation with the prescribing treatment provider. In this scenario it should be noted that the client has already been taught the techniques of CBT-I to help make sleep better while on a steady dose of hypnotic. In some cases, the client is sleeping well with the medication so there may be little sleep restriction in the initial CBT-I; in other cases, sleep remains poor even on medication. Even if sleep is poor on medication, it is important to remain cautious about safety in those taking sleep medications. The goal during a taper is to reduce the weekly dose of medication by 25 percent per week, or whatever the pre scribing physician sees as appropriate. The therapist explains the protocol and rationale for noncontingent use and gradual reduction and solicits feedback on the plan. The client and therapist review the relapse prevention plan for what to do after a poor night (i.e., after rebound insomnia) as well as a coping with fatigue plan. Sometimes clients feel confident early and want to go completely drug-free. Likewise, some physicians may feel that a quicker taper would be suitable for their patient. For many medications at low doses this can be an acceptable way to engage in the CBT-I + taper treatment. However, in cases wherein withdrawal can have dangerous conse quences (e.g., benzo - diazepine dependence, abnormally high doses), it is important to go slowly under medical supervision. Group Therapy CBT-I There is evidence that group therapy is an effective modality for CBT-I (Bastien, Morin, Ouellet, Blasi, & Bouchard, 2004; Verbeek, Konings, Aldenkamp, Declerck, & Klip, 2006). In some ways CBT-I is a perfect candidate for group therapy because psychoeducation, Stimulus Control rules, sleep hygiene rules, Cognitive Therapy as well as counter arousal strategies fit nicely with a group format. However, the sleep scheduling aspect of SRT 32 Cognitive Behavior Therapy for Insomnia

is very challenging in a group format. The idea of scheduling is very personal to clients and linked to their particular presentation. “Scheduling” can have different meaning to different clients; for some it equates to conformity, having a boring lifestyle, or it activates memories of hurt experiences with an autocratic parent. Some clients hear recommendations to change habits as an accusation that they “caused” their insomnia, or they are in some way to blame. Additionally, deriving a schedule must take into account current sleep time production, chronotype, individual life demands, and relationship dynamics, so managing these issues in a group of 6 or more people, can become challenging. One possible way to achieve this is to devote an entire group session to deriving a schedule in which the group members exchange sleep diaries with a partner in the group, and together they calculate the total sleep time, total time in bed and total wake time of their partner’s diary. Together, the group calculates the time-inbed prescription of their partner’s sleep diary and then they collaborate on a schedule in dyads. The group shares any possible difficulties encountered during the derivation of the schedule and together they engage in trouble-shooting. The facilitator uses questioning to help group members arrive at solutions for the other group members. There are very few resources available for learning group delivered CBT-I, so a template is provided below and contrasts it with an individual therapy schedule. For an example of a schedule and topics, see Table 3.1. Applications (apps) and Alternative Modes of Delivery Smart Phone Applications Smart phone applications that provide sleep estimates are very popular and widely available. Such apps are not used clinically because of their inferior reliability and in Cognitive Behavior Therapy for Insomnia 33 Table 3.1 Sample schedule and topics in individual versus group delivery Week Group Individual 1 Psychoeducation, SC and Sleep Hygiene Psychoeducation, SC, SRT, Sleep Hygiene 2 Troubleshoot adherence, SRT 3 Troubleshoot adherence, determine if Troubleshoot adherence, determine if changes necessary to schedule, add changes necessary to schedule, add counter arousal counter arousal and cognitive therapy 4 Troubleshoot adherence, determine if changes necessary to schedule, add cognitive therapy 5 Troubleshoot adherence, determine if Troubleshoot adherence, determine if changes necessary to schedule, continue changes necessary to schedule, continue with cognitive therapy, introduce with cognitive therapy, introduce termination issues, relapse prevention termination issues, relapse prevention homework homework 6 No meeting No meeting 7 Troubleshoot adherence, determine if Troubleshoot adherence, determine if changes necessary to schedule, cognitive changes necessary to schedule, cognitive therapy, termination issues and relapse therapy, termination issues and relapse prevention prevention

some cases dubious validity. For example, some apps purport to track and sense the “right” time to wake up clients. The websites associated with these apps give no detail as to how they work but the phone is placed on the bed and there is reference to the phone tracking movement so presumably, the application is collecting data with an accelerometer. There are no particular movements associated with optimal waking. The best time to wakeup may be arguably during REMs but the only way to determine the presence of REMs is to measure brain wave activity via electrodes on the scalp, not movement. Other apps provide an “objective” estimate of total sleep time via the accelerometer, similar to a clinical device called an actigraph. The method of placing the accelerometer on the bed has not been tested and is presumably less reliable than wearing an accelerometer (e.g., it can be subject to false input via pets, kids, and other bed partners). There are, of course, wearable accelerometers, and one such popular device was tested and compared with clinically validated actigraphs as well as poly somnography (Montgomery-Downs, Insana, & Bond, 2012). The popular device overestimated total sleep time by over an hour when compared with PSG and over 24 minutes compared to the actigraph. Both the actigraph and the device were particu - larly poor (i.e., showed greater error) in those with poor sleep; arguably the people most drawn to such devices. Some apps are treatment specific, such as CBT-I COACH. This app accompanies CBTI treatment and was developed from the CBT-I materials for the VA training rollout. Such apps typically provide sleep diaries, help with calculating sleep prescriptions, psychoeducation materials, and capability for reminder messages with tips, motivation, and alarms to change sleep habits. These are essentially the same as the materials provided with treatment but the delivery mode is different and there may be some advantages to using an app on a Smartphone. For example, it is more readily accessible and discreet to complete forms such as a thought record using a phone than carrying a paper form and completing it in public. Additionally, calculating sleep diary indices can be daunting for some clients, so these apps can make it far easier. Self-Help Books Self-help books (i.e., bibliotherapy) are a popular mode of delivery for people. Therapy is expensive and many people cannot take time off from work or family each week to attend sessions, while others, particularly in rural areas, may not have ready access to live therapists. Some also may feel uncomfortable talking to a professional about their problems. Bibliotherapy has the potential to increase access to empirically supported treatments in written format. The main drawback to this approach is that for the most part these products are not significantly vetted and so anyone can publish a self-help book and there is no guarantee about the strength of the material presented. In other words, all bibliotherapies are not equal and may not be empirically supported. However, there are books written by experts and voted on by other experts to recommend, e.g., the VA CBT-I training rollout selected a self-help book (Carney & Manber, 2009) available commercially for their training. In addition, there may be no opportunity to receive individual advice when there are issues not covered in the book and the client runs into problems. This has been shown to be important because in tests of bibliotherapy, there is evidence that it is effective (Mimeault, 1999), however the effect 34 Cognitive Behavior Therapy for Insomnia

was enhanced when telephone consultation was added. Other studies have similarly reported that bibliotherapy with telephone consultation was equally effective as individual, traditional psychotherapy (Bastien et al., 2004; Currie, Clark, Hodgins, & El-Guebaly, 2004). Thus, although there is support for bibliotherapy, the best support is when there is individual follow-up as well. For those with MDD-I there are few books available, with one exception (Carney & Manber, 2009), written with clients with complex comorbidities like depression, pain, or anxiety in mind. Internet Delivered CBT There is evidence for successful CBT-I treatment using sophisticated interactive software programs at home or delivered over the internet (Espie et al., 2012; Ritterband et al., 2009; Strom, Pettersson, & Andersson, 2004; Vincent & Lewycky, 2009). This may be a particularly helpful mode for those with poor access to CBT-I or those in remote areas. Such interactive programs may be an important way to increase access to CBT-I although there is some concern about high attrition (24–33 percent) (Strom et al., 2004; Vincent & Lewycky, 2009) so it is important to conduct moderator studies to understand who benefits most from this modality. Perhaps they may be best utilized as an initial step in a stepped-care model of delivery. As such, those that do not do well nor drop out might be encouraged to move on to the next step in care. To avoid “inoculation” against more intense levels of treatment, it may be important to alert clients to the concept of stepped care from the start so that there is understanding and buy in that if earlier steps do not succeed that other levels of treatment are available. In this way clients may be less likely to simply give up if the initial steps do not work. Resources The Anxiety and Depression Association of America is a resource for those with depression and/or anxiety. There is information and resources for finding therapists, self-help materials, and applications. Website: www.adaa.org/ The Mood Disorders Society of Canada is an organization devoted to support and advocacy for those with Mood Disorders, including MDD. Website: www.mooddis orderscanada.ca The Canadian Association for Cognitive and Behavioral Therapies (CACBT) has a list of Canadian practitioners who have been certified in Cognitive Behavior Therapy. Website: www.cacbt.ca The Association for Behavioral and Cognitive Therapy (ABCT) has a find-a-therapist listing as well as a listing of self-help resources, and information about disorders. Website: www.abct.org/home/ The National Sleep Foundation is a site devoted to providing information and advocacy about sleep. Website: www.sleepfoundation.org The American Academy of Sleep Medicine (website: www.aasm.net): There is an accred - itation process in the United States for medical sleep specialties. More information, Cognitive Behavior Therapy for Insomnia 35

including a list of providers and sleep centers accredited by the American Academy of Sleep Medicine can be found on at www.aasmnet.org/accreditation.aspx The Depression and Bipolar Support Alliance provides support for those with depres - sion. Website: www.dbsalliance.org Summary • CBT-I is a highly efficacious and effective treatment, shown to be effective in those with depression, and to enhance the treatment of depression. • Contraindications for CBT-I include: untreated or suboptimally treated sleepdisordered breathing, narcolepsy, or periodic limb movement disorder with accom - panying excessive daytime sleepiness, unstable condition, substance abuse. CBT-I should be used with caution in those sensitive to sleep deprivation such as those with bipolar disorder, panic disorder, epilepsy, and parasomnias. • CBT-I has been shown to be effective in very brief formats (one to two sessions) and as delivered by non-sleep and non-mental health treatment providers. • There is evidence for other modalities of delivery including group therapy, some internet delivery, telephone delivery and bibliotherapy. It would be useful to have moderator data on alternative modes so that we could determine for whom these modes work best. • It is unnecessary to discontinue sleep medications before starting CBT-I but it is important to establish non contingent use at a stable dose and time each night before proceeding with CBT-I. • Although there are many dubious sources of information on the internet, there are also reputable internet sites available to locate treatment providers certified in CBT-I, and to learn more about sleep or depression, and/or for clients to obtain support. 36 Cognitive Behavior Therapy for Insomnia

4 Assessment of Insomnia in Those with Depression Assessment should be regarded as an ongoing activity throughout CBT-I, rather than a single event at the beginning of treatment. It is essential to continuously assess for changes in sleep patterns, varying levels of sleepiness, and client adherence, and remain open to emerging evidence. Consider the following example: at the sleep assessment session, you meet a 41 year old female with average body habitus, no knowledge of whether she snores, no hypertension, and a normal, albeit elevated score on sleepiness scale. Such findings are not particularly suggestive of sleep apnea. If, however, over the course of treatment, there is high adherence to treatment, a very quick sleep onset latency, even when the time spent in bed has been lengthened, there are complaints of subjective sleepiness and a report of many very brief wake-ups in the second half of the night, one should reconsider whether there may be an occult sleep disorder, such as sleep apnea. The goals of the initial assessment session are to establish a diagnosis of insomnia and initial conceptualization of the case, rule out other sleep disorders or conditions contraindicated for CBT-I, assess for comorbidities, substances and medications, establish treatment goals, and obtain family, medical, sleep, and previous treatment histories. That said, new information about any of these factors may emerge throughout treatment and should be revisited. History of the Insomnia All assessments begin with a discussion of consent and limits to confidentiality followed by a history of the sleep problem. Of course, it is important in psychotherapy to get a history of other issues, including current and past interpersonal, occupational, and health details, but since these remain the same for all problems, we will not go into these general psychotherapy issues here. Instead, we will remain focused on sleep and mood related details. Later we provide a general guide for assessment that we find helpful clinically. The first order of business is typically a question such as, “What brings you here?” or “Please tell me about your sleep problem.” The goal of this question is manifold. What is the nature of the current problem? Is the primary complaint about nighttime or daytime difficulties? When did it start? Is it a lifelong problem, i.e., are there family stories about difficulties as a baby, through childhood, teenage years right up until the present? In some cases, there will be a report of a lifelong insomnia but after beginning work together, it will become apparent that this is not the case. Such is the case with Kelly, a case example presented in Chapter 10 and throughout the book. In such cases,

this can reflect an all or none way of viewing oneself as a “bad sleeper.” Such beliefs likely will be targeted for modification at some point in therapy. How did the problem start (i.e., is the client aware of a contiguous stressor or did it occur unexpectedly)? What is the client’s explanation for what is going on (i.e., to what do they attribute the insomnia)? When providing psychoeducation (see Chapter 5), it will be important to emphasize a case-specific explanation. For example, I recall that you had said that initially the insomnia began in the weeks before your wedding, and you were puzzled by the fact that it continued even after the stress of the wedding subsided. I would like to talk about some possibilities for why the insomnia persisted even after the wedding . . . Continue querying about whether the problem changed over time, how long the problem has persisted and the reason for seeking treatment now. It is important to understand how they have tried to fix the situation (i.e., what has been tried with respect to medication or a change in habits), as this is the information the therapist needs to assess sleep effort and to help debunk other possible failed attempts. For example, if the client ceased caffeine in an attempt to fix the situation, it is important to address why this did not work and what other measures are necessary to manage the insomnia. Otherwise, any mention of caffeine will be met with skepticism because it was already tried. In addition, such debunking should help to raise hope for the client that this time their efforts may be more likely to succeed. Lastly, it is important to have agreement on the goals for treatment. Unrealistic goals (e.g., “I want to sleep like I did as a teenager,”) are helpful to uncover because it permits cognitive modification of unrealistic beliefs about sleep. It also serves to demonstrate that the way clients view sleep can have an important effect on both how well they sleep and how they feel during the day. The treatment goals discussion at the end of the assessment session is often the start of the intervention. That is, once realistic expectations are stated (i.e., “I would like to spend less time awake during the night,”), the therapist and client can easily agree on such goals and the therapist can discuss a conceptualization and treatment plan for moving forward with the client. Diagnosis of Insomnia The diagnostic criteria for an Insomnia Disorder require a complaint of difficulty initiating or maintaining sleep or non-restorative sleep for a minimum of three months (American Psychiatric Association, 2013). There is no guidance as to what numeric value would constitute difficulty initiating or maintaining sleep for a number of reasons. First, it is important to note that insomnia is a subjective disorder. Certainly, “non-restorative sleep” is a subjective term that would be difficult to quantify except perhaps on an EEG. Whereas a cutoff of sleep disruption greater than or equal to 31 minutes is a reasonable proposal (Lichstein, Durrence, Taylor, Bush, & Riedel, 2003), this proposal lacks evidence for optimal sensitivity and specificity (Lineberger, Carney, Edinger, & Means, 2006). Another important factor in this diagnosis is the presence of one or more of the daytime symptoms of insomnia listed in the Research Diagnostic Criteria for Insomnia (Edinger et al., 2004), including fatigue or malaise, attention or concentration problems, negative 38 Assessment of Insomnia

mood, social or vocational dysfunction, or poor school performance, somatic symptoms such as tension headaches and gastrointestinal symptoms in response to sleep loss, motivation or energy or initiative reduction, daytime sleepiness, and worry about sleep. Without the presence of these daytime sequelae, the disruption in sleep alone would have to be seen as a consequence of different problems such as short sleep (i.e., someone who requires less sleep than the average) or perhaps mania. However, with both the sleep disruption and daytime sequelae present, it is no longer relevant to consider if the disorder is “related” to another Axis I disorder, as there is poor evidence of validity for the distinctness of these types of insomnia (i.e., secondary insomnia) (Edinger et al., 2011). Diagnostic and Measurement Pitfalls The most recent DSM update (DSM5) (American Psychiatric Association, 2013) was characterized by significant changes, including a renaming of the Sleep Disorders section to Sleep-Wake Disorders. The renaming of the section denotes an acknowledg - ment that insomnia and other sleep disorders are a 24-hour phenomenon; that is, they have both nighttime and daytime sequelae. In a chart review study, the best predictor of whether a patient was diagnosed with depression was whether they complained of insomnia (Krupinski & Tiller, 2001). The best predictor of a depression diagnosis should be the presence of one of the MDD criteria in section A (i.e., depressed mood or anhedonia). Indeed, these are the discriminating symptoms for differentiating those with insomnia only from those with MDD-I; insomnia and fatigue are not discriminating items (Carney, Ulmer, Edinger, Krystal, & Knauss, 2009). When the patients in the chart review study diagnosed with MDD were followed-up with diagnostic interviews, just over one quarter actually met diagnostic criteria for MDD; the 72 percent incorrectly diagnosed with MDD had undiagnosed insomnia (Krupinski & Tiller, 2001). As noted above, the DSM5 eliminated the distinction between an insomnia related to a mental disorder versus an insomnia that was considered primary, mainly because this distinc - tion lacks reliability and validity (Edinger et al., 2011). In addition, when patients suffer from a comorbid mental disorder, studies suggest that treatment providers are less likely to consider conditioning, beliefs or poor sleep habits as treatment targets or maintaining factors (Nowell et al., 1997), even when the evidence suggests that these are primary factors for such patients (Carney et al., 2010a; Kohn & Espie, 2005). Historically, insomnia has been under diagnosed and consequentially, undertreated, and the changes to the DSM will hopefully improve this problem. With regard to depression and insomnia, perhaps part of the issue relates to the degree of overlap between the two conditions. Daytime symptoms for insomnia include: fatigue, cognitive complaints, mood disturbance (including dysphoria), and impaired functioning (American Psychiatric Association, 2013; Edinger et al., 2004). Indeed, there are very few discriminating items for these disorders (Carney et al., 2009). In a comparison of those with MDD and those with ID only, the only items that discrim - inated the two groups were: depressed mood, anhedonia, guilt, pessimism, thinking about past failures, self-dislike, crying, agitation, hypersomnia, and decreased appetite. Clinical cutoffs for mild and moderate depression on the second edition of the Beck Depression Inventory (BDI-II) (Beck, Steer, & Brown, 1996) have slightly less support when insomnia is present (i.e., specificity is decreased). Thus, the concern is that some Assessment of Insomnia 39