10/11/17. Nothing to disclose. What is it? Mindy Cetel, M.D., F.A.A.S.M. Integrative Insomnia & Sleep Health Center. October 2017

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1 Mindy Cetel, M.D., F.A.A.S.M. Integrative Insomnia & Sleep Health Center October 2017 Nothing to disclose. What is it? 1

2 Transient insomnia: episodic Acute stress or illness Jet lag or shift change Environmental disturbance Short-term insomnia: few days to 3 months Major life event Chronic insomnia: longer than 3 months Chronic illness One or More of the Following Symptoms Must be Present Difficulty Initiating Sleep Difficulty Maintaining Sleep Waking Up Earlier Than Desired Associated with Clinically Significant Distress or Impairment At Least 3 Month Duration (3x/Week 1 ) 1. International Classification of Sleep Disorders 3 rd Ed Initiation and maintenance complaints commonly occur together. Complaints often merge over time - sleep onset complaints subsequently develop sleep maintenance complaints and vice versa. Complaints of poor quality, unrefreshing or nonrestorative sleep do not solely suffice as insomnia disorder Quality complaints often accompany onset and maintenance complaints 2

3 In adults greater than 30 minutes to fall asleep or 30 minutes awake after asleep connote clinical significance if concomitant reduced total sleep time Fatigue - lack of energy motivation, desire to reduce activity cognitive function : concentration, attention, memory mood, irritability performance at work and school (errors, productivity) Impaired social functioning Somatic symptoms often associated with sleep difficulties i.e. more pain,headaches, G.I. dysfunction Subjective complaints ofdaytime sleepiness are reported Typically absence of objective sleepiness Seldom fall asleep spontaneously in day. Typically can not sleep when attempting to nap in the daytime. MSLT objective sleepiness test: normal range Contrasts with sleep apnea, primary hypersomnias such as Narcolepsy or voluntary sleep deprivation. Discrepency between subjective and objective sleepiness may be due to hyperarousal 3

4 Complaint of difficulty initiating or maintaining sleep WITHOUT daytime complaints IS NOT INSOMNIA! Can be short sleep requirement (as low as 4 hours documented), sleep misperception, excessive time in bed, etc. Serial monitoring typically shows marked night tonight variability in all sleep measures as well as in recorded bed and rising times. Variability is greater than good sleepers. Patients with insomnia underestimate total sleep time by 1 hour on average. Good sleepers tend to overestimate sleep duration and underestimate sleep latency and awakenings relative to objective sleep. This subjective objective mismatch may be related to physiological hyper- arousal, one of the core features of insomnia. Hypnotic medication users may sleep well when they take medications. However without their medication they would meet the chronic insomnia criteria. Insomnia diagnosis applies to patients who voice concerns about their inability to sleep without their medications. 4

5 Studies suggest increased physiological arousal (24 hour hyperarousal) increased heart rate altered heart rate variability increased whole body metabolic rate elevated cortisol elevated ACTH elevated CRF particularly near sleep onset increased body temperature increased high frequency EEG activity during non- REM sleep Studies imply heightened activity of the sympathetic nervous system and HPA axis across sleep and wakefulness This is thought to perpetuate sleep wake dysfunction. Physiological dysregulation may be more evident in subgroup with extreme short objective sleep duration Insomnia pts with objective or subjective sleep maintenance difficulty showed regional increased glucose metabolism in Non-REM sleep Areas involve thalamocortical networks in frontal, anterior temporal, and anterior cingulate distribution, and pontine tegmentum. Suggests overactivity in phylogenetically older brainstem arousal systems as well as in higher order centers for emotional and cognitive processing. Nofzinger 2004 A J Psychiatry 5

6 NMR spectroscopy shows reduced GABA in sleep regulating regions that correlate with objective sleep continuity. Such changes may decrease arousal thresholds and increase perceptions of wakefulness in insomnia Predisposing factors Personality Family history Sex Circadian tendency Coping mechanisms Age Precipitating factors Situational Environmental Medical Psychiatric Medications Perpetuating factors Conditioned arousal Poor sleep hygiene Performance anxiety Circadian rhythm disturbance Chronic comorbid illness Hypnotic use Excessive attention to sleep Speilman et al. (1987) 6

7 Difficulty sleeping during stressful times Habitual light sleepers Personality factors that produce anxious over concern about health, general well-being, or daytime functioning Comorbid psychiatric conditions particularly mood and anxiety disorders Comorbid restless leg syndrome or medical disorders such as GERD, conditions that result in chronic pain, breathing difficulties or immobility Major life change are often precipitating circumstances Acute medical problem; surgery, hospitalization Pain Onset Excessive focus on and worry about sleep difficulties and their daytime consequences. Thoughts about sleep difficulties may occur through the day and amplify as bedtime approaches Conscious effort to try to sleep. 7

8 Sleep difficulties persist after the initial triggering factor has disappeared. Vicious cycle of poor sleep, daytime impairments, apprehension of insomnia and further sleep disturbances. 70% with insomnia continue reporting insomnia one year later 50% still have insomnia three years later Persistent insomnia increases risk for depression Conditioned arousal in response to cues in their bedroom May fall asleep easily at bedtime outside of their bedrooms when not trying to sleep, but show cognitive and physiological arousal lying down in bed with the intention to fall asleep. May sleep better away from home. Sleep Difficulty Sympathetic Arousal Negative Cognitions Negative Emotions 8

9 Cardiovascular diseases Ischemic heart disease Nocturnal angina Respiratory diseases Chronic obstructive pulmonary disease Bronchial asthma Gastrointestinal diseases Peptic ulcer disease Gastroesophageal reflux Neurological diseases Parkinson s/alzheimer s Rheumatic disorders Fibromyalgia Osteoarthritis Psychiatric disorders (many) Dyspnea (from any cause) Endocrine syndromes Diabetes Menopause Hyperthyroidism Pain (from any cause) Associated sleep disorders Sleep apnea Restless legs syndrome Periodic limb movement disorder Miscellaneous conditions Dermatologic Chronic fatigue syndrome HIV/AIDS Lyme disease Systemic cancer Pregnancy Medical treatment induced Pain is not usually the sole cause of insomnia. Chronic insomnia disorder applies when the insomnia symptoms show some independence from pain. What factors invoke a separate insomnia diagnosis? Are there times that the sleep complaints occur in the absence of pain? How much of the time does the sleep difficulty arise directly with pain? Have perpetuating cognitive or behavioral factors arisen, suggesting an autonomous aspect to the insomnia? i.e. (negative expectations, conditioned arousal, sleep disruptive habits) 9

10 Co-occurrence of pain and insomnia is highly impactful. Chronic pain and chronic insomnia are independently linked to disability, medical morbidity, psychiatric morbidity, and decreased quality of life. 50 to 70% of chronic pain patients have significant sleep disturbance and consider it a major quality-of-life issue. Viscious Cycle: Chronic pain precedes or exacerbates sleep disturbances. Insufficient sleep can amplify pain perception. Theoretically improving sleep should improve pain. Experimental sleep deprivation in healthy adults reduces pain threshold, amplifies negative mood and causes somatic symptoms (Kundermann, Pain Res Manag 2004, Smith MT, Sleep 2007) Poor night sleep associated with increased pain the following day. Vicious cycle resulting in physical and mental anguish (Raymond, Pain 2001, Chapman, Pain Med 2006) 10

11 Normal sleepers undergoing experimental painful stimuli to deep muscle and joint : reduced deep sleep higher EEG frequencies associated with more shallow sleep Consistent with an arousal effect (Drewes, Sleep 1997) Cortical arousals not full awakenings are induced experimentally by heat on skin (Lavigne, Pain 2000) Muscle pain stimuli in contrast to vibratory and auditory stimuli to healthy sleepers results in subjectively lower quality sleep (Lavigne Pain 2004 ) Prospective study of pain in fibromyalgia patients predicts subsequent insomnia (Affleck Pain 1996 and Nicassio Pain 2006) Pain is usually blamed as the main cause of sleep disturbance with chronic pain. 66% of chronic pain patients report poor or interrupted sleep and fatigue as secondary complaints (Lavigne Sleep and Pain 2007). > 50% of patients at pain specialist clinic have moderate to severe insomnia 63% to 90% with insomnia and pain report onset of insomnia at or shortly after pain onset. Studies demonstrate correlation between pain intensity and insomnia severity Morin Clin J Pain 1998 Smith, Perlis J Behav Med 2000 Power, Arthritis Rheum 2001 Tang, J Sleep Research 2007 Imperative to improve sleep in pain patients given that sleep disturbance heightens pain sensitivity and is associated with increased disability. If untreated both insomnia and chronic pain may have severe negative impact on mental and physical health and ability to function. Theadom A. J Psychosomatic research 2007;62 11

12 Treatment for insomnia in chronic pain is important because insomnia is likely to persist. Large longitudinal study found 69% persistence of insomnia at one year. (Morphy, Sleep 2007) Negative impacts of insomnia (tiredness, poor concentration, irritability) deplete coping resources and make it more difficult to manage the pain. Counterpoint studies subsets with high pain have normal sleep or even good sleep. Smith, J Behav Med 2000 Power, Arthritis Rheum 2005 In some studies variance in sleep explained by pain was minimal ie 5% and became nonsignificant controlling for psychological variables such as pain attention Persistent insomnia in chronic pain patients better predicted by : general mood disturbance (Harman Sleep 2002) pain focused attention (Pilowksy Pain 1985) affective pain appraisal (Tang, J Sleep Res 2007) Pre-sleep pain rumination (Smith, J Behav Med 2001) Pain alone does not sufficiently predict persistent insomnia Factors triggering insomnia are different than those maintaining insomnia Although many insomnia cases in chronic pain are precipitated by pain onset, the contribution of pain decreases as the insomnia persists, and as other factors perpetuate insomnia. Similar to primary insomnia, perpetuating factors are often cognitive behavioral and develop as a result of maladaptive coping : i.e. extending time in bed to catch up on sleep), inactivity, emotional reactions to these problems, with anxiety, depression, frustration. Tang, Current Rheum Reports

13 Insomnia is both a risk for depression and a consequence of depression Depressed patients with insomnia have worse outcomes, higher remission rates, and greater instability in treatment response 1 Insomnia does not always resolve with antidepressant treatment 2 Depression is more likely to resolve with treatment of insomnia Insomnia may be the prodromal symptom in recurrent depression 3 1 Buysse et al. (1997) 2 Dew et al. (1997) 3 Perlis et al. (1997) 95 Insomnia Impacts Quality of Life P<.0001 SF-36 Scale Score N=362 Control Insomnia 35 Body Pain General Health Mental Role Emotional Role Physical Social Vitality Health Functioning Physical Functioning Significant differences were observed between insomnia and control subjects on all scales of the SF-36, all significant at the P<.0001 level Zammit et al. (1999) Chronic insomnia occurs in about 10% of the population. More common in women and in those with medical, psychiatric, substance disorders and in people in lower socioeconomic strata. 13

14 Subtype with objectively short sleep duration averaging less than six hours per night. Documented association with elevated morbidity HTN Obesity DM2 HPA axis activation Autonomic activation: increased heart rate, 24-hour metabolic rate, and impaired heart rate variability?mortality in men Pharmacological 1. Zolpidem 2. Ezopiclone 3. Zaleplon 4. Temazepam 5. Clonazepam 6. Lorazepam 7. Alprazolam 8. Flurazepam 9. Triazolam 10. Trazodone 11. Suvorexant 12. Amitriptyline 13. Mirtazapine 14. Doxepin 15. Ramelteon 16. Melatonin 17. Diphenhydramine 18. Doxylamine Succinate 19. Quetiapine 14

15 Large meta-analysis 2012: 13 studies, 4378 patients (Z drugs) BZRAs had only modest objective effect of 22 minutes decrease in sleep latency = time it took to fall asleep. Effect size is below NIH effect size for clinical significance. Similar modest effect size on subjective decrease in sleep latency compared to placebo. Improved by addition of a small but significant placebo effect (and likely amnestic effect). No consistent effect found on secondary outcomes: Wake after sleep onset # of awakenings Total sleep time Sleep efficiency Subjective sleep quality BMJ 2012; 345 Heudo- Medina Morning sedation Habituation and Rebound insomnia Fatigue Ataxia Anterograde amnesia Sonambulism/complex sleep behavior Respiratory depression benzodiazepine with opioid Worse sleep apnea benzodiazepine (less with BZRA which do not relax muscle tone) Rebound insomnia: sleep may worsen relative to baseline for 1-3 days post-discontinuation Recrudescence: return of original insomnia symptoms Withdrawal: new cluster of symptoms not present prior to treatment i.e. tremor, anxiety 15

16 Kripke et al. (2012) Large scale matched cohort study showed association between hypnotics and mortality as well as increased cancer risk Multiple classes of hypnotics implicated Hazard ratio for death ranged from 3.60 with 0.4 to 18 doses to 5.32 with >132 doses > 132 doses increased cancer risk by 35% Causality was however not demonstrated Anecdotal evidence of sleep benefit exists Low level evidence supporting efficacy Poor quality control (not FDA regulated) Examples: Valerian 5-HTP Passion flower Skullcap Lavender Hops Demonstrated efficacy for sleep onset insomnia associated with delayed sleep phase Studies on the effect of melatonin on sleep onset latency in non-circadian insomnia have shown mixed findings. Rogers et al. (2003) 16

17 B1 blockers (atenolol, metoprolol) block sympathetic signaling to pineal, suppressing nighttime melatonin. 3 wks melatonin 2.5 mg taken one hour before bed improved sleep c/w placebo Increased TST 37 minutes Increased stage 2 by 41 minutes Decreased latency to stage 2 by 14 mins Increased Sleep Efficiency by 7.6% No rebound or withdrawal effect Scheer; Sleep

18 Behavioral (Non-Drug) Paradoxical Intention Relaxation Training, Meditation Imagery Training Biofeedback, Neurofeedback Bright Light Therapy / Blue Blocker Glasses Multi-Component Cognitive Behavioral Therapy Hypnosis Ebb forehead cooling device Transcranial Magnetic Stimulation Indications: Chronic Insomnia Psychophysiological Inadequate Sleep Hygiene Sleep State Misperception Comorbid Insomnia* With a medical condition With a psychiatric disorder *pre-condition for CBTI is that the primary medical or psychiatric condition should be optimally managed 18

19 1. Sleep Hygiene 2. Sleep Restriction Therapy 3. Stimulus Control Instructions 4. Relaxation Training 5. Cognitive Therapy Foster sleep-promoting behaviors and eliminate sleep-antagonistc behaviors Ensure the bedroom environment is conducive to sleep Maintain a regular sleep-wake schedule Avoid naps Limit the use of stimulants (i.e., caffeine, nicotine) Limit the use of alcohol Get physical exercise during the day Establish a consistent, relaxed evening routine Do not eat a heavy meal late in the evening Avoid watching the clock at night 19

20 Limit time in bed as a therapeutic intervention People struggling with insomnia often spend excessive hrs. in bed attempting to sleep and catch up on sleep. Vicious cycle: Longer times in bed assure longer periods of wakefulness. Adversive conditioning - Bed becomes associated with wakefulness. Corrects the mismatch between amount of time spent in bed and the amount of time spent sleeping. Limits time in bed to the average time spent asleep in past week per sleep diary. Theoretically not decreasing the amount of sleep, just the amount of time spent awake in bed. (likely are decreasing sleep in actuality in view of underestimation of sleep with insomnia) Rise at the same time each day, regardless of amount of sleep obtained. (earlier rise time is ok if unable to sleep) Use an alarm. This strengthens the biologic clock and determines when you should feel sleepy at night. 20

21 10/11/17 Instruct to go to bed only when sleepy, at or later than the prescribed bedtime. Wait until feel a wave of sleepiness before attempting sleep. Sleep only during this time window for 1-2 weeks Sleep only during this time window for 1-2 weeks Keep sleep diary Expect daytime sleepiness at first If sleep efficiency >85%, add 15 minutes to sleep window per week until feeling refreshed by sleep. 21

22 On the first night of treatment patients time in bed was restricted to a mean prescribed time in bed of five hours 39 minutes which represents a reduction of two hours 20 minutes from the mean time in bed of eight hours reported in the baseline sleep log Mean sleep latency for the group decreased from a baseline of 48 minutes to 19 minutes by the end of treatment. Mean total awake time decreased rapidly at the start of treatment, remained low throughout the eight week treatment, and was reduced by one hour 49 minutes at the end of treatment. Only 71% completed treatment. 22

23 Based in classical conditioning theory Assumes a learned association between the bedroom (stimulus) and arousal (conditioned response) Evidenced by paradoxical arousal phenomenon To undo the perpetuating conditioned response, the patient must not spend excessive time awake in the bedroom Go to bed only when very sleepy If unable to fall or remain asleep after minutes, move to another room Engage in pleasant sedentary activity in dim light Return to bed only when sleepy Repeat as necessary 23

24 Helps to train brain: Bed = Sleep Plan in advance activities and comfortable place to go Number of times patient got out of bed Days of therapy Bootzin, et al The BUSY BRAIN Wait a minute Did I floss? 24

25 Compartmentalize worrying and planning to daytime, not in bedroom. Schedule appointment with Planning book. Write down things on your mind. Write down next steps. Close the book. When worries emerge in bedroom, remind yourself you will deal with it at tomorrow s appointment. (new habit takes time) Can I get my co-pay back? I suppose you ve tried counting sheep. Permit only positive or neutral thoughts and emotions in bedroom. Set intention to be done for the day. Do not worry or try to solve problems once in bed. (they ll wait till the morning) Quieting a busy brain : count your breaths in groups of 10; count your blessings, say your prayers) 25

26 Diaphragmatic Breathing Progressive Muscle Relaxation Meditation / Guided meditation Relaxation / Guided Imagery CDs for Sleep Counting Breaths meditation Paced Breathing app (Breathe2Relax) Identify and modify maladaptive beliefs and attitudes that perpetuate insomnia Five domains hypothesized to contribute to insomnia: 1. Worry and rumination ( to do list ) 2. Attentional bias and monitoring for sleeprelated threat (I won t be quick witted tomorrow ) 3. Dysfunctinal beliefs about sleep (lack of sleep causes Alzheimers) 4. Misperception of sleep and daytime deficits Sleep Education A little good information goes a long way toward reducing sleep-related anxiety by de-mystifying good sleep and establishing realistic expectations. Sleep is not a coma. Wake ups are normal. Body takes the core sleep it needs most early in night. Don t need to catch up sleep hour for hour. 26

27 Changing how you think can change the way you feel and how well you sleep. Consider these alternative thoughts: I've done this before so I know I can do it again I will survive even if I don't sleep at all tonight I can tolerate this I have functioned well before even after not sleeping well I have functioned poorly before even after I did sleep well One night of poor sleep is not the end of the world From App: Cbti Coach Randomized Controlled Trials 37 studies N = 2246 subjects/pts examined CBT in primary insomnia, five of which were randomized, controlled clinical trials Overall, CBT had greater improvement on sleep diary and PSG variables than control conditions Twenty-six studies provided follow-up data, indicating the durability of behavioral treatment over short, intermediate, and long (>12 months) periods Morin, et. al. (2006) 27

28 As individual strategies, the evidence is strongest for stimulus control, relaxation, and sleep restriction as stand alone interventions for chronic insomnia. Compared to pharmacologic treatment, as effective as hypnotics. Improvements are generally well-maintained three months up to two years. CBTi achieves moderate to large treatment effect sizes : SOL: # Awakenings : WASO: Total Sleep Time: Sleep Quality: Older adults with maintenance insomnia (n=78) Treatment : 8 weeks Active Treatments: CBTI: 8 weekly 90 min. group sessions temazepam 7.5 to 30 mg (2-7 nights/week) Follow up at 3, 12, & 24 months Morin et al. JAMA,

29 70 60 WASO min Pre Post 3 mo 12 mo 24 mo 10 0 CBTI Temazepam CBTI+Tem Placebo SII Score Placebo Temazepam CBTI+Tem CBTI Pre Post 3 mo 12 mo 24 mo PRIMARY COMORBID Subjective WASO (min) CBTI SH CBTI SH Pre Post 6 mo 29

30 CBTI is has demonstrated efficacy for improving insomnia symptoms including: sleep latency, wake time after sleep onset, and sleep efficiency CBTI is superior to sleep medication in the long term CBTI targets underlying causes of insomnia, not just the symptoms CBT I has been used successfully to treat insomnia associated with chronic illnesses, geriatric groups, psychiatric disorders and a variety of pain conditions CBT for pain (CBT-P) is an evidence-based intervention for chronic pain 30

31 Pain patients indicate that better sleep is one of the most important outcomes they desire aside from pain reduction. Study explored efficacy of pain management programs vs. CBT I designed for primary insomnia in treating insomnia in patients with pain related insomnia Focusing treatment on either pain or insomnia is based on the assumption that there is a reciprocal therapeutic relationship between them. Tang Current Rheum Reports 2009 ViV Pain management programs using cognitive behavioral principles are a treatment of choice. Delivered in groups by multidisciplinary teams. Most PMPs include a sleep educational component different than CBTi but often do not evaluate sleep as an outcome measure in clinical trials 31

32 CBT pain components include : Cognitive therapy identifying and changing unhelpful pain beliefs. pain psychophysiology education Guided relaxation training pacing, activity planning Dealing with the psychological effects of pain and stress goalsetting, gradual return to self-care, work, social and physical activities. communication skills flare up planning relapse prevention Sleep education (not CBTi) Meta-analysis of PMPs (CBT-P)show that they produce only minimal benefits in sleep despite helping manage pain. Blunting pain symptoms does not necessarily lead to better sleep. Chronic insomnia in pain patients is maintained by cognitive behavioral factors not addressed in PMP s : excessive time in bed, poor stimulus control,dysfunctional beliefs and attitudes about sleep Tang, Current Rheum Reports 2009 Sleep Hygiene verbal instruction not shown t be effective in chronic insomnia for non pain pts either. Need to address pain related insomnia as an individual disorder rather than as symptom of chronic pain. This can be achieved by offering pain patients a full course of CBT for primary insomnia. Tang, Current Rheum Reports

33 Three RCTs assess efficacy of CBTi in chronic non-cancer pain. All of these trials measured pain and mood after treatment to assess the wider impact. All three with differing CBTi treatments showed significant improvements in sleep measured with diary and validated questionnaires. Two demonstrated persisting gains at 3 and 6 month follow-up. Redondo 2004, Gustavsson 2006, Becker 2000 The pre-and post treatment effect sizes obtained for sleep measures were strong and comparable to if not better than those reported for CBT I for primary insomnia: SOL: 0.79 to 2.15 WASO: 0.8 to 1.45 TST: 0.21 to 0.99 SE: 0.99 to 2.01 Sleep Quality: Remission rate in sleep translates to 16% to 57% based on definitions of remission among the three studies BUT.. 33

34 Using more stringent criteria to determine the clinical significance of outcomes the non-remission rates are moderate 43% to high 84%. CBT I may insufficiently improve sleep in chronic pain patients to help them regain a normal sleep pattern The 3 three RCTs relied more on behavioral than on cognitive sleep interventions. The 3 RCTs were limited by homogeneous populations that intentionally excluded comorbid major depressive and anxiety disorders Although it is assumed that non-drug treatment can do no harm, caution should be applied when offering CTI to patients with chronic pain. Sleep restriction therapy reduces the amount of sleep or rest in bed. May increase discomfort, pain, and daytime sleepiness especially during the initial stage. Attention should be paid to potential effect of sleep loss adding to concurrent medication effects, medical or psychiatric problems i.e. diabetes, hypertension, depression CBTI potential adverse effects include objective daytime sleepiness, decreased reaction time Non-responders May be harsh in population with comorbidities which may not be perfectly controlled 34

35 Contrary to hypothesis of a reciprocal relationship between sleep and pain, consolidation in sleep was not accompanied by significant reduction is in pain severity ratings. Only non-significant trends in improved pain rating Sleep improvements had more effect on enhancing mood, promoting subjective well-being and increasing confidence in coping with pain than in reducing pain. 35

36 Reciprocal relationship may not be as apparent in a therapeutic context as it is in an experimental setting. The reviewed RCTs showed that a reduction in pain had only a minimal positive impact on sleep, and conversely improved sleep neither relieves pain at the acute treatment phase or 3 to 6 month follow-up. If the relationship between sleep and pain may not be reciprocal in the treatment context, then hybrid interventions to simultaneously address pain and insomnia may be the way forward. Explore integration of CBTi and CBTp treatment strategies Pilot study combining CBT for pain and insomnia Compared efficacy of combined versus CBTI vs CBTP on pain, sleep and mood 10 weekly individual sessions by CBT psychologist N= 21 randomized open label completers vs waitlist controls CBT-P included pain psychophysiology education, relaxation training, pacing, pain specific cognivitive therapy, activity planning, problem-solving, communication skills, flare up planning and relapse prevention. CBT included sleep education, sleep restriction therapy, stimulus control therapy, sleep hygiene, sleep specific cognitive therapy, relaxation training, and relapse prevention. Combined CBT I/P included all components of both therapies. Tang, 2012 Behav Res and Therapy CBT pain: no sleep improvement compared to waitlist. CBTI alone and combined CBT I/P: significant improvements in insomnia, significant improvements in fatigue, and depression All groups experienced non-significant improvements in pain disability. CBT pain had largest but NS improvement on pain outcomes. (Might have expected combined intervention to have the largest effects on pain outcomes). Tang, 2012 Behav Res and Therapy 36

37 Some counterpoints for contemplation: People who are disabled and a lacking in daily structure tend to spend excessive durations in bed attempting to sleep. Even a gentle sleep restriction to 8 hours will better maintain the circadian rhythm. Sleep disturbance perpetuates and takes on a life of its own Fixing pain does not always improve sleep. Fixing depression does not always improve sleep. Fixing sleep with CBTi can help depression. Adaptations of CBTi for pain population may be of benefit Fixing sleep with CBTi needs more study to see if it helps pain. 37