cbt-i for chronic pain · 2016-06-01 · 10 20 30 40 50 60 70 80 nights per week with sleep onset...
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© Associated Professional Sleep Societies, LLC 1
CBT-I for
Chronic Pain
Michael T. Smith, Ph.D.Johns Hopkins University
School of Medicine,Department of Psychiatry
06/116A Fakir in India , Photograph by M. Bourke-White
© Associated Professional Sleep Societies, LLC 2
Conflict of Interest DisclosuresSpeaker: Michael Smith
1. I do not have any potential conflicts of interest to disclose, OR
2. I wish to disclose the following potential conflicts of interest:
Type of Potential Conflict Details of Potential Conflict
Grant/Research Support NIH (NIDA, NIDCR, NINDS); Merck
Consultant Three Wire Inc., FitBit, Inc., PainCare, LLC.
Speakers’ BureausFinancial support
Other BMED Interactive, Inc., Director
3. The material presented in this lecture has no relationship with any of these potential conflicts, OR
4. This talk presents material that is related to one or more of these potential conflicts, and the following objective references are provided as support for this lecture:
© Associated Professional Sleep Societies, LLC 3
AIMS1) Provide an overview of the sleep-pain relationship
and the discuss the promise of integrating CBT-I into the treatment of chronic pain
2) Discuss assessment issues when evaluating someone with chronic pain and insomnia
3) Review Existing Studies of Cognitive Behavior Therapy for Insomnia (CBT-I ) in Chronic Pain
4) Discuss Issues related to Tailoring CBT-I for Pain Creating Hybrid Therapies (Combine CBT-I & CBT-P) Modifying Standard CBT-I Adding Additional components (light therapy, melatonin)
© Associated Professional Sleep Societies, LLC 4
Sleep Deficiency and Chronic Pain Conditions
Are Major Health Epidemics
Chronic Pain
11.5-55.2%
50% - 88%
CDC (2009): Approx One third of US adults obtain
insufficient sleep
Chronic Insomnia
10-15%
Sleep Apnea4-20%
39-75%Webster et al. 2008
© Associated Professional Sleep Societies, LLC 5
What is Pain?
“Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage,"
International Association for the Study of Pain.
Sensory-Discriminative “sharp, dull”
Affective-Motivational “Unpleasant”
Cognitive-Evaluative
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Lavigne et al: Pain 2000; Clin Neurophysiol, 2001; Pain, 2004;
Sandrini et al 2001, Wang et al. 2004, Bentley, 2003)
What Experimental Pain Does to Sleep
• Multiple studies have delivered a variety of noxious stimuli to sleeping subjects (laser pulses, Heat, hypertonic saline injections, etc)
1) Noxious stimuli can cause arousal from all sleep stages
2) Degree of physiologic response depends on intensity & duration
3) Nociceptive processing is attenuated durign sleep, particularly in SWS relative to other sleep stages.
Degree of thermal stimuli required to induce arousal from SWS = daytime pain tolerance (Bentley, 2003)
PAIN AROUSAL INSOMNIA
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Chronic Pain is a Complex Biospychosocial Problem - Multiple Factors in Addition to Pain, Impact sleep quality.
CentralSensitization
CentralSensitization
Coping & BeliefsCoping & Beliefs
PersonalityPersonality
MoodMood
Self-efficacySelf-efficacySocial ContextSocial Context
SleepSleep
CultureCulture
GeneticsGenetics
Persistent Pain
Historical EventsTrauma
Historical EventsTrauma
neuroendocrineneuroendocrineMedicationsMedications
InflammationInflammation
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What is Chronic Pain? Pain that persists beyond expected time of healing ? (3 mos ?)
• Chronic Pain is conceptualized as a neurologic disorder [Melzack, R (1999)]
• Central Sensitization
DeLeo, 2006
Dysregulation of supraspinal inhibitory & facilitatory mechanisms that modulate nociception & regulate spinal sensitization
• Sleep disturbance: may alter these descending systems (Smith et al. 2007)
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How Are Sleep and Pain Inter-related ?
PAIN AROUSAL Sleep Disruption
1) Traditional Linear View
Lentz (1999); Onen (2001); Kundermann (2004); Roehrs, et al (2006); Kundermann (2008)
2) Reciprocal View (Moldofsky, 1975)
Sleep deprivation:
a) Hyperalgesia
Thermal sensitivity
Mechanical sensitivity
b) Spontaneous pain (Haack, 2005, Smith 2007)
Sleep extension decreases pain sensitivity in sleepy adults (Roehrs et al., 2012)
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Summary of Polysomnographic Findings of Sleep in Chronic Pain
Sleep Continuity Disturbance (Wittig et al., 1982)
Sleep Spindles [sigma 12-14hz]
(Harman, 2002, LBP)(Landis, 2004, FM)
Slow Wave SleepNielsen (1994), Drewes (1995)
Alpha EEG AbnormalityEspecially rheumatologic
– Moldofsky (1983); Roizenblatt (2001)
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What do the longitudinal clinical data show ?
• In chronic pain: relationship is bidirectional (Sleep Pain) e.g., (Affleck, 1996; Stone,1997; Smith, 2010)
• Poor sleep increases odds of developing widespread pain (WP) In general population [Gupta (2007)] ---3 fold increased risk over 15 Mos. In those with a regional pain disorder [Mikkelsson (1999)]
• Restorative sleep linked to 3 fold remission rate from WP[Davies (2008)]
• Insomnia Increases risk of chronic pain after acute injury [Castillo (2006)]
Burn InjurySleep Onset Insomnia During Hospitalization Predicts
Rate of Improvement in PainControlling for:
Premorbid mental health sx, general health
In hospital pain severity, total burn surface area, total graft area, mental health SX, ICU time N = 333; Smith et al. Pain (2008)
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Assessment Issues: Other Sleep D/O’s
Smith et al., Pain 2009
Rates of ICSD / RDC Sleep Disorder Diagnoses in TMD
No DX
32%
68% ICSD Sleep D/O
Primary Insomnia (PI)
26%
SI (TMD/Psych) 9.5%
OSA, 28.4% (73% mild range)
RLS / PLMS 7.6%
RDC BRUX, 17.3 %
Other SD 7.6%
% Overall Sample N = 53
43% > 2 disorders
13% RDC good sleepers
40
40.5
41
41.5
42
42.5
43
43.5
44
44.5
Heat Pain Threshold – Ventral ForearmMean, 95% Confidence Intervals
Deg
rees
Cen
tigra
deNo DXn = 17
PI n = 14
OSAn =15
RDC BRUX n = 9
• PI, OSA, & Sleep Bruxism all associated
with Clinical Pain Severity (BPI), P<.05
Pain patients have overlapping risk factors for sleep apnea: obesity, older age
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Effects of Analgesic Drug Classeson Sleep Architecture
CLASS NREM SleepNREM 1&2 SWS REM
Opioids ↑ ↓ ↓
NSAIDs - ↓ -TCAs (e.g., amitriptyline)
Varies ↑ ↓
SNRI’s (e.g., duloxetine) - - ↓Anti-Convulsants (gabapentin)
↓ Arousal (newer agents)
↑ (newer agents)
-
Anti –Spasmotics(baclofen) ↑ - ↑
Assessment Issues: MedicationsHow do analgesic regimens promote or impede sleep quality?
• Adequate nighttime analgesia is critical
• **Consider effects of opioids on sleep & central apnea (Yue et al. Med. Clin N. AM, 2010)
• Some anticonvulsants may be effective for insomnia [gabapentin (Lo et. al., 2010)]
Cairnes, BE in Sleep & Pain (2007)
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Clinical Syndrome
Depression symptom severity
Assessment Issues: Psychiatric Comorbidity
Major Depression: 5%-85%– depends on setting
– ranges from 30-50% in tertiary care settings
Anxiety d/o: 30-80% (Fishbain, Pain (1986)
PTSD (Beckham, J. psychosom res., 1997)
Bair, et al. Arch. Intern Med, 2003
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Assessment Issues: Suicidality
0
10
20
30
40
50
60
70
80
Nights Per Week With Sleep Onset Disturbance
Perc
enta
gePredictors of SISleep Onset Insomnia
Pain Intensity
Controlling for:Depression
Medications
Pain Interference
Affective Distress
10/12 ideators accurately classified, P<.0001
No Suicidal Ideation, n=39
Suicidal Ideators, n= 12
Smith et. al (2004) Clin. J. of Pain
Insomnia is an independent risk factor for Suicide in Mental Health Populations, e.g., Nrugham et al. 2008)
Suicidality is elevated in chronic pain, Tang et al., 2006)
• 90% of planned Suicides occur within 1 year of onset of ideation (Kessler, 1999)
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PRE-MORBID ACUTE EARLY CHRONIC
BEHAVIORAL MODEL OF INSOMNIA
PERPETUATING FACTORS
PRECIPITATING FACTORS
PREDISPOSING FACTORS
THRESHOLD
Maladaptive Coping: retire to bed when in pain (conditioned pain-related arousal, decreased physical activity, pain catastrophizing, etc.
Spielman et al. 1987
Do Models of Primary Insomnia Inform Insomnia Comorbid with Chronic Pain?
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In some cases pain might not be the main cause of insomnia on a nightly basis?
0
50
100
150
200
250
300
350
P. Insomnia CP+Pain CP- pain
SLWASOTSTSE %
•No Difference on any sleep parameters on nights with pain and nights without pain
•No Difference between groups on Alpha EEG abnormalities or SWS deficits
N=25 N=10 N=14
Mixed Chronic Patients Unmedicated,
4-week washout
Schneider-Helmert, 2001;
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Cognitive-Behavioral Treatment (CBT-I)
Hyperarousal Chronobiologic Dysregulation
Homeostatic Dysregulation
BEHAVIOR
• Targets Maintaining Factors
•Data Driven— Diaries / Actigraphy
— Chart weekly progress
• Addresses Compliance
• Individual or groups
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Cognitive-Behavior Therapy for Insomnia:Multi-component Treatment Approach
COMMON COMPONENTS (not exhaustive)1) Stimulus Control
2) Sleep Restriction
3) Sleep Hygiene
4) Relaxation therapy
5) Bright Light Therapy (Lack, 2007)
6) Cognitive Therapy
Overwhelming Empirical Support
Ineffective as a monotherapy
Not as effective as SRT and SCT [Morin et al., Sleep (2006)]
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SEX
READ IN BED
SEX
TV
AWAKE IN BED
WORRY IN BED
EAT IN BED
WORK IN BED
PROBLEM SOLVE
GOOD STIMULUS CONTROL STIMULUS DYSCONTROL
ODDS 1 IN 2 ODDS 1 IN 9
Stimulus - Response Contingencies
SLEEP SLEEP
Classic Stimulus Control Theory
BEDROOM BEDTIME
BEDROOM BEDTIME
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SEX BEDROOM BEDTIME
READ IN BED
SEX
TV
AWAKE IN BED
WORRY IN BED
EAT IN BED
WORK IN BED
CLEAN BDRM
GOOD STIMULUS CONTROL W/ STIMULUS CONTROL TX
ODDS 1 IN 2 ODDS 1 IN 2
SLEEPSLEEP
BEDROOM BEDTIME
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Stimulus Control InstructionsRichard Bootsin
Decondition Arousal & Re-associate Bed With Sleep• Do not use your bed or room for anything but sleep• Go to bed only when sleepy• If not asleep in 15-20 mins get out of bed• Return to bed only when sleepy• Repeat as often as necessary• Get up at the same time every day!• No napping
A
H
C
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Sleep RestrictionSpielman et al, 1987
7AM11PM Bedtime 10AM
2AM Bedtime 7AM
1:45AM New Bedtime 7AM
BaselineInsomnia
Week 1SR
Week 2SR
Uses Sleep Debt to Consolidate Sleep
A C
H
1) Fix Rigid WT
2) Curtail Sleep Opportunity to match TST
3) Titrate 15 min. weekly bedtime advances contingent of SE = 95% benchmark
© Associated Professional Sleep Societies, LLC 24
Clinical Trials of CBT-I in Chronic Pain
Name Pain Type N Sleep Outcomes1. Currie et al. (2000) Mixed Pain 60 ↑ Sleep Continuity: Diary &
Actigraphy, 3 Mo. FU2. Edinger et al. (2005) Fibromyalgia 42 ↑ Sleep Continuity: Diary &
Actigraphy, 6 Mo. FU3. Vitiello et al (2009) Osteoarthritis 51 ↑ Sleep Continuity: Diary, 1YR
FU4. Jungquist et al. (2010) Neck and Back 28 ↑ Sleep Continuity: Diary, FU
data in preparation
• Standard, multi-component CBT-I: SRT and SCT• Effect Sizes: Moderate to Large & comparable to CBT-I for PI• Outcomes maintained at follow-up (3 mos -1 Year)CAVEATS
No PSG outcomes All were attentional or waitlist control, No Double –blinded studies
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Does CBT-I Improve Pain ?
Name Pain Type N Pain Outcomes1. Currie et al. (2000) Mixed Pain 60 No: cohen’s d @ 3 mo’s = .41
2. Edinger et al. (2005) Fibromyalgia 42 No, but Sort of (Sleep hygiene subgroup that spontaneously adopted SRT and SCT
3. Vitiello et al (2009) Osteoarthritis 51 Yes (on some but not all measures)
4. Jungquist et al. (2010) Neck and Back 28 Pain No, but Pain-related interference YES
• Most of studies were not designed to answer this question
• Effect Sizes of CBT-I on Pain are promising
Effect Sizes on Pain, Jungquist (2010)
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The effects of CBT for Pain on Pain are Modest: new approaches are needed.
-0.18
-0.21
-0.28
-0.18
-0.72
-0.18
-0.15
-0.35
-1 -1 0 1 1
Pain
Depression
Anxiety
Psychological disability
Active coping
Self-efficacy
Physical disability
Joint swelling
• Morley et. al, 1999: d = .33 pain, .54 Disability• Williams et. Al. 2013: Small effects on disability, CAT, not
pain, with active controls
Effect sizes of CBT-P in Arthritis (Dixon et al. 200)
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New Directions: Developing Hybrids
Intergrating CBT-I and CBT-PCore elements of CBT-P blend well with CBT-I1) Cognitive restructuring of maladaptive pain-related beliefs and
cognitions
2) Relaxation Training
3) Behavioral Activation
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Pain-Related Thoughts & Beliefs Predict Pain & Disability, Across
Multiple Chronic Pain Conditions:
(See Keefe, JOP for review (2004)
Magnification & Exaggeration
Rumination & HypervigilanceHelplessness & Pessimism
A set of negative cognitions, emotions, attitudes, and beliefs related to pain(which has trait and state characteristics)
PAIN CATASTROPHIZING:Fear of Movement Causing Intense pain / (re) injury
KINESIOPHOBIA:
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Pre-sleep cognitive hyper-arousal is a nearly universal feature of chronic insomnia
General Pain-Related Thoughts* 36%
Negative Sleep-Related Thoughts 26%
Daytime Review 15%
Friends and Family 14%
Environmental Stimuli 10%
Most Common Pre-Sleep Thoughts in Mixed Chronic Pain (n=54)
(Smith et al 2000 & 2001; J. BMED)
Is Pre-Sleep Pain Catastrophizing Associated with Sleep?
“General pain-related thoughts” predicted 15% of variance in sleep latency, controlling for nighttime pain, etc.
53% of variance in Wake After Sleep Onset Time explained by thoughts about environment (28%) and nighttime pain severity
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Hybrid Treatments:Relaxation Training
• Efficacy for pain is well established (Palermo, 2010)– Especially musculoskeletal pain
• Most of the Data evaluates “Westernized” Relaxation Therapies– Abdominal (Diaphramatic) Breathing– Progressive Muscle Relaxation– Guided Imagery (hypnosis)
• Efficacious for Insomnia, but as a monotherapy, relaxation has smaller effect sizes than SRT or STC [Morin et al., Sleep (2006)]
• YOGA & Mindfulness Meditation – In RA: ↓ IL-6, Zautra & Irwin, 2008– Promising preliminary findings in insomnia (Khalsa,
2004)– Practice During a time of relative low pain
Behavioral Sleep Medicine Specialist
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Hybrid Treatments: Behavioral Activation Activity goals
– Pacing (Strategic use of activity-rest cycles)– Discussion of fear of pain (Kinesiophobia) and
avoidance of activities that elicit pain (prevent deconditioning)
– Strategic use of activities• ↑ Pleasure and ↑ Sense of Mastery (self-accomplishment)
Exercise Goals– Strong Evidence: Cardiovascular Exercize is an Effective
Treatment in Fibromyalgia (↓Tender Point) • Goldenberg, Burckhardt, Crofford, JAMA (2004)
– Exercise improves sleep adults – systemic review• Yang PY et al. J. Physiother (2012) – Moderate effects
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Studies of CBT-I/P Hybrids
Name Pain Groups N RX elements Outcomes
Pigeon, et al. (2012)
Mixed 1. CBT-I 2. CBT-P3. CBT-IP4 WLC
21 10 SessionsFull CBT-P (beh. Activation, activity pacing, cognitive TX, pain education, relaxation, imagery, CBT mood, etc.) & full CBT-I (SRT, SCT, etc.)
CBT-P: pain, Not InsomniaCBT-IP: insomnia > CBT-I >
WLC
CBT-IP Between group effect size on pain = .34
Tang et. al. (2012)
Mixed CBT-IP vs.SX Monitor
20 4 Sessions- SRT& SCT- Behav. Activation- CBT for pain
CBT-IP: insomnia CBT-IP: pain interference CBT-IP: No impact, Pain Severity (ES = .05)
Vitiello et. al(2013 & 2104)
Knee OA
1) CBT-P2) CBT-IP3) EDU
367 6, 90 min. GroupsFull CBT-P Combined CBT-I
Over 9 Mos.CBT-IP, insomnia; not CBT-PCBT-IP NO pain (ES = .1)CBT-P NO painAT 18 Mos:NO overall Insomnia or Pain*Subgroup hi Baseline I&P; CBTIP: Pain and Insomnia
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Conclusions about Hybrids
• Hybrids are feasible• Larger trials with longer-term follow ups needed• As currently conducted (Kitchen sink) not especially effective for
pain • Flooding patients with too many skills ? • Sequencing and adapting specific skills may be needed?• Effects on Pain seen on longer term follow up• Treatment optimization studies are needed to build a better hybrid
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Tailoring CBT-I for Pain
Modifications to Standard CBT-I: Sleep Restriction
0
1
2
3
4
5
Baseline Partial 1 Partial 2 Partial 3 Total Recovery
ControlFARSO
Spontaneous Painful Symptom Frequency
PILL, 10 painful symptoms Composite (0-40)
0 =no symptom – 4 very much)
• Partial Sleep Loss is Hyperalgesic ! (Roehrs et al, 2006 )
Typically sleep loss to SRT is minor and short-term (first 2 weeks)
Sleep fragmentation may be more hyperalgesic than curtailment (Smith et al., 2007)
Smith et al. Sleep (2007)
• Less aggressive restriction (or sleep compression)
• 85% benchmark to increase sleep opportunity
• Change titration amount from 15 min. to 30 min.
• Titrate faster in weeks 2+ (3 days)
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Tailoring CBT-I for Pain
Modifications to Standard CBT-I: Stimulus Control
• Be aware of pain specific compliance & safety issues Patients with lower extremity pain have trouble with Stimulus Control.
Consider and manage fall risks
Sedatives including BZRAs & narcotics ↑ fall risk
Mobility and frailty
• Functional Analysis of what patients do and where they go during episodes of severe pain (how these coping strategies impact sleep) Retiring to bedroom to rest or be alone may associate pain with sleep
environment (poor stimulus control)
Develop alternative places & pain mgmt coping strategies for flares
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Tailoring CBT-I for Pain
Modifications to Standard CBT-I: Sleep Hygiene • Pain may be associated with reduced sleep spindle
activity [(sensory motor gating); Landis 2000 in FM, Harmen, 2002 in LBP]
• Increased awareness of environmental stimuli @ Sleep onset is associated with WASO in CP (Smith et al. 2001)
White Noise Machine May be Particularly Helpful
• Decreased SWS is common in Chronic Pain (Nielsen, 1994; Drewes, 1995)
• Some sleep deprivation studies suggest that SWS deprivation is hyperalgesic (Moldofsky, 1976; Lentz, J. Rheumatol, 1999)
Passive Body Heating May increase SWS (Liao WC, 2002, Bunnel PE, Sleep, 1988)
30 min. hot bath 2 hrs prior to sleep
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Circadian Dysrythmia May Be a Neglected Consequence and / or Cause of Pain and Insomnia
N= 105 Older Adults, 2 weeks of Actigraphy Monitoring (R01 AR054871):1. Pain Free Good Sleepers (n= 26) , 2. Primary Insomnia (n= 16),
3. Knee OA No Insomnia (n= 13), 4. Knee OA Insomnia (n=50 )
• Insomnia and OA Pain independently associated with less robust circadian rythmicity (P,<05)- Controlling for RDI, BMI, age, sex
Good Sleeper Control Knee Osteoarthritis
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Tailoring CBT-I for Pain
Optional Components: Light Therapy / Melatonin
• Mu Opioid receptors located in the SCN (Desjardin et al, Brain Res., 1990)
• Mu opioid receptor activation may produced phase advances (Vansteensel (2003) J. of Bio Rhythms)
• Melatonin has analgesic properties
• Literature on abberant melatonin profiles in CP is mixed - small studies,
• Clinical trials of melatonin and light therapy in chronic pain are needed.
N= 52
PCA Tramadol Usage
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Case Example: Inactivity & Circadian Dysrythmia In Context of Pain
• 50 Year old Female• Chronic Neck and Back Pain due
to Motor Vehicle Accident• HX Posttraumatic Stress Disorder• Spends 24 to 36 hrs in bed trying
to sleep or read• Reduced social activity• Drinks ETOH, 35 ounces /wk to
sleep
Successfully Treated in Clinic • CBT for Insomnia (rigid schedule)• Light therapy• Behavioral Activation
12:00 AM
12:00 AM
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Example of Multi-component Protocol
• Session 1: Evaluation (Meds, Depression, Apnea, SI)
• Session 2: Modified SCT & SRT
• Session 3: Sleep Hygiene & Assess Maladaptive Beliefs / Cognitions Passive Body Heating
Light therapy and or melatonin if applicable
Behavioral activation / exercise goals
• Session 4) Cognitive Restructuring
Pain Catastrophizing, Kinesiophobia
Session 5: Relaxation Training
Session 6: Consolidation of Skills
Session 7: Relapse Prevention & Maintenance of Gains
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Take Home Messages
• Sleep disruption may causally influences pain trajectory
• Thorough assessment of pain patient with insomnia is critical (Meds, opioids, apnea, SI, depression)
• Standard CBT-I works well for sleep and may improve pain-related outcomes, especially pain-related interference in function– May need to modify SRT and SCT.– Need to take into account disease specific issues (e.g., knee OA & SCT)– Longer term outcomes studies are needed 1 year +
• Further development & testing of novel hybrids needed– Hybrids are feasible– More thought needs to go into sequencing and number of skills deployed– Add Relaxation therapy and cognitive restructuring (catastrophizing and
kinesiophobia)– Future studies should consider directly addressing circadian dysrhythmia
• Light Therapy / melatonin(mood and regulate circadian rhythm)
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THANK YOU!
• Johns Hopkins Behavioral Medicine Laboratory• Jennifer Haythornthwaite, Ph.D.• Robert Edwards, Ph.D.• Luis Buenaver, Ph.D• Claudia Campbell, Ph.D.• Virginia Coryell, Ph.D.• Patrick Finan, Ph.D.• Michelle Polley• Mercedes Robinson• Sara Bounds• Lea McCauley• Jim Stone