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 06/116 A Fakir in India , Photograph by M. Bourke-White

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Page 1: CBT-I for Chronic Pain · 2016-06-01 · 10 20 30 40 50 60 70 80 Nights Per Week With Sleep Onset Disturbance Percentage Predictors of SI Sleep Onset Insomnia Pain Intensity Controlling

© 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

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© 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:

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© 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)

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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

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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

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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