3/13/2019

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TALKING TO PATIENTS ABOUT PAIN

WE NEED TO DO BETTER

Damian Keter, PT, DPT

Board Certified Orthopaedic Clinical Specialist

Cert. Chronic Pain Rehabilitation

Louis Stokes Cleveland VA Medical Center

VAU.S. Department of Veterans Affairs

Veterans Health Administration

VA Northeast Ohio Healthcare System

DISCLOSURES

• No disclosures

OBJECTIVES

1. Understand why we as healthcare providers need to do better discussing pain with

our patients.

2. Understand what pain is, how it is produced, and the different types of pain which

can be experienced.

3. Understand the effects our words have on patient outcomes related to pain.

4. Understand the role of Placebo and Nocebo effects when discussing pain

5. Understand research regarding patient perception and role of education on pain

management.

6. Learn clinical examples to be utilized with patients to strengthen efficacy of pain

education.

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WHY DO WE NEED TO TALK ABOUT PAIN?

• “We have learned more about the physiology of pain in the last ten years than in the

previous thousand years”

• Lorimer Moseley

• #CHOOSEPT

• Pain Science Education in DPT programs is lacking

• The most powerful tool we can give our patients is the ability to manage their pain

Two important shifts in our understanding of pain: (Neuromatrix Theory)

1.) The brain and spinal cord are what produce pain, not tissue damage

2.) Various parts of the central nervous system work together to produce pain

WHAT IS PAIN?

• “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 (IASP)

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“UNPLEASANT SENSORY AND EMOTIONAL EXPERIENCE “

• We know there is an emotional component

• Stress, fear, patient expectations

• Pain - Emotions

• Link between chronic pain and psychological conditions including depression and

anxiety is well established

“ASSOCIATED WITH ACTUAL OR POTENTIAL TISSUE DAMAGE”

• Actual OR Potential

• Something ‘might’ be wrong

• Is the brain always right?

• You can have pain when nothing is actually mechanically/musculoskeletally wrong!

• Imaging?

IS PAIN AN OUTPUT OR INPUT?

• Previous definitions/theories emphasizing pain as input

(Different fibers carrying ‘pain’ signals)

• Current understanding is that pain is produced by the brain and independent of

peripheral input.

• Nociceptive input can influence

• In the lack of peripheral input pain is still able to be produced

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PAIN IS AN OUTPUT NOT AN INPUT

• Pain is not something that travels to the brain (although nociception does)

• The brain CREATES the feeling of pain

• To promote taking steps to reduce nociceptive input

• Pain is considered to be a Homeostatic Emotion NOT a sensation

HOMEOSTATIC EMOTION

• Uncomfortable feeling/urge created by the brain when it senses a problem with

homeostasis

• Goal- to motivate behavior to restore homeostasis

• Emotions consist of a sensation and a motivation with direct autonomic effects.

• Pain is one of many distinct homeostatic emotions that directly reflect the condition of

the body.

• Thermoregulation, Thirst, Hunger, Itch

CLINICAL EXAMPLE

1.) Body senses

abnormality in blood

volume/salt concentration

2.) Body creates urge to

drink (thirst)

3.) Drink water and thirst

goes away.

BUT WAIT!

It takes more than 5 minutes for

liquid to get absorbed and effect

salt/blood volume??!!

Brain knows that problem has

been addressed therefore

removes urge (thirst)

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Does love come from the genitals?

“Does anger come from your fist? Does lust come from your

genitals? Does love come from your heart? Does pain really

come from your back? The answer to all the above is ‘no’. Pain

is a bit like anger, love, and lust- it’s a conscious experience

constructed by your brain, not your back. Sure it takes into

account information provided by the back, but ultimately the

brain is boss. So just like you wouldn’t look to your genitals for

your love problems, so too your back can only provide limited

answers for your pain problems. You need to consider what’s

going on in your brain for the best pain treatment”

From Explain Pain Supercharged (2017) P176, Moseley & Butler, Noigroup Publications

© Neuro Orthopedic Institute Australasia | Used with permission

Nociceptive Pain

PERIPHERAL NOCICEPTIVE PAIN

• Generally related to injury, inflammation, and repair

• ‘Typical pain’

• Painful at site of injury and in proportion to

injury/harm

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PERIPHERAL NOCICEPTIVE PAIN

• In true Nociceptive pain the nervous system is functioning properly

• Direct correlation between stimulus intensity and response (Eudynia)

PERIPHERAL NOCICEPTIVE PAIN-MODULATION

• Control at the spinal level; affects A-Delta Fibers by stimulation of a-Beta Fibers

• Gate Control

• Descending pain inhibition pathways- subconscious inhibition of pain through

inhibitory descending pathways in the brain on the dorsal horn cells

• ~75% of the sensory nerves enter CNS through dorsal horn spinal nerves

• Conscious Inhibition

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PERIPHERAL NOCICEPTIVE PAIN

• Treatment Goals

• Reduce irritation

• Reduce Inflammation (PRICE)

• Return to “normal” mechanics

• Reduce muscle guarding/compensation patterns

• Exercise progression to return to previous activity level

• Strong evidence for Manual Therapy to return to normal mechanics

Neuropathic Pain

Peripheral

Central

Sympathetically maintained

NEUROPATHIC PAIN

• Subsets

• Peripherally generated:

• Cervical or lumbar radiculopathy, nerve lesions, brachial or lumbosacral plexopathies,

peripheral nerve compression/injury

• Centrally generated:

• involves injury to the central nervous system at the level of the spinal cord or above.

• Sympathetically maintained:

• may be generated peripherally or centrally

• characterized by localized autonomic dysregulation

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PERIPHERAL NEUROPATHIC PAIN

• “Pain directly caused by lesion or disease affecting the somatosensory system”

(International Association for the Study of pain)

• Reflects nervous system injury/impairment

• Abnormal signals arising both from injured axon as well as surrounding conjoining

axonal structures

• Pathological- it serves no purpose

• Common causes include: - Trauma

- Inflammation

- Autoimmune

Disease (MS)

- Metabolic disease

(Diabetic Neuropathy)

- Infection (Herpes)

- Tumors/Cancer

- Toxins

- Primary

neurological disease

PERIPHERAL NEUROPATHIC PAIN

• Can be continuous or episodic

• Evidence of sensory involvement

• Burning, tingling, prickling, shooting, electric-like, aching, spasm, cold

• Increased pain without notable provocation

PERIPHERAL NEUROPATHIC PAIN

• Treatment

• Removal of cause (treat infection, address blood sugar, etc)

• Medication management

• Exercise

• To maintain function and mobility

• Preliminary evidence for WB exercises to promote neuroplastic changes

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CENTRAL NEUROPATHIC PAIN

• Pain caused by primary lesion or dysfunction of the CNS

• Burning, numbing, tingling, shooting

• With or without sensory loss

• Allodynia and hyperalgesia

• Causes: Ischemia (CVA), tumors, trauma (SCI), Demyelination, Syrinx

• Clinical Examples: Pain associated with MS and CVA

• Treatment

• Pain medications- min-nil effect

• Tricyclic antidepressants (nortriptyline) or anticonvulsants (Neurontin)

• Lowering stress levels has been shown to reduce pain

• Goals of PT should be related to increasing function and patient education to avoid

maladaptive coping

CENTRAL NEUROPATHIC PAIN

SYMPATHETICALLY MAINTAINED NEUROPATHIC PAIN

• Pain that is maintained by sympathetic nervous system activity

• Burning, throbbing, shooting, pressing

• Associated ANS dysregulation and trophic changes

• Clinical Examples: CRPS, Phantom limb pain, Post-herpetic Neuralgia

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Nociplastic Pain

NOCIPLASTIC PAIN

• Nociplastic pain: Pain that arises from altered nociception despite no clear

evidence of actual or threatened tissue damage causing the activation of peripheral

nociceptors or evidence for disease or lesion of the somatosensory system causing

the pain. –IASP

• An amplification of neural signaling within the CNS that elicits pain hypersensitivity

• Nociceptor inputs can trigger a prolonged but

reversible increase in excitability and synaptic

efficacy of neurons in central nociceptive

pathways.

• Manifests as pain hypersensitivity, dynamic

tactile allodynia, secondary pressure

hyperalgesia, aftersensations, and enhanced

temporal summation

• Results in secondary changes in brain activity

which can be detected by electrophysiological

and imaging techniques.

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NOCIPLASTIC PAIN

• Pain we experience MAY NOT reflect the presence of a peripheral noxious stimulus

• Interpretation of non-nociceptor and nociceptor activation as pain even without

noxious stimulation

• Uncoupling of clear stimulus-response relationship

• DOES NOT mean that pain is not real, however is not true noxious stimulation, also

can no longer be termed nociceptive

• Previously related to drug-seeking, secondary gain, etc.

DESCENDING INHIBITION

From Why do I Hurt (2013) Louw . International Spine and Pain Institute ©| Used with permission

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MECHANISMS OF PAIN ACTION

• Input (sensory)

• Peripheral Nociceptive

• Mechanical/chemical irritation

• Ischemia, tissue damage, inflammation

• Peripheral Neuropathic

• Stimulation of neural tissue distal to dorsal horn

• Central Neuropathic

• Stimulation/Irritation of neural tissue in CNS contributing to pain perception

MECHANISMS OF PAIN ACTION

• Processing

• Centrally evoked (nociplastic)

• Central sensitization; brain and spinal cord symptoms remain once stimulus is removed and

tissue is healed

• Strong Cognitive/Affective component

• Thoughts and understanding of pain, dysfunction, and interventions (cognitive)

• Emotions- fear, anxiety, anger (affective)

• Output

• Sympathetically maintained

Pain

• Trauma/Mechanism

• Swelling/Bruising

• Pain localized

• Intensity in correlation with stimulus

Nociceptive Pain

• Acute/Subacute

• Insidious onset

• Nerve distribution related

complaints (peripheral vs

dermatomal)

• Spreading/Radiating/non-localized

• Diffuse pain distribution (not typical nerve

distribution)

• Burning/Numbness/Tingling

• Acute/Subacute/Chronic

• Repeatable and predictable mechanical provocation

• Unpredictable provocateurs

• Hypersensitivity at multiple areas

• Allodynia

• Myotomal weakness

>3 months

• Psychological factors present

• Unpredictable

• Non-consistent with

biomechanical stressors

Peripheral Neuropathic Pain Nociplastic PainCentral Neuropathic Pain

• LMN Signs

• UMN Signs

• History of CNS disorder

• Distribution within body region

effected by CNS disorder

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TRANSITIONING OUR UNDERSTANDING PAIN

• Biomedical model (Cartesian model of pain)

• Typically taught medical professional programs

• Focus on medical/mechanical deficits contributing to pain

(pain = tissue injury)

• More than 350 years old

• Biopsychosocial model

• Focus on multifactorial causation related to chronic pain including psychosocial factors.

MORE THAN 0-10

• Qualities of pain

• Location and does it move/radiate?

• Aggravating factors

• Relieving factors

• Previous treatments (and response to those treatments)

• Other Characteristics- Allodynia?, Hypersensitivity? Numbness/tingling?

PATIENT EDUCATION

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PATIENT EDUCATION

• Goal of any pain education program is to reduce connection between pain and tissue

pathology

• As long as person in pain links their pain to tissue damage then strategies that don’t ‘fix’

tissue damage will not be effective in reducing pain

• patients will seek treatments to specifically target ‘injured tissue’

• Credentials of person providing education?

• Trust

PATIENT EDUCATION

• Self –management programs should encourage patients to take ACTIVE role in the

management of their condition

• Patient education on pain and disease

• Relaxation and stress management skills

• Pacing and graded exercise

• Coping strategies and problem solving training

PRINCIPLES OF EDUCATION

• Patient friendly language

• Focus on brain, including education on role of thoughts, attitudes, perceptions, and

superstitions as well as tissue damage and healing

• Pain NOT associated with tissue damage but rather an individuals response (output)

to threat, real OR perceived.

• In absent of acute complaint

• Emphasis on plasticity of nervous system as it relates to pain

• Common misconception that patients cannot comprehend education related to pain

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EDUCATION

• Should aim to support ongoing care of chronic pain conditions

• It may not ‘go away’

• Active role in pain management

• “What are YOU doing to control your pain?”

• Plan for flare-up

• Thermostat not thermometer

Louw A, et. al 2014

– with permission

DIFFERENCES WHEN DEALING WITH CHRONIC PAIN

• Research confirms:

• acute/subacute pain involves somatosensory cortex

• chronic pain is confined ONLY to emotion related circuitry

• Following injury/trauma

• At several months, stimulation resolves in acute regions and is either gone (pain is

resolved) or transitions to emotional circuits (chronic pain)

• How does this relate to the way which we treat chronic vs acute pain? (role of education?)

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WHY ADDRESS PSYCHOSOCIAL FACTORS?

• Carragee et al (2004)

• 100 subjects with known mild persistent low back pain

• Imaging (Radiograph and MRI) as well as Psychosocial screening

• No intervention provided

• 5 year follow up to determine status

“The development of serious LBP disability in a cohort of subjects with both structural and

psychosocial risk factors was strongly predicted by baseline psychosocial variables. Structural

variables on both MRI and discography testing at baseline had only weak association with back

pain episodes and no association with disability or future medical care.”

VA/DOD GUIDELINES ON LBP/EDUCATION 2017

EDUCATION ALONE?

Pain neuroscience education for adults with chronic musculoskeletal pain: a mixed-

methods systematic review and meta-analysis (Watson et el 2018)

• PNE can facilitate patients’ ability to cope with their condition.

• PNE doesn’t produce clinically significant reductions in pain.

• PNE doesn’t produce clinically significant reductions in disability.

• PNE does produce clinically significant reductions in kinesiophobia.

• PNE does produce clinically significant reductions in catastrophising.

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ROLE OF PLACEBO/NOCEBO

PLACEBO/NOCEBO

• Placebo effect is REAL; Placebo is not “nothing”

• Imaging studies has confirmed physiological changes with placebo based treatment

• Activation of areas involved in opioid analgesia (prefrontal cortex)

• Should be utilized to enhance efficacy of treatment

• Therapy, Medication, Self-management

• Control of supraspinal can not only produce analgesic effects (placebo) but can also

enhance pain (nocebo)

PLACEBO/NOCEBO

• Placebo effects have demonstrated increased effect with repetitive conditioning

while nocebo has not (does not require conditioning to have effect)

• Placebo/nocebo has shown to be more effective than medication itself in some cases.

• Stimulant vs muscle relaxant

• Placebo vs non-opioid analgesic

• Nocebo/placebo effect has shown to decrease or increase action at opioid receptors

therefore interfering with pharmacodynamic properties of painkillers.

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HOW EFFECTIVE IS PLACEBO?

Placebo effects of Sham Opioid solution: a Randomized controlled study in patients with

chronic low back pain- Klinger et al 2017

• N= 48

• All received placebo

• Group 1 was told it was opioid and should reduce pain

• Demonstrated decreased pain, increased functional capacity and increased ability to perform daily

tasks

• Group 2 was told it was Placebo

• No effect on pain or functional capacity as compared to baseline

THE POWER OF PLACEBO

• Louw et al, 2016; Sham Surgery in Orthopedics; A systematic review of the Literature

• 6 RCT, N=277

(rated as ‘very good’ methodological quality)

“This review suggests that sham surgery has shown to be just as effective

as actual surgery in reducing pain and disability; however, care should

be taken to generalize findings because of the limited number of

studies.”

• Sham surgery vs Labral Repair vs Bicep Tenodesis-

Shroeder et al; 2016

• 218 participants with Arthroscopically revealed

SLAP II lesions

• Randomly assigned to either labral repair (n=40),

biceps tenodesis (n=39) or sham surgery (n=39)

• “There were no significant between-group

differences at any follow-up in any outcome. “

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• Subacromial decompression surgery for adults with shoulder pain: a systematic review

with meta-analysis; Lahdeoja et al; 2019

• 1014 patients

• Subacromial decompression surgery vs placebo surgery vs Physical Therapy

• “Subacromial decompression surgery provided no important benefit compared with

placebo surgery or exercise therapy, and probably carries a small risk of serious harm”

2016- Orthopedic Surgeon Ian

Harris;

“For many complaints and

conditions, the real benefit from

surgery is lower and the risks are

higher than you or your surgeon

think.”

Ian Harris.

“The scalpel is probably the

most powerful placebo

known to modern medicine”

- Patients expectations play a

LARGE role in the effects of

Placebo

- The more likely something is to

work (surgery vs pill) the more

placebo effect it has.

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EDUCATION- EXERCISE

• Grading of Exercise

• Why to take the graded exposure approach to pain rehabilitation

• Psychological progression/trust

• Delayed onset muscle soreness

• Therapists response to pain during exercise

• “knock on the door of the pain”

WHY DOES EXERCISE HELP WITH PAIN?

• Peripheral Mechanisms

• Decreased nociceptor activity

• Alteration in local immune cell function (increased anti-inflammatory cytokines)

• Central Mechanisms

• Multiple serotonin and opioid pathways to decrease sensitivity at brain and spinal cord

level

• Neuropathic and Psychosocial Mechanisms also present

• Wording/education related to manual therapy can increase efficacy

• Utilize reversible terminology

• Stuck/Irritated/stiff

• Avoid permanent/more severe terminology

• Out of place/torn/unstable

EDUCATION - MANUAL THERAPY

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WHY DOES MANUAL THERAPY HELP WITH PAIN?

• Peripheral Mechanisms

• Activation of peripheral analgesic system (cannabinoid and adenosine)

• Alteration in local immune cell function (increased anti-inflammatory cytokines)

• Central Mechanisms

• Activation of descending inhibitory pathways

• Oxytocin pathway (Massage)

• Serotonin, Noradrenaline, cannabinoid (Mobilization)

• Reduction in glial cell activation in spinal cord

• Reduction in temporal summation (Manipulation)

• Neuropathic and Psychosocial Mechanisms also present

REVIEW- WORDING

• Avoid harmful and non-reversible words, without description and comforting factors

• Slipped, broken, torn etc

• Utilize Placebo to your advantage WITHIN ETHICAL LIMITS

• Utilize promising and optimistic terminology related to what you are doing

• “get things moving normally”

• “teach the muscles how to work more normally again”

• “Re-Teach the joint that this isn’t a harmful movement”

IMAGING AND PAIN

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WHICH PATIENT IS EXPERIENCING MORE PAIN?

IMAGING

• Degenerative changes

are normal and imaging

has POOR correlation with

Low Back pain and

disability

• Boden et al 1990

• MRI Study

• Asymptomatic Patients > 60 y/o

• 36% had a herniated disc

• 21% had spinal stenosis

• 90% had a degenerated or bulging disc

Imaging Finding 20 30 40 50 60 70 80

Disk degeneration 37% 52% 68% 80% 88% 93% 96%

Disk signal loss 17% 33% 54% 73% 86% 94% 97%

Disk height loss 24% 34% 45% 56% 67% 76% 84%

Disk bulge 30% 40% 50% 60% 69% 77% 84%

Disk protrusion 29% 31% 33% 36% 38% 40% 43%

Annular fissure 19% 20% 22% 23% 25% 27% 29%

Facet degeneration 4% 9% 18% 32% 50% 69% 83%

Spondylolisthesis 3% 5% 8% 14% 23% 35% 50%

W. Brinjikji, 2015

AGE-SPECIFIC PREVALENCE ESTIMATES OF DEGENERATIVE SPINE IMAGING FINDINGS IN

ASYMPTOMATIC SUBJECTS

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NOT JUST AT LUMBAR SPINE

IMAGING FINDINGS IN OLYMPIC LEVEL ATHLETES

Evaluation of spine MRIs in athletes participating in the Rio de Janeiro 2016 Summer

Olympic Games’- Wasserman et al 2018

• 100 MRI’s were completed on Olympic Athletes

• “Fifty-two of the 100 (52%) athletes who received cervical, thoracic and/or lumbar

spine MRI showed moderate to severe spinal disease.”

• moderate/severe degenerative disc changes with varying degrees of disc bulges and

herniations, Spondylosis, etc.

• NOT acute injuries

DOES THIS MEAN IMAGING SHOULD BE AVOIDED?

• Education prior to imaging results regarding likely findings

• Breaking connection between findings on imaging and pain experienced.

• ‘things are irritated’

• ‘Normal age related changes’

• ‘It’s like grey hair’

• ‘Many of these findings would be present in people without pain’

• ‘If they took an x-ray of my back’

• Discuss the research with them (if appropriate patient)

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IMAGING

• You are lying to your patient when you tell them there pain is related to….

• There is POOR correlation between most orthopedic imaging findings and pain

• Spend the 1 minute explaining things to patients rather than them looking to Google

for answers

• Yes this is what your imaging found HOWEVER no that does not mean you have to be in

pain.

VA/DOD GUIDELINES ON LBP/IMAGING 2017

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• Darlow et al 2013

• Impact of what clinicians say to people with Low Back Pain

• Structured interview

• Strong evidence that patients belief about low back pain associated with their

clinicians beliefs.

• Moderate evidence that patient and clinicians fear avoidance beliefs are also

associated.

WHAT WE SAY MATTERS!

WHY WHAT WE SAY MATTERS

If you don’t believe me…..

• ‘Do Patients perceptions of provider communications relate to experiences of

physical pain’- Ruben at al 2018

• 1027 Veterans

• More positive provider communication was related to higher self-efficacy, which has

shown direct correlation with reducing pain and reducing interference with patients lives.

CLINICAL EXAMPLES- THE EFFECT OF BRAIN PERCEPTION ON PAIN

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FREE EDUCATIONAL RESOURCES

• http://www.greglehman.ca/pain-science-workbooks/

• https://bodylogic.physio/resource/turning-the-volume-down-on-persistent-pain/

• https://www.tamethebeast.org/

WE CAN DO BETTER

• Trust

• Wording

• Don’t feed into Nocebo; Utilize the placebo effect to increase efficacy of treatment

• Don’t create fear or facilitate idea that ‘pain will never go away’

• It’s okay to tell a patient that there is nothing orthopedically wrong

• Education can and should be utilized as an adjunct to almost any treatment

• Does not require a large amount of time

TAKE IT WITH A GRAIN OF SALT..

• You do not want to be the therapist that “only talks to people”

• Be careful when listening to ‘gurus’; simply because they suggest something does not

make it evidence based

• Don’t cherry pick

information- you can

find information to

support almost

ANYTHING.

• Evidence Changes

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QUESTIONS?

DAMIAN.KETER@GMAIL.COM

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