talking to patients about pain...3/13/2019 1 talking to patients about pain we need to do better...
TRANSCRIPT
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?
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