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Morten Høgh MSc Pain: Science & Society
Specialist Physical Therapist in Musculoskeletal Physiotherapy (COMT), Specialist Physical Therapist in Sports Physiotherapy (RISPT)
Affiliations: Center for Neuroplasticity and Pain (CNAP) Aalborg University - www.videnomsmerter.dk - FysioDanmark Aarhus/Fysiocenter
Disclosure: I receive fee for authorship of ‘Smertebogen’
Pain measurement and registration in non-verbal patients
“If color was a sense, then red is pain. But how would you determine the color and the nuances if not by asking the patient”.
The Biopsychosocial Model๏ Biochemical reactions do not translate directly into an illness
๏ Biological derangements do not shed light on the meaning of the symptoms in the patient
๏ Finding biology and treating patients require different skill sets
๏ Adopting a sick role does not require any biological derangement
๏ The success of biological treatments are influenced by
• Psychosocial factors (including placebo/nocebo)
• Adherence to treatment (therapeutic alliance)
• Patients are influenced by their clinicians - and visaversa
Engel (1977/1980) Borrell-Carrio et al. (2004)
Nociception
Pain experience
Adapted from Hume (1748)
Causation
if… then
Correlation
oftenif…
Pattern (in theory)
if… ?
then maybe
adapted from ‘An Enquiry Concerning Human Understanding’ by David Hume (1748)
“When two things occur at the same time or within the same place we
tend to believe that they are causal”
Nociception?
Pain experience
Adapted from Hume (1748)
How this relates to pain๏ Pain is not caused by nociception
๏ because you can be in pain when there is no nociception
๏ Nociception does not cause pain ๏ because you can have an injury and not feel it
๏ Pain correlate with nociception ๏ experimental pain depends on a relationship between pain and nociception
๏ We have many excellent theories (patterns) regarding the relationship between pain and nociception (neurophysiology) ๏ i.e. sensitisation and descending signals
๏ But current theories only seem to work if the stimulus is nociception ๏ current theories are insufficient at explaining pain without nociception
What causes pain?๏ No one knows!
๏ But we know that tissue damage alone should not be a theory for pain because it wrongly implies that ๏ pain is causally related to tissue damage = tissue-damage-repair is the only
sensible solution (and everything else is ‘psychogenic’ or ‘covering up’)
๏ pain (and all it correlates with) must go away if the tissue is healed
๏ more pain must mean more damage or be a sign of insufficient healing
๏ there must be undiscovered tissue damage if pain continues
๏ Clinical implications ๏ Understand the patient (‘patient-centred’)
๏ Focus on what pain does rather than what it is
๏ Understand mechanisms that may explain hyperalgesia (rule in/rule out)
Pain will most likely always:๏ Attract you attention
๏ Be aversive or unpleasant
๏ Be experienced in your body (including phantoms)
๏ Motivate you to get away from it by ๏ learning from the situation you are in (find patterns)
๏ behave adequately according to the context you are in (social)
๏ prioritise behaviours, thoughts and actions that are believed to be pain relieving
๏ Influence your well-being, mood and communication
๏ Reflect changes that you need to pay attention to
VA
S
100
Days Weeks Months Years
Is all pain equal?Acute vs. Chronic Pain
Acute pain๏ Intense and highly motivating
๏ ‘Get away and learn to avoid it’
๏ Usually acknowledged by society and peers ๏ ‘I have had it myself’ and ‘don’t worry you will get over it’ responses
๏ Usually highly predictive ๏ ‘Give it a day or two and come back if it hasn’t changed, or if it gets worse’
๏ More obstructive than worrying for most people ๏ ‘…but it’s just bad timing. I really don’t have time for this right now’
๏ Usually very responsive to treatments (any kind) ๏ Why do you think that most treatments don’t show significant effect after 6-12
weeks (regarding NSLBP - check out Artus et al. 2010 and 2014)
๏ But acute pain does not have to correlate with nociception
Normal (acute?) pain
It hurts!!!
I must remember to brush my teeth
Like the last time…
I guess there must be bacteria in my teeth
Chronic pain๏ Exhaustive and discouraging ๏ Unacknowledged by society and peers and HCPs ๏ Unpredictable stimulus-response (e.g. movement:pain) ๏ All absorbing: Is there a future? ๏ Often associated with mood changes and stress ๏ Loneliness: Social support becomes much more necessary
๏ ‘who will believe me’, ‘what can I believe’, ‘who should I trust’??
๏ Life quality: The pain sensation becomes less of a problem than the effect on life
๏ Cure does occur but no treatment is known to be curative
Complex It hurts
Should I be scared!
Will it go away?
Does my dentist know what’s going on with me?
What am I doing wrong?
They don’t believe me!
I should have never…
Never again will I…
Brush my teeth? How?!?
It’s in my teeth
Attention
Genes
Imune system
Culture and social heritage
Expectations
Placebo
Nocebo
Nociception
PERCEPTION
and much more?
Friends, beliefs and knowledge
Experience
Adapted from Moseley (2007)
What is it in this person that make
her hurt in this context?
Butler & Moseley Explain Pain (2003)
Hierarchy of Pain Assessment Techniques
Self-report
Search for Potential Causes of Pain
Observe Patient Behaviors
Surrogate Reporting (family members, parents, caregivers) of Pain and Behavior/Activity Changes
Attempt an Analgesic Trial
Adapted from Herr et al Pain Manag Nurs. 2006;7(2):44-52
Pain is complex - always…
How effective the patient believes the
treatment is
How well the patient can work
and be social
Daily functions
Mood
Social support
StressSleep
NRS (0-10)NRS (0-100)
How are you today?๏ Mood changes (including depression and anxiety) ๏ Sleep disturbances ๏ Cardio-vascular fitness (including metabolic syndrome) ๏ Immune responses ๏ Muscular responses (muscle dysfunction, sarcopenia-like effects) ๏ Reduced self-confidence and meta-cognitive capacity ๏ Socio-economic deroute (job, marriage, parental role…) ๏ Perceived injustice and insufficient support (HCPs, spouse,
family, work…) ๏ Feeling guilty (medication abuse, not doing enough, receiving
passive treatments…)
Patient reports
0 1 2 3 4 5 6 7 8 9 10
Værst tænkeligesmerter
Ingensmerter
Milde s
merter
(1-3
)
Moder
ate sm
erter
(4-6
)
Volds
omme s
merter
(4-7
)
Ingen
smer
ter
(0)
Evaluation of the pain intensity
VAS
NRS
VRS
Faces Pain Scale
Anbefales til ældre uden eller
med mild demens
Pain drawing
Palpation
Patient Specific Functional Scale
Adapted from:Stratford, P. (1995). Assessing disability and change on individual patients: a report of a patient specific measure. Physiotherapy Canada.
Pain provoking functions (disablities)Describe the function:
How would you rate your best, worst and average pain?
Does pain stop you from this activity?
How does the pain react to accumulation of activity?
How long does it take for the pain to reach baseline again?
0-100 (NRS) - best and worse during this activity?
0 = cannot perform the task at all10 = can functionally perform with no restrictions/as before
#2: Search for potential causes of pain
Self-report
Search for Potential Causes of Pain
Observe Patient Behaviors
Surrogate Reporting (family members, parents, caregivers) of Pain and Behavior/Activity Changes
Attempt an Analgesic Trial
๏ Expectations
๏ Mood
๏ Sleep
๏ Social support
๏ Acceptance and understanding
๏ Health Care (providers, payers, law…)
๏ The attitudes of the dentists (and significant others)
๏ Genetics
๏ Tissue damage
๏ High threshold stimuli
๏ Sensitisation (LTP)
๏ Genetics?
๏ Cognition?
PAINNOCICEPTION
Nociceptive Withdrawl Reflex• ‘The Sherrington Reflex’
• Motor response to nociceptive (and other) stimuli
• No strong correlation with other nociceptive responses
The FLARE response
• axonal reflex
• not nociceptive specific
• possible correlation with skin irritants (including pain)
Peripheral terminal
Axon
Cell nucleus
Central terminal
Axon hillock
other neurons
Central neuron
Free nerve endings
Receptors
Acute tissue injury
Axonal reflex
Neural CellularVacular
Peptide exocitose
Proteins released from injured cells
Chemokines, bradykinin, serotonin, histamine,
neutrophils, macrophages
Destruction of bacteria and removal of debris
Vasodilation
Increased permability
Chemotaxis of neutrophils, macrophages, plasma, T-
Cells, mast cells etc.
Cytokine release
NGF/GDNF release from Schwannske Celler
CGRP Sub P
Vasocontriction
Is neuro imaging the answer we are looking for?
What’s causing the activity?
Legrain et al. (2011)
“The pain neuromatrix is dead and it is time for pain research to be more critical”
“Stimulus-specificity can be falsified”
Adapted from prof. Iannetti @ Wellcome Trust scientific congress,
Cambridge 2015
Salience rather than nociception?
Legrain et al. (2011)
Can pain be a conditioned
(learned) response?
Edwards RR et al. (2011)
Placebo mechanisms
Benedetti F (2010)
Fear and learning120 J. Zaman et al. / Neuroscience and Biobehavioral Reviews 51 (2015) 118–125
Fig. 1. Evolution of discrimination acuity and perception of bodily sensations during chronic pain. During acute pain fear learning can result in reduced perceptual discrim-ination, i.e., a reduced ability to discriminate between the CS and similar stimuli (more or less intense stimuli), in this example on the intensity dimension (left panel). Therelationship between discrimination acuity and physical distance between the CS and similar stimuli is represented by the gray ellipses. The ellipses represent compromisedacuity in discriminating between the CS and similar stimuli despite increased physical dissimilarity between stimuli. In addition to decrements in discrimination acuity withdisease progression, the perception of the CSs might also change. CSs can acquire US properties (right panel) and therefore shift on the axis in a non-linear fashion (expo-nential decay). As a consequence of this shift, discrimination impairments that previously applied to these interoceptive and proprioceptive stimuli, result in an impaireddiscrimination of painful and non-painful sensations. CS = conditioned stimulus; US = unconditioned stimulus.
developed an internet-delivered cognitive behavioral therapy pro-tocol that included an exposure procedure in which subjects aregradually exposed to irritable bowel syndrome (IBS) symptoms byengaging in various activities such as eating symptom provokingfoods or physical activities (Ljótsson et al., 2014, 2013, 2011). Therationale of these interventions is that persistence of avoidancebehavior results in the maintenance of fear responses, and interfer-ence with daily activities. In addition, there is emerging evidenceshowing fear learning or extinction deficits in chronic pain patients.Fibromyalgia patients displayed reduced contingency awarenessand safety learning compared to healthy controls in a differen-tial fear conditioning paradigm (Jenewein et al., 2013; Meulderset al., 2015). Schneider et al. (2004) showed elevated conditionedresponses during extinction in chronic back pain patients comparedto controls in addition to acquisition differences. Following pairingof a visual cue with a painful stimulus applied to the abdomen,IBS patients had higher skin conductance responses during extinc-tion compared to controls (Labus et al., 2013). Further support foraltered fear learning and extinction comes from studies on anxietydisorders which often co-occur with chronic pain (Bouton et al.,2001; Lissek et al., 2005; Mineka and Oehlberg, 2008).
1.3. Fear learning, perception and chronic pain
While acknowledging that behavior is an important and treat-able component of chronic pain, less scientific attention has beenpaid to how associative fear learning affects the perception of bodilysensations in general and pain perception in particular. Here, weargue that the effects of associative fear learning on the perceptionof bodily sensations, which may be mediated through perceptualdiscrimination (i.e., reduced discrimination acuity of bodily sen-sations), are especially relevant for contemporary chronic painmodels. Fear learning during acute pain is thought to impair one’sability to discriminate between bodily sensations (CSs) associatedwith pain (see Fig. 1). As a consequence of these learning processes,pain-related expectations arise in response to the CS (Vlaeyen andLinton, 2000, 2012), which bias perceptual decision-making towardpain (Wiech et al., 2014). The combination of these processes mayresult in a lower perceptual accuracy of pain-related sensations(Wiech et al., 2014). Note that perceptual accuracy and discrimina-tion are closely related but not identical, as the former is considered
to be an outcome, while the latter is a process that changes overthe course of the chronification process. Over time, the perceptionof interoceptive and proprioceptive stimuli associated with painchanges. The driving mechanism behind these changes remainsunclear but contemporary theories assign a critical role to anxietyand fear (Vlaeyen et al., 2012; Vlaeyen and Linton, 2012), as theyare thought to bias perception toward pain (Apkarian et al., 2011,2009). Thus, due to their association with pain these bodily sen-sations become aversive (De Houwer, 2007; De Peuter et al., 2011;Van Oudenhove and Aziz, 2013; Vlaeyen and Linton, 2000) and withtime elicit sensations of pain. As a consequence of this shift, discrim-ination impairments that previously applied to these interoceptiveand proprioceptive stimuli, result in an impaired discrimination ofpainful and non-painful sensations (see Fig. 1). Within this frame-work, the role of attentional process should be further explored,especially the concept of hypervigilance given its association withpain (Van Damme et al., 2006; Vlaeyen and Linton, 2000). Hyper-vigilance originates as a consequence of a heightened perceptionof threat and might bias pain perception, as the body is scanned forthreats (Crombez et al., 2005). This detection of potentially threat-ening stimuli could be at the expense of a more thorough processingof sensory input and might result in the misclassification of bodilysensations as painful.
2. Perceptual discrimination and chronic pain
Interoceptive stimuli are often complex constellations of fea-tures on multiple dimensions (e.g., modality, intensity, location,unpleasantness). Their representation consists of a graded pat-tern of activation across a range of units for multiple dimensionssimultaneously (McLaren and Mackintosh, 2000). Perceptual dis-crimination is the ability to distinguish stimuli that differ in at leastone dimension. In the context of chronic pain it can apply to the abil-ity to distinguish between different non-painful bodily sensations(CSs vs. similar stimuli, e.g., more or less intense stimuli), betweendifferent sensory qualities of pain (burning vs. pricking), or betweenpainful and non-painful bodily sensations.
Despite a few exceptions (Peters and Schmidt, 1992, 1991), themajority of the clinical studies point to an impaired perceptual dis-crimination in individuals suffering from chronic pain. Most studieshave investigated discrimination between non-painful bodily
Stress and pain
Stress-induced analgesiaFear/anxiety related pain (nocebo)
Stressor (e.g. context)
Pain(inhibition through
endogenous opioids)
Att
entio
n
Stressor(e.g. context)
Pain(via CCK)A
ttention
Adapted from Benedetti (2011) Oxford Press
Could pain be pain-reducing?
Modulation is all about balance
PRO-NOCICEPTIVE MECHANISMS
ANTI-NOCICEPTIVE MECHANISMS
Think about modulation as a way for the body to get just the right amount of response in any given situation. And remember that it is plastic!
Communication
Clinician
Care-taker Patient
The tool box
Skills needed in ‘BPS’ practice • patient-education (teaching)
• tools of motivation and negotiating
• awareness to non-verbal communications
• indirect data collection and influence via significant others
• task-specific qualifications (e.g. dental surgery)
E.M.P.A.T.H.Y.
Riess & Kraft-Todd, Academic Medicine, Vol. 89, No. 8 / August 2014
Eye
cont
act
Facial muscles
Posture
E.M.P.A.T.H.Y.
Riess & Kraft-Todd, Academic Medicine, Vol. 89, No. 8 / August 2014
Aff
ecti
ve s
tate
s
E.M.P.A.T.H.Y.
Riess & Kraft-Todd, Academic Medicine, Vol. 89, No. 8 / August 2014
Tone of your voice
E.M.P.A.T.H.Y.
Riess & Kraft-Todd, Academic Medicine, Vol. 89, No. 8 / August 2014
Hea
ring
the
who
le p
atie
nt
and
seei
ng t
he c
onte
xt
E.M.P.A.T.H.Y.
Riess & Kraft-Todd, Academic Medicine, Vol. 89, No. 8 / August 2014
(Your response)
affective vs
cognitive empathy!
#3: Observe patient behaviours
Self-report
Search for Potential Causes of Pain
Observe Patient Behaviors
Surrogate Reporting (family members, parents, caregivers) of Pain and Behavior/Activity Changes
Attempt an Analgesic Trial
Observations
• Grimassing
• Behaviour
• Verbalising
What signs would you look for in the face of a patient to support
your hypothesis of pain?
Bemærk musklerne omkring øjne, øjenbryn og næsen
Verbalising & behaviour• Sighing
• Moaning
• ‘Growling’ and ‘Grunting’
• Shouting
• Loud respirations or irregular respiration
• Asking for help or attention
• Agression (words, gestures or behaviour)
• Rigidity
• Tension
• Protective gestures or behaviors
• Rocking movement
• Reduced ROM or other (sudden) changes in mobility
#4: Surrogate reporting
Self-report
Search for Potential Causes of Pain
Observe Patient Behaviors
Surrogate Reporting (family members, parents, caregivers) of Pain and Behavior/Activity Changes
Attempt an Analgesic Trial
Possible data sources
• Significant others (spouse, partner, child/parent)
• Friends and other family
• Caregivers and GP
• Colleagues, neighboughs and business partners
Attention
Genes
Imune system
Culture and social heritage
Expectations
Placebo
Nocebo
Nociception
PERCEPTION
and much more?
Friends, beliefs and knowledge
Experience
Adapted from Moseley (2007)
Educate๏ Sharing knowledge that gives you confidence
in the benign nature of the condition ๏ Make sure the patient knows why you think it
is valid for them (not for ‘someone like them’) ๏ What’s wrong with me? ๏ What will happen to me? ๏ How do I explain this (once I buy it)
๏ Share and exercise explanations, diagnosis and narratives
๏ Focus on the role of the spouse/family if the patient is cognitively impaired
Hunter Integrated Pain Service and Hunter Urban Medicare Local thank our colleagues in Denmark at the Slagelse GenoptraeningsCenter and Morten Hoegh for their contribution to this work.
Understanding Complex Pain
NU
TR
ITIO
N A
ND
LIF
ESTYLE
MY
STORY
MOVEMENT AN
D FU
NC
TIO
N
M E D I C A L T R E A T MENTS
THOUGHTS AND
EMO
TION
S
How big
an impact
are pain
and mood
having on
my wel lbeing?
Is there still somethingwrong with my body?
Maybe my diet and lifestyle are contributing to a sensitized nervous system
Finding new meaning...has stress taken over my body?
Without movement I won’t do well
health
relationships
money
my past
pain
fear
acceptance
My management plan:
Watch YouTube video“Understanding pain and what to do about it in less than 5 minutes”
Information on
complex pain:
www.hnehealth.
nsw.gov.au/pain
Retrain yourbrain!
#5: Attempt analgesic trial
Self-report
Search for Potential Causes of Pain
Observe Patient Behaviors
Surrogate Reporting (family members, parents, caregivers) of Pain and Behavior/Activity Changes
Attempt an Analgesic Trial
Pharma• Local anesthetics
• Non-opioids
• Paracetamol
• NSAIDs
• Opioids
• Anti-depressants
• Anti-convulsants
Although mechanism-based
it will rely heavily on probability if you don’t have patient reports
www.videnomsmerter.dk
Thank you for your attention you may find pdf of the slides at: