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Pain and Exercise:
Mechanisms and Theories
AJ Lamb, MS, CSCS, PES
December 19th, 2018
1
2
Contents
• Introduction
• Background into our current understanding of chronic pain
• Affective aspects of pain
• How might allowing painful exercises mitigate pain
• Conclusion and implications
3
Introduction
“Exercise interventions are the cornerstone of management for
musculoskeletal pain conditions, with the benefits being well-established.”
• Mechanisms are still not totally understood
• Optimal dosage / type of exercise is unclear
• Exercise-based treatments have shown to be effective, but reliability is not
excellent
 Prescription variability
 Individual variability = inconsistent results
4
Introduction
• Traditional pain model = largely Biomedical
5
Introduction
• Therapeutic exercises are often to be performed largely “pain-free”
• New evidence shows that protocols allowing painful exercises has shown
benefit over pain-free exercises; (Smith et al. 2017)
 Defined as exercises that are prescribed with instructions clearly stating that
pain may be experienced, but the exercise is safe
• This review is a narrative… (not a systematic review or meta-analysis)
 The objective is to build a discussion regarding theoretical mechanisms of
painful exercises; after briefly touching on what is now known from previous
mechanistic data
 This review focuses on three mechanisms that influence exercise and
musculoskeletal pain:
 Central pain mechanisms, peripheral pain mechanisms, and the
immune system 6
Our Current Understanding of Chronic Pain
Mechanisms for Central and Peripheral Pain Sensitization
• Central Sensitization: increased responsiveness of nociceptive
neurons in the central nervous system to normal input
 Increased relative response to the presence and intensity of noxious
peripheral stimuli
 Central sensitization is an umbrella term. Beneath which are 4 key
characteristics:
 Hyperalgesia
 Allodynia
 Temporal summation of pain (TSP)
 Diffuse noxious inhibitory control (DNIC)
7
Our Current Understanding of Chronic Pain
Hyperalgesia
 Increased pain response to a normally painful stimulus
 Hypersensitive to mild-pain phenomena
 Example: pin prick near knee
 Normal conditions (2/10)
 Hyperalgesic from chronic PFPS (9/10)
Allodynia
 Pain response to a stimulus that is not typically painful
 Hypersensitive to “normal” phenomena
 Example: Give me a hug!
 Chronic LBP complains of pain during hug
8
Our Current Understanding of Chronic Pain
Temporal summation of pain (TSP)
• Progressive increases in pain perception in response to repeated stimuli of the
same intensity
• Thought to represent central pain facilitation occurring at the dorsal horn
neurons with incoming nociception
 Dorsal vs ventral horn…
• Temporal summation is commonly assessed in humans with heat, cold,
pressure, or electrical current
 Example: Patient with PFPS complains of increasing pain with more
repetitions of the same exercise
9
10
Our Current Understanding of Chronic Pain
Diffuse noxious inhibitory control (DNIC)
• Describes a broad descending endogenous pain modulation system
• Any mechanisms that may overlap/contribute to modulating/inhibiting pain
• Two primary mechanisms to date:
 Activation of descending nociceptive inhibitory mechanisms
 Release of endogenous opioids
• Example “pain inhibits pain”:
 Patient may report lower pain scores for a primary complaint, say LBP, in the
presence of a secondary stimuli, say placing hand in cold water
………..muscular acidosis??
11
Our Current Understanding of Chronic Pain
Role of the Immune System
• Thought to play a critical role in chronic pain states
 Long-term development of hyperalgesia and allodynia
• Consider the innate immune response of inflammation..
 Activated by exposure to microbial cell wall fragments, toxins, irritant
chemicals, and autoimmune reactions. These are detected by toll-like
receptors (TLR’s) which regulate the CNS’s immune response.
 TLR’s are predominantly made up of glial cells and sense the presence of
damage or danger (exogenously or endogenously).
 The immune system may influence hyperalgesia and allodynia through
alterations in glial cells from normal immune function to being capable of
acting on dorsal horn neurons as a nociceptor.
• Previous literature has reported increased glial activity in individuals with
chronic pain. Mechanisms are unclear, but clearly influences central
sensitization
12
Affective Aspects of Pain
Biopsychosocial model
• Recognized with some musculoskeletal ailments: Kinesiophobia,
catastrophizing, low self-efficacy, anxiety, depression
(Blair et al. 2008; Gureje, O. 2008)
• Evidence suggests that these psychological factors might affect the quality
of life and modulation of an individual’s pain experience
(Ossipov, Campbell, and Edwards 2009; Moseley and Arntz 2007; Harvie et al. 2015; Lobanov et al. 2014, Chou and Shekelle 2010; Moseley 2007)
• Systematic Review of self-management interventions for chronic
musculoskeletal pain (16 studies, n=4047) showed that self-efficacy and
depression were the strongest prognostic factors.
 Strongest mediating factors were reducing catastrophizing and increasing
physical activity
(Miles et al. 2011)
13
Affective Aspects of Pain
Pain-related fear is likely to amplify the experience of pain
• Pain is experienced at higher magnitudes when there is a greater
attention placed on it
• Pain-related fear creates a poor attention bias
• Pain-related fear may influence central sensitization via:
 Increasing nociceptive transmission via spinal gate mechanism
 Via modulation of descending/efferent pathways
 Temporal summation where dorsal horn neurons are activated,
increasing glutamine sensitivity, thus producing a pain response
disproportionately larger than the stimulus
14
Allowing painful exercises to mitigate pain
• Traditional explanations by which exercise improves pain:
 Biomechanics, strength, mobility, tissue structure, etc..
 Fail to recognize the biopsychosocial spectrum of cofactors
• Painful exercises have the potential to reconceptualize pain-related fear
 Challenge a patient to think differently about pain / tissue damage
 Opportunity to reintroduce movement that was previously perceived as a
threat
 Tolerance or tissue – or maybe cognitive pathways
• The amygdala is deemed the “fear center” of the brain
 Re-shape the response to fear more positively than poor memories
 Chronic pain states reinforce disadvantageous perception (amygdala) 15
Allowing painful exercises to mitigate pain
• Contemporary thinking- avoidance precedes the development of pain
• By allowing painful exercises, with appropriate safety cues, new
associations can be made
• These new associations compete with previously conditioned
fear/response
• “Your shoulder is painful because it has become deconditioned and not
used to movement. We need to exercise your shoulder, so it will become
strong and conditioned to enable you to do what you need to do.”
16
Allowing painful exercises to mitigate pain
• Medial prefrontal cortex (mPFC) is associated with learning new inhibitory
associations
 Patients with PTSD have presented decreased activity of the mPFC, and
increased amygdala activity
• Allowing painful therapeutic exercises could reduce threat perception
 Enhancing the mPFC
 Altering the amygdala’s response
 Positively modulating nociceptive inhibitory systems
• Pain-related activity may never be fully eliminated
17
Allowing painful exercises to mitigate pain
Central pain processes
• Exercised-induced hypoalgesia (EIH)- resultant analgesic effect of an
acute bout of exercise
 Cardiovascular, resistance, isometric, isotonic
• B-endorphins secretion from the pituitary and hypothalamus
 Activating u-opioid receptors peripherally and centrally
• Hypothalamus has a variety of direct descending nociceptive inhibitory
mechanisms
18
Allowing painful exercises to mitigate pain
Immune function
• Regular exercise has been shown to reduces susceptibility to
viral/bacterial infection
 Why not immune responses from pain as well
• Inflammation is largely correlated with sympathetic tone and
amygdala activity
 Increase parasympathetic tone, suppress sympathetic system, chronic
inflammation, and resultant perceived pain
19
20
21
Conclusion and Implications
• Delivery of exercises that reconceptualize pain as safe and
nonthreatening MAY facilitate advantageous outcomes
 Or may not!
• Evidence highlights various psychological cofactors worth
respecting:
 Pain-related fear
 Self-efficacy
 Catastrophizing
Pain is complex and not well understood!!!
22
Conclusion and Implications
My challenge to you:
Think more abundantly about individuals with (chronic) pain
I have no formal education in pain management.
Refer to a well-read practitioner.
Pain is complex and not well understood!!!
23

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Pain and Exercise: Mechanisms and Theories

  • 1. Pain and Exercise: Mechanisms and Theories AJ Lamb, MS, CSCS, PES December 19th, 2018 1
  • 2. 2
  • 3. Contents • Introduction • Background into our current understanding of chronic pain • Affective aspects of pain • How might allowing painful exercises mitigate pain • Conclusion and implications 3
  • 4. Introduction “Exercise interventions are the cornerstone of management for musculoskeletal pain conditions, with the benefits being well-established.” • Mechanisms are still not totally understood • Optimal dosage / type of exercise is unclear • Exercise-based treatments have shown to be effective, but reliability is not excellent  Prescription variability  Individual variability = inconsistent results 4
  • 5. Introduction • Traditional pain model = largely Biomedical 5
  • 6. Introduction • Therapeutic exercises are often to be performed largely “pain-free” • New evidence shows that protocols allowing painful exercises has shown benefit over pain-free exercises; (Smith et al. 2017)  Defined as exercises that are prescribed with instructions clearly stating that pain may be experienced, but the exercise is safe • This review is a narrative… (not a systematic review or meta-analysis)  The objective is to build a discussion regarding theoretical mechanisms of painful exercises; after briefly touching on what is now known from previous mechanistic data  This review focuses on three mechanisms that influence exercise and musculoskeletal pain:  Central pain mechanisms, peripheral pain mechanisms, and the immune system 6
  • 7. Our Current Understanding of Chronic Pain Mechanisms for Central and Peripheral Pain Sensitization • Central Sensitization: increased responsiveness of nociceptive neurons in the central nervous system to normal input  Increased relative response to the presence and intensity of noxious peripheral stimuli  Central sensitization is an umbrella term. Beneath which are 4 key characteristics:  Hyperalgesia  Allodynia  Temporal summation of pain (TSP)  Diffuse noxious inhibitory control (DNIC) 7
  • 8. Our Current Understanding of Chronic Pain Hyperalgesia  Increased pain response to a normally painful stimulus  Hypersensitive to mild-pain phenomena  Example: pin prick near knee  Normal conditions (2/10)  Hyperalgesic from chronic PFPS (9/10) Allodynia  Pain response to a stimulus that is not typically painful  Hypersensitive to “normal” phenomena  Example: Give me a hug!  Chronic LBP complains of pain during hug 8
  • 9. Our Current Understanding of Chronic Pain Temporal summation of pain (TSP) • Progressive increases in pain perception in response to repeated stimuli of the same intensity • Thought to represent central pain facilitation occurring at the dorsal horn neurons with incoming nociception  Dorsal vs ventral horn… • Temporal summation is commonly assessed in humans with heat, cold, pressure, or electrical current  Example: Patient with PFPS complains of increasing pain with more repetitions of the same exercise 9
  • 10. 10
  • 11. Our Current Understanding of Chronic Pain Diffuse noxious inhibitory control (DNIC) • Describes a broad descending endogenous pain modulation system • Any mechanisms that may overlap/contribute to modulating/inhibiting pain • Two primary mechanisms to date:  Activation of descending nociceptive inhibitory mechanisms  Release of endogenous opioids • Example “pain inhibits pain”:  Patient may report lower pain scores for a primary complaint, say LBP, in the presence of a secondary stimuli, say placing hand in cold water ………..muscular acidosis?? 11
  • 12. Our Current Understanding of Chronic Pain Role of the Immune System • Thought to play a critical role in chronic pain states  Long-term development of hyperalgesia and allodynia • Consider the innate immune response of inflammation..  Activated by exposure to microbial cell wall fragments, toxins, irritant chemicals, and autoimmune reactions. These are detected by toll-like receptors (TLR’s) which regulate the CNS’s immune response.  TLR’s are predominantly made up of glial cells and sense the presence of damage or danger (exogenously or endogenously).  The immune system may influence hyperalgesia and allodynia through alterations in glial cells from normal immune function to being capable of acting on dorsal horn neurons as a nociceptor. • Previous literature has reported increased glial activity in individuals with chronic pain. Mechanisms are unclear, but clearly influences central sensitization 12
  • 13. Affective Aspects of Pain Biopsychosocial model • Recognized with some musculoskeletal ailments: Kinesiophobia, catastrophizing, low self-efficacy, anxiety, depression (Blair et al. 2008; Gureje, O. 2008) • Evidence suggests that these psychological factors might affect the quality of life and modulation of an individual’s pain experience (Ossipov, Campbell, and Edwards 2009; Moseley and Arntz 2007; Harvie et al. 2015; Lobanov et al. 2014, Chou and Shekelle 2010; Moseley 2007) • Systematic Review of self-management interventions for chronic musculoskeletal pain (16 studies, n=4047) showed that self-efficacy and depression were the strongest prognostic factors.  Strongest mediating factors were reducing catastrophizing and increasing physical activity (Miles et al. 2011) 13
  • 14. Affective Aspects of Pain Pain-related fear is likely to amplify the experience of pain • Pain is experienced at higher magnitudes when there is a greater attention placed on it • Pain-related fear creates a poor attention bias • Pain-related fear may influence central sensitization via:  Increasing nociceptive transmission via spinal gate mechanism  Via modulation of descending/efferent pathways  Temporal summation where dorsal horn neurons are activated, increasing glutamine sensitivity, thus producing a pain response disproportionately larger than the stimulus 14
  • 15. Allowing painful exercises to mitigate pain • Traditional explanations by which exercise improves pain:  Biomechanics, strength, mobility, tissue structure, etc..  Fail to recognize the biopsychosocial spectrum of cofactors • Painful exercises have the potential to reconceptualize pain-related fear  Challenge a patient to think differently about pain / tissue damage  Opportunity to reintroduce movement that was previously perceived as a threat  Tolerance or tissue – or maybe cognitive pathways • The amygdala is deemed the “fear center” of the brain  Re-shape the response to fear more positively than poor memories  Chronic pain states reinforce disadvantageous perception (amygdala) 15
  • 16. Allowing painful exercises to mitigate pain • Contemporary thinking- avoidance precedes the development of pain • By allowing painful exercises, with appropriate safety cues, new associations can be made • These new associations compete with previously conditioned fear/response • “Your shoulder is painful because it has become deconditioned and not used to movement. We need to exercise your shoulder, so it will become strong and conditioned to enable you to do what you need to do.” 16
  • 17. Allowing painful exercises to mitigate pain • Medial prefrontal cortex (mPFC) is associated with learning new inhibitory associations  Patients with PTSD have presented decreased activity of the mPFC, and increased amygdala activity • Allowing painful therapeutic exercises could reduce threat perception  Enhancing the mPFC  Altering the amygdala’s response  Positively modulating nociceptive inhibitory systems • Pain-related activity may never be fully eliminated 17
  • 18. Allowing painful exercises to mitigate pain Central pain processes • Exercised-induced hypoalgesia (EIH)- resultant analgesic effect of an acute bout of exercise  Cardiovascular, resistance, isometric, isotonic • B-endorphins secretion from the pituitary and hypothalamus  Activating u-opioid receptors peripherally and centrally • Hypothalamus has a variety of direct descending nociceptive inhibitory mechanisms 18
  • 19. Allowing painful exercises to mitigate pain Immune function • Regular exercise has been shown to reduces susceptibility to viral/bacterial infection  Why not immune responses from pain as well • Inflammation is largely correlated with sympathetic tone and amygdala activity  Increase parasympathetic tone, suppress sympathetic system, chronic inflammation, and resultant perceived pain 19
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  • 22. Conclusion and Implications • Delivery of exercises that reconceptualize pain as safe and nonthreatening MAY facilitate advantageous outcomes  Or may not! • Evidence highlights various psychological cofactors worth respecting:  Pain-related fear  Self-efficacy  Catastrophizing Pain is complex and not well understood!!! 22
  • 23. Conclusion and Implications My challenge to you: Think more abundantly about individuals with (chronic) pain I have no formal education in pain management. Refer to a well-read practitioner. Pain is complex and not well understood!!! 23