npta western intro to painpain ≠ damage 16 uhoh! herzog 2016-mri variability-49 distinct findings...
TRANSCRIPT
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NPTA: Western District
Persistent Pain Part 1: Neurophysiological Foundations
Presenter:Dr. Justin Dunaway PT,DPT,OCS,Cert-SMT/DN
Dip. Extremity ManipulationTherapeutic Pain Specialist
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Why is this so important?• US: 43% of population reported chronic pain• 2nd highest in developed nations (1st in dev/non dev for depression) (Tsang
2008)• US has 4.6% of the world population and consumes 80% of worlds opioid supply
(99% of hydrocodone) (Manchikanti 2008)
• 28,647 deaths (2014) from prescription opioid/heroin ODs- 33,000 (2015) 64,000 (2016) 70,000 (2017) (CDC.gov/overdose)
• 45% of Heroin users addicted to prescription opioids- CDC 2015• As of 2016 Opioid overdose is now the leading cause of death of people under
50 yrs old in the US
• As of 2017- Life expectancy in US declining secondary to opioid epidemic
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Objectives:• Part 1: Foundation
• Have a foundational understanding of adaptive nociceptive driven pain mechanisms • Have a foundational understanding of neuroplasticity and its relationship to pain
• Have a foundational understanding of persistent maladaptive pain and its mechanisms and physiology
• Have a foundational understanding of beliefs and expectations and their role in persistent pain
• Part 2: Eval and treatment concepts
• Understand Pain Dominance theory
• Apply Pain Dominance theory to evaluation and treatment concepts
• Understand the basics of Left/right discrimination, Graded Motor Imagery, and Graded Exposure
• Have a framework for applying Graded exposure techniques in the clinic.
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* DesCartes- Treatise on Man 1633
What pain isn’t!!!!
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Nociception vs Pain
• Nociception: The process by which information about actual or potential tissue damage (noxious thermal, mechanical, chemical) is relayed to the brain
• Pain: An unpleasant sensory and emotional experience associated with actual or potential damage or described in terms of such (International Association for the Study of Pain)
• Pain : “A multiple system output activated by the brain based
on a perceived threat”- Moseley
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From Nociception to “the experience of pain”
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1st order Afferents: Nociceptors- A delta and C fibers
• High threshold thermal, mechanical, chemical, polymodal
2nd order Afferents: Synapse in dorsal horn and project to supraspinal regions via the Spinothalamic Tract
• Wide Dynamic Range- intensity
• Nociceptive Specific- localization and type
From Nociception to “the experience of pain”
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Interneurons
Excitatory and Inhibitory Interneurons• Act Pre and Post synapse at dorsal horn• Augment excitation of 1st and/or second order afferents
• Allow for modulation of signal at dorsal horn• Local and cortical controls
Dorsal Horn• Sorting of information• Volume Control
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• Brainstem (Pons/Medulla)- Alert consciousness, motor/reflex/autonomic function, descending pain modulation
• Tectum- auditory and visual processing
• Periaqueductal Grey (PAG)- pain inhibition
• Limbic System- emotion, behavior, motivation, long term memory, olfaction
• Thalamus- major relay center for nearly all inputs
Spinothalamic TractProjections
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Thalamic Projections
• Thalamus- Major relay station
• Projects to Cingulate Gyrus (cingulate gyrus with amygdala)
• Function in behavioral/motor response coordination and planning
• Function in emotional valence
• Projects to Amygdala
• Primary role in emotions and drives
• Also functions in olfaction, memory, autonomic/endocrine control
• Projects to S1 & S2
• Somatotopic organization of nociceptive input (homunculus)
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Neural correlates of the interindividual differences in the subjective experience of pain (Coghill 2013)
Methods: 8 woman, 9 men, healthy, 21-40 years old
• Five 30 sec 49 deg painful stimulus with 30 sec rest (35 deg)
• Subjects rated their pain 0-10
Results: Pain ranged from 1.05-8.9/10
• Also ran fMRI at the same time
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Neural correlates of the interindividual differences in the subjective experience of pain (Coghill 2013)
S1: Localization
ACC: Motivational/Goal Oriented Processes/Negative Emotional Valence
PFC: Intensity, memory, affect, attention
Results: Significant differences in cortical activation between “high” and “low” pain
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Neural correlates of the interindividual differences in the subjective experience of pain (Coghill 2013)
Discussion:
• Pain is defined by the first-person experiential perspective and must be diagnosed and treated with significant consideration of the subjective report. Thus, even if unique patterns of brain activity have been characterized in large numbers… the subjective report will likely remain the single most reliable index of magnitude of pain.
• … the present findings validate the subjective report
• … the finding that individuals with similar patterns of activation… provide similar subjective reports of pain magnitude suggest that they can accurately capture their conscious experience via introspection.
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Abnormal Findings on Magnetic Resonance Images of the Cervical Spines in 1211 Asymptomatic Subjects (Nakashima 2015)
• 87.6% had disc bulging
• ≈ 75% in 20’s
Associations between MRI findings
And LBP: 10 yr analysis (Tonosu 2017)Disc bulge, spndy, Modic changes:
• NOT associated with pain
• Progression not associated with pain
• Baseline MRI not associated with future
painMRI not predictive of future pain 16
Pain ≠ Damage
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Uhoh!
Herzog 2016- MRI variability-49 distinct findings Where pt obtains MRI and who reads It directly impacts DX, TX, and outcome
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Endogenous Pain Modulation
What we know now:• There is more to pain than
peripheral stimulus• 2 people with the same
stimulus can have entirely different but real pain experiences
• Damage (images) doesn’t seem to correlate with pain or future pain
What we don’t know yet:• Why?
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Intraspinal Pain Modulation: Inhibitory interneurons act pre and post synaptically at the dorsal horn
• i.e. Gait Control Theory
Bulbospinal Pain Modulation: Inhibitory and excitatory interconnections between Pons and Medulla
• Send projections to interneurons in Lamina of dorsal horn
• Pons houses specialized “on/off” cells that “turn up/down” information coming up from cord
Endogenous Pain Modulation
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Midbrain Modulation: PAG
• Receives input from cingulate gyrus, limbic system, hypothalamus, Spinothalamic tract (PSTT division)àmodulate activity of PAG
• PAG modulates activity of the Pons/Medulla• Causes release of serotonin, GABA, dynorphin, encephalin,
norepinephrine into dorsal horn• These systems all “work together” for volume control to
cortex• Overall systemic inhibition
Cortical Modulation:• Modulate descending systems• Reinterpretation of nociceptive signal
Endogenous Pain Modulation
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Pulling it all togetherMature Organism Model• Pain is a normal adaptive experience• Alter behavior to enhance the processes of
recovery and chances of survival
• Brain/CNS- “Central Scrutinizing Center”• Logic Engine samples info from:
• Periphery: Nociceptive input • External Context: Environment • Internal Context: Past experiences,
knowledge, beliefs, culture, past successful behaviors, past success observed in others, failures
• Info integrated to create output to respond for best advantage for body/genes
Gifford 1998
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Endogenous Pain Modulation
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Persistent Pain & Neuroplasticity
Neuroplasticity: Hebbian Theory
The dark side of neuroplasticity
Acute/ChronicOr
Adaptive/Mal-Adaptive
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• Ion Channel Concentration
• Ion Channel Type
• Abnormal impulse generators• Retrograde firing – inflammatory chemicals i.e substance
P
Peripheral Plasticity
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Increased Ion channel concentration and interneuron death
• Increased sensitivity, spontaneous discharge, poor localization, proprioceptive deficit
(Woolf 2011)
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• The location of CoG and map volume were correlated with onset of TrAEMG during rapid arm movements
• …preliminary evidence of reorganization of trunk muscle representation at the motor cortex in individuals with recurrent LBP, and suggest this reorganization is associated with deficits in postural control (TSAO 2008)
Maladaptive Cortical Plasticity
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Somatosensory Cortex, Midbrain, and Brainstem Plasticity
Smudging and Grey matter density changes in Somatosensory cortex, midbrain, and brainstem correlate with: • increased pain/ chronicity/ unpleasantness • distortions in perceived body image (size, shape, swelling, position sense,
localization, laterality) • Decreased threshold for noxious/non-noxious stimulus
• Incorrect localization
• Proprioceptive deficitsPAG-RVM shifts from inhibition to maladaptive facilitation (Hover parent mode)
(Flor 1997, Wilke 2006, Pelletier 2015)
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Mesolimbic and Prefrontal Maladaptive Plasticity
“Most impressive and possibly most important” (Pelletier 2015)
• Areas involved in- Cognitive/Affective aspects of pain, behavior response, fear, emotions, negative conditioning, attention
• Strong correlations with chronicity
• Increased vigilance/decreased ability to disengage from pain
• Strong influence over PAG/RVM pathway
• Correlates with pain catastrophizing /Fear Avoidance which can cause further reorganization cortically due to disuse
“vicious cycle where injury, pain, altered sensory transmission, sensorimotor changes, behavioral changes, salience, attention, and fear-avoidance may feed off one another perpetuating the disability”
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The subjective experience of pain: Where expectations become reality (Koyama 2005)
Methods: 10 healthy subjects, 24-46 years old, exposed to thermal noxious stimulus of 46, 48, and 50 deg. fMRIs taken during and in between heat stimulus.Length of periods between stimulus signaled intensity. (7.5, 15, 30 sec)30 trails performed Results: pain decreased 28.3% + expectationfMRI
• Expectation: thalamus, insula, PFC, ACC• Pain: S1, insular cortex, PFC, ACC
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The subjective experience of pain: Where expectations become reality (Koyama 2005)
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The subjective experience of pain: Where expectations become reality (Koyama 2005)
Discussion: Positive expectations produce a reduction in perceived pain (28.4%) that rivals the effects of a clearly analgesic dose of morphine. (.08 mg/kg of BW for a 25% reduction in pain)
The potent modulation evoked by positive expectations underscores the potential of cognitive therapy for the treatment of pain.
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Background: Physical therapy influences chronic pain by means of the specific ingredient of an intervention as well as contextual factors including the setting and Therapeutic Alliance (TA) between provider and pt.
Methods: 117 subjects with CLBP were divided into four groups. Active or Sham IFC with enhanced TA (ETA) or limited TA (LTA). All subjects were told intervention was “effective pain relieving tx”
• LTA- 5 min interaction and therapist did not converse with subject• ETA- 1st 10 min PT asked about symptoms, lifestyle, cause of
condition. Interaction advanced through verbal behaviors, active listening, tone of voice, empathy
Enhanced Therapeutic Alliance Modulates Pain Intensity and Muscle Pain Sensitivity in Patients with CLBP
(Fuentes et al 2014)
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*Increased pain(adverse event): 1 in AL and 1 in EL
Enhanced Therapeutic Alliance Modulates Pain Intensity and Muscle Pain Sensitivity in Patients with CLBP
(Fuentes et al 2014)
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Conclusion: The context in which physical therapy interventions are offered has the potential to dramatically improve therapeutic effects. Factors other than the specific ingredient of a treatment may have a large role in achieving positive clinical outcomes, and exploring them is central to physical therapist practice.
Enhanced Therapeutic Alliance Modulates Pain Intensity and Muscle Pain Sensitivity in Patients with CLBP
(Fuentes et al 2014)
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Descending analgesia- When the spine echoes what the brain expects (Goffaux 2006)
Descending Noxious Inhibitory Control(DNIC): Spinal-bulbo-spinal pathway
Methods: 20 participants divided into 2 groups and sural nerve withdrawal reflex was measured. Group 1 told cold water immersion will decrease sural stimulus pain, Group 2 told immersion will increase sural nerve pain.
Results:
• Positive Expectation Group: 77% decrease in sural nerve pain, 23% decrease in R-III reflex amplitude
• Negative Expectation Group: .05% decrease in sural nerve pain, 24 % increase in R-III reflex amplitude
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Discussion: ”Expectations of hyperalgesia completely blocked the analgesic effects of descending inhibition on spinal nociceptive reflexes”
“This means that a valid pain treatment can lose its clinical efficacy if patients do not expect pain relief.”
Descending analgesia- When the spine echoes what the brain expects (Goffaux 2006)
From a neurophysiological standpoint: BELIEFS AND EXPECTATIONS ARE THE FOUNDATION THAT OUTCOMES ARE BUILT ON!
If beliefs are so important where do they come from?
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The Effect of Treatment Expectation on Drug Efficacy: Imaging the Analgesic Benefit of the Opioid Remifentanil (Bingel 2011)
4 Experimental Pain (Heat) Trials:• Normal Saline- NPRS 66• Opioid Secret (control)- NPRS 55• Remifentanil (positive)- NPRS 39• “No Drug” (negative)- NPRS 64
fMRI:• (+) increased descending inhibition• (-) increased fear/anxiety/mood
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The Enduring Impact of What Clinicians Say to People With Low Back Pain (Darlow 2013)
• Health care professionals had the strongest influence upon attitudes and beliefs
• Information from single encounter can influence beliefs of pts for many years
• Much information resulted in increased vigilance, worry, guilt, and frustration
• “Clinicians can contribute to avoidance beliefs directly by focusing upon what patients should not do and indirectly by providing management advice and pathoanatomic explanations, which are interpreted as meaning the spine is vulnerable and requires protection.”
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Easy to Harm, Hard to Heal (Darlow 2015)
• Beliefs combined to create negative misrepresentation of the back
• Beliefs augment perceived threat
• Results in selective attention to threatening information, potentially perpetuating back pain
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Misconceptions and the Acceptance of Evidence-based Nonsurgical Interventions for Knee Osteoarthritis. A Qualitative Study (Bunzili 2019)
• Pts on waiting list for TKA• All believed it was ”Bone on Bone”
• Most believed it was caused by wear and tear
• Loading would increase damage
• Pain would get worse over time
• PT and exercise would increase pain
“Once the participants in this study had been “diagnosed” with “bone-on-bone” changes, many disregarded exercise- based interventions which they believed would damage their joint, in favor of alternative and experimental treatments, which they believed would regenerate lost knee cartilage. “
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Do the “math”
Gifford 1998
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• “A Substantial part of the therapeutic benefit patients experience when undergoing medical treatment is caused by their brain’s response to the treatment context”
The Neuroscience of placebo effects: connecting context, learning, and health (Wager 2015)
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Maladaptive Neuropasticiy
(laterality/mirror box/ location
discrimination/ graded exposure)
Internal Context (education/fear
elimination/positive expectation)
External Contextual Factors (leveraging
placebos)
Peripheral Dysfunction
(MT/Loading)
Dorsal Horn/Descending Pain Modulation
(Manual therapy/exercise)
I would rather know the person who has the disease than the disease the person has. -Hippocrates
Pulling it all together!
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Justin Dunaway
Instagram/twitter: DrDunawayDPTwww.StandHaitiProject.org
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