Chronic Pain Physiology

1. Chronic Pain Physiology Will Hamilton, PhD and Libby Hinsley, PT, C-IAYT AYC, October 2019

2. Part 1: Pain

3. Acute Pain 1) Noxious Stimulus: (Chemical, Thermal, Mechanical) impacts nociceptor 2) Fast, Myelinated A-delta fibers- Sharp instant pain, well-localized 3) Slow, unmyelinated C-fibers- Persisting, throbbing, achy, less localized ( Frequency of Impulse Pain Severity

4. 4) Dorsal Horn/Ganglion (back of spine) The First of Many Gates Impulses compete with other nerve impulses Pain Inhibition from competing stimuli- Eg. pressure, vibration, cold

5. Melzack and Wall (1965) “Gates” that either allow or bar entry Of the nerve impulses up the spine Competition from other nerve impulses (touch, cold, Proprioception, pressure) e.g. The diagnosis trap  How relevant is the pain signal? Based on inhibitory interneurons in spine Should also include descending pathway • Part of Placebo (kind face, assurance of safety, dentist pinch) • Or Nocebo response (MRI death sentence, trauma impact on how quickly return to safety)

6. 5) Ascending Pathway Through Brainstem and Thalamus 6) At Thalamus- nerve impulses turn Into pain and relayed to rest of Brain- Which then relay to many areas Including structures related to: A) Attention (ACC and Insula) B) Somatic Perception C) Emotion & Memory D) Movement & Cognition

7. Anterior Cingulate Cortex and Insula “Should I even notice this?”

8. Somatosensory Cortex e.g. Where is it? What am I currently doing?

9. Emotional and Memory Centers (e.g. amygdala, hippocampus, parietal lobes) e.g. What do I know about this? Where am I? How dangerous is this? Movement/Cognition (Prefrontal Cortex) e.g. What does this mean? What do I do? Pain Severity Primitive Response

10. Pain Neuromatrix Integrated thalamo-cortical-limbic structures Multiple Different Selves, A Parliament of Selves Similar to Emotion- E.g. a pattern of primed body sensations, cognitions, memories, perceptions, and behavioral repertoires

11. Descending Pathway: Can have either amplifying or inhibiting effects on pain perception The Neuromatrix selectively controls signal transmission  e.g. How relevant is it to continue perceiving this? Ex- Running after being attacked Ex- Lorimer Moseley and the Eastern Brown Snake

13. Part 2: The Transition to Chronic Pain https://www.medpagetoday.com/resource-centers/pain-management/does-acute-pain-become-chronic/1040

14. If Pain Persists… “Inflammatory soup” at injury site: peptides (e.g., bradykinin), neurotransmitters (e.g., serotonin), lipids (e.g., prostaglandins), and neurotrophins (e.g., NGF); Reduced circulation, ischemic tissue Reduces threshold activation for pain receptors Norepinephrine/adrenaline increases firing of pain pathways in thalamus Which can create a runaway feedback loop of: “Yes! This pain is really relevant! Pay it lots of attention! Stop using that body part” Even well after the tissue has healed and danger is gone. Central Sensitization

15. Why Does Some Pain Become Chronic? • Many factors are thought to contribute: • Peripheral and central sensitization • Altered cortico-limbic processing (emotional brain) • Behaviors and learning mechanisms • Genetic factors • Lifestyle factors - inflammation, autoimmunity, sedentary, deconditioning • History of trauma or past chronic pain episode • And others… • Nervous system gets “stuck” in a habit of pain

16. Central Sensitization • Increased excitability of dorsal root ganglion (peripheral sensitization) • Increased excitability and sensitivity of dorsal horn neurons (more receptors, and lower threshold for activation) • Allodynia and hyperalgesia • Broken “alarm system” • Changes in motor and sensory cortex (smudging, disorganization)

17. Motor Cortex and Sensory Cortex

18. Smudging • Decreased ability to differentiate and control key muscle groups including multifidus • Decreased proprioception and body awareness • Decreased coordination and motor control • Decreased sense of graphesthesia • Decreased left/right discrimination https://www.coreconcepts.com.sg/article/multifidus-smallest-yet-most-powerful-muscle/ https://medical-dictionary.thefreedictionary.com/graphesthesia

19. Broad Effects of Central Sensitization • Sympathetic nervous system on hyper-alert • Endocrine response: increased stress hormones • Immune response: pro-inflammatory

20. Broad Effects of Central Sensitization • Pain linked more to thoughts and feelings • Pain linked to any perceived threat • Increased sensitivity for all senses • Pain persists, spreads, worsens, becomes less predictable https://www.allaboutvision.com/conditions/lightsensitive.htm

21. Broad Effects of Central Sensitization • Increase in pain with any type of movement and at smaller thresholds • Pain patterns not consistent with expected clinical findings related to injury or mechanical dysfunction • No clear position of comfort • Fear and Avoidance/Kinesiophobia • Life gets progressively smaller and more exhausting https://www.facebook.com/AppliedYogaIntegration/posts/kinesiophobia

22. Reduced movement leads to reduced opportunities to mechanically clear the inflammation Reduced competition from other nerve impulses (e.g. proprioception, cold, pressure) As tissues get deconditioned, pain signal worsens Pain Neuromatrix gets more conditioned to attend to pain, perceive it as threatening, respond in more primitive ways, remember more times where pain has been impairing, and generalize pain activation across context “Better safe than sorry”

24. Allodynia- non-pain sensations perceived as pain Hyperalgesia- increased sensitivity to pain Secondary Hyperalgesia- Areas nearby original injury increase in pain Smudging- decreased discrimination of body map (worse performance on Two Point Test)

32. Yoga can be transformative for body, mind, and spirit!

34. Part 3: How Can We Turn It Around? https://itunes.apple.com/us/podcast/depression-180-turn-it-around/id681924022?mt=2

36. Some Techniques for Turning it Around • Education about pain decreases pain • Mindful movement: SLOW • Body awareness: Differentiation of parts • Left/Right Discrimination • Cross-lateral movement • Contralateral movement • Proprioception • Interoception • Mental practice/motor imagery • Novel movements, in novel settings • Active, participatory strategies • These and other strategies can help re-wire and re-organize the brain

37. Some Techniques for Turning it Around • Themes of safety, friendliness and curiosity • Build confidence in the body; notice what works • Internal locus of control (“I’m in charge”) • Link movement with breath • Movement vs. posture (“exploring” vs. “correctness”) • Nudge the edges of discomfort, but avoid setting off the alarm system (Graded exposure) • Breath Practices – Slow and steady, no forcing, lengthen Exhale

38. Avoid The Trap of Diagnosis • A diagnosis may or may not be relevant • Prevalence of DDD (Teraguchi et al, 2014) • 71% in men and 77% in women aged <50 years, and >90% in both men and women aged >50 years. • Prevalence of lumbar disc pathology in 98 asymptomatic subjects (Jensen et al, 1994) • 36% had normal discs at all levels • 52% had a bulge at at least one level • 27% had a protrusion • 38% had an abnormality at more than one level • 14% showed signs of facet arthropathy • Beware of imaging in the context of chronic pain • DON’T GET ON THE FEAR TRAIN https://www.spineuniverse.com/conditions/degenerative-disc-disease

39. Pain Management is remarkably complex • But that means there are lots of ways • To intervene, including: • Changing how pain is attended to • Changing what pain means to us • Changing how we feel about pain • Changing how we communicate • Changing how we respond to pain • Managing our stress response • (sleep, diet, breathing, social, etc) • Clearing inflammation from the body • Taking effective medications • Moving our body improve circulation • Add other signals besides pain • (massage, acupuncture, ice, vibration, etc)

40. citations • Jensen, MC, et al. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med. 1994 Jul 14;331(2):69-73. • Teraguchi et al. Prevalence and distribution of intervertebral disc degeneration over the entire spine in a population-based cohort: the Wakayama Spine Study. Osteoarthritis and Cartilage Volume 22, Issue 1, January 2014, 104-110.