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Central Sensitization

Explore central sensitization and its impact on pelvic health. Learn from Denise Jagroo's insights and expertise during her London lecture. Discover the complexities of neural signaling amplification and its implications for pain hypersensitivity. Uncover the physiological responses that lead to central sensitization and its manifestations. Gain valuable knowledge to enhance rehabilitation practices and improve patient care.

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Central Sensitization

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  1. Central Sensitization Denise Jagroo London 2016

  2. WHY? • Why do all my pelvic pain patients seem just like…. ME?

  3. Why???....

  4. ???

  5. Its like playing whack-a-mole

  6. About Denise.. New York University: Undergraduate and Graduate • Doctorate in Physical Therapy 2002 • Manual Therapy Certification • University of St. Augustine

  7. About Denise… • Certificate of Achievement in Pelvic Physical Therapy • American Physical Therapy Association Women’s Health Section • Board Certified Specialist in Women’s Health • American Physical Therapy Association Women’s Health Section

  8. About Denise…. • Established a Pelvic Rehab Clinic at the Manhattan Veteran’s Hospital 2009 • Owner of Private Practice In New York • Staten Island • Denise Jagroo Physical Therapy

  9. About Denise Lecture nationally and internationally to health clinicians regarding Pelvic Health and Rehabilitation

  10. About Denise… • Author: • “Your Best Pregnancy” • Host Webseries on YouTube • Exercise equipment • Blogger

  11. Sensitization • Before we talk about central sensitization, what is sensitization? • Sensitization- an increase in the excitability of neurons, so they are more sensitive to stimuli or sensory inputs • Natural physiological response to help us avoid pain

  12. What? Sun Burn!

  13. What is Central Sensitization? • Type of neuronal plasticity (woolf , 2007) • Activity-dependent synaptic plasticity in the spinal cord that generates post-injury pain hypersensitivity

  14. HUH? • The connection between neurons can CHANGE in strength! • Either due to using it too much or using it too little

  15. Abnormal Changes in the CNS Peripheral Input Hypersensitive painful and prolonged response (fibromyalgia)

  16. Central Sensitization • Benign inputs begin to produce painful responses. • Or worse, no input, such as phantom limb pain.

  17. What is Central Sensitization? Simply put: An amplification of neural signaling within the CNS that elicits pain hypersensitivity - (Woolf 2007)

  18. It’s not as simple as a telephone wire

  19. Ok, so far… • Not as simple as we thought • There are changes that can happen in the CNS • Can change the effect of a stimulus • Remember to think of our patients…

  20. Sensitization: the 70’s

  21. ? • Injury • Afterwards it doesn’t take as much to make someone say ‘ouch!’ • Something seems more painful than it should be…

  22. By the 1980s.. • Realization that synapses were subject to a form of use-dependent plasticity that could increase their strength or efficacy

  23. Woolf 1983

  24. ? • Stim • Then NO STIM! • But still feeling the effects!! Even after stim taken away!

  25. Neural windup? • NO! • This phenomenon (central sensitization) differed from windup, which represented a progressively increasing output during the course of a train of identical stimuli

  26. Central Sensitization

  27. Central Manifestation

  28. In simple terms… Central sensitization: • Pain that’s more intense = (Hyperalgesia) • Pain where there shouldn’t be pain = (SecondayHyperalgesia) • Pain from something that shouldn’t be painful = (Allodynia)

  29. Central Sensitization Skin Effects LaMotte 1991 & 1992 -1% Intradermal Capsaicin injections in humans - in receptive field of peroneal nerve (below knee) studied via subcutaneous microelectrode -TRPV1 (detection/regulation of body temp, sensation of scalding heat/pain)

  30. Central Sensitization • Injection Site: • Intense pain lasting minutes (at injection site) • 3 zones: heat hyperalgesia 1-2 hours • Dynamic tactile allodynia: several hours & beyond heat area • Largest zone to pinprick—WAY OUTSIDE—24 HOURS

  31. Biomarkers • FMRI: Functional magnetic resonance imaging or functional MRI (fMRI) is an MRI procedure that measures brain activity by detecting associated changes in blood flow

  32. Biomarkers • Increased excitability of neurons in somatosensory cortex evoked by low threshold aB stim within secondary hyperalgesia • Brainstem changes • Cerebral processing

  33. Visceral Effects Brock 2010 • GI Tract: esophageal stim thermal & mechanical pain hypersensitivity in RECTUM

  34. Visceral Effects

  35. Again… Central sensitization: • Pain that’s more intense = (Hyperalgesia) • Pain where there shouldn’t be pain = (SecondayHyperalgesia) • Pain from something that shouldn’t be painful = (Allodynia)

  36. Cross Talk

  37. Cross-Talkin’ • GOOD: Close neural connections in the sacral spinal cord are ESSENTIAL complex coordinated visceral functions in the pelvis • BAD: Intimate connections also allow neuroinflammation to spread from involved to uninvolved neurons via dorsal horn

  38. Viscero-somatic reflexes • Visceral somatic reflexes: afferent stim from a visceral source can affect somatic structures • Nerve cell bodies in dorsal horn of spinal cord and other CNS regions receive convergentinput from both somatic and visceral structures

  39. Viscerovisceral & Viscerosomatic Convergence (Di Saia 2012) • Afferent signals converge —aberrant interactions that can result In painful sensations from organs that are not directly inflamed or stimulated (cross-talk) and from nearby somatic structures (cross-sensitization)

  40. Viscerovisceral & Viscerosomatic Convergence The concept of viscerovisceral & viscerosomatic convergent helps explain why there is so much overlap in the presence of conditions such as • endometriosis • Interstitial Cystitis (PBS) • IBS • Vulvodynia

  41. Cross –Talkin’ • End terminal stimulatedsubstancePretrogade traveling down C andA delta fibersincreased expression of sodium channels & sensitization distally at the terminal nociceptors PAIN organ system to organ system & spread of pathologies • Central connection

  42. Cross Talkin’ • Noxious Prodromic • (PeripheralCentral) noxious afferent stim from an irritated pelvic organ leads to

  43. Cross-Talkin’ • Andromic (CentralPeripheral) • Afferent stim & co-sensitization of another non-irritated pelvic organ

  44. Cross-Talkin’ • Reflexive pathways may occur: • Locally via axon collaterals (dichotomizing afferents) • Spinal cord (DRG) • CNS

  45. Cross Talkin’ • SOOooooo… • Neuroinflammation via andromicpathwaysfunctional changes in the Uninsultedorgan with little or no evidence of an organic etiology

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