This document discusses the challenges of treating pain in orthopedic clinics. It outlines emerging evidence supporting a multi-system model of pain involving the nervous, immune, and endocrine systems. A new paradigm is needed that considers multiple treatment domains beyond just biomechanics. Assessment of pain should classify it as nociceptive, neuropathic, or central sensitization based on history and exam findings. Treatment requires addressing tissue dysfunction, maladaptive cognitions, and stress responses through manual therapy, education, pacing exercise, and reducing fear beliefs. Placebo effects and expectations also influence treatment outcomes.

1. Pain in the Orthopedic Clinic Roderick Henderson, PT Board Certified Orthopedic Specialist Strength and Conditioning Specialist

2. Orthopedic PT Stereotype Formulaic Protocol-driven Boring…

3. What We Really See Tremendous variability Rehab protocols rarely fit each patient Loads of evidence…much of it conflicting Only boring and formulaic if we stop paying attention!

4. Challenge #1 Orthopedic PTs classically trained as clinical biomechanists Emerging evidence scrutinizing the link between biomechanics and clinical syndromes

5. Challenge #2 We don’t like “chasing pain” and would rather just fix the problem Emerging evidence suggesting a frequent mismatch between symptoms and tissue dysfunction

6. Emerging Paradigm Multiple treatment domains Biomechanics Neuroscience Immunology Endocrinology Challenge #3: Keeping new evidence organized!

7. Objectives Challenges of pain in the orthopedic clinic Pathobiological mechanisms of pain and tissue dysfunction Assessment and treatment proposals

8. Traditional Injury Model Symptoms Pathology Halderman S. Presidential Address, North American Spine Society: Failure of the pathology model to predict back pain. 1990; Spine 15:718-724.

9. Expectations Symptoms Pathology Halderman S. Presidential Address, North American Spine Society: Failure of the pathology model to predict back pain. 1990; Spine 15:718-724.

10. Expectations Ideally pathology and symptoms should improve with treatment Clinical and anatomic evidence indicates this rarely occurs

11. A Growing Trend Symptoms Pathology Halderman S. Presidential Address, North American Spine Society: Failure of the pathology model to predict back pain. 1990; Spine 15:718-724.

12. A Growing Trend Patients with significant symptom behavior Often occurring beyond the point of tissue healing Halderman S. Presidential Address, North American Spine Society: Failure of the pathology model to predict back pain. 1990; Spine 15:718-724.

13. A Growing Trend Symptoms Pathology Halderman S. Presidential Address, North American Spine Society: Failure of the pathology model to predict back pain. 1990; Spine 15:718-724.

14. A Growing Trend Pathological signs present without symptoms (false positives) Seen with increasing regularity HNP Bone spur Significant questions for the utility of structural diagnoses in chronic cases

15. Where to Start? Anatomy and biomechanics necessary but insufficient treatment guides Emerging evidence supporting a multi-system model of tissue injury and rehabilitation Chapman CR, Tuckett RP, Song CW. Pain and Stress in a Systems Perspective: Reciprocal Neural, Endocrine, and Immune Interactions. Journal of Pain. 2008;9(2): 122-145

16. Evolution of Pain Theory Specificity Gate Pain Matrix

17. Specificity Rene Descartes Book titled Treatise of Man (1664)

18. Principles Tissues have “pain” receptors Pain-specificfibers carry pain signals

19. Key Assumptions Pain is an input to the CNS Direct and invariant relationship between stimulus and experience Pain enters here

20. Upside of Specificity Definite step up from mysticism! Acknowledged the nervous system

21. Limitations of Specificity Pain in the absence of tissue Pain after neurolysis of peripheral nerves

22. Limitations of Specificity Pain with non-noxious stimuli Pain is a non-linear event

23. Specificity M.I.A. Paper cuts! Minimal harm but loads of hurt! Severe trauma under stress Massive trauma but pain not often felt until after the event

24. Wanted: New Model Need acknowledgement of the nervous system Account for limitations of specificity Enter Ronald Melzack…

26. Saw limitations of specificity

28. Key Assumptions Pain not an input Nociception modulated by dorsal horn and CNS Output is the “pain experience”

29. Limitations of the Gate Widespread or chronic pain syndromes? Pain in paraplegia? Bizarre pain syndromes Melzack R. From the Gate to the Neuromatrix. Pain Supplement. 1999; 6:S121-S126.

30. Key Observations Brain involved but not at one specific site Immune and endocrine systems response seems to interact with the nervous system Very broad responses to similar conditions

31. Wanted: Another Evolution Melzack returns New model incorporates Nervous system Immune system Endocrine system Also addresses varied patient responses

32. Enter the Matrix Melzack R. Pain and the Neuromatrix in the Brain. Journal of Dental Education. 2001;65(12):1378-1382

33. Dissecting the Matrix Inputs to the nervous system Processing by multiple structures Outputs from the patient

34. Cognitive Inputs Thoughts and ideas Attentionand vigilance Active versus passive coping

35. Significance Brain strongly influences nociception Not capable of eliminating nociception i.e. we can’t “think” pain away

36. Sensory Inputs State of the injured tissue Mechanical deformation Chemical irritation Visual and auditory stimuli Closely tied to somatosensation See “mirror box” on youtube!

37. Affective Inputs Persistent activation of immune / endocrine response Connections topara inflammatory states? Obesity Tobacco

38. Therapeutic “On-Ramps” Movement / Exercise Manual care / SMT Education / Reassurance

39. Implications Multiple avenues to pain relief Most PT “schools” have one or more of these elements! Maybe why bogus treatments seem so effective?

40. Next Up…Processing Determined by synaptic architecture Connections solidified with practice Constantgathering input and interpreting outputs Tracey I, Mantyh PW. The Cerebral Signature for Pain and its modulation. J Neuron. 2007;55:377-391

41. Processing is Dynamic Body is constantly asking “How seriously should I take this input?” All inputs evaluatedto determine the best response or output Resultant output is studied and learning occurs

42. Where it Goes Wrong Severe and persistent pain states many inputs deemed threatening Dysfunction of one or more elements of this processing Tissue Cognition Stress response

43. Outputs Tracey I, Mantyh PW. The Cerebral Signature for Pain and its modulation. J Neuron. 2007;55:377-391

44. Ouch! That Hurt! How the patient expresses pain is an output Intensity Facial expression / emotion Motor behavior Postures Antalgic gait Listening and observation provides clues to output!

45. Outputs: What We See

46. Behind the Scenes Complex information gathering, signaling, and outputs Loads of this happening “offline” Tracey I, Mantyh PW. The Cerebral Signature for Pain and its modulation. J Neuron. 2007;55:377-391

47. Implications Effects of injury distributed across several systems Changes in pain reflects a changes to one or more of these systems Tracey I, Mantyh PW. The Cerebral Signature for Pain and its modulation. J Neuron. 2007;55:377-391

48. We Didn’t Sign Up for This… We know anatomy and biomechanics not behavioral psychology nor immunology Unfortunately patients present with these elements They stay relevant whether we acknowledge them or not!

49. What’s Next? Orthopedic assessment within the context of pain science Treatment approaches to patients in pain

50. Assessment of Pain Need a clearer classification system International Association of the Study of Pain (IASP) helps us out here

51. Taxonomy of Pain (IASP) Pain classified as Somatic or visceral Nociceptive or neurogenic Referred or radicular Still some debate over this taxonomy but it is the best we have right now Loeser JD, Treede RD. The Kyoto protocol for IASP pain terminology. Pain. 2008;137:473-477.

52. Risks of Poor Classification

53. Nociceptive Pain Activation of high-threshold afferent fibers is the primary input Mechanical deformation Chemical irritation Seen most often in acute or traumatic injuries Ankle sprains Post-op TKA

54. Nociceptive Pain Familiar patterns of presentation Predictable stimulus-response relationship Consistent aggravating and easing factors

55. Neurogenic Pain Direct mechanical or chemical stimulation of peripheral nerve Examples: Carpal tunnel syndrome Nerve root compression

56. Practical Examples in LBP Nociceptive back pain Nociception arising from ZAJ, Disc, etc… Local, dull, aching Somatic referred pain Expands into wider areas due to convergence Can be proximal OR distal referred Bogduk N. On the definitions and physiology of back pain, referred pain, and radicular pain. Pain. 2009;147:17-19

57. Practical Examples in LBP Radicular pain Ectopic discharges from DRG due to HNP Previously considered “sciatica” but this term should be phased out Radiculopathy Conduction blockade along a nerve root Sensory or motor involvement in a dermatomal distribution Bogduk N. On the definitions and physiology of back pain, referred pain, and radicular pain. Pain. 2009;147:17-19

58. Neurogenic “Wind-Up” Hyperalgesia Allodynia Useful measures of sensitization and central changes

59. Sources of Wind-Up Two possible origins Persistent nociceptive drive Failure of central mechanisms Possible targets of Education Physical activity SMT?

60. Proposed Assessment Model History Clinical exam

61. Assessing Pain: Questionnaires Visual analog scale Numeric pain rating scale Fear-avoidance beliefs questionnaire McGill Pain Inventory Fritz J, George SZ, Delitto A. The role of fear-avoidance beliefs in acute low back pain: relationships with current and future disability and work status. Pain;94(1):7-15

62. History Activity limitations Patient’s perception of problem Behaviors of symptoms

63. Clinical Exam Basic clinical exam AROM PROM Resisted testing Special provocative testing Severity ROM at painful point Neurodynamic testing David Butler Michael Shacklock

64. Exam Considerations History indicating peripheral / nociceptive mechanisms Green light for a thorough mechanical exam Combination of peripheral and central mechanisms Yellow light Strong indications of central mechanisms Minimalist exam

65. Determining “Central” Recent proposed model of assessment by Nijs and colleagues Diagnosis of central sensitization based on Diagnosis History Clinical exam Nijs J, Van Houdenhove BV, Oostendorp RA. Recognition of central sensitization in patients with musculoskeletal pain: Application of pain neurophysiology in manual therapy practice. 2010;14:1-7.

66. Diagnoses Associated with CS Characteristic of the Disorder Chronic whiplash Fibromyalgia Chronic fatigue Irritable bowel syndrome Present in a Subgroup Chronic LBP Subacute whiplash TMD Myofascial pain syndrome OA RA Chronic HA Nijs J, Van Houdenhove BV. From acute musculoskeletal pain to chronic widespread pain and fibromyalgia: Application of pain neurophysiology in manual therapy practice. Manual Therapy. 2010:1-7.

67. Historical Features of CS Characteristic of CS Hypersensitivity Light Noise Mechanical pressure Temperature Possibly related to CS Fatigue Poor sleep Difficulty concentrating Limbs feel “swollen” Paresthesias Nijs J, Van Houdenhove BV. From acute musculoskeletal pain to chronic widespread pain and fibromyalgia: Application of pain neurophysiology in manual therapy practice. Manual Therapy. 2010:1-7.

68. Clinical Testing for CS Assess sensory modalities at sites distant to injury Pain thresholds Touch Temperature Joint end feels Brachial plexus provocation Nijs J, Van Houdenhove BV. From acute musculoskeletal pain to chronic widespread pain and fibromyalgia: Application of pain neurophysiology in manual therapy practice. Manual Therapy. 2010:1-7.

69. Potential Combinations Current model suggests all mechanisms likely at play to some degree in determining pain Example: Patient s/p TKA with 3 year history of Knee pain Gait deviations Fear avoidance

70. Treatment Proposal Nijs J, Van Houdenhove BV. From acute musculoskeletal pain to chronic widespread pain and fibromyalgia: Application of pain neurophysiology in manual therapy practice. Manual Therapy. 2009;14:3-12.

71. Key Points Resolution between multiple variables (local, central, distributed) Treat local problems in the absence of strong psychosocial influences Address graded exposure to movement in the presence of strong psychosocial influences

72. Reducing Threat Inhibition of nociception Pain free manual or exercise intervention Careful not to activate non-nociceptive threats (fear / anxiety) Non-nociceptive threat reduction Pain education Explain Painby Moseley and Butler Caution against strict biomechanical explanations Butler D, Moseley L. Explain Pain. Adelaide, AUS: NoiGroup Publications 2003

73. Patient Guides Treatment Moseley GL A pain neuromatirx approach to patients with chronic pain. Manual Therapy. 2003; 8,3: 130-140.

74. Patient Guides Treatment Moseley GL A pain neuromatirx approach to patients with chronic pain. Manual Therapy. 2003; 8,3: 130-140.

75. Pacing and Graded Exposure Start with low baselines Build up tolerance gradually and systematically Take regular rest between activities Butler D, Moseley L. Explain Pain. Adelaide, AUS: NoiGroup Publications 2003

76. Pacing and Graded Exposure Do small amounts often rather than doing everything at once Avoid prolonged activity and avoid prolonged rest Do not rush to increase activity/exercise levels. Butler D, Moseley L. Explain Pain. Adelaide, AUS: NoiGroup Publications 2003

77. Pacing and Graded Exposure Justmaintaining the program can be beneficial Slow gradual approach enables long-term change

78. Additional Considerations Placebo response Aerobic exercise Environment of recovery

79. Placebo Response Expectation of pain increase shown to activate the thalamus, insula, and ACC Expectation of relief has similar but opposite effect and has been the focus of much investigation Negative and positive expectation-induced modulation of pain deserves consideration Colloca L, Sigaudo M, Benedetti F. The role of learning in placebo and nocebo effects. J Pain. 2008;136:211-218.

80. Placebo and Manipulation Does expectation influence outcome of SMT? Sixty healthy volunteers underwent quantitative sensory testing (QST) followed by manipulation Before the manipulation however…. Bialosky JE, et al. The influence of expectation on spinal manipulation induced hypalgesia: An experimental study in normal subjects. BMC Musculoskeletal Disorders. 2008;9(19)

81. Expectations were Primed Group 1 - “SMT is a very effective form of manipulation used to treat low back pain and we expect it to reduce your perception of heat pain.” Group 2 – “SMT is an ineffective form of manipulation used to treat low back pain and we expect it to temporarily worsen your perception of heat pain.“ Group 3 – “SMT is a form of manipulation used to treat low back pain that has unknown effects on perception of heat pain.“ Bialosky JE, et al. The influence of expectation on spinal manipulation induced hypalgesia: An experimental study in normal subjects. BMC Musculoskeletal Disorders. 2008;9(19)

82. Results All groups demonstrated hypoalgesic responses in the lower extremities to SMT regardless of expectation Hyperalgesia was present in the low back in subjects provided with negative expectations Bialosky JE, et al. The influence of expectation on spinal manipulation induced hypalgesia: An experimental study in normal subjects. BMC Musculoskeletal Disorders. 2008;9(19)

83. Conclusion? Evidence exists for the role of expectation as a mediator of the response to treatment Placebo response Nocebo response The role of expectation in any intervention must be accounted for before assigning specificity to the intervention itself Bialosky JE, et al. The influence of expectation on spinal manipulation induced hypalgesia: An experimental study in normal subjects. BMC Musculoskeletal Disorders. 2008;9(19)

84. Aerobic Exercise Very effective in reducing threat value of movement Reduction in sympathoexcitatory response to activity Reduction in sympathetic-sensory coupling SE Dicarlo, LK Stahl, VS Bishop. Daily exercise attenuates the sympathetic-nerve response to exercise by enhancing cardiac afferents. Am J Physiol - Heart Circ Physiol, 1997;42:H1606-H1610

85. Even Resistive Exercise! Study of 31 women with knee OA Acute resistive exercise 25 sets of 10 reps at 60% (whew) Significant increase in anti-inflammatory cytokine (IL-10) compared to controls Helmark IC, Mikkelson UR, Borglum J, et al. Exercise increases interleukin-10 levels both intraarticularly and perisynovially in patients with knee osteoarthritis: a randomized clinical trial. Arthritis Res Ther. 2010. July 1;12(4):R126 (ahead of print)

86. Environment of Recovery Progress visual and auditory intensity Less potential for activating pain neurosignature Use distraction during sensitizing movements Conversation Music the patient enjoys Butler D, Moseley L. Explain Pain. Adelaide, AUS: NoiGroup Publications 2003

87. Environment of Recovery Make treatment pleasant Feel free to laugh with your patient Sense level of self-consciousness Ensure early successes Affirmative language and priming Counsel proper sleep habits

88. Take Home Understand the development of modern pain theory Overview of the systems-based response to injury Basic and clinical research support for a broader approach to orthopedic cases

89. Remember! Orthopedics can be Formulaic Protocol driven Integration of multi-system approach Evidence informed Patient centered EFFECTIVE

90. Recommended Reading Butler D, Moseley L. Explain Pain. Adelaide, AUS: NoiGroup Publications 2003. Butler D. Sensitive Nervous System. Adelaide, AUS: NoiGroup Publications 2002. Jones M, Rivett D. Clinical Reasoning for Manual Therapists. Elsevier: 2004.

91. Questions or Comments Email roderickmpt@gmail.com

92. Thank You!