1. Conservative Management of Joint Pain John C. Hughes, D.O. Aspen Integrated Medicine
2. Overview: Osteopathic Treatment of Joint Pain Osteopathic Medicine: DO defined, Principles DO techniques for knee, back, hip, shoulder pain: Direct versus Indirect Focus: Counterstrain Injectional Therapy for joint pain Pathophysiology of Joint injury Proliferative Therapy Medications/ Supplementation for Pain
3. Osteopathic Medicine: DO history Developed in the late 1800’s alongside allopathic (M.D.) medicine Founded by A.T. Still, M.D., who rejected the harsh drug treatments used then for manual medicine Still was accepted by the medical community but chose to start his own schools because his holistic philosophy was fundamentally different
4. Osteopathic Medicine: DO Defined Many D.O.’s practice in typical allopathic settings as surgeons, internists, or primary care settings Traditional osteopathic doctors make up about 10% of all those trained and are those who continue to utilize their hands to manually treat patients.
5. Osteopathic Medicine: DO Defined A D.O. is different than the other therapists because, in the U.S., a D.O. is a medical physician Traditional osteopathic doctors use very specific forms of manual medicine, unlike any other manual therapist. An important note: A D.O. is not a therapist. When an osteopathic doctor places his or her hands on a patient, he or she is practicing medicine. Insurance companies reimburse D.O.’s at a higher rate for osteopathic manual medicine than any other manual therapies
6. Osteopathic Medicine: DO Principles 1) The body is a unit; one cannot treat a part of the body without consider its entirety. 2) Structure and function are reciprocally interrelated. 3) The body is capable of self-regulation, self-healing, and health maintenance. 4) The nervous system controls, influences, and integrates all bodily functions. 5) Rational treatment is based on an understanding of these principles.
7. Osteopathic Techniques for Joint Pain counterstrain indirect balancing myofacial release cranial therapy lymphatic drainage facilitated positional release HVLA, muscle energy
8. Osteopathic Techniques: Direct Direct: Attempt to direct body parts into and often through their physiological and anatomical barrier Examples: Muscle Energy, HVLA (High Amplitude, Low Velocity), Stretching, ROM exercises Demo Great for Cervical, Mid-Back, Low back somatic dysfunctions (facet joints, intercostal areas, some tight muscles, “frozen” shoulders) in young, healthy patients Used by Chiropractors, Physical Therapists frequently
9. Osteopathic Techniques: Direct Pros: Often provides quick relief for patients, can encourage healthy physiology Cons: Rarely provides permanent changes to the tissue, patient has to return frequently to find relief Rationale: The body cannot adapt and hold to the often abrupt changes created by these often rapid lengthening therapies (that go beyond the physiologic barrier) Dangers: Can be damaging to body tissues, joints
10. Osteopathic Techniques: Indirect Indirect: Attempt to direct body tissues (muscle, bone, fascia, tendons) away from their anatomic or physiological barrier Examples: counterstrain indirect balancing myofacial release cranial therapy
11. Osteopathic Techniques: Indirect Pros: More sophisticated techniques as they work with the body’s own physiology; great for older, post- surgical patients, after trauma; very effective and calming to the body; provide lasting, often permanent changes; not forceful–minimal risk of damaging tissue Rationale: The body can adapt to the physiological changes fostered by indirect techniques Cons: Require more patience and more time to do techniques; difficult for patients to do own their own; do not provide immediate “popping” sounds
12. Indirect Techniques: Counterstrain Used mostly by traditional osteopathic doctors, some chiropractors, and a few physical therapists Counterstrain: Developed by Laurence Jones, D.O. Definition: “a passive positional technique that places the body in the position of greatest comfort, thereby relieving pain by reduction and arrest of inappropriate proprioceptor activity that maintains somatic dysfunction”
13. Counterstrain: How does it help? A “somatic dysfunction” might be defined as any body part dysfunction that presents itself with a restriction of motion, tissue texture changes, asymmetry, or temperature changes For example: A knee joint sprain presents with restriction of motion The knee joint motion is most restricted at one point Likewise, the knee joint is also least restricted at one point Demo
14. Counterstrain: How Does It Work? Technique: Could be thought of as the opposite of stretching (as the goal is to find the greatest position of ease) Directed not at tissue damage itself but to the “aberrant neuromuscular reflexes within the tissue” In particular, counterstrain is directed at muscle spindles within the extrafusal fibers of muscles Muscle spindles are highly specialized sensory receptors which consist of a connective tissue sheath holding 5-12 intrafusal fibers (about 3mm long each)
15. Counterstrain: How Does It Work for Pain? On the polar, contractile ends of these intrafusal fibers, there are gamma motor neurons that terminate there after originating on the ventral horn The contractile ends of the intrafusal fibers are sensitive to changes in length (that occurs with muscle stretching) When the extrafusal fibers of the muscle are stretched, the intrafusal fibers are activated to resist the stretch through an efferent neurofeedback to the gamma motor neurons
16. Counterstrain: How does it Work for pain? The gamma motor neurons thus provide a necessary CNS control to allow appropriate stretching and resistance With more stretching of the large extrafusal muscle fibers (as often occurs with trauma, aka somatic dysfunction), there is more gamma motor stimulation so there is a greater reflexive resistance to the stretch created by feedback from the intrafusal muscle fibers
17. Counterstrain: How does it Work for pain? In short, the greater the trauma/ the greater the stretch, the more gamma excitement is present in the CNS Counterstrain works by approximating the muscle by passive shortening in order to decrease gamma gain (aka gamma excitement) to turn off the reflexive contraction by initiated by the intrafusal fibers of the muscle spindles A muscle that has been approximated can then return to its lengthened form allowing increased range of motion, less spasm, and ultimately less pain
18. Counterstrain: How does it Work?
19. Counterstrain: Figures
20. Counterstrain: Figures
21. Clinical Data: Counterstrain “Effect of Counterstrain on Stretch Reflexes, Hoffmann Reflexes, and Clinical Outcomes in Subjects With Plantar Fasciitis” JAOA • Vol 106 • No 9 • September 2006 • 547- 556 Conclusions: Clinical improvement occurs in subjects with plantar fasciitis in response to counterstrain treatment. The clinical response is accompanied by mechanical, but not electrical, changes in the reflex responses of the calf muscles. http://www.jaoa.org/cgi/content/full/106/9/547
22. Clinical Data: Counterstrain “Stretch Reflex and Hoffmann Reflex Responses to Osteopathic Manipulative Treatment in Subjects With Achilles Tendinitis” JAOA • Vol 106 • No 9 • September 2006 • 537-545 Conclusion: The reduction of stretch reflex amplitude with OMT, together with no change in H-reflex amplitude, is consistent with Korr’s proprioceptive hypothesis for somatic dys-function and patient treatment. Because subjects’ soreness ratings also declined immediately after treatment, decreased nociceptor activity may play an additional role in somatic dysfunction, perhaps by altering stretch reflex amplitude. http://www.jaoa.org/cgi/content/full/106/9/537
23. Counterstrain: Further References Korr’s Theory http://www.jiscs.com/PDFs/CH13SCS.pdf “Immediate effects of the strain/counterstrain technique in local pain evoked by tender points in the upper trapezius muscle” Clinical Chiropractic, Volume 9, Issue 3, Pages 112-118 http://linkinghub.elsevier.com/retrieve/pii/S14792354060007 33 osteopathic treatment when compared to standard medical treatment helped patients with chronic injuries find pain relief in less visits and less medication http://content.nejm.org/cgi/content/abstract/341/19/1426
24. Injectional Therapy for joint pain: Physiology of Acute Sprains Inflammation phase–damaged cells release cytokines and other mediators that cause vascular dialation and permeability PMLs, followed by macrophages enter the scene and along with other cells, stimulate the migration and proliferation of fibroblasts Proliferative phase of connective tissue healing–fibroblasts encourage synthesis of procollagen matrix (2-3 days after injury) Vascular buds form increasing blood supply (3-4 days) and new tissue forms
25. Injectional Therapy for joint pain: Physiology of Acute Sprains Remodeling phase: Collagen type I changes to collagen type III and fibrils increase along lines of stress to become tightly packed (2-3 weeks) Collagen thickens and increases to preinjury length but with only 50 to 70 % tensile strength (without additional injury to stimulate fibroblasts) With severe injury, the healing process may stop before the tissue is sufficiently competent for everyday use The term “degenerative” is often used to describe this inadequate healing and resulting body structure (other terms include chronic tendonitis, DDD, OA, etc.)
26. Injectional Therapy for joint pain: Degenerative, Chronic Tissue-Why painful? “Nerve density at periosteum and periosteal attachments of tendons and ligaments is 2nd only to skin” Without functional sufficiency, pain mechanoreceptors function as chronic nociceptors
27. Injectional Therapy for Joint Pain: Is blocking inflammation the answer? Cortisone injections: block inflammation, stop the healing cascade, decrease immune function (risking microbial infection), cause tendon weakening, atrophy, or ruptures Antinflammatory medications: block healing cascade
28. Injectional Therapy for joint pain: What is Proliferative Therapy? Prololiferative therapy (or Prolotherapy) is defined as the injection of irritant or proliferant solutions into the affected ligaments, tendons, and/or joints. This type of injection leads to local inflammation in the injected area. The localized inflammation triggers a wound healing cascade, resulting in the deposition of new collagen, New collagen shrinks as it matures. The shrinking collagen tightens the ligament that was injected and makes it stronger
29. Injectional Therapy: History of Prolotherapy The concept of Prolotherapy originated in the non-surgical treatment of hernias, varicose veins, and hemorrhoids, If the connective tissue in the veins becomes weakened, hemorrhoids and varicose veins form. Weakness in the collagen, of course, causes ligament laxity and tendon degeneration with resultant chronic pain. Most of the early innovators in injection treatment method were surgeons who were looking for methods to improve surgical outcomes or replace surgery with more conservative methods.
30. Injectional Therapy: History of Prolotherapy The injection of hernias, varicose veins, and hemorrhoids was called Sclerotherapy, because the injection “sclerosed,” or scarred, the area. Hippocrates, the father of Western medicine, introduced heated metal probes into the dislocated and painful shoulders of javelin throwers. He believed that this would tightened the shoulder capsule by creating tough scar tissue and that the scar tissue would keep the shoulder in place. Dr. George S. Hackett developed modern prolotherpy beginning in 1939; Unlike the sclerotherapists, Hackett used an irritant that helped proliferate healthy collagen
31. Prolotherapy: Solutions, Technique Proliferative substances have varied over the decades but have included phenol, glycerin, sodium bicarbonate, dextrose, sodium morruhate, hypertonic saline Dextrose is commonly used as a proliferant today These substances are injected at the bony attachments of tendons and ligaments to improve their integrity
32. Prolotherapy: Explained Dextrose is thought to “dehydrate” the injected tissues, causing an injury signal for the body, and initiating the healing process. Dextrose has been shown to be a growth stimulant on it’s own as well. This healing process is one of inflammation restarts the normal healing cascade that would occur with an acute injury
33. Prolotherapy: Clinical Evidence 1800 patients followed for 2 years; 80% showed marked improvement in upper and lower body pain; Hackett GS: Prolotherapy in whiplash and low back pain. Postgrad Med 27:214-219, 1960 Two RCTs (160 participants) found that prolotherapy injections, given with spinal manipulation, exercise, and other therapies, are more effective than control injections for chronic low-back pain and disability. http://www.cochrane.org/reviews/en/ab004059.html
34. Prolotherapy: Clinical Evidence 60% increase in collagen fibril diameter measured at 3 months after 6 weekly injections in patients with low back pain; Klein RG, Dorman TA, Johnson CE: Proliferant Injections for Low Back Pain: Histological Changes of Injected Ligagments and Objective Measurements of Lumbar Spine Mobility Before and After Treatment J Neurol Orthop Med Surg 10: 141-144, 1989 Osmolarity studies: Elevation osmolarity by as little as 50 mOsm has been found to activate multiple growth factors including PDGF
35. Prolotherapy: Clinical Evidence Response of Knee Ligaments to Prolotherapy in a Rat Injury Model; Am J Sports Med July 2008 vol. 36 no. 7 1347-1357 Conclusion: Dextrose injections increased the cross- sectional area of MCLs compared with saline-injected and uninjured controls. Dextrose injections did not alter other measured properties in this model.
36. Prolotherapy: Clinical Evidence A systematic review of four injection therapies for lateral epicondylosis: prolotherapy, polidocanol, whole blood and platelet-rich plasma; British Journal of Sports Medicine 2009;43:471-481 Conclusions: There is strong pilot-level evidence supporting the use of prolotherapy, polidocanol, autologous whole blood and platelet-rich plasma injections in the treatment of LE.
37. Medications/ Supplementation for Pain Oral Supplements: Traumeel Systemic Enzymes Curcumin SOD Oral Medications: 1st choice: Ultram 2nd choice: Percocet or Tylenol Not recommended: Ibruprofen, other Cox 2, steroids
38. Medications/ Supplementation for Pain Topical Medications: Lidocaine cream (post- operative neuralgia) Topical Supplements: DMSO Traumeel Capsaicin
39. Other Supplements/ Medications: Glucosamine Hyaluronic Acid (Injections): occasional
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