Integrative Treatment of Degenerative Disease

REHABILITATION OF NEURO-ORTHOPEDIC CHRONIC PAIN

Simon Voitanik, MD, PhD

What are the major advantages of integrative pain management and why does the traditional approach to chronic pain fail to give expected results?

To understand integrative pain management, consider these concepts:

I . Abandon linear thinking in which it is presumed that pain and inflammation are coming from a specific and identifiable source. Consider instead that pain is seated within a neuromatrix (40), in which pain may originate within a dysfunctional central nervous system.

2. The central nervous system may create or maintain peripheral inflammation via a dorsal root reflex (29). This process can be triggered by injury and inflammation in a site that is remote from where the patient perceives the pain. This is why local treatment may be useless for chronic pain.

Clinicians in our network are trained in manual medicine, prolotherapy, nerve blockade and acupuncture, which they integrate with neurology, orthopedic and sports medicine, and behavioral medicine, enabling them to understand and treat the complex mechanisms involved in chronic pain.

Exciting research in the neurophysiology of pain, such as the role of intraosseous pressure as a cause of pain, provide our physicians with additional modalities to provide relief to patients who have failed other pain treatment approaches.

Chronic pain is often the result of injury or deterioration of the body's connective tissue, coupled with a dysfunctional response to painful stimuli by the body's own nervous system. Thus, a muscle strain, joint sprain or bone bruise might provoke abnormal discharges in peripheral nerves, or in central nervous pathways, that perpetuate or even augment the pain. Our treatment program alleviates chronic pain by addressing these critical components of the pain control system. The following information is provided to aid your understanding of our treatment program.

PATHOGENESIS OF NEURO-ORTHOPEDIC PAIN

Degeneration of the spine and extremities results from normal wear and tear on bones, joints and their supporting structures. Overuse and injury cause additional deterioration, and in some persons, there is a genetic predisposition to premature degeneration of connective tissue. DIAGRAM #1

Genetic predisposition, repeated micro and macro injuries lead to degeneration of the connective tissue and result in pain and inflammation. For example, in degenerative disease of the spine, it has been shown that pain is generated by receptors within degenerated discs, facet joints, ligaments, compressed nerves, and other local tissues that are affected by degeneration. It also has been shown that increase of intraosseous pressure can augment pain perception. The spinal cord carries these painful stimuli to the brain which should, but doesn't always, respond by appropriate release of inhibitory neurotransmitters. The interconnections between the pain from damaged connective tissue and its mediation through the peripheral and central nervous system, give the pain specialist various levels at which the pain cycle can be interrupted.

SPINAL PAIN MODEL

Studies of the relationship between vertebral microtrauma and intraosseous pressure show that the subchondral endplate is the site most vulnerable to injury (35, 36). Damage to the endplate of the vertebral body affects diffusion to the disc and causes increased intraosseous pressure that induces pain (10, 22). Degeneration of discs is coupled with ligamentous weakness and subsequent instability of the spinal motion segments (two vertebrae, one disc, two zygapohyseal joints with associated muscles and ligaments). It leads to pain and a protective spasm of the small intervertebral and larger paravertebral muscles that support and mobilize the spine. Prolonged pain and muscle spasm leads to shortening of these muscles with accumulation of fibrotic tissue. The fibrous tissues are perceived as painful knots or "trigger points " in the body of the muscles. Such dysfunction of muscle due to shortening, fibrosis and spasm leads to increased intramuscular pressure and decreased blood flow, which has also been implicated in the pathogenesis of back pain (18). Additionally, shortening of the muscles decreases spinal mobility which puts increased stress on the already damaged ligaments as the individual continues to try to flex, extend and rotate his spine in the accomplishment of life's most basic tasks. Shortening of muscles also compresses nerves and blood vessels, further contributing to additional inflammation and pain. Patients may experience still more pain as neurons in the dorsal roots of the spinal cord become sensitized by the continuous pain impulses from the peripheral stimuli. Once sensitized, these neurons show increased background electrical activity, increased receptive field size, and increased response to peripherally applied stimuli. A retrograde pain stimulus may then result as dorsal root reflexes within the spinal cord release inflammatory neuropeptides from the terminals of the primary afferent nerves at the site of the original joint or muscle injury (29).

INTRAOSSEOUS PRESSURE

Bone is a dynamic composite of tissue with nociceptive neuropeptides present. It is particularly striking that adjacent bones of the vertebral column are united by large extraosseous veins in the spinal canal which are in continuity with the spinal veins (Fig.1.). Because the veins unite one vertebra with its neighbours, extensive regions of the column can be regarded from the vascular standpoint as a unit. It is also probable that venous drainage of the vertebral column is promoted by the pumping action of the muscles which have extensive attachments, particularly to the neural arch and its processes. It is noteworthy that rheumatoid and ankylosing spondylitis affect not isolated parts but considerable lengths of the vertebral column. It seems likely that venous impediment is a factor in the progress of these disorders, because the beneficial effects of physical medicine in their treatment can be attributed in no small measure to the promotion of venous drainage from the vertebral column. Wardle (52) and Helal (16) demonstrated radiographically in cases of osteoarthritis of the knee that venous congestion of the cancellous bone is present. They suggested that the beneficial effects of osteotomy in the surgical treatment of osteoarthritis, particularly the relief of pain when severe deformity has developed in the joint, seems to be due to surgical decompression of the veins of cancellous bone. A review of the literature by Sala D., et al (40)on patella hyperpressure measurement, clinical manifestation, diagnosis, and treatment indicates that there is sufficient evidence to consider patellar intraosseous hyperpressure as an important etiologic factor in patellar pain syndrome. As is well known, osteoarthritis of the spine affects not one but many joints, possibly because of the diffuse venous drainage of the vertebral column which takes in many joints in one vascular territory. It is this anatomical venous factor which gives osteoarthritis of the spine its generalized distribution, as distinct from that of the appendicular skeleton, where it is common for large joints to be singly attacked by the disease process

DIAGNOSIS AND REHABILITATION OF NEURO-ORTHOPEDIC PAIN

Our treatment of the patient with chronic pain includes diagnosis and alleviation of: muscle shortening, restricted range of joint motion, increased intraosseous pressure, radiculopathy, and central nervous system processes that perpetuate and/or augment pain (DIAGRAM 2.)

TISSUE INFILTRATION

If nociceptive impulses are thought to arise from a particular site then the injection of local anesthetic into that site should be of help in establishing the diagnosis. Painful scars generally are thought to be caused by the development of small neuromas. While some scars are diffusely tender, most scar pain is associated with very localized areas of tenderness. Injection of a small amount of local anesthetic into the affected muscle, joint, tendon sheath, scar, bursa, etc. helps to determine whether local anesthetic injection relieves the pain at rest as well as the pain produced by maneuvers that usually aggravate the pain.

MUSCLE SHORTENING

Muscle shortening, palpable as a taut muscle band, is treated by needling and infiltration (N&I) with local anesthetic. The anesthetic is injected into trigger points, myotendinal junctions, and tendinous attachments to bone, and is followed by needling these same areas (12, 14, 15). N&I breaks up pockets of fibrous tissue where nerve endings are entrapped with inflammatory, irritative substances (32, 50).

In addition, amide local anesthetics have potent and long-lasting anti-inflammatory properties (4). When paravertebral muscles are involved, N&I is preceeded by a somatic or medial branch block to decrease the pain of needling. N&I is often followed by electrical stimulation and ultrasound to improve blood circulation, stimulate tissue regeneration, and enhance needling effects. Botox, which inhibits muscle contraction by blocking the release of acetylcholine from peripheral nerves, appears to be an effective treatment for refractory myofascial pain syndrome (43, 44, 45).

RESTRICTED RANGE OF JOINT MOTION

The range of motion of the intervertebral joints can be diagnosed by manually examining "joint play" (20). With the patient prone, the examiner exerts a springing pressure against the different aspects of the spinous process. Healthy joints allow the adjoining vertebrae to deflect in the direction of the pressure, with little or no associated pain. But abnormal joints allow minimal deflection and induce pain. The manual technique of diagnosing vertebral joint dysfunction was determined to be as accurate as radiologically controlled diagnostic nerve blocks in a double blinded study (14). The restriction of the intervertebral joints may be a result of spasm or shortening of local muscles, shrinking of the joint capsule, or entrapment of the fat pads or meniscoids ( parts of the inner membrane of the joint capsules) between the articular surfaces of adjoining vertebrae. It is critical to realize that the restriction of intervertebral joints in a particular area of the spine may be the result of injury or dysfunction in a remote part of the spine. The entire musculoskeletal system behaves as a functionally linked kinetic chain and a localized tissue injury can produce functional biomechanical adaptations at locations some distance from the primary site of injury (33). It is therefore imperative that the clinician evaluates the entire spine with particular attention paid to the most susceptible to injury transitional zones, where the spine curvatures change between the kyphosis of the thorax and sacrum to the lordosis of the neck and low back. Treatment of restricted movement of the spinal motion segments involves manual manipulation/mobilization techniques. The therapist mobilizes a joint by passively moving it through its physiologic range. Smooth, repetitive passive joint oscillations at the limit of the joint's available range of motion can mechanically enhance the joint's mobility . Researchers have demonstrated that joint tissue can be manipulated to a level of "plastic deformation" along a "stress-strain curve" (26). Mobilization techniques have also been demonstrated to have neurochemical effects such as restoration of axonal transport and reduction in pain by stimulation of large-fiber joint afferent nerves with an associated release of endorphins (19). The patient is also taught self-mobilization and postisometric relaxation techniques that help maintain the effect of mobilization techniques performed in the office.

INCREASED INTRAOSSEOUS PRESSURE

Bone is a dynamic composite tissue containing nociceptive neuropeptides. The periosteum and the epiphyseal marrow appear to be the most richly innervated structures. At sites of fleshy muscle attachments the fibrous periosteurn is extremely tenuous, so that the intramuscular and periosteal circulations are continuous.

Bone pain can be caused by increased intraosseous pressure secondary to a variety of injuries and processes (1, 2, 17). It has also been shown that overstimulation of the intraosseous receptors enhances pain transmission (28). Bone pain can be effectively treated by several modalities: periosteal injection with 1% procaine improves bone blood supply. Stimulation of periosteal receptors with electroaccupuncture or infiltration with a 5 - 10% dextrose solution has been shown to have an analgesic effect on intraosseous receptors involved in pain transmission (5, 16). Intraosseous injection of 1% lidocaine can further decrease intraosseous pressure and enhance the success of local nerve blocks (23, 27, 25).

RADICULOPATHY

Radicular pain is usually the result of nerve compression due to disc herniation, paravertebral muscle spasm or both. The presence and degree of sensory nerve compression and degeneration can be diagnosed by "quantitative sensory testing," (QST) an office procedure whereby the patient"s responses to calibrated heat and cold are evaluated along neurodermal distributions (8, 24). Treatment for radicular pain includes epidural injections and/or nerve blocks. Research implicates the nervi nervorum, the small nerves that innervate the large nerve roots, in the pathogenesis of radicular pain (31) that can be treated by infiltration with a local acting anesthetic and or corticosteroids. If treated early, nerve root injury caused by an extruded nucleus pulposus or herniated disc, can be reduced by injection of lidocaine (34). Nerve root injury can also be alleviated by treating the spasm of paraspinal muscles by the needling and infiltration and physical therapy methods already mentioned. It has also been shown that paravertebral muscle spasm, caused by irritation from spinal disc herniation, can be alleviated by injection of a saline or dextrous solution into the capsule of the associated zygapophysial joints (15)

PROLOTHERAPY

Prolotherapy is a form of medical treatment of chronic soft tissue injuries. By injecting a substance (ordinarily 12,5% Dextrose with 1% Lidocaine ) designed to create a mild inflammatory reaction the physician can re-create the chemical environment of a acute injury and trigger the proliferation of a collagen. Clinical research studies (41, 42) have shown a 75% success rate in chronic musculoskeletal pain patients treated by this technique.

CENTRAL NERVOUS SYSTEM

An important concept in chronic pain is the tendency for constant C-fiber stimulation to sensitize pain transmission pathways in the spinal cord resulting in increased release of inflammatory neurotransmitters. Thus the central nervous system response to pain can keep increasing even though the painful stimulus from the periphery remains steady. This "wind-up" phenomenon in deep dorsal neurons can dramatically increase the patient's sensitivity to the pain. This mechanism of sensitization or wind-up can be alleviated by activation of descending pathways that stimulate inhibitory neurons that may help suppress pain. Methods of treatment include appropriate use of antidepressant pharmaceutical agents and acupuncture. Central nervous system pain control mechanisms can also be impacted by treatment of peripheral nerve pathways. For example, PENS therapy (percutaneous electrical nerve stimulation) can relieve pain by stimulating A and B fibers in the sclerotomal and myotomal distribution which correspond to the patient's pain pattern (3) Pain relief may be further enhanced by pre-injecting 0.5% lidocaine, which blocks A-delta and C fibers from transmitting painful stimuli.

Expected Results of Treatment

Though there are many variables that will influence treatment outcome, including duration and degree of pathology, the typical patient can expect four to six treatment sessions to reduce pain approximately fifty percent and to be able to increase physical activity about thirty percent.

Summary of Neuro-Orthopedic Pain Management

References

1. Arnoldi CC, Djurhuus JC, Heerfordt J, Karle A Intraosseous phlebography, intraosseous pressure measurements and 99mTC-polyphosphate scintigraphy in patients with various painful conditions in the hip and knee. Acta Orthop Scand 1980 Feb;51(1):19-28

2. Arnoldi CC, Lemperg K, Linderholm H Intraosseous hypertension and pain in the knee. J Bone Joint Surg [Br] 1975 Aug;57(3):360-3

3. Ahmed AA, Craig WF, White PF, Huber P: Percutaneous Electrical Nerve Stimulation (PENS): A Complementary Therapy for the Management of Pain Secondary to Bony Metastasis. The Clinical Journal of Pain, 14: 320-323, 1998

4. Ben-David B et al: Comparison of i.m. and local infiltration of ketorolac with and without local anesthetic. Br J Anesth, 75(4):409-412, 1995

5. Bilibin DP, Sokov EL, Chodorovich HA, Churukanov BB, Shevelev OA: Visceral afferentation and pain. Moscow 1998 pp. 143-189

6. Bove GM, Light AR: The nervi nervorum. Missing link for neuropathic pain? Pain Forum, 6(3):181-190, 1997. 91 References Institute of Medical Biology, Dept of Anatomy & Cell Biology, Odense University, Campusvej 55, 5230 Odense M, Denmark (Dr GM Bove) TN.01 MY9811/131 ã1998

7. Castro-Lopes JM, Tavares I, Tolle TR, Coimbra A: Carrageenan-induced inflammation of the hind foot provokes a rise of GABA-immunoreactive cells in the rat spinal cord that is prevented by peripheral neurectomy or capsaicin treatment, Pain 56; 193-201, 1994

8. Chado HN: The current perception threshold evaluation of sensory nerve function in pain management. Pain Digest: 5:127-134, 1995

9. Dray A; Inflammatory mediators of pain. Br J Anesth, 75(2); 125-131, 1995

10. Esses SI, Moro JK Intraosseous vertebral body pressures Spine 1992 Jun;17(6 Suppl):S155-9

11. Fischer AA, New Approaches in Treatment of Myofascial Pain Physical Medicine and Rehabilitation Service, Veterans Affairs Medical Center, Bronx; and the Department of Rehabilitation Medicine, Mount Sinai School of Medicine, City University of New York, New York, New York. From: PHYSICAL MEDICINE AND REHABILITATION CLINICS OF NORTH AMERICA V'OLUME 8 - NUMBER I - FEBRUARY 1997

12. Gunn CC: The Gunn Approach to the Treatment of Chronic Pain. New York, Churchill Livingstone, 1996

13. Gunn CC, Milbrandt WE, Little AS, et al: Dry needling of muscle motor points for chronic low-back pain: A randomized clinical trial with long-term follow-up. Spine 5:279-291,1980

14. Jull G, Bogduk N, Marsland A: The accuracy of manual diagnosis for cervical zygapophysial joint pain syndromes. The Medical Jornal of Australia Vol. 148 March 7, 1988 pp 233-236

15. Indahl A, Kaigle AM, Reikeras O, Holm SH "Interaction between the porcine lumbar intervertebral disc, zygapophysial joints, and paraspinal muscles." Spine 1997 Dec 15;22(24):2834-40

16. Ishimaru K, Kawakita K, Sakita M Analgesic effects induced by TENS and electroacupuncture with different types of stimulating electrodes on deep tissues in human subjects. Pain 1995 Nov;63(2):181-7

17. Kiaer T, Gronlund J, Sorensen KH Subchondral pO2, pCO2, pressure, pH, and lactate in human osteoarthritis of the hip.Clin Orthop 1988 Apr;(229):149-55

18. Konno S, Kikuchi S, Nagaosa Y The relationship between intramuscular pressure of the paraspinal muscles and low back pain. Spine 1994 Oct 1;19(19):2186-9

19. Korr IM: Neurochemical and neurotropic consequences of nerve deformation. In Glasgow EF et al (eds): Aspects of Manipulative Therapy. Melbourne, Churchill-Livingstone, 1985, pp 64-71

20. Maigne R: Diagnosis and Treatment of Pain of Vertebral Origin. Baltimore, Williams & Wilkins, 1996

21. Mense S: Nociception from skeletal muscle in relation to clinical muscle pain. Pain, 54: pp241-289,1993

22. Moore MR, Brown CW, Brugman JL, Donaldson DH, Friermood TG, Kleiner JB, Odom JA Jr Relationship between vertebral intraosseous pressure, pH, PO2, pCO2, and magnetic resonance imaging signal inhomogeneity in patients with back pain. An in vivo study. Spine 1991 Jun;16(6 Suppl):S239-42

23. Nusstein J, Reader A, Nist R, Beck M, Meyers WJ Anesthetic efficacy of the supplemental intraosseous injection of 2% lidocaine with 1:100,000 epinephrine in irreversible pulpitis. J Endod 1998 Jul;24(7):487-91

24. Nygaard OP, Mellgren SI: The function of sensory nerve fibers in lumbar radiculopathy. Use of quantitative sensory testing in the exploration of different populations of nerve fibers and dermatomes. Spine 1998 Feb 1;23(3):348-52;

25. Parente SA, Anderson RW, Herman WW, Kimbrough WF, Weller RN Anesthetic efficacy of the supplemental intraosseous injection for teeth with irreversible pulpitis. J Endod 1998 Dec;24(12):826-8

26. Paris S: Mobilization of the spine. Phys Ther 59:988-955, 1979

27. Reitz J, Reader A, Nist R, Beck M, Meyers WJ Anesthetic efficacy of the intraosseous injection of 0.9 mL of 2% lidocaine (1:100,000 epinephrine) to augment an inferior alveolar nerve block. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998 Nov;86(5):516-23

28. Shevelev OA, Sokov EL The characteristics of the modulation of the afferent reactions during stimulation of the intraosseous receptors Biull Eksp Biol Med 1993 Jun;115(6):587-9

29. Sluka KA Pain mechanisms involved in musculoskeletal disorders. J Orthop Sports Phys Ther 1996 Oct;24(4):240-54

30. Sokov EL Intraosseous blocks--the pathogenetic treatment of the pronounced neurological manifestations of lumbar osteochondrosis.Ter Arkh 1993;65(11):74-7

31. Sorkin LS et al: Role of the nervi nervorum in neuropathic pain. Innocent until proven guilty. Pain Forum, 6(3):191-192, 1997. 11 References Dept of Anesthesiology 0629, University of California, San Diego, 9500 Gilman Dr., La Jolla, CA 92093-0629

32. Sorkin LS et al: Neural changes in acute arthritis in monkeys. IV. Time-course of amino-acid release into the lumbar dorsal horn. Brain Res Rev 17: 39-50, 1992

33. Tollison CD, Satterthwaite JR, Tollison JW: Handbook of Pain Management Second Edition pp 91-93

34. Yabuki S et al.: Effect of lidocaine on nucleus pulposus-induced nerve root injury. A neurophysiologic and histologic study of the pig cauda equina. Spine, 1998, Nov 15;23(22):2383-9

35. Yoganandan N, Maiman DJ, Pintar F, Ray G, Myklebust JB, Sances A Jr, Larson SJ Microtrauma in the lumbar spine: a cause of low back pain. Neurosurgery 1988 Aug;23(2):162-8

36. Yoganandan N, Larson SJ, Gallagher M, Pintar FA, Reinartz J, Droese K Correlation of microtrauma in the lumbar spine with intraosseous pressures. Spine 1994 Feb 15;19(4):435-40

37. Zimmerman M: Components of pain and pain-associated phenomena in the rnusculo- skeletal system. In Jayson MIV, Sweziey RL, Knoplich J, et al: Back Pain, Painful Syndromes and Muscle Spasm: Current Concepts and Recent Advances. New Jersey, The Parthenon Publishing Group Ltd, 1990, pp 29-52

38. Zohn DA: Musculoskeletal Pain. Boston, Little, Brown and Company, 1988

39. Willis WD Jr: An alternative mechanism for neuropathic pain. Nervi nervorum. Pain Forum, 6(3):193-195, 1997. 28 References Dept of Anatomy and Neurosciences, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1069 (Dr WD Willis, Jr)

40. Melzack, R "Pain ? an overview" Acta Anesthesiol Scan 1999; 43: 880-884

41. KLEIN RG, EEK BC, DELONG WB, MOONEY V A RANDOMIZED DOUBLE-BLIND TRIAL OF DEXTROSE-GLYCERINE-PHENOL INJECTIONS FOR CHRONIC, LOW BACK PAIN. SANSUM MEDICAL CLINIC, DEPARTMENT OF ORTHOPAEDIC MEDICINE, SANTA BARBARA, CA J SPINAL DISORD 1993 FEB;6(1):23-33

42. Ongley MJ, Klein RG, Dorman TA, Eek BC, Hubert LJ A new approach to the treatment of chronic low back pain. Lancet 1987 Jul 18;2(8551):143-6

43. Cheshire WP, Abashian SW, Mann JD Botulinum toxin in the treatment of myofascial pain syndrome. Pain 1994 Oct;59(1):65-9

44. Porta A comparative trial of botulinum toxin type A and methylprednisolone for the treatment of myofascial pain syndrome and pain from chronic muscle spasm. M Pain 2000 Mar;85(1-2):101-5 45. Wheeler AH, Goolkasian P, Gretz SS A randomized, double-blind, prospective pilot study of botulinum toxin injection for refractory, unilateral, cervicothoracic, paraspinal, myofascial pain syndrome. Spine 1998 Aug 1;23(15):1662-6; discussion 1667