QuestionHi, I have some queries to my neck and shoulder pains, I was invovled in a car accident. At that time i was alighting, and the door was half opened when the car was being moved forward. The Door closed hit my elbow and i got a jerk back to the chair as i was not having the seat belt on. Now the pain is pretty consistent its like hard muscles and aching in the mornings when i wake up. Not much of a peaceful sleep. My xray states that my neck could have been ultered to straight during the whiplash. I would like to know if you can advise on what is the possible cures and remedy to this. Thanks.
AnswerDear Ellen,
Whiplash injuries often compromise the structure of the spine in the neck due to the transfer of energy. The fact that you were half in the car at the time of impact compounds the issue because the kinematics are changed from a purely liner collision. The bottom line is that you probably have disk injuries as well as ligamentous injuries in the neck. In addition to spinal adjustments, these "soft tissue injuries" need to rehabilitated with resistive exercises, disk decompression (axial traction), and structural directional traction to restore the lost curve. It is an intense program, but serves to limit the injury and restore function. This is the same protocol I use daily in my clinic, and has been formulated from years of research, training and clinical judgement.
Unfortunately, I cannot help you personally with the rehab program, but I will include the written copy of my treatment protocols along with the research behind them. I can help you with the nutritional aspects though, as I can facilitate connection with metabolic testing for nutraceutical management of inflammation, tissue repair, and pain relief by hooking you up with the companies I utilize daily with my patients...just call the clinic, or e-mail me through my website and I will get you the information. Until then read over the below treatment protocols, show them to your doctors, and additionally check out the below websites:
www.ideaslpine.com
www.srisd.com
Respectfully,
Dr. J. Shawn Leatherman
www.suncoasthealthcare.net
CHIROPRACTIC TREATMENT PROTOCOLS FOR CRASH INJURIES
Risks and Benefits of Management Options: There is a risk that chiropractic treatment will have a temporary increase in the pain experienced by the patient due to mobilization of inflammatory mediators that are present in injured and inflamed tissues such as; cytokines, proteolytic enzymes elastase, trypsin, chymotrypsin, plasmin, cathepsins & collagenase, growth factors (PDGF & TGF-?, chemotactic agents for neutrophils (12-HETE, PF-4, & PAF), enzyme inhibitors (alpha-1- antitrypsin, alpha-2-macroglobulin), clotting factors, serotonin, thromboxane A-2, platelet activating factor, platelet factor-4, interlukin-1-? thromboglobulin-? tumor necrosis factor (TNF), and substance P. (2,4,6,12,14,16,17,25,28,30,31,32,38,40,44,56,61,68) All of these mediators are released in the acute inflammatory process and persist into the secondary phase of inflammation. Many have been connected to nociceptive (pain promoting) input to the tissues. TNF and IL-1 have also been shown to contribute to joint injury and bone resorption. (56) They may also act as pyrogens similar to prostaglandins/eicosanoids. (16)
Benefits of care are that with passive modalities, controlled early mobilization of injured tissues through chiropractic adjustments, and proper nutritional supplementation; aberrant processes can be limited and sometimes reversed by supplying increased oxygen and blood supply to the tissues. Therefore, pathways are established inducing proper nutrient delivery for repair, stimulated lymphatic channels pull inflammatory mediators away from injured tissues, and normal neurological input is instituted to the brain for improved proprioception through the dorsal columns. Pain control is modulated locally due to the gate theory reflexes. Activation of the opiate receptors, stimulate the descending inhibitory pathways of the peri-aquaductal grey regions in the reticular formation of the lower brain. The nucleus raphe magnus is stimulated and serotonergic projections extend down the cord, synapse with interneurons in the superficial dorsal horn, which release enkephalins and result in inhibition of the nociceptive system. (22,23) According to Wyke, these are the same inhibitory neurons that are stimulated as joint mechanoreceptor afferents are depolarized from a chiropractic adjustment. (66)
揝oft tissue injuries?encompass anything that is not bone including organ systems, nervous tissue, cartilage, musculature, ligaments, tendons, and fascial tissue. Muscle has a high reparative capacity and sufficient regenerative capacity, but extensive damage results in scarring and atrophy of the fiber bundles. (17) In contrast, tendons and ligaments are notably slow to heal! Even after forty weeks, collagen may still not be present in normal concentration and organization. (21) Articular cartilage, which is found in every zygapophyseal joint in the spine, has a notoriously limited potential for either healing or regeneration. (48) The ability of articular cartilage to heal will depend on the severity of injury. Patients requiring surgery are the least likely to heal. (48) In relation to acceleration/deceleration type trauma from vehicular crashes, the cartilaginous surfaces of the facet, (a.k.a. the synovial folds), are exposed to tremendous loading moments with sheer, compression, tensile, and torsional forces. Major cartilaginous damage is probable throughout the spine along with ligament disruption and is responsible for sclerotogenous pain patterns experienced by patients.
Regarding patient care, immobility is a main factor that promotes degeneration. The restoration of mobility seems to curtail degeneration. Previous research has demonstrated that the tensile strength of ligaments and tendons respond to changes in physiologic stress and motion that aid the healing process. Improving mobility can even enhance cartilage healing after traumatic injuries as well as the strength and stiffness of ligamentous structures. Furthermore, after trauma, healing occurs by an unspecified form of collagen, scar tissue, which frequently causes adhesions and fibrotic changes that must be dealt with therapeutically. Chiropractic adjustments improve and restore motion and movement patterns in the zygapophyseal joint at the facet articulations which include the ligamentous, myotendinous, and fascial complexes. With the addition of carefully progressed passive and active rehabilitation programs, further mobility can be achieved due to increased stretch and flexibility.
Instructions/Explanations for Treatment: Acute phase-emphasis is placed on limiting the inflammatory response and reducing pain. The use of interferential current aids this process by increasing lymphatic drainage as well as increasing blood flow, oxygenation and nutrient delivery to the injured tissues. We use specific nutraceuticals in the early phase of treatment such as pro-enzymes; malic acid, magnesium, omega III fatty acids, bromelain, tumeric, and zinc. These agents have been proven to inhibit and reduce inflammation, maximize the bioavailablity of repair materials for soft tissue healing, and provide neurological support. (6,7,8,9,10,11,18,19,26,29,33,34,35,37,39,43,46,47,49,51,52,54,56,62) Cryotherapy is an important part of this early phase for its analgesic and anti-inflammatory effects. Passive techniques are used mostly in this phase of care. Massage may be utilized as well to facilitate the relaxation of myospasm, mobilize fascial slings and bands, and inhibit trigger points with Nimmo technique. (13)
Sub-acute phase-emphasis is on the incorporation of active participation of the patient in their care. Home exercises and stretches are taught in this phase and are to be performed either three times weekly or daily depending on patient progress and tolerance. (31) This will facilitate increases in the mobility of injured tissues while limiting the formation of adhesions and abnormal scar tissue. (5,20,53,64)) Nutritional supplementation continues throughout this stage as well as chiropractic adjustive techniques. Ultrasound techniques may be used to increase the microcirculation, break up deeper adhesions and/or trigger points and muscle spasms that are becoming chronic, promote increased oxygen uptake, and increase the plasticity of collagen. (42,67) Patients will generally have their first re-evaluation in this stage of care to ensure that they are ready for active rehabilitation.
Physical rehabilitation phase-emphasis in this stage is to continue with reduction of pain, actively stimulate joint mechanoreceptors, Golgi tendon organ and muscle spindle cells to increase proprioceptive information as well as focusing on building strength, stability, and increasing active functional ranges of motion. (31) Substantial evidence exists confirming that ligaments serve important roles as signal sources for the reflex systems of the locomotor apparatus, (63) therefore effort should be made to normalize and mimic normal function after trauma. The introduction of significant amounts of proprioceptive training in the rehabilitation process is paramount, and aids in the reorganization of the tissue. (65) Reorganization of collagenous scar tissue is important. It creates increased tensile strength as well as promoting the break down of the abnormal cross bridges, aligning the scar along the physiological action of the muscle, tendon or ligamentous complex. (27,41,45,55,57) Healing times for intra-articular collagen are such that it may take up to 3 months to achieve 50 percent of the normal strength and 6 months before a functional strength of 70 percent is reached. (15,69) Essentially, collagen forms 70 percent of the dry weight of the ligament, turning over slowly with a half-life of 300 to 500 days. (24) Maximum functional improvements may take over 2 years for resolution.
Chiropractic adjustive techniques remain the cornerstone of the program to ensure that the zygapophyseal joint biomechanics are proper as facets continue to articulate correctly and send mechanoreceptive information to higher brain centers, and to reduce the neoneuralization of scar tissue. Neoneuralization increases pain transmission to the brain via nociceptive input from the synaptic arborization of c-afferent fibers. The goal is to limit and inhibit this process so that neurological wind-up does not occur and lead to chronic pain and residual disability. Stretching/AROM, resistance training incorporating bands and weights, physioball training, dynamic spinal traction and postural exercises are utilized for maximum benefit.
Dynamic spinal traction for structural remodeling and rehabilitation is utilized to maximize the physiological effects of creep, hysteresis, and set that occur in viscoelastic tissues such as ligaments. (64) The ligamentous complex is the limiting factor in effective rehabilitation. (36,53) Only sustained incremental loading of the ligamentous tissues with low force of long duration, in a consistently applied manner, will have the desired structural viscoelastic effect of plastic changes. (31,59,60) Cryotherapy is also utilized in traction due to research indicating that tissues stretched under heating conditions and then allowed to cool under tensile conditions maintain a greater proportion of their plastic deformation than do structures allowed to cool in the unloaded state. Cooling under tension may allow the collagenous microstructure to stabilize at the new stretched length. (36,60)
**Our office protocols have been established to facilitate application of the above techniques, nutrition/ supplementation and information; therefore maximizing injury repair, pain suppression, and patient recovery. Specific treatment differences will exist from patient to patient in relation to their individual injuries, severity of injuries, as well as tolerance to rehabilitation.**
J. Shawn Leatherman, BA, BS, DC, CCST, CCSP?
Director of Clinical Rehabilitation
REFERENCES
1. Aguayo S. Neuropeptides in inflammation and tissue repair. In Henson & Murphy eds. Mediators of the Inflammatory Process, Handbook of Inflammation. New York: Elsevier, 1989: p.219-44
2. Alberts B, et al. Molecular Biology of the Cell (2nd ed). New York: Garland Publishing; 1989
3. Ammon H, et al. Inhibition of leukotriene B-4 formation in rat potential neutrophils by ethanolic extract of the gum resin exudates of Boswellia serrata. Planta Med 1991;57:203-07
4. Arend W. Cytokines and growth factors. In Kelley W, et al. eds. Textbook of Rheumatology (4th ed). Philadelphia: W.B. Saunders; 1993: p.227-47
5. Bersch DF, Bauer E: Structure and mechanical properties of rat tail tendon. Biorheology 17:84, 1980
6. Bollet A. Nutrition and diet in rheumatic disorders. In shills M, Young V.eds. Modern Nutrition in Health and Disease (7th). Philadelphia: Lea & Febieger; 1988: p.1471-81
7. Bollet A. Nutrition and diet in rheumatic disorders. In shills M, et al.eds. Modern Nutrition in Health and Disease (8th). Philadelphia: Lea & Febieger; 1994: p.1362-1390
8. Bucci L. Nutrition Applied to Injury Rehabilitation and Sports Medicine. Boca Raton: CRC Press, FL; 1995
9. Bronsgeest-Schoute H, et al. The effect of various intakes of n-3 fatty acids on the blood lipid composition in healthy human subjects. Am J Clin Nutr 1981; 34:1752-57
10. Budowski P, Crawford Mu-linolenic acid as regulator of the metabolism of arachidonic acid: dietary implications of the ratio, n-6:n-3 fatty acids. Proc Nutr Soc 1985; 44:221-29
11. Callegari P. Botanical lipids: Potential role in modulation of immunologic responses and inflammatory reactions. Rheum Dis Clin N Am 1991;17(2):415-25
12. Capron A. Platelets as effectors of hypersensitivity reactions. In Kay A. ed. Allergy and Inflammation. New York: Academic Press; 1987 p. 125-38
13. Chamberlain G. Cyriax抯 friction massage: A reviews. J Ortho Sports Phys Ther 1982;4(1):16-22
14. Cooper R. The role of epidural fibrosis and defective fibrinolysis in persistence of post laminectomy back pain. Spine 1991;16(9):1044-18
15. Cooper RR, Misel S: Tendons and ligament insertion. J Bone Joint surg (Am)52:1, 1970
16. Cotran, Kumar & Robbins. Robbins?Pathologic Basis of Disease (4th ed). Philadelphia: W.B. Saunders; 1989
17. Davidson J. Wound repair. In Gallin, Goldstein & Synderman eds. Inflammation: Basic Principles and Clinical Correlates (2nd ed). New York: Raven Press; 1992: p.809-19
18. Drevon C. Marine oils and their effects. Nutr Rev 1992;50(4):38-45
19. Dyerberg J. Linolenate-derived polyunsaturated fatty acids and prevention of atherosclerosis. Nutr Rev
20. Elliott DH: The biomechanical properties of tendon in relation to muscular strength. Ann Phys Med 9:1, 1967
21. Engles M. Tissue response. In Donatelli R & Wooden R. Orthopedic Physical Therapy (2nd ed). Churchill Livingston; 1994: p.1-31
22. Fields H. PAIN. New York: McGraw Hill; 1987: p.92,213
23. Guyton A. Basic Neuroscience (2nd ed). Philadelphia: W.B. Saunders; 1991
24. Hardingham TE, Muir H. Binding of hyaluronic acid to proteoglycans. Biochem J 139:565, 1974
25. Harland B. et al. Calcium, phosphorus, iron, iodine, and zinc in the 揟otal diet?.J Am Diet Assoc 1980;77:16-20
26. Higgs G. The effects of dietary intake of essential fatty acids on prostaglandin and leukotriene syntheses. Proc Nutr Soc 1985;44:181-87
27. Hirsch G: Tensile properties during tendon healing: a comparative study of intact and sutured rabbit peroneus brevis tendons. Acta Orthop Scand (Suppl) 153:1, 1974
28. Hurri H. Fibrinolytic defect in chronic back pain. Acta Orthop Scand 1991;62(5):407-09
29. Hwang D, Carroll A. Decreased formation of prostaglandins derived from arachidonic acid by dietary linoleate in rats. Am J Clin Nutr 1980;33:590-97
30. Jayson M. Chronic inflammation and fibrosis in back pain syndromes., in Jayson, M. ed. The Lumbar Spine and Back Pain (3rd ed). New York: Churchill Livingstone; 1987: p.411-18
31. Jayson M. The role of vascular damage and fibrosis in the pathogenesis of never root damage. Clin Ortho Rel Res 1992;279:4048
32. Kottke F. Therapeutic exercise to maintain mobility. In Kottke F, Lehmannn J. eds. Krusens?Handbook of Physical Medicine and Rehabilitation (4th ed). Philadelphia: W.B. Saunders; 1990:p.436-51
33. Kremer J. Nutrition and rheumatic diseases. In Kelley W. et al. eds. Textbook of Rheumatology (4th ed). Philadelphia: WB Suanders; 1993: p.484-97
34. Leaf A. Weber P. Cardiovascular effects on n-3 fatty acids. New Eng J Med 1988;318(9):549-56
35. Leaf A. Health Claims: Omega-3 fatty acids and cardiovascular disease. Nutr Rev 1992;50(5):150-54
36. Lehmann JF, Masock AJ, Warren CG et al: Effects of therapeutic temperatures on tendon extensibility. Arch Phys Med Rehabil 51:481, 1970
37. Linder M. Nutritional Biochemistry and Metabolism (2nd ed). New York: Elsevier; 1991
38. Mainardi C. Fibroblast function and fibrosis. In Kelley W. et al. eds. Textbook of Rheumatology (4th ed). Philadelphia: W. B. Saunders; 1993:p.337-49
39. Marshall L, Johnston P. Modulation of tissue prostaglandin synthesizing capacity by increased rations of dietary alpha-linolenic acid to linoleic acid. Lipids 1982;17(12):905-13
40. Nissley S. Growth factors. In Becker K et al. Principles and Practice of Endocrinology and Metabolism. Philadelphia: J. B. :Lippincott; 1990: p.1315-21
41. Noyles FR, Torvik PJ, Hyde WB et al: Biomechanics of ligament. II. An analysis of immobilization, exercise, and reconditioning effects in primates. J Bone Joint Surg (Am) 56:1406, 1974
42. Paaske WP, Hovind H, Sejrsen P: Influence of therapeutic ultrasonic irradiation on blood flow in human cutaneous, subcutaneous and muscular tissue. Scand J Clin Invest 31:388, 1973
43. Pike M. Anti-inflammatory effects of dietary lipid modification. J Rhematol 1989;16(6):718-20
44. Pountain A. Impaired fibrinolytic activity in defined chronic back pain syndromes. Spine 1987;12(2):83-86
45. Reid DC: Functional Anatomy and Joint Mobilization. University of Alberta Press, Edmonton, 1975
46. Ross R. Atherogenesis. In Gallin I et al. Inflammation: Basic Principles and Clinical Correlates (2nd ed). New York: Raven Press; 1992:p.1051-59
47. Salmon J, Terano T. Supplementation of the diet with eicosapentaenoic acid: a possible approach to the treatment of thrombosis and inflammation. Proc Nutr Soc 1985;44:385-89
48. Salter R. Continuous Passive Motion. Baltimore: Williams & Wilkins; 1993
49. Sanders T, Younger K. The effect of dietary supplements o n-3 polyunsaturated fatty acids on the fatty acid composition of platelets and plasma choline phophoglycerides. Brit J Nutr 1981;45:613-18
50. Sapega AA, Quedenfeld TC, Moyer RA et al: Biophysical in range of motion exercise. Physician Sports Med 9:57, 1981
51. Simpoulos A. Omega-3 fatty acids in health and disease and in growth and development, Am J Clin Nutr 1991;54:438-63
52. Sinclair H. The relative importance of essential fatty acids of the linoleic and linolenic families: Studies with an eskimo diet. Prog Lipid Res 1981;20:897-99
53. Stromberg D, Wiederhielm CA: Visco-elastic description of a collagenous tissue in simple elongation. J Appl Physiol 26:857, 1969
54. Terano T et al. Eicosapentanoic acid as a modulator of inflammation. Biochem Pharmacol 1986;35(5):779-85
55. Vailas AC, Tipton CM, Matthes RD et al: Physical activity and its influence on the repair process of medial collateral ligaments. Connect Tissue Res 9:25, 1981
56. Valone F. Platelets. In Kelley W et al. ed. Textbook of Rheumatology (4th ed). Philadelphia: W.B. Saunders; 1993:p.319-26
57. Van der Meulen JCH: Present state of knowledge on processes of healing in collagen structures. Int J Sports Med 3:4, 1982
58. Wahl L. Inflammation. In Cohen, Diegelmann, Lindbald eds. Wound Healing: Biochemical and Clinical Aspects. Philadelphia: W.B. Saunders; 1992: p.49-62
59. Warren CG, Lehmann JF, Koblanski JN: Elongation of rat tail tendon: effect of load and temperature. Arch Phys Med Rehabil 52:465, 1971
60. Warren CG, Lehmann JF, Koblanski JN: Heat and stretch procedures : evaluation using rat tail tendon. Arch Phys Med Rehabil 57:122, 1976
61. Werb Z. Phagocytic cells: Chemotaxis and effector function of macrophages and granulocytes. In Stites et al. eds. Basic and Clinical Immunology (6th ed). Norwalk :Appleton & Lange; 1987:p.96-113
62. Willis A. Nutritional and pharmacological factors in eicosanoid biology. Nutr Rev 1981;39(8):289-301
63. Woo SLY, Buckwater JA: Injury repair of the musculoskeletal soft tissues. Am Acad Orthop Surg Workshop, Savannah, GA, June 1987
64. Woo SLY: Mechanical properties of tendons and ligaments. Biorheology 19:385, 1982
65. Wyke B: Articular neurology: a review. Physiotherapy 58:94, 1972
66. Wyke B. The neurology of low back pain. In Jayson M ed. The Lumbar Spine and Back Pain (3rd ed). Churchill Livingstone; 1987:p.56-99
67. Wyper DJ, McNiven DR, Donnelly TJ: Therapeutic ultrasound and muscular blood flow. Physiotherapy 64:321, 1978
68. Zimmerman G. Platelet-activating factor: A fluid-phase and cell-associated mediator of inflammation. In Gallin, Goldstein, Snyderman eds. Inflammation: Basic Principles and Clinical Correlates (2nd ed). New York: Raven Press; 1992:p.149-76
69. Zuckerman J, Stull GA: Ligamentous separation force in rats as influenced by training, detraining. Med Sci Sports: 5:44, 1973.
