QuestionOn May 29, 2008 I was involved in a serious automobile accident. The truck that I was a passenger in hit a the bed of a semi truck after it pulled in front of us. I received a severe cut on my left frontal part of my forehead. The CAT scan and subsequent MRI showed no breaks or fractures. I have been getting treatment from my local chiropractor. I do not know what kind of Dr he specializes in. They say that I have a bulged disk in my lower back. They also say that I have a severe bone bruise on my left knee. I have been seeing this DR for months now and I am no better. I am still in constant pain. My question is this. A friend recommended that I visit her Chiropractor that is a DC. I have been considering going to an orthopedic DR. Do you think that I should continue with the same treatment, knowing that it just takes time? Go to a different Chiropractor, or change venues completely?
AnswerDear Terri,
You should print this out it is extensive.
If you are seeing a chiropractor his educational degree has to be DC, however, all chiropractors are not created equally. Most are very scientific in their approach but may not have special knowledge in the area of automobile/acceleration injuries. This is a specific topic and most doctors of all disciplines have very little training in these injuries. However the chiropractic profession has literally written the most comprehensive book on diagnosing and managing these injuries (Whiplash Injuries: The cervical acceleration deceleration syndrome, third edition; Foreman & Croft).
Although these injuries do take an appreciable amount of time to recover from, going to a chiropractor who only adjusts the spine and does not employ active care protocols is a mistake. So maybe you should switch providers. However, I would look to a doctor who has specialized training in car crash injuries. You can contact the Spine Research Institute of San Diego, www.srisd.com or The International Chiropractic Association, www.chiropractic.org to find doctors who have completed and passed their respective programs of study on spinal injury post motor vehicle crash. I have completed them both, and they are the best programs available on these types of injury.
The above programs shaped how I have structured my treatment programs for crash patients due to the intricacy of injuries sustained in these crashes. Just so you can get an appreciation of what our protocols are I will copy them to this correspondence. See below.
Hope this helps Terri. Feel free to write back or contact me through my website if needed.
Respectfully,
Dr. J. Shawn Leatherman
www.suncoasthealthcare.net
CHIROPRACTIC E/M COUNSELING RECORD: SUPPLEMENTAL INFORMATION
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-β), 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-β, thromboglobulin-β, 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 anisotrophic 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) Chiropractic Biophysics traction protocols are substantially researched and documented. There are over 80 clinical papers in the index medicus, and are too bulky to be listed in this document. (**) Cryotherapy is utilized in traction and post-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 load may allow the collagenous microstructure to stabilize at new stretched lengths. (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.
REFERENCES
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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
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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
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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
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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
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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
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37. Linder M. Nutritional Biochemistry and Metabolism (2nd ed). New York: Elsevier; 1991
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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
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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
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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
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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
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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
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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
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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
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67. Wyper DJ, McNiven DR, Donnelly TJ: Therapeutic ultrasound and muscular blood flow. Physiotherapy 64:321, 1978
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** Pubmed/Medline桽earch: Chiropractic Biophysics, Harrison, Calliet, Haas, Ferrantelli, Calloca, Keller, & Meyer.
E/M Counseling Supplement for Patient Treatment
Traumatic Brain Injury/Mild Traumatic Brain Injury/Concussion
Motor vehicle trauma is the single most important factor in both fatal and mild brain injuries. Early reports ranged from 40% to 60% caused by motor vehicle crash (MVC) with concussion being the most common diagnosis given. (15,27,57) More recent accounts report MVC as the origin of 60% to 67% of all occurrences. (1,21) Many of these MVC-related injuries are the result of blunt head injury, which describes contact with some object without penetration of the skull, such as striking the steering wheel, dash board or the B pillar of the doorframe. However, it has been shown that non-contact concussion is a common result of acceleration type injuries. The term of choice today is traumatic brain injury (TBI) or mild traumatic brain injury (MTBI). (15)
Mechanism of Injury: Previously thought to be a direct shearing of axons, the actual mechanism is from abrupt acceleration and deceleration of brain tissue. (39) The initial shear effect creates the activation of a degenerative cascade. During a low speed whiplash injury, (7 mph) the head may be accelerated at 9-18g. (58) Since the brain is a soft structure, shear strains are created as the outer part of the brain moves at a different pace than the inner part of the brain. This is intensified as the momentum of the head changes rapidly in a sagittal direction during a whiplash trauma, and when head impact occurs inside the vehicle. The most important factors in whiplash-induced concussion are angular acceleration, flexion/extension of the neck, and increased intracranial pressure gradients. (40,41,52)
Animal studies confirm the real issue of induced concussion from acceleration/deceleration even though animals did not lose consciousness. (32,33) Portnoy et al. reported that significant increases in intracranial pressure were measured in baboons exposed to whiplash. Examination discoveries included suprascapular intramuscular hemorrhages. (47) Hemorrhages were not from contact. Acceleration, deceleration, and shear were mechanisms of injury. Non-centroidal motion in the coronal plane was found to be the most injurious and non-centroidal acceleration in the sagital plane to be least injurious concerning brain injury. (22,38,56) Although this infers that lateral whiplash motions of the head are more likely to produce concussion or diffuse axonal injury (DAI) than frontal or rear impacts, MTBI and DAI have been found in both types of collisions.
According to the work of Hinoki, the integrity of the brainstem reticular formation is largely responsible for maintaining levels of consciousness. A study by Jane et al. proved conclusively that non-centroidal accelerations of the head (without contact) could produce damage to axons in the inferior colliculus, pons, and dorsolateral medulla, which are in close proximity to the reticular formation. (25) The authors discussed the previous work of Povlishock et al., who presented the pathogenesis of DAI. Their proposed mechanism of trauma is not necessarily an immediate shearing of axons, but rather a reactive degeneration secondary to trauma. (48,49) Others have corroborated this concept of continuing degeneration, such as Gennerelli, in statements that MTBI should be considered a process rather than an event. (21). In addition we know that the spinal cord becomes stiffer as rates of strain increase, therefore creating a higher susceptibility to injury. (5)
Pathophysiology: The precise nature of DAI is thought to be a reactive swelling of damaged axons and capillaries throughout the brain (29,48,49) 揇irect brain trauma results in intra-axonal changes in the 68-kd neurofilament subunit which then loses its alignment and interferes with axoplasmic transport. This causes axonal swelling and eventual disconnection. The neurofilament change may be the result of either direct damage to the cytoskeleton or a biomechanical event that results in neurofilament disassembly. The temporal progression of those events is related to the severity of the injury? (16,42)
At time of injury, the brain is subjected to massive depolarization from acceleration/deceleration, and tissues are damaged due to shear currents/forces that increase intracranial pressure and mechanically deform axons. It is postulated that such events terminate with neuronal death involving the production of free radicals, and tissue acidosis. (6,7,53) In 1997, Connor and Connor showed in the American Journal of Clinical Nutrition that free radicals amplify inflammation by up regulation of genes that encode for pro-inflammatory cytokines and adhesion molecules. It is known that free radicals damage lipids, proteins, membranes and DNA. (2,8,13,18,19,28)
Micro hemorrhages develop between 12 and 96 hours post injury, arachadonic acid is released, CSF lactic acidosis is present, and lipid peroxidation occurs from membrane disruption and squalor. Free radical scavengers such as large doses of antioxidants and iron chelators have been proposed as therapeutic devices. (59) Antioxidant supplementation as well as Omega III fatty acid supplementation, (DHA-docosahexanoic acid & EPA-eicosapentanoic acid), inhibit the degradation of tissue by the reduction of oxidative stress. Oxidative stress is due to free radical damage, arachadonic acid production, lipid peroxidation/degradation, prostaglandins (pge2), and leukotrienes. (9,10,11,20,24,31,34,46,51,54) In particular, bioflavonoids play a significant role as they have been proven to act as intracellular and extra cellular antioxidants, reduce platelet aggregation, repair damage in vessel walls and have anti-inflammatory action. (12,14,17,30,35,36,44,45,50)
Even in relatively mild brain injuries, an excessive release of excitatory neurotransmitters such as acetylcholine and glutamate, contribute to the pathologic neuronal apoptosis (cell death) in the brain. The results are permanent deficits! MTBI can produce diffuse reactions in cerebral metabolic activity and can disrupt the blood brain barrier allowing an increase of excitotoxic effects. (6,7,23) Recent research affirms that brain injury leads to increased glutamate release, which in turn activates the NMDA (N-methyl d-aspartate) receptor in cortical neurons allowing an increased calcium influx. (26) This channel complex contributes to excitatory synaptic transmission at sites throughout the brain and the spinal cord, and is responsible for neuronal plasticity. When continually activated neuronal death and chronic pain may result. Specific areas known to be vulnerable to injury include the parieto-occipital lobe, the temporal lobe, amygdala, anterior frontal lobe, and para-sagital sinuses. (43) Antioxidants, magnesium and omega III fatty acid supplementation all inhibit circulating Excitotoxins and down-regulate the NMDA receptor.
Post concussion syndrome (PCS) can develop after MTBI. Posttraumatic headaches are exceedingly common residuals, and may last for years. (55) First headaches begin with a concussion and can continue for weeks or months. The head usually hurts where the head is struck if blunt force trauma was the mechanism of injury. Etiological factors in posttraumatic headaches are blunt head trauma, 57.3%, whiplash, 43.6%, Object hit head, 13.7%, other, 13.7%, and body shaken, 9.4%. (3) It has been suggested by one of the preeminent experts in this area that patients suffering from recurrent post-traumatic headaches or other elements of the PCS should be treated for migraine. (37) Other symptoms of PCS are as follows: Dizziness: Light headedness, vertigo and nausea, which is caused by injury to the semicircular canals, changes in endolymph or perilymph pressure, or direct damage to the vestibular cochlear nerve. Serious symptoms of hearing loss such as hyperacusis may occur as the result of damage to the actual hearing mechanism. Cranial nerve and brain dysfunction: Disruption of smell and taste, information speed and processing, attention, articulation, memory, new information acquisition, reaction time and sleep disturbances such as lethargy, drowsiness, and fatigue are common sequelae. (4)
**In relation to the research above, Suncoast Healthcare Professionals uses nutritional supplementation to decrease the cyto-toxic attack on neuronal tissue after resultant concussive episodes. Due to the fragile nature of brain tissue as well as the physiological makeup, it is evident that nutritional supplementation is paramount in the treatment of mild traumatic brain injury post motor vehicle trauma. The application of ant-inflammatory and antioxidant agents should be utilized initially and sequentially for a minimum period of 6 months post injury. Our office procedures and this supplementation is in line and adapted from protocols used in hospitals for the preservation of brain tissue after concussion, coma, transient ishemic attack and strokes, as well as brain surgery.**
REFERENCES
1. Abu-Judeh HH, Parker R, Singh M, El-Zeftaway H, Atay S, Kumarm, Naddaf S, Aleksic, S, Abdel_Dayem HM. SPET brain perfusion imaging in mild traumatic brain injury without loss of consciousness and normal computed tomography. Nuclear Medicine Communications 20, 505-510, 1999.
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4. Beers, MH, Berkow R, (editors). The Merck manual. 17th Edition. Section 14, chapter 175, pp.1428-1430.
5. Bilston LE, Meaney DF, Thibault LE: The development of a physical model to measure strain in a surrogate spinal cord during hyperflexion and hyperextension. International Conference on the Biomechanics of Impact, Eindhoven, Netherlands, September 8-10, 225-226, 1993.
6. Blaylock R. Excitotoxins: The Taste That Kills. Albuquerque, NM. Health Press 1994.
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9. 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
10. 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
11. 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
12. Catapano AL. Antioxidant effect of flavonoids. Angiology 1997;48:39-44.
13. Cotran, Kumar &Robbins. Robbins?Pathologic Basis of Disease (4th ed.). Philadelphia: W.B. Saunders; 1989, page 10.
14. Craig W. Phytochemicals: Guardians of our health. J Am Diet Assoc 1997:97(10 suppl 2):s199-s204.
15. Croft AC, Foreman S: Whiplash Injuries: The cervical acceleration/deceleration syndrome. 3rd ed. Lippincott, Williams & Wilkins, 2002. p. 336-373.
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