QuestionHi, I was in a low impact car accident 6 months ago, the car hit my stationary car from the rear and it was going really slow. But my seat came off the floor and I hit my knees on the dash etc etc. From this I end up with a lower disc problem but my oesteopath helped fix this, but my neck problem hasnt resolved, the lower back still has manipulation on my visits. The pain from my neck is incredible when it is triggered on average twice a month. It affects my left side - eye droops, shoulder arm , tingling fingers no grip and the pain from the back of my head the front is unbearable, no one has seen me like this except my family as by the time I manage to get an appointment the sapams? have preety much ended, but I had one at work and ended up needing to go to hospital for pain relief so I could sit in a car to get home. I also seem to go really stupid, my words getr muddled.. This happens about 1-2 times a month. The professional views are mixed, hospital staff who saw me during this pain said I will probably have this for rest of my life, GP said it may go but he's not a fortune teller, oesteopath said he will fix it. Oesteopath said pain is due to bone locked in my my neck restricting blood flow to my head (brain?) and trapping a nerve.
I am quite scared as family say during spasm period I look like I had a stroke. I dont know what to do to manage this except the route I am taking, ice pain relief and oesteopath twice a month which is reducing to once a month I go in when it triggers again.
I am I at risk of having a stroke from this? Can I still do my mandatory training in a few months which is 5 days of quite difficult physical - control and restraint. I find it hard to concentrate these days as well even when not having spasm.
I would apperciate some advice whether this will get any better or do I statrt to adjust my life around this more?
thank u for your time.
AnswerDear Tracy,
Whiplash is no joking matter and often injuries can be quite severe to include the cervical nerve roots, the sympathetic chain, the brachial plexus and even the brain. Unfortunately when the injury is in the brain, it is often overlooked because most diagnostic tests are not specific enough to pick up the cellular injuries. Has the osteoptah run tests on blood flow and brain perfusion, metabolic activity in the brain, MRI of the neck to look at the nerve roots for inflammation, how about a nerve conduction velocity, not to mention have you had flexion and extension x-rays of the neck to determine and document ligament instability (tearing/disruption). All of these things needs to be considered... Please print this answer and read it carefully as there is a lot of detailed and complex information. You should review all of this material with your physicians and demand that they take a further look!!
Whiplash: mechanism of Injury:
Upon impact, the target vehicle begins to move forward into the occupant, making contact mostly through the seat back. In accordance with Newton抯 1st law of motion, the occupant抯 inertia resists this motion. As the seat back continues to move forward, the occupant must yield. Initially, the thoracic curve is flattened by the seat back. This results in a vertical/axial compressive force, which is transmitted through the spine. (Research has not yet been able to establish this flattening mechanism in the lumbar spine.) As the vertical compressive force continues up the spine, some rise of the torso in the seat occurs. This is called ramping and is halted after 1-3 inches of vertical displacement, usually due to the restraining effect of the seatbelt/shoulder harness and the weight of the torso.
Meanwhile, as the torso is experiencing this vertical and forward acceleration, the head ?also acting in according with Newton抯 1st law ?attempts to remain at rest. As the vertical force extends upward into the neck it initiates flexion of the upper cervical vertebral segments and hyper-extension of the lower cervical vertebral segments. Compression then quickly gives way to tension as the upward moving head and now downward moving torso attempt to disengage. As the torso moves forward in relation to the head, significant amounts of horizontal/shear force occur in the neck roughly parallel to the facet joint line. As this is initiated under conditions of compression, the overall stiffness of the neck may be diminished as a result of the ligamentous slack, which offers less resistance to shear and thus less resistance to the injury mechanism. Realize that at the time of initial impact, compression and shear combine to shift the IAR of C5 from its normal location in the body of C6 to a higher position in its own body.
As the torso continues to move forward, the neck begins to pull the head along with it. This has the effect of further flexing the upper cervical spine and hyper-extending the lower cervical spine (primarily the C5-C6 segments) and the spine assumes an S-shaped configuration. The s-shaped configuration and curve reversals have both been shown through clinical research to predict a poor outcome for the occupant and possibly lead to chronicity.
The head is also induced to extend along with the neck as the head takes up the backset (distance between head and restraint) during the head lag phase. Depending on specific head restraint geometry (occupant抯 position relative to the head restraint), head restraint contact will usually occur in about 100 milliseconds at which time head translational acceleration will peak. Any stored energy in the seat back from its deflection (usually about 5-15 degrees) will be released as the occupant begins to move forward into the re-entry phase. This effectively increases the torso and head speed known as 搊verspeed? It抯 the reason why the occupant抯 torso is accelerated more than the vehicle, and why the occupant抯 head is accelerated more than the torso.
As the change from forward motion to rearward motion occurs, the direction of horizontal shear reverses rapidly and the rearward bending moment immediately changes to a forward bending moment. Depending on the initial position of the occupant with respect to seat belt and shoulder harness, the seat and shoulder portions of the restraint system will halt the forward moving torso, this will rotate the upper torso to some extent and will effectively magnify the neck抯 bending moment due to the head抯 inertia, and may affect discal pressures in the lumbar spine, acting in accordance with Newton抯 1st law of motion. This is coupled with the addition of some angular motion forward in the neck along with acceleration.
Therefore, it is likely that in many cases injury occurs in the initial phase as a result of head lag, compression, tension, and shear loading along the facet articulations. Lower cervical hyperextension during the s-shaped phase is also associated with injury. Global hyper-extension of the neck can occur depending on the head restraint geometry, but it is interesting to note that researchers have produced injuries in volunteers well within the normal anatomical ranges of motion of the neck. Thus, injury can occur without hyper-extension or hyper-flexion.
NOTE: Several studies have demonstrated the potential to ramp up the seat back after rear impact collision. This tendency is even greater in out-of-position occupants. The initial effect of ramping will be abrupt axial stretch of the lumbar spine with compression of the cervical spine. This stretch will still be felt if the pelvis is firmly anchored by the lap belt and ramping is thus prevented. Many occupants slouch and/or lean forward in their car seats. In either case, the first area of the body to be accelerated by the seat back will be the pelvis. This bending moment will effectively flex the lumbosacral spine until the thorax comes into full contact with the seat back.
As the seat back is loaded with elastic energy from the inertia of the occupant, it will extend backward in proportion to these forces--a movement that can exceed 30 degrees. At this time significant slack can develop in the restraint belts (particularly the shoulder belt) and the excess webbing may not be spooled back into the retractors. Then, as the head and torso decelerate in the forward direction, carried along by a combination of their own inertia and the released elastic energy from the seat back, this slack is overcome suddenly, resulting in acute peaks in deceleration forces and subjecting the lumbar spine to its second flexion injury, this time in combination with the shear force provided by the restraining lap belt. In this case the inertia of the pelvis and lower extremities may be relatively unrestrained and can carry the lower half of the body against the belt.
Occular dysfunction is common following whiplash injury, with the most common complaint being blurred vision. Patients often have disturbed accommodation and impaired adaptation to light intensity, an sensitivity to light. However, from what you have described Tracy, you seem to have the presentation of Horner's syndrome as well. Although this is rare in whiplash, it has been reported. Horner's syndrome is a clinical syndrome caused by damage to the sympathetic nervous system. Horner syndrome can be caused by any interruption in the sympathetic nerve fibers, which start in the part of the brain called the hypothalamus and run to the face, or it can be due to the sympathetic connection of the peripheral nerves in the neck and brachial plexus.
Sympathetic nerve fiber injuries can result from:
1. Injury to the main artery to the brain (carotid artery)
2. Injury to the nerves running down the arm (brachial plexus)
3. Migraine or cluster headaches
4. Stroke or lesion in the brainstem
5. Tumor in the top of the lung
Symptoms:
1. Decreased sweating on the affected side of the face
2. Drooping eyelid (ptosis)
3. Sinking of the eyeball into the face
4. Small (constricted) pupil
Diagnostic tests may include:
1. Blood tests
2. Carotid ultrasound
3. Chest x-ray
4. CT angiogram or magnetic resonance angiography (MRA)
5. CT scan of the chest
6. Eye drop tests
7. MRI of the head
This is a critique written by Dr. Art Croft on some recent literature on occular dysfunction and Horner's syndrom issues post whiplash injury:
Over the past couple of dozen years, a number of papers have appeared in the medical literature which attempted to explain the not uncommon complaint of visual disturbances among whiplash patients. Generally, this is attributed to a loss of accommodation and impaired light adaptation. As the current author notes, none of the studies have been controlled to date. The most commonly reported visual complaints or findings among the whiplash population are blurred vision, visual disturbances, and defective accommodation. The author recruited 19 whiplash patients (both acute and chronic, and all attributed to motor vehicle crash injury). The majority had headaches and all had neck pain. But this was a selected group in that 17 of them complained of visual disturbances. Thus, the subjects of this study are probably not representative of all whiplash patients.
In addition to the whiplash patients, a control group was also evaluated. In both cases, accommodation was evaluated by having patients read lines of text at a standard 6 m distance. The author then blurred the lines from the baseline at which the patient had the highest visual acuity by adding a lens of 1-2 D and then gradually reducing the strength of the lens until the subject could once again read the line. This represented minimal accommodation. This was repeated by adding lenses of increasing strengths of concave 0.25 DS until the subject could no longer read the line, and this represented maximal accommodation. Other forms of accommodation, such as proximally induced accommodation and convergence were not tested. The results were that the whiplash group had a statistically significant reduction in accommodation amplitude compared to the matched controls. Note that a loss is also seen with age, but this was controlled for in this study.
The author explored the current thinking in this area, concluding that the issue of exact causation remains unsettled. However, based on the balance of literature, it appears that accommodation is chiefly facilitated by the parasympathetic nervous system and that the sympathetic nervous system acts as an antagonist. Brown believed that injury to the sympathetic nerves in the cervical spine was a plausible explanation for the observed accommodation errors. The hypothesis proposed, he noted, has been that either interruption,
which would cause a Horner's syndrome, or excitation, which may cause changes in accommodation and pupillary dysfunction, can occur. Brown concluded that it is interruption in the sympathetic fibers that probably best explains these findings.
However, if the parasympathetic nervous system plays the predominant part in accommodation (as it also does in light adaptation, which, very importantly I believe, is a prominent complaint in this subgroup of patients and one that the author did not happen to mention), would an interruption of the sympathetic nervous system have a significant effect if, as recent reports indicate, it plays only a minor role? I tend to think not. Moreover, disturbance/irritation of the sympathetic nervous system in the cervical spine, which is proposed as the mechanism in this accommodation disorder, is also thought to be the cause of reflex sympathetic dystrophy (RSD), which is a potentially crippling condition and one that is rare in whiplash trauma.
Horner's syndrome (anhydrosis, ptosis of upper lid, and constriction of the pupil) is only rarely seen in whiplash patients and suggests that dysfunction or suppression of the sympathetic nervous system does not often occur in this group and is not a plausible component of this disorder. Thus, it seems more likely to me that dysfunction of the parasympathetic nervous system is the more common cause of this disorder. It would produce precisely what we see in these visual disturbance patients: a diminished accommodation and impaired adaptation to light. Note that these parasympathetic nerve fibers start in the midbrain and are derived from the accessory oculomotor (Edinger-Westphal) nucleus and travel with the oculomotor nerve. Note also that lesions to the tectum of the midbrain in the area of the superior collicular bodies will interfere with the decussating light reflex fibers in the periaqueductal area. Is there any connection? Brain stem and midbrain injuries can be a factor in some CAD cases and cranial nerve palsies are also not uncommon.
Moreover, there are preganglionic parasympathetic fibers in the facial, glossopharyngeal, vagus, and accessory nerves, as well as the third and fourth sacral nerves. The vagus, of course, has important cardiac, gastric, pulmonary, and intestinal branches. This is perhaps particularly interesting in light of a Canadian study which reported that persons having experienced whiplash injury in the past are significantly more likely to develop cardiovascular disorders, breathing disorders, digestive disorders, low back pain, and allergies (Cote P, Cassidy JD, Carroll L. Is a lifetime history of neck injury in a traffic collision associated with prevalent neck pain, headache and depressive symptomatology? Accid Anal Prev 32:151-159, 2000).
Below Tracy you will find my office treatment protocols after injury has been documented. This includes Mild Traumatic brain Injury.
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 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.**
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.
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, memory or 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.
2. Allen R. Free radical and differentiation: The interrelationship of developmental aging. In Yu B. ed. Free radicals in aging. Boca Raton: CRC Press, 1993: p.11-37.
3. Barnat MR: Posttraumatic headache patients I: demographics, injuries, headache and health status. Headache 26:271-277, 1986.
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.
7. Blaylock R. Health and Nutrition Secrets That can Save Your Life. Albuquerque, MN. Health Press 2002:p.171-200, 311-326.
8. Block G. The data support a role for antioxidants in reducing cancer risk. Nutr Rev 1992;50(7):207-213.
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.
16. Croft AC: Whiplash and Brain Injury Traumatology; Module 1: advanced topics; the fundamental science. page 100.
17. de Groot H, Rauen U. Tissue injury by reactive oxygen species and the protective effect of flavonoids. Fundamentals in Clinical Pharmacology 1998; 12(3):249-55.
18. Demopoulos H. Control of free radicals in biologic systems. Fed Proc 1973;32:1903-1908.
19. Demopoulos H. The development of secondary pathology with free radical reactions as a threshold mechanism. Journal of the American College of Toxicology 1983;2:173-184.
20. Drevon C. Marine oils and their effects. Nutr Rev 1992;50(4):38-45
21. Gennarelli TA: Biomechanics of Head Injury. Conference on the biomechanics of impact trauma. Association for the Advancement of Automotive Medicine, Chicago, Il, November 13-14, 1995.
22. Gennarelli TA, Thibault LE, Tomei G, et al.: Directional dependence of axonal brain injury due to centroidal and non-centroidal acceleration. SAE 872197, in Proceedings of the Thirty-First Stapp Car Crash Conference, Society of Automotive Engineers, 49-53, 1987.
23. Hayes RL, Dixon CE: Neurochemical changes in Mild head injury. Sem Neurol 14(1):25-31, 1994.
24. Higgs G. The effects of dietary intake of essential fatty acids on prostaglandin and leukotriene syntheses. Proc Nutr Soc 1985;44:181-87
25. Jane Ja, Steward O, Genneralli TA: Axonal degeneration induced by experimental noninvasive minor head injury. Journal of Neurosurgery 62:96-100, 1985.
26. Kao CQ, Goforth PB, Ellis EF, Satin LS: Potentiation of GABA(A) currents after mechanical injury of cortical neurons. Journal of Neurotrauma 2004 Mar;21(3):259-270.
27. Kraus JG, Nourjah P: The epidemiology of mild, uncomplicated brain injury. J Trauma 28(12), 1988.
28. Kremer J. Nutrition and Rheumatic diseases. In Kelley W. et al. eds. Textbook of Rheumatology (4th ed). Philadelphia: Wb Saunders; 1993: p.484-497.
29. Levi L, Guilburd JN, Lemberger A, et al.: Diffuse axonal injury: analysis of 100 patients with radiological signs. Neurosurgery 27(3):429-432, 1990.
30. Lindahl M, Tagesson C. Flavonoids as phospholipase A2 inhibitors: importance of their structure for selective inhibition of group II phospholipase A2. Inflammation 1997;21:34-56.
31. Linder M. Nutritional Biochemistry and Metabolism (2nd ed). New York: Elsevier; 1991
32. Liu YK, Chandran KB, Heath RG, Unterharnscheidt F: Subcortical EEG changes in rhesus monkeys following experimental hyperextension-hyperflexion (whiplash) Spine 9(4):329-338, 1984.
33. Liu YK, Wickstrom JK, Saltzberg B, Heath RG: Subcortical EEG changes in rhesus monkeys following experimental whiplash. 26Th ACEMB, 404, 1973.
34. 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
35. Mascolo N, Pinto A, Capasso F. Flavonoids, leukocyte migration and eicosanoids. J Pharm Pharmacology 1988;40:293-295.
36. Machiex JJ, Fleuriet A, Billot J. Fruit phenolics. Boca Raton: CRC Press; 1990;p.272-273.
37. Margulies S. The postconcussion syndrome after mild head trauma ?Part II: is migraine underdiagnosed? Journal of Clinical Neuroscience 2000;7:495-499.
38. Marguilles SS, Thibault LE, Genneralli TA: Physical model simulations of brain injury in the primate. Biomechanics 23(8):823-836, 1990.
39. Ommaya Ak, Gennarelli TA: Cerebral concussion and traumatic unconsciousness. Brain 97:6330654, 1974.
40. Ommaya AK, Hirsch AE: Tolerances for cerebral concussion from head impact and whiplash in primates. Journal of Biomechanics 4:13-21, 1971.
41. Ommaya AK, Hirsch AE, Martinez JL: The role of whiplash in cerebral concussion. 660804 197-203, 1996.
42. Ommaya AK, Yarnell P: Subdural hematoma after whiplash injury. Lancet 237-239, Aug 2. 1969.
43. Otte A, Ettlin TM, Nitsche EU, Wachter K, Hoegerle S, Simon GH, Fierz E, Moser E, Mueller-Brand J: PET and SPECT in whiplash syndrome: a new approach to a forgotten brain? Neuro Neurosurg Psychiat 63:368-372, 1997.
44. Packer L. Oxidants, antioxidant nutrients and the athlete. Journal of Sport Science 1997;15(3):353-363.
45. Packer L. The Antioxidant Miracle. 1999. John Wiley & Sons.
46. Pike M. Anti-inflammatory effects of dietary lipid modification. J Rhematol 1989;16(6):718-20
47. Portnoy HD, Benjamin D. Brian M, et al.: Intercranial pressure and head acceleration during whiplash. 14th Stapp Car Crash Conference 700900 SAE 152-168, 1970.
48. Povlishock JT, Becker DP: Fate of reactive axonal swellings induced by head injury. Laboratory Investigations 52(5):540-552, 1985
49. Povlishock JT, Becker DP, Cheng CLY, et al.: Axonal changes in minor head injury. J Neuropathol Exp Neurol 42:225, 1983.
50. Robbins RC. Flavones in citrus exhibit anti-adhesion action on platelets. Internat J Vit Nutr Res 1998;58:418-422.
51. 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
52. Siegmund GP, King DJ, Lawrence JM, Wheeler JB, Brault JR, Smith TA: Head/neck kinematic response of human subjects in low-speed-rear-end collisions. SAE Technical Paper 973341,357-385, 1997.
53. Siesko BK,: Basic mechanisms of traumatic brain damage. Annals of Emergency Medicine 22(6):959-969, 1993.
54. Simpoulos A. Omega-3 fatty acids in health and disease and in growth and development, Am J Clin Nutr 1991;54:438-63
55. Solomon S. Posttraumatic headache. Medical Clinics of North America. 2002;85:987.
56. Thibault LE, Margulies SS, Genneralli TA: The temporal and special deformation response of a brain model in inertial loading. SAE 87, in proceedings of the 31st Stapp Car Crash Conference, Society of Automotive Engineers, 267-272, 1987.
57. Vazquezbarquero A, Vazquezbarquero JL, Austin O, et al: The epidemiology of head injury in Cantabria. European Journal of Epidemiology 8(6):832-837, 1992.
58. West DH, Gough JP, Harper TK: Low speed collision testing using human subjects. Accident reconstruction Journal 5(3):22-26, 1993.
59. White BC, Krause GS: Brain injury and repair mechanisms-the potential for pharmacologic therapy in closed-head trauma. Annals of Emergency Medicine 22(6):970-979, 1993.
Tracy, I know this is overwhelming and complicated, but I wanted you to see some of the bredth of information available even though this is just touching the surface. Additionally, I would recommend that you check out the Spine Research Institute of San Diego's website: WWW.SRISD.COM, it is packed with additional information and resources. Good Luck Tracy,
Respectfully,
Dr. J. Shawn Leatherman
Director of Clinical Rehabilitation
Suncoast Healthcare Professionals
www.suncoasthealthcare.net
