QuestionI have been having daily back and neck pain since I was rear-ended 1 year ago on the highway. I have been to physiography-therapy for about 16 weeks, had an x-ray about 4 months ago on my lower back which came out ok. My family doctor and physiotherapist believe it to soft-tissue damage..
I always have a sore and stiff neck, occasional headaches. It cracks about 90% of the time while turning my head and sometimes it feels like something is moving and i worry that oneday it may not actually go in place.
My lower to mid back gets really sore when bending forward or sitting too long and i usually change positions to help the problem but some days are worse than others.
I have done back and neck stretches & strengthening exercises about 3-4 times a week for the past year.
Not sure where to go from here really with this one.
AnswerDear Ken,
The symptoms you are experiencing are common from rear impact vectored collisions. These types of collisions, "whiplash", frequently produce significant soft tissue injuries that can remain symptomatic for years. Common injuries are in the myofascial structures, ligaments, disks, and nerve roots. Now that the injury has been longstanding without appropriate treatment, you are experiencing chronic pain which is even harder to control due to scar formation, new pain nerve growth into the tissue, and the fact that your tissue is now sensitized to pain transmission which means that even low stimulus can excite pain fibers and transmit pain signals to the brain.
Unfortunately most medical doctors don't know how to treat these types of injuries (some do) and usually will brush you off with a prescription of pain meds and muscle relaxers. They get no formalized training in the diagnosis or treatment of soft tissue injuries, especially regarding the specific nature of vehicle crash dynamics and occupant kinematics. Even when you go to the physical therapist, they are unlikely to do much more than general stretching and exercises. Chiropractors have performed the majority of research on these injuries in the past 15 years due to the fact that we treat them most often, and they foremost experts on vehicle crash injuries are tow chiropractic physicians here in the United States. I have taken both of their programs and have been certified on a few separate occasions, so I understand what you have experienced.
Ken, I would recommend that you seek out the care of a chiropractic physician who has been specifically trained in the diagnosis and treatment of crash injuries. Many physicians will say they understand the nature of these injuries, but most don't even understand the causation mechanism, let alone the tissue damage, pain referral or effective treatment approaches. the best place to look for a qualified physician is on the Spine Research Institute of San Diego's website: www.srisd.com
Moreover, you need to educate yourself on these injuries and what to expect. Below I am going to explain the mechanism of injury, and then provide my office treatment guidelines for you to read and appreciate. You may want to print this information as it is fairly extensive, and will probably require a few reads to understand. You will likely have questions as well...feel free to write back for specific explanations if needed.
Respectfully,
Dr. J. Shawn Leatherman
www.suncoasthealthcare.net
MECHANISM OF INJURY: Upon impact, the target vehicle (the vehicle that has been struck), 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 injury.
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. This configuration has 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 overspeed and is the reason why the occupant is accelerated more than the vehicle.
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 acting in accordance with Newton抯 1st law of motion. This is coupled with the addition of some angular motion forward and 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. It is likely that further injury can occur in the forward phase, and this is somewhat more likely in females and smaller individuals due to their lower inertia/body mass which results in increased acceleration. It is important to note that in multiple vehicle collisions, (3 or more vehicles); second or third impacts may aggravate the second phase by imposing additional decelerative effects and accentuating neck bending moments and shear forces.
MY OFFICE GUIDELINES: 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-?, 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.** Please check out www.idealspine.com for more information on spinal traction for structural repair.
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