QuestionQUESTION: Dear Dr:
Thanks for your time in advance. I had a car accident in the beginning of May, 2007. My car got hit in the driver front side. At the time I felt some pain when I looked up. This is my first time to have auto accident. I need your advice very much. I got my MRI report last week and here is impression:
1. 1.8mm central disc extrusion in the C5-6 disc space with central compression of the thecal sac. No lateralization occurs to either side of the canal. Contact with the ventral surface of the cord is present.
2. Note is made of a 2.3mm central disc extrusion in the T1-2 disc space flattening the thecal sac and abutting the cord surface.
Because it is not my fault in car accident, but I don抰 know how serious problem I have from the report. I can feel pain around neck back but not very severe pain. Only a little bit of numbness of my left arm. I am very nervous about it. I heard this possibly cause paralyze. Could you tell me how serious this injury and can I get recovery by some treatment instead of surgery? I would appreciate it so much!
ANSWER: Dear Jessica,
Your MRI results are not great. You have two significant bulges of the disk material into the spinal cord area. The thecal sac which is compressed by both bulges is the outer covering of the spinal cord...the cerebral spinal fluid is contained within the thecal sac. Contact of the ventral surface means that the bulge is pressing into the front of the spinal cord at that level. Although the injury is fairly serious, you can get conservative care for the problem.
Chiropractic care is very effective in helping with these problems, but should include some physical rehabilitation of the neck to include some traction to alleviate the gravitational stress on the disks. A home traction device you should look into is called the Posture Pump...more information: www.posturepro.com. To find a chiropractic physician who has been certified in car crash injuries, check out the Spine Research Institute of San Diego: www.srisd.com. The website is also a great source of information.
In addition to the MRI findings, it is likely that you have ligament damage in the neck as well...most of the time this is not checked for on MRI, unless the ordering physician requests it to be looked at. Therefore, you need to make sure the chiropractor takes flexion and extension views of the spine to look for it. This is a very significant finding and needs to be addressed and documented.
Below you will find more information I have compiled on vehicle crashes (Cervical acceleration/deceleration injuries or whiplash injury), along with my clincial treatment guidelines. Side impact and rear impact crashes result in whiplash injuries. The information is dense, but important to understand...you may want to print it out to read, and show it to the treating physician. Good luck in your recovery Jessica.
Respectfully,
Dr. J. Shawn Leatherman
www.suncoasthealthcare.net
Experience affirms that automobile insurance company claim adjusters, defense attorneys, and defense medical/chiropractic examiners maintain that an individual within a vehicle involved in a collision cannot be injured if their vehicle sustains only minimum structural damage. Yet there is no doubt that individuals involved in minimum structural damage collisions develop symptomatology consistent with whiplash type neck distortion soft tissue injuries. Practicing health care providers, who examine 搘hiplash?patients, document findings that are consistent with occult soft tissue trauma. Alterations of segmental motion, alterations of joint end play, abnormal regional posture, alterations of normal tissue textures, abnormal sensitivity to local pressure, etc?are some of those findings. Despite adamant claims by patients that their symptoms are genuine and by doctors that their findings are real, the insurance company perspective is that the patient抯 prime objective is secondary gain and that of the doctor抯 is greed. The mathematical principles of collision physics are complex and unique for each accident. Yet they can be simplified, as many of the forces involved are so small that for practical purposes they are negligible. Importantly, these principles often support the position of the patient and their doctor.
1998 Yoganandan et al. Cervical Spine Vertebral and Facet joint kinematics under whiplash. Journal of Biomechanical Engineering 120:305-307.
Yoganandan et al applied reflective targets to adjacent facet joints to track motion during whiplash using high speed video. They commented that, 揘eck injuries secondary to whiplash during rear end vehicular crashes have become a national and international problem. They often result in no discernable radiographic trauma. In contrast, soft tissue damage such as excessive deformation is an expected outcome of these loading sequelae,?and proposed that compression and sliding motions of the facet joints might lead to joint fiber excitation which could be productive of pain, while the head lag portion would allow head translations producing soft tissue injuries result in occipital headaches.
1955 Severy et al. Controlled automobile rear-end collisions梐n investigation of related engineering and medical phenomena. Medical Aspects of Traffic Accidents, Proceedings of the Montreal Conference pp 152-184.
1955 Severy et al. Controlled automobile rear-end collisions梐n investigation of related engineering and medical phenomena. Canadian Services Medical journal 11:727-758.
1958 Severy et al. Automobile barrier and rear-end collision performance. Presented at the Society of Automobile Engineers summer meeting, Atlantic City, NJ, June 8-13.
Severy抯 group were the first to show that the acceleration of the human head in low speed rear impact collisions could be up to 2-3 times or more higher than the occupant抯 vehicle. This is due to the unique and complex occupant-vehicle coupling of this type of crash.
**HOW THE SPINE IS INJURED**
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. Spine Research Institute of San Diego {SRISD})
The type of injuries chiropractic physicians treat, resulting from rear impact motor vehicle collisions, are classified as 搃nertial acceleration injuries.? Popular terminology within our profession is 揷ervical acceleration / deceleration syndrome,?or CAD (Foreman and Croft). The acceleration that results in passenger inertial injury is the result of energy. The acceleration achieved by the struck vehicle in a rear impact is dependent upon the weight and speed of the striking vehicle. (Macnab).
Understanding energy is the key to understanding the physics of automobile rear impact collision vehicle damage and passenger injury. Published experts in motor vehicle collisions have completed experiments (Navin, Emori) or made observations which conclude that the degree of patient/passenger injury from automobile collisions is not related to the size, speed, or magnitude of damage of the involved vehicles.
Motor vehicle collision patient/passenger injury and clinical prognosis for recovery IS NOT related to the damage of their vehicle! Rather, injury and prognosis are coupled with direction of impact, awareness, and head/neck rotation.
揟he amount of damage sustained by the car bears little relationship to the force applied. To take an extreme example: If the car was struck in concrete, the damage sustained might be very great but the occupants would not be injured because the car could not move forward, whereas, on ice, the damage to the car could be slight but the injuries sustained might be severe because of the rapid acceleration permitted.?br>
Macnab, in The Spine. Saunders, 1982, p. 648.
揈ach accident must be analyzed in its own right. Auto speed and damage are not reliable parameters.?br>
Ameis, Cervical Whiplash: Considerations in the Rehabilitation of Cervical Myofascial Injury. Canadian Family Physician, September, 1986.
揟he Amount of damage to the automobile may bear little relationship to the forces applied to the cervical, spine and to the injury sustained by the cervical spine.?br>
Hirsh, Whiplash Syndrome. Orthopedic Clinics of North America, October 1988, p. 791.
搮neck extension becomes almost 60 degrees which is a potential danger limit of whiplash, at collision speed as low as 2.5 km/h.?br>
Emori, Whiplash in Low Speed Vehicle Collisions, SAE, Feb, 1990, p. 108.
**AWARENESS FACTOR**
Being caught by surprise or being unaware prior to impact worsens the prognosis.
揑f the passenger is aware of and anticipates a collision, and makes his neck muscle tense, he can tolerate more sever impact.?br>
Emori, Whiplash in Low Speed Vehicle Collisions, SAE, Feb, 1990, p. 108.
Injury results because the neck is unable to adequately compensate for the rapidity of head and torso movement resulting from the acceleration forces generated at the time of impact. This is particularly true when the impact is unexpected and the victim is unable to brace for it.?br>
Teasell & McCain, in Painful Cervical Trauma, Williams and Wilkins, 1992, p. 293.
In a whiplash injury, the acceleration-deceleration movements of the neck are typically completed within 250 ms. The brevity of this period precludes any voluntary or reflex muscle response that might arrest, limit, or control the movements of a cervical motion segment. Without muscle control the normal arcuate movement of a cervical motion segment must be disturbed, and the forces to which individual segments are subjected can be resisted only by passive ligamentous for a variety of possible injuries.
Lord, in Spine: State of the Art Reviews: Cervical Flexion-Extension/Whiplash Injuries, Hanley & Belfus, Sept. 1993, p. 374.
揑njury is greater when the impact is unexpected and the victim is unable to brace.?br>
Teasell, in Spine: State of the Art Reviews: Cervical Flexion Extension/Whiplash Injuries, Hanely & Belfus, Sept. 1993, p. 374.
**POSITION OF THE HEAD FACTOR**
The head being turned at the moment of impact increases injury.
揥hen the direction of force is from the side, or when a frontal or rear force occurs while the head is turned to one side, the spine is less flexible and the force is expended upon the articulations where the small bone elements may be fractured.?br>
Turek, Orthopaedics Principles and their Applications, Lippincott, 1977, p. 740.
If the head is turned at the moment of impact, there is increased injury on the side to which the head is turned, as: 搉ot only will the already narrowed foramen be compressed more, but the torque effect on the facets, capsules, and ligaments will be far more damaging.?br>
Cailliet, Neck and Arm Pain, F.A. Davis Company, 1981, p. 85.
搃n a crash, when the hyperflexion-hyperextension occurs with head rotation present, the pattern of tissue injury is different and the extent of damage produced is always more severe. Rotation increases stress in certain soft tissue structures, which then reaches their limit of motion at an earlier point, thus resulting in more severs injury with less application of force.?br>
Webb, Whiplash: Mechanisms and Patterns of Tissue Injury, Journal of the Australian Chiropractors?Association, June, 1985.
揑t has also been shown that extension with preexisting rotation is more likely to rupture the anterior longitudinal ligament than simple extension.?br>
Webb, Whiplash: Mechanisms and Patterns of Tissue Injury, Journal of the Australian Chiropractors?Association, June, 1985.
揑f the head is in slight rotation, a rear-end impact will force the head into further rotation before extension occurs. This has important consequences because cervical rotation pre-stresses various cervical structures, including the capsules of the zygopophseal joints, intervertebral discs, and the alar ligament complex, making them more susceptible to injury.?br>
Barnsley, in Spine: State of the Art Reviews: Cervical Flexion-Extension/Whiplash Injuries, Hanley & Belfus, Sept. 1993, p. 329
揑njuries are greater when nonsymmetrical loads are applied to the spine. This occurs when the spine sustains a rotary injury. The injuries are increased because the facet joints lock-out spinal motion, making the neck rigid, less resilient, and more susceptible to injury. When the head is rotated 45 degrees to one side, the amount of extension that side of the spine is capable of is decreased by 50%. This results in increased compressive loads on the facet joints, articular pillars on the ipsilateral side, and increased tensor loads at the facet joints on the contralateral side. The intervertebral foramen are smaller on the side of rotation and lateral flexion, and the neurovascular bundles are more vulnerable to compressive injuries.?br>
Havsy, Whiplash Injuries of the Cervical Spine and Their Clinical Seaquelae, Am Journal of Pain Management , January, 1994.
**PRE-CRASH DEGENERATIVE JOINT DISEASE FACTOR**
Pre-existing degenerative joint disease renders such joints less capable of adequately handling and dispersing the forces of a new injury; therefore, injury to these articulations and the surrounding tissues is greater, there are more long term subjective, objective, and functional residuals; and the probability of accelerated progression of additional degenerative joint increases to 55% probable.
揟he injury may be compounded by the presence of degenerative disease of the spine.?br>
揥ith advancing age, especially in the presence of degenerative disease, the tissues become inelastic and are easily torn.?br>
Turek, Orthopedics Principles and their Applications, Lippincott, 1977, p. 740.
揟he pre-existence of degeneration may have been quiescent in that no symptoms were noted, but now minor trauma may 揹ecompensate?the safety margin and symptoms occur.?br>
Calliet, Neck and Arm Pain, F. A. Davis Company, 1981, p. 103.
揇egenerative joint disease is recognized as a major influence on subsequent tissue damage both in severity and pattern.?br>
揑n any individual where changes consistent with degenerative joint disease are present, one can expect the injury to produce severe symptoms requiring prolonged treatment.?br>
Webb, Whiplash: Mechanisms and Patterns of Tissue Injury, Journal of the Australian Chiropractors?Association, June, 1985.
揊or the elderly, neck injury can be very serious. The degenerative spine, is biomechanically 搒tiffer,?behaving more like a single long bone than like a set of articulating structures. Deforming forces are less evenly dissipated, and more damage is done.?br>
Ameis, Cervical Whiplash: Considerations in the Rehabilitation of Cervical Myfoascial Injury, Canadian Family Physician, September, 1986.
揑f present, degenerative changes should be duly noted as they may affect the prognosis.?搮preexisting degenerative changes adversely affected the outcome.?br>
Dunn, Soft-Tissue Injuries of the Lower Cervical Spine, Instructional Course Lectures, Am Academy of Orthopedic Surgeons, 36, 1987.
揟he analysis of the radiological results showed that pre-existing degenerative changes in the cervical spine are strongly indicative of a poor prognosis.?br>
Mairmaris, Whiplash injuries?of the neck: a retrospective study, Injury: the British Journal of Accident Surgery, 1988.
揟he films should be inspected especially for evidence of pre-existing structural changes or for alteration, which are frequently associated with a more difficult, more prolonged, and less complete recovery. These changes may include the presence of osteophytes, foraminal encroachment on the oblique projections, and the presence of intervertebral disc space narrowing. When hyperextension injury occurs in the presence of pre-existing osteophytes formation, there is further narrowing of the spinal canal, which increases the potential for injury to the nerve roots or cord.?br>
Hirsh, Whiplash Syndrome, Fact of Fiction?, Orthopedic Clinics of North America, October, 1988.
搮the presence of preexisting degenerative changes, no matter how slight, appears to alter the prognosis adversely.?br>
Foreman and Croft, Whiplash Injuries, The Acceleration/Deceleration Syndrome, Williams & Wilkins, 1988, p. 389 and p. 395.
揚re-existing degenerative changes may worsen the prognosis.?br>
Porter, Neck Sprains After Car Accidents, British Medical Journal, April, 1989.
揑n a follow-up study of patients with similar injuries but with preexisting degenerative changes in the neck, it was observed that after an average of 7 years 39% had residual symptoms, and reontgenographic evidence of new degenerative change at another level occurred in 55%.?br>
Holm, Soft-Tissue Neck Injuries, in The Cervical Spine, The Cervical Spine Research Society, Sherk editor, Lippincott, 1989, p. 440.
揚atients with degenerative change initially have more symptoms after 2 years than those with normal radiographs at the time of injury.?br>
Watkinson, Prognostic factors in soft tissue injuries of the cervical spine, Injury: the British Journal of Accident Surgery, No. 4, 1991.
**DAMAGE IS SOMETIMES SUBTLE**
A very large proportion of injuries occur at speeds below those needed to cause permanent damage to vehicles. However, there may be subtle signs of damage in the form of damaged or sprung seat backs, witness marks (stretch marks) on the seat belt, scrape marks on bumper isolators (if the vehicle has isolators), and damage to the frame and bumper systems that is not visible from the exterior of the vehicle. This result is a paradoxical relationship due to the elastic, not plastic nature of LOSRIC--the ability for the materials used in automobiles to bounce back instead of deform under pressure. The apparent paradox of the inverse relationship between property damage and injury potential is a real one. (Spine Research Institute of San Diego)
1995 Waltz and Muser. Biomechanical aspects of cervical spine injuries. SAE Tech Paper 950658 45-51. 揟he greater the vehicular damage, the less biomechanical loading (and the inverse).?br>
2000 Chapline et al. Neck pain and head restraint position relative to the driver抯 head in rear-end collisions. Accident Analysis and Prevention 32:287-297.
In this study, the largest category of injury crashes was graded as having no damage. In these, 38% of females and 19% of males had symptoms. When damage was rated as minor, these percentages rose to 54% and 34% respectively.
**DAMAGE THRESHOLDS**
The National Highway Transportation Safety Association, NHTSA, has reported that shoulder and lap belts reduce the risk of fatal injury by 45% and the risk of moderate injury by 50%. The risk of fatality in a crash is approximately 5x抯 higher for an unbelted occupant. However, while the seatbelt and shoulder harness use has decreased the number of fatalities and serious facial and chest trauma, it has significantly increased the amount or minor and sometimes disabling cervical, thoracic, and lumbar injuries as well as numerous types of abdominal injuries.
1987 Dunn & Blazar. Soft-tissue injuries of the lower cervical spine. Instructional Course Lectures, American Academy Orthopaedic Surgeons, Vol XXXVI, 499-512.
1985 Allen et al. The effect of seatbelt legislation on injuries sustained by car occupants. Journal of Injury 16:471.
1991 Hayes et al. Seat belt injuries: radiological and clinical correlation. Radiographics 11:23-26
**I have 20 more references to this phenomenon.
May 1st, 1998 issue of Spine cites references that indicate:
?The damage threshold for a 1980 Toyota Tercel was 8.1 mph.
?The damage threshold for a 1977 Honda Civic was 8.2 mph.
?The damage threshold for a 19809 Chevrolet Citation was 8.4 mph.
?The damage threshold for a 1979 Pontiac Grand Prix was 9.9 mph.
?The damage threshold for a 1979 Ford e-150 van was 9.9 mph.
?1981-1983 Ford Escorts could withstand multiple impacts at 10 mph without sustaining vehicle damage.
?The damage threshold for a 1981 Ford Escort was 10.2 mph.
?The damage threshold for a 1978 Honda Accord was 11.0 mph.
?The damage threshold for a 1979 Ford F-250 pick up was 11.7 mph.
?The damage threshold for a 1983 Ford thunderbird was 12.1 mph.
?The damage threshold for a 1989 Chevrolet Citation was 12.7 mph.
(Spine Research Institute of San Diego Module program)
You can see that forces great enough to cause injury in the occupant frequently will result in no vehicle damage. Vehicles are now becoming stiffer, deform less in crashes, and the energy is transmitted to the occupant.
-36% of injuries occurred at velocity rate changes below 9.3 mph.
-20 % of injuries occurred at velocity rate changes above 9.3 mph indicating the inverse correlation to vehicle damage and occupant injury,
-18% of injuries occurred at speeds below 6.2 mph.
-60 % of injuries occurred at speeds between 6.2 and 12.4 mph.
Freeman M, et al. Spine, Volume 23, Number 9, 1998, p.1046
Question: Is there a magnitude of collision at which it can be assumed that no passenger injury could have occurred?
Answer: YES. This is known as zero probability.
Question: Can 搝ero probability?of injury be assessed by determining the damage to the passenger抯 vehicle?
Answer: NO!
**Decreasing the forward acceleration of the patient抯 vehicle decreases patient injury匱hings that decrease forward vehicle acceleration include: large patient vehicle, small striking vehicle, dry road conditions, patient抯 vehicle stationary at time of impact, brakes firmly on, manual transmission in low gear.
**Increasing the forward acceleration of the patient抯 vehicle increases the patient injury?Things that increase forward vehicle acceleration include: small patient vehicle, large striking vehicle, icy road conditions, patient抯 vehicle moving at time of impact, brakes are not on, automatic transmission in patient抯 vehicle.
This information is just a touch of the research and literature compiled throughout the years that validate the ability to be injured, as well as the fact that people are injured in rear-end low speed collisions. This document is not meant to be comprehensive. It is to give insight to the tactics used by insurance companies to deny patient treatment, show that the insurance companies?reasons for denial are invalid, as well as provide quality information to further didactic education, literature review and research, and build upon as a knowledge base.
CHIROPRACTIC Evaluation and Management 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.**
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
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---------- FOLLOW-UP ----------
QUESTION: Dear Dr:
Thanks so much for your professional answer. I have made an appointment with a Nero surgeon next week, but I want to do some home or office exercise when I get a break but I dont know what exercies I can do so that I will not hurt more until I can see the specialist. Could you give me some advice? Thanks a lot!
AnswerDear Jessica,
The reason I sent you so much information is because I really think you should consider trying a good chiropractic physician before you see the neurosurgeon, as their only means of treatment is drugs or surgery...they don't do any conservative care. Although you may be sent to a physical therapist, PT's have no training in vehicle injuries or the documentation of such.
Concerning specific exercises, there really aren't any, other than gentle range of motion activities and mild stretching. Other specific exercises may be incorrect for you...unless I know what the spine looks like on x-ray, it is very difficult for me to guide you on that. All exercises should be tailored to help the spinal structure and alleviate pressure on the spine.
On thing for sure is that you definitely need to do traction to reduce the weight bearing stress on the disk spaces. I hope you looked at the Posture Pump device...it would be perfect to utilize for what was found on your MRI.
Sorry I can't offer more than that, but without more radiographic information and physical exam findings, I can't really opine of what would be appropriate for a specific program.
Respectfully,
Dr. J. Shawn Leathertman
www.suncoasthealthcare.net
