QuestionMy daughter was recently in a car accident 3 days ago to be exact. A boy ran a stop sign and hit her in the drivers side door. The hit was hard enough to spin the car aroung twice and face the car in the opposite direction when the car stopped. She went to the hospital they did chest x-rays and found that she had several ribs bruised. She also told them of her back hurting. They sent her home to take ibuprofen and a few days of rest. Now her left leg hurts and her butt bone hurts to the point that she is in tears at times. I have taken her back to our family doctor that said that her hip, pelvic bone was probably bruised and to continue to take iburpofen. What should we do?
AnswerDear Jimi,
Print this answer it is lengthy and complicated.
Bottom line here is that she likely has ligamentous, facet joint, sacroilliac joint and possible disk injury from the crash. Medical professionals are often not trained well in the soft tissue of the body, and do not understand the pain patterns well or effective rehab techniques, especially after crash injury. They just aren't trained well in this field.
These things can be really complicated due to the nature of the forces generated in the initial impact as well as the changes of velocity to the body reacting to the transfer of energy from one vehicle to the other. Below you will find more details on the approximate mechanism of injury from the side impact, pain patterns, and how we treat these injuries in our clinic. I would suggest that you also go to www.srisd.com to lean more about auto crash injuries as well as look for local physicians who have been trained to diagnose and treat these injuries. Good luck Jimi.
Respectfully,
Dr. J. Shawn Leatherman
www.suncoasthealthcare.net
Side Impact Mechanism of Injury
Side impacts are some of the most dangerous crashes because of the lack of structural protection and the relative aggressiveness of most vehicles' front-end components compared to their sides and occupant kinematic response. Making matters worse, of course, is the disparity between vehicle masses, ride heights, and structure (i.e., frame rail design vs. unibody or monocoque). Increasing ride height and mass of the bullet vehicle have been shown experimentally to result in deeper penetration of the target vehicle and greater potential for injury. The most important factor in side impact crashes is the match-up between the longitudinal components of the bullet vehicle and the door-sills of the target vehicle. If the door-sill is too low or the longitudinal frame is too high, intrusion will be significant.
Mechanism of Injury:
Upon impact, the target vehicle begins to move laterally pulling the occupant, due to the vehicle抯 restraint system. In accordance with Newton抯 1st law of motion, the occupant抯 inertia resists this motion. Initially, the thoracic curve is laterally flexed by the restraint, but impact inside the vehicle (such as with the driver) can mitigate or reverse the bending moment. This results in a compressive force on the impact side and a tensile force on the opposite side, which is transmitted through the spine, again due to the restraining effect of the seatbelt/shoulder harness and the weight of the torso.
Meanwhile, as the torso is experiencing this bending, compression and tension, the head ?also acting in according with Newton抯 1st law ?attempts to remain at rest. The force extends upward into the neck, initiating lateral bending of the cervical vertebral segments. The compression then quickly gives way to tension as the opposite moving head and torso attempt to disengage. This is asymmetrical loading, which is often magnified when the head is turned in either direction
Significant amounts of horizontal/shear force occur in the neck near 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 forces and thus less protective resistance to the side-impact vectored injury mechanism and this may actually increase the transfer of energy to the occupant.
As the change of motion from side to side occurs (abruptly in this case due to the head impact with the driver), the direction of horizontal shear reverses rapidly to the opposite 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 lateral and forward motions of the torso to the limits of the restraint system, and this rotates the upper torso to some extent and will effectively magnify the neck抯 bending moment due to the head抯 inertia. This is coupled with the addition of some angular motion forward and backward in the neck due to the yaw experienced by the vehicle. Therefore, it is more likely than not, that injuries occur in the initial phase and the re-entry phase complicated by the fact that head contact was made. Injuries are a result of head lag, compression, tension, and shear loading along the facet articulations and adjacent ligaments. Thus, injury can occur with or without a pathological range of motion, and without blunt impact trauma.
The Misunderstood Pain: Sclerotogenous Referral Pain
Presenting Situation: The patient states, 揑 have back pain that shoots into my leg? but the neurologist states the NCV (Nerve Conduction Velocity) EMG (Electromyogram) and MRI (Magnetic Resonance Imaging) are all normal. Is the patient embellishing? The answer is probably no. While it is true that some patients magnify their symptoms, they are usually not sophisticated enough to feign symptoms into a specific reproducible pattern. Why then were the imaging and electrodiagnostic tests negative? The answer is simple. The tests are either not sensitive enough to demonstrate the lesion, not designed to find the existing lesion or improperly performed and interpreted. For example, a negative MRI may suggest that there is no visualized compression of neural structures by discs or bone spurs. Negative NCV抯 and EMG抯 may suggest that there was insufficient compression or no compression of the large diameter nerves, which would result in a measurable abnormality. But what about the small diameter sensory nerves, what about ligament tearing, is there fatty infiltration of the muscle fibers, what about the other soft tissue structures? The truth is that researchers have shown an association between low back pain or leg pain and the lumbar facet joints many times, which is not generated by the disc, spinal nerve or spinal cord (1,2,3).
In fact, patients with referred pain often do not have nerve compression. Sounds good, right? Unfortunately it抯 not that simple. The most common referred pain seen in trauma cases are vascular, neurologic, visceral and sclerotomal. Neurologic pain (dermatomal pain), such as seen with disc herniations and nerve root compression, is the most frequently looked for type of pain. Less common are the vascular referred pains such as those seen with thoracic outlet syndromes. Visceral referred pain can happen with contusion to the body抯 organ systems. However, the most common and frequently overlooked origin of referred pain is from the soft tissues of the spine, also known as sclerotomal or sclerotogenous pain. An example: referred pain experienced with myofascial trigger points. While trigger points are common they are only one of the many sources of sclerotomal pain. Other sources would include the disc itself, facet joint capsules, facet joint cartilage, tendons, ligaments, etc?br>
Sclerotomal: The name suggests pain can come from any tissue of the same embryonic origin. A sclerotome is an embryonic region, which during fetal development differentiates into a variety of different body structures. These parts may or may not be neurologically connected but are understood to have some physiological relationship. Researchers have demonstrated these relationships repeatedly over the years and mapped out their referral distributions quite well. In fact, sclerotomal referral patterns have been published in many indexed medical journals beginning with the early work of Kellgren in 1939, Inman and Saunders in1944, and Feinstein et al. in 1954. One of the most well respected anatomical researchers, Bogduk, confirmed earlier findings in 1988.
Sclerotomal/referred pain has some unique characteristics. For example, in the lumbar spine (lower back) a Sclerotomal pain is usually more severe than dermatomal pain. Sclerotomal pain may not radiate down the entire leg and will usually stop at the knee or calf. There is no weakness or muscle atrophy with scerotomal pain. Referred pain can often be reproduced by applying pressure to the tissue site. In the cervical spine (neck) referral patterns to the cranium, chest, upper extremities and thoracic spine (upper and middle back) are common.
Referred pain has been overlooked as a source of pain by many clinicians because of the difficulty in treatment and diagnosis. Defense doctors, independent medical examiners, file reviewers, and insurance carriers, who have little or no experience with managing these types of injuries, often classify patients as malingerers or symptom magnifiers, and limit their treatment by cutting insurance benefits. Over time these patients may become chronic pain patients and eventually develop symptoms consistent with Fibromyalgia and Chronic Fatigue Syndrome.
Early Discovery: Many years ago Kellgren (4) conducted his now-classic research into the nature of referred pain. He injected hypertonic saline into paraspinal and other soft tissues and observed that the volunteers felt not only a local pain at the site of injection, which was to be expected, but also a pain radiating some distance away. Volunteers often complained of deep somatic pain or autonomic symptoms such as sweating, pallor, or palpitations. Kellgren mapped these referred patterns and found that there was a fair amount of consistency from one person to the next.
Rediscoveries: Some time later, Inman and Saunders (5) conducted similar research, again injecting fluid into the paraspinal tissues and documenting the patterns and nature of the resultant referred pain. In both instances they found that fairly consistent patterns of referred pain could be reproduced. Usually this referred pain began shortly after the injection and grew gradually. Most volunteers described it as gripping, aching, burning, heavy, or cramp-like. The important findings of Inman and Saunders are listed below.
Findings of Inman and Saunders
1. A time lag of minutes to several hours between injection and referred pain existed.
2. Volunteers had difficulty localizing the stimulus.
3. Periosteum and its attachments were most sensitive; muscle was least sensitive.
4. Greatest radiation occurred when periosteum or attachments were stimulated.
5. Muscles in referral areas were tender and sore.
6. Autonomic symptoms occurred when thoracic areas were stimulated.
7. The pain could last for several days.
Refinements: In an elegant experiment, Feinstein et al. replicated the earlier work of Kellgren, Inman and Saunders (6). They injected the brachial plexus of one volunteer with procaine. The complete regional block that resulted also included the autonomic nervous system (ANS), as evidenced by the temporary Horner's syndrome that was produced. In this way they had removed both the peripheral nervous system (PNS) and the autonomic nervous system from the list of contributors to the pain. Another paraspinal injection of saline solution into this volunteer's neck resulted in the same referred arm pain experienced before the regional block. Therefore, this mechanism of referral was not mediated or conveyed by either the ANS or the PNS, but was in fact a central phenomenon. The findings of Feinstein et al. are summarized below.
Findings of Feinstein et al.
1. Upper cervical stimulation resulted in head pain.
2. A segmental relationship existed, whereby injection of a muscle whose innervation was C5-6 would result in soreness in other muscles innervated by those levels.
3. Muscle soreness and spasm was noted in referred pain areas.
4. Hypesthesia was noted over referred areas.
5. Phantom limb pain could be reproduced in amputees (even in those who had not experienced it at the time of their amputation).
6. **The ANS and PNS are not mediators of the pain.
Perhaps most interesting about this referred or sclerotogenous pain, is the observation that the levels of referral, while reproducible from patient to patient, do not seem to follow known dermatomal or myotomal patterns. In fact, the body maps created by Feinstein and coworkers are re-created in Foreman and Croft抯 Textbook: Whiplash Injuries: the cervical acceleration/deceleration syndrome [3rd edition, pp 396-404]. These body maps demonstrate that, very often, injection at one spinal level results in pain referral to areas innervated two to four spinal segments away. And often, referral is to not one, but several segment levels. This serves to confuse the issue all the more. For example, an injection at C7 may result in referred pain in areas innervated by C5, C6, C7, C8 and T1.
Since it is most common for clinicians to view the human body with the neurogenic pain model, a ligamentous injury at C7, resulting in the above referred pain pattern, might confuse the uneducated physician. Diagnostic options may include: multiple disc lesions, brachial plexopathy, thoracic outlet syndrome, or outright malingering, which is often the impression many doctors arrive at. The patient is branded a faker, and left without answers.
Non-classical neurological findings in CAD/whiplash trauma are common (7) and should not be used to suggest that patients are disingenuous. These non-dermatomal sensory abnormalities, as common as they are, qualify one for a DSM-III psychiatric diagnosis! Some have argued that they are common in Multiple Personality Disorder. As stated previously, anatomical studies and electrodiagnostic studies will generally be normal, although plain films often demonstrate some instability. Again, this only serves to confound the uneducated physician, and muddle diagnosis.
Recent Corroboration: Bogduk and Marsland (8,9) demonstrated that cervical facet joints could be the source of neck pain. Over 50% of their chronic CAD injury group had facet pain (8,10). Dwyer et al. (11) injected the cervical facet joints of human volunteers with saline solution and dye and recorded their responses. They found that the upper cervical joints, C2-3, were associated with suboccipital headaches when injected (they did not inject C1-2 or OCC-C1, but presumably these would have resulted in headaches as well). Lower levels were productive of neck and shoulder pain, not surprisingly. In part II of their study (12), they used the pain maps created from injecting normal volunteers to predict the spinal levels involved in a group of patients who complained of neck and/or shoulder pain. Their success rate with this method was 100% (Limitations- fairly small study group).
Although this work by Bogduk and Marsland (9) and Dwyer et al. (11) seems to suggest that discrete scleratomes exist in the cervical region, the high degree of overlap at lumbar levels noted by some observers precludes the description of such a construct there. Kellgren (4) and Inman and Saunders (5) described discrete scleratomes at lumbar levels, but more recent researchers have been unable to confirm such consistency (13,14). McCall et al. (15), for example, injected facet joints at L1-2 and L4-5 and found much overlap even though a general pattern of flank pain was seen at upper levels, whereas buttock and groin pain was seen at lower levels. In essence, these studies argue against 搕rue scleratomes," in the lumbar spine while the phenomenon of scleratogenous pain is still very real. Scleratomal pain, it turns out, was a poor term for the phenomenon. Nevertheless, Bogduk and Lord (16) continue to use the term and give a good review of pain and whiplash injury. The figure below points to the differences between dermatomal and scleratomal pain.
The broadly referring pattern of facet joints is at least partially explained by a recent set of experiments. Ohtori et al. (17) used retrograde neurotracing methods with Fluoro-Gold (FG), to trace the level of dorsal root ganglions (DRGs) innervating the C1-C2, C3-C4, and C5-C6 facet joints and their pathways in rats. Neurons labeled with FG were present in the DRGs from C1 through C8 in the C1-C2 group, from C1 to T2 in the C3-C4 group, and from C3 to T3 in the C5-C6 group, which illustrates the redundancy of innervation at multiple levels. No wonder an injured facet joint may refer pain so broadly.
The prognosis for sclerotogenous pain from traumatic insult is dependent upon many factors. The extent of damage, pre-exiting illnesses, compliance with care and early detection by the physician, all contribute to the potential outcome. Damaged soft tissues tend to heal in a disorganized manner even with regular management. Active care protocols applied in a controlled manner are essential in managing the resultant scar formation in sclerotogenous structures and reducing chronic pain. The fibrotic replacement tissue is never as competent as the original tissue and is prone towards re-injury and hypersensitivity. Even with prompt attention the prognosis for complete recovery may be only fair to poor.
References:
1. Carrera GF: Lumbar facet joint injection in low back pain and sciatica. Neuroradiology 137:665-667, 1980
2. Fairbank JCT, Park WM, McCall IW, O'Brien JP: Apophyseal injection of local anesthetic as a diagnostic aid in primary low-back pain syndromes. Spine 6(6):598-605, 1981.
3. Destouet JM, Gigula LA, Murphy WA, Monsees B: Lumbar facet joint injection: indication, technique, clinical correlation, and preliminary results. Radiology 145:321-325, 1982.
4. Kellgren JH: On distribution of pain arising from deep somatic structures with charts of segmental pain areas. Clin Sci 4:35-46, 1939.
5. Inman VT, Saunders JBdeCM: Referred pain from skeletal structures. J Nerv Ment Dis 99:660-667, 1944.
6. Feinstein B, Langton JNK, Jameson RM, Schiller F: Experiments of pain referred from deep somatic tissues. J Bone Joint Surg 36A(5):981-997, 1954.
7. Bogduk N: Post whiplash syndrome. Aust Fam Phys 23(12):2303-2307, 1994.
8. Barnsley L, Lord S, Wallis BJ, Bogduk N: The presence of chronic cervical zygapophyseal joint pain after whiplash. Spine 20(1):20-26, 1995.
9. Bogduk N, Marsland A: The cervical zygapophyseal joints as a source of neck pain. Spine 13(6):610-617, 1988.
10. Lord SM, Barnsley L, Wallis BJ, Bogduk N: Chronic cervical zygapophyseal pain after whiplash. Spine 21(15):1737-1745, 1996.
11. Dwyer A, Aprill C, Bogduk N: Cervical zygapophyseal joint pain patterns I: a study in normal volunteers. Spine 15(6):453-457, 1990.
12. Aprill C, Dwyer A, Bogduk N: Cervical zygapophyseal joint pain patterns II: a clinical evaluation. Spine 15(6):458-461, 1990.
13. Hockaday JM, Whitty CWM: Patterns of referred pain in the normal subject. Brain 90(3):481-496, 1967.
14. Sinclair DL Jr, Feindel WH, Weddell G, et al.: The intervertebral ligaments as a source of pain. J Bone Joint Surg 30B:515-525, 1948.
15. McCall IW, Park WM, O'Brien JP: Induced pain referral from posterior lumbar elements in normal subjects. Spine 4(5):441-446, 1979.
16. Bogduk N, Lord SM: Cervical spine disorders. Cur Opin Rheumatol 10:110-115, 1998.
17. Ohtori S, Takahashi K, Chiba T, Yamagata M, Sameda H, Moriya H. Sensory innervation of the cervical facet joints in rats. Spine 26:147-150, 2001.
CHIROPRACTIC E/M COUNSELING RECORD: SUPPLEMENTAL INFORMATION
Risks and Benefits of Management Options: There is a risk that chiropractic treatment will have a temporary increase in the pain experienced by the patient due to mobilization of inflammatory mediators that are present in injured and inflamed tissues such as; cytokines, proteolytic enzymes elastase, trypsin, chymotrypsin, plasmin, cathepsins & collagenase, growth factors (PDGF & TGF-β), chemotactic agents for neutrophils (12-HETE, PF-4, & PAF), enzyme inhibitors (alpha-1- antitrypsin, alpha-2-macroglobulin), clotting factors, serotonin, thromboxane A-2, platelet activating factor, platelet factor-4, interlukin-1-β, thromboglobulin-β, tumor necrosis factor (TNF), and substance P. (2,4,6,12,14,16,17,25,28,30,31,32,38,40,44,56,61,68) All of these mediators are released in the acute inflammatory process and persist into the secondary phase of inflammation. Many have been connected to nociceptive (pain promoting) input to the tissues. TNF and IL-1 have also been shown to contribute to joint injury and bone resorption. (56) They may also act as pyrogens similar to prostaglandins/eicosanoids. (16)
Benefits of care are that with passive modalities, controlled early mobilization of injured tissues through chiropractic adjustments, and proper nutritional supplementation; aberrant processes can be limited and sometimes reversed by supplying increased oxygen and blood supply to the tissues. Therefore, pathways are established inducing proper nutrient delivery for repair, stimulated lymphatic channels pull inflammatory mediators away from injured tissues, and normal neurological input is instituted to the brain for improved proprioception through the dorsal columns. Pain control is modulated locally due to the gate theory reflexes. Activation of the opiate receptors, stimulate the descending inhibitory pathways of the peri-aquaductal grey regions in the reticular formation of the lower brain. The nucleus raphe magnus is stimulated and serotonergic projections extend down the cord, synapse with interneurons in the superficial dorsal horn, which release enkephalins and result in inhibition of the nociceptive system. (22,23) According to Wyke, these are the same inhibitory neurons that are stimulated as joint mechanoreceptor afferents are depolarized from a chiropractic adjustment. (66)
揝oft tissue injuries?encompass anything that is not bone including organ systems, nervous tissue, cartilage, musculature, ligaments, tendons, and fascial tissue. Muscle has a high reparative capacity and sufficient regenerative capacity, but extensive damage results in scarring and atrophy of the fiber bundles. (17) In contrast, tendons and ligaments are notably slow to heal! Even after forty weeks, collagen may still not be present in normal concentration and organization. (21) Articular cartilage, which is found in every zygapophyseal joint in the spine, has a notoriously limited potential for either healing or regeneration. (48) The ability of articular cartilage to heal will depend on the severity of injury. Patients requiring surgery are the least likely to heal. (48) In relation to acceleration/deceleration type trauma from vehicular crashes, the cartilaginous surfaces of the facet, (a.k.a. the synovial folds), are exposed to tremendous loading moments with sheer, compression, tensile, and torsional forces. Major cartilaginous damage is probable throughout the spine along with ligament disruption and is responsible for sclerotogenous pain patterns experienced by patients.
Regarding patient care, immobility is a main factor that promotes degeneration. The restoration of mobility seems to curtail degeneration. Previous research has demonstrated that the tensile strength of ligaments and tendons respond to changes in physiologic stress and motion that aid the healing process. Improving mobility can even enhance cartilage healing after traumatic injuries as well as the strength and stiffness of ligamentous structures. Furthermore, after trauma, healing occurs by an unspecified form of collagen, scar tissue, which frequently causes adhesions and fibrotic changes that must be dealt with therapeutically. Chiropractic adjustments improve and restore motion and movement patterns in the zygapophyseal joint at the facet articulations which include the ligamentous, myotendinous, and fascial complexes. With the addition of carefully progressed passive and active rehabilitation programs, further mobility can be achieved due to increased stretch and flexibility.
Instructions/Explanations for Treatment: Acute phase-emphasis is placed on limiting the inflammatory response and reducing pain. The use of interferential current aids this process by increasing lymphatic drainage as well as increasing blood flow, oxygenation and nutrient delivery to the injured tissues. We use specific nutraceuticals in the early phase of treatment such as pro-enzymes; malic acid, magnesium, omega III fatty acids, bromelain, tumeric, and zinc. These agents have been proven to inhibit and reduce inflammation, maximize the bioavailablity of repair materials for soft tissue healing, and provide neurological support. (6,7,8,9,10,11,18,19,26,29,33,34,35,37,39,43,46,47,49,51,52,54,56,62) Cryotherapy is an important part of this early phase for its analgesic and anti-inflammatory effects. Passive techniques are used mostly in this phase of care. Massage may be utilized as well to facilitate the relaxation of myospasm, mobilize fascial slings and bands, and inhibit trigger points with Nimmo technique. (13)
Sub-acute phase-emphasis is on the incorporation of active participation of the patient in their care. Home exercises and stretches are taught in this phase and are to be performed either three times weekly or daily depending on patient progress and tolerance. (31) This will facilitate increases in the mobility of injured tissues while limiting the formation of adhesions and abnormal scar tissue. (5,20,53,64)) Nutritional supplementation continues throughout this stage as well as chiropractic adjustive techniques. Ultrasound techniques may be used to increase the microcirculation, break up deeper adhesions and/or trigger points and muscle spasms that are becoming chronic, promote increased oxygen uptake, and increase the plasticity of collagen. (42,67) Patients will generally have their first re-evaluation in this stage of care to ensure that they are ready for active rehabilitation.
Physical rehabilitation phase-emphasis in this stage is to continue with reduction of pain, actively stimulate joint mechanoreceptors, Golgi tendon organ and muscle spindle cells to increase proprioceptive information as well as focusing on building strength, stability, and increasing active functional ranges of motion. (31) Substantial evidence exists confirming that ligaments serve important roles as signal sources for the reflex systems of the locomotor apparatus, (63) therefore effort should be made to normalize and mimic normal function after trauma. The introduction of significant amounts of proprioceptive training in the rehabilitation process is paramount, and aids in the reorganization of the tissue. (65) Reorganization of collagenous scar tissue is important. It creates increased tensile strength as well as promoting the break down of the abnormal cross bridges, aligning the scar along the physiological action of the muscle, tendon or ligamentous complex. (27,41,45,55,57) Healing times for intra-articular collagen are such that it may take up to 3 months to achieve 50 percent of the normal strength and 6 months before a functional strength of 70 percent is reached. (15,69) Essentially, collagen forms 70 percent of the dry weight of the ligament, turning over slowly with a half-life of 300 to 500 days. (24) Maximum functional improvements may take over 2 years for resolution.
Chiropractic adjustive techniques remain the cornerstone of the program to ensure that the zygapophyseal joint biomechanics are proper as facets continue to articulate correctly and send mechanoreceptive information to higher brain centers, and to reduce the neoneuralization of scar tissue. Neoneuralization increases pain transmission to the brain via nociceptive input from the synaptic arborization of c-afferent fibers. The goal is to limit and inhibit this process so that neurological wind-up does not occur and lead to chronic pain and residual disability. Stretching/AROM, resistance training incorporating bands and weights, physioball training, dynamic spinal traction and postural exercises are utilized for maximum benefit.
Dynamic spinal traction for structural remodeling and rehabilitation is utilized to maximize the physiological anisotrophic effects of creep, hysteresis, and set that occur in viscoelastic tissues such as ligaments. (64) The ligamentous complex is the limiting factor in effective rehabilitation. (36,53) Only sustained incremental loading of the ligamentous tissues with low force of long duration, in a consistently applied manner, will have the desired structural viscoelastic effect of plastic changes. (31,59,60) Chiropractic Biophysics traction protocols are substantially researched and documented. There are over 80 clinical papers in the index medicus, and are too bulky to be listed in this document. (**) Cryotherapy is utilized in traction and post-traction due to research indicating that tissues stretched under heating conditions and then allowed to cool under tensile conditions maintain a greater proportion of their plastic deformation than do structures allowed to cool in the unloaded state. Cooling under load may allow the collagenous microstructure to stabilize at new stretched lengths. (36,60)
Our office protocols have been established to facilitate application of the above techniques, nutrition/ supplementation and information; therefore maximizing injury repair, pain suppression, and patient recovery. Specific treatment differences will exist from patient to patient in relation to their individual injuries, severity of injuries, as well as tolerance to rehabilitation.
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