Ranges of Motion as a Utility for Outcome Assessments

Chiropractic Taking a Lead Role in Rendering Accurate Assessments for Spine

By William J. Owens

Mark Studin

The Academy of Chiropracitc has had quite few questions over a long period of time related to patient treatment outcomes and inquires as to the most accurate ways in which to both measure and document them.  Bombardier (2000) published a paper in Spine entitled “Outcome Assessments in the Evaluation of Treatment of Spinal Disorders: Summary and General Recommendations.” This paper comprehensively reviewed not just outcome assessments, but how the assessment categories are broken down.  Although many in the field utilize outcome assessment forms, when working in both clinical and academic environments across the globe, most doctors fall severely short with regard to comprehension of the tools they are using.  Most of the time we see that doctors are simply repeating what they hear without understanding it and memorialize it in clinical notes, thereby rendering inaccurate outcomes to the detriment of the patient and the profession.

Outcome assessments were originally created as “tools” for research purposes, specifically to objectify whether specific treatments were working on a global scale within a population.  Measurement of the effectiveness of treatment is important for the clinician, but the history related to outcome assessment is based upon making assumptions on large groups of people to make a homogenous statement or predictive statement based on a large group of very different people.  In research, investigators want to “group everybody together” and generalize so that they can obtain a starting point to understand the issue they are researching. In this case, the research topic is the effectiveness of a specific treatment, response to chiropractic care in our offices. 

With it comes to patient treatment in general and proving effectiveness in an individual patient, we want to be explicit in regard to a specific diagnosis for that specific patient, it is not a process whereby we work off of generalizations.  An experienced practitioner shouldn’t conclude a definitive prognosis based on what’s going on with the rest of the world or even with larger groups of patients. A prognosis should be based upon that particular patient’s response at that particular time. As an example, if a patient were to lose a pinky finger in a work-related accident and that patient was a forest ranger, his day would most likely consist of hiking through the woods. That would render one set of conclusions regarding outcomes and his ability to function. However, if that sample patient earned his living as a concert pianist, there would be a major difference in perceived outcomes and his ability to function in their respective occupations.  Although we could give both men an impairment rating for the loss of that digit, how that loss might affect their lives is very different and specific to each patient. That is what “patient centered care” is all about, focusing on the individual patient not on the population to which that patient is part.  A lot of the most outcome assessment tools are designed give providers treatment pathways, however, to obtain the complete picture, you need to asses each patient’s complete clinical documentation, such as changes in pain levels, motor and sensory function, range of motion, location and degree of muscle spasm, neurological function or any other clinically valid finding.  Initially in care, perhaps only modalities could be utilized, but later, it could be possible to render chiropractic spinal adjustments, changing the prognosis and plan for future outcome improvements. Therefore, the utilization of a “single assessment tool” can do harm to a patient if not all tools available are considered.    

Based upon the last sentence, the inclusion of any “single” assessment tool would appear to be as irresponsible as the exclusion of any “single” assessment tool. You must consider multiple parameters, both in clinical evaluations combined with a detailed history to conclude an outcome.

Bombardier (2000) wrote, “Clinicians and researches increasingly recognize the importance of the patient’s perspective in the evaluations of effective of treatment” (p. 3100). This statement is consistent with Sackett, Rosenberg, Gary, Haynes and Richardson (1996) who stated, “Evidence based medicine is not restricted to randomized trials and meta-analyses. It involves tracking down the best external evidence with which to answer our clinical questions” (p. 73).

Both articles realized that effective healthcare requires more than just published research and must include patient feedback is valid in helping to determine the direction of care and outcomes. However, it cannot stop here and therein lies the problem. It is not possible to determine permanencies or lack thereof with a simple “subjective response” to make a conclusive prognosis. Evidence-based care includes 1) published research, 2) the doctor’s experience and input, and 3) the patient’s input, both verbally and through test results so that the care can be “evidence-based.”  The “evidence” for care comes from three distinct areas and therefore the results of the intervention must also meet the same level of complexity.  There are no shortcuts.

Bombardier (2000) also reported, “A core set of measures should include the following five domains” (p. 3100). This information is leaning a little bit more towards research, however, if you can grasp this general concept, you will begin to understand the miscommunication relating to outcome assessments and what is required to tell the patient’s “true story.” “A core set of measures should include the following five domains: back specific function, generic health status, pain, work disability, and patient satisfaction” (Bombardier, 2000, p. 3100).

When looking at a specific region of the spine, one should focus on these five domains and generically inquire as to what the patient’s presentation is overall. Is he/she an obese smoker? Is he/she fit and active? Are there other comorbidities such as diabetes, a missing limb, etc.?  His/her pain should be documented in detail including whether he/she is completely or partially disabled, what his/her work duties are, and, ultimately, whether he/she is satisfied with his/her care. We know that patient satisfaction is a driver of compliance and if we have compliant patients, then we have people that are adhering to their treatment plan, and historically we’re going to get better outcomes. 

When it comes to specific back function, there are two main outcome assessments: The Roland-Morris Disability Questionnaire and the Oswestry Disability and both are related directly to spine, specifically the lower back.  Historically, chiropractic has considered the spine to be one contiguous organ, but many within the profession are now considering treating the spine segmentally and ignoring the whole. Medicine, conversely started by treating the spine segmentally and is now embracing a whole spine model which in part, is based upon the scientific papers published in neurosurgery journals (following chiropractic’s historic lead). Spinal biomechanics dictates that a whole spine model is critical in spinal stability and long-term spinal health.   If you do not consider creating a homeostatic model, then any corrections made will be temporary at best and perhaps undo any compensatory mechanisms within the spinal system.  Proper full spine biomechanical analysis is being embraced by the neurosurgical community at a very high level particularly, since it is been shown to influence spinal surgery outcomes and chiropractic shares the same goal; to create a homeostatic, biomechanically balanced spine “post-treatment.”

Scheer et al. (2016) wrote:

Patients with thoracolumbar deformity [scoliosis] without preoperative CD [cervical deformity aka loss of cervical lordosis] are likely to have greater improvements in HRQOL [health related quality of life] after surgery than patients with concomitant preoperative CD. Cervical positive sagittal alignment [cervical lordosis] in adult patients with thoracolumbar deformity is strongly associated with inferior outcomes and failure to reach MCID [minimal clinically important difference] at 2-year follow-up despite having similar baseline HRQOL to patients without CD. This was the first study to assess the impact of concomitant preoperative cervical malalignment in adult patients with thoracolumbar deformity. These results can help surgeons educate patients at risk for inferior outcomes and direct future research to identify an etiology and improve

patient outcomes. Investigation into the etiology of the baseline cervical malalignment may be warranted in patients who present with thoracolumbar deformity. (p.109)

Neither Roland-Morris nor Oswestry takes into consideration whether the patient’s entire spine is involved. As an example, the lumbar spine is in pain, but is it a compensatory lesion with the primary lesion being in the cervical region?  Roland-Morris and Oswestry continue to fragment the spine into regions which really are not regions at all, but part of an entire model or organ system. That is a significant drawback in that they’re only “assessing” one part of the spine and, therefore, only a portion of an organ system and ultimately only part of the patient’s real spinal dysfunction.

When it comes to the generic measures like health status, the SF-36 is highly regarded in that arena. To find more, do a computer search using the search terms “SF-36 outcome measure.”

According to Rand Health (n.d.):

As part of the Medical Outcomes Study (MOS), a multi-year, multi-site study to explain variations in patient outcomes, RAND developed the 36-Item Short Form Health Survey (SF-36). SF-36 is a set of generic, coherent, and easily administered quality-of-life measures. These measures rely upon patient self-reporting and are now widely utilized by managed care organizations and by Medicare for routine monitoring and assessment of care outcomes in adult patients. (https://www.rand.org/health/surveys_tools/mos/ 36-item-short-form.html)

Bombardier (2000) commented:

Moreover, the SF-36 Bodily Pain Scale provides a brief measure of pain intensity and pain interference with activities. Health-related work disability should include a minimum of measure of work status and work-time loss...No single measure of patient satisfaction is clearly preferred but guiding principles are provided to choose among available measures. (p. 3100)

Generic health status in the SF-36 includes pain and working disability. It also looks at status and time lost which are important factors that contribute to an accurate diagnosis, prognosis and treatment plan. In addition, our issue with many written, form-based tools is that they’re time consuming and can be difficult, particularly with patients of differing socioeconomic status, level of education and language. This issue is addressed by the SF-36. Consistency in patient care is critical and implementing a system that allows all patients to utilize it will render a consistent outcome measure. We don’t want to have an electronic interface in the waiting room for outcome measure that can only be utilized by 10% of patients while the other 90% have difficulty because of various issues such as literacy challenges, generations that are not used to technology, or general sloppiness when inputting data (i.e. reversing the 1-10 scale). In those cases, your “data in” is the garbage that you must deal with. In addition, too many doctors “scantily” review the patient portion of the history and if it is not accurate, it creates an inaccurate picture.

Very few individual measures are clearly superior and we must understand that it is the totality of your findings and your patient reports in their entirety that create an accurate picture. If a lawyer, an insurance adjuster, or a medical doctor asks what type of outcome measures you use, the proper answer is, “I use the patient’s objective clinical findings correlated to his/her subjective improvement.  That objective data is obtained every visit through my touching the patient, feeling for spasm, determining if the patient can move, stressing joints, and correlating those findings to his/her pain and the historical etiology of the accident/injury/episode, as well as basic and advanced imaging.”  It reflects the comprehensive patient assessment performed and becomes close to “bulletproof!”

If you are exclusively using only one of the five assessments, either the Roland-Morris, Oswestry, NPI indexes or pain scales, you are measuring only one of five domains.  If you’re not doing all five, you are not rendering a complete assessment and potentially doing the patient a disservice and adding an inaccurate statistic to the treatment rendered (not technique, but the chiropractic as a profession).  Back specific function, generic health status, pain/disability status and patient satisfaction must be part of your outcome assessment; however, you will still need to add the clinical findings that should correlate and all modalities inclusive of ranges of motion as considered.

Bombardier (2000) wrote:

A generic measure is particularly important in populations with comorbidities…since disabilities from these comorbidities may influence the patients’ response to treatment…Generic measures also provide a more comprehensive picture of the patient health status because back specific instruments do not include measures of patients’ mental or social health. (p. 3100)

Therefore, managed care, from a business model perspective, has reaped windfall profits because it categorizes people into large populations and creates generic care paths requiring practitioners to be complicit in their profit generation by utilizing these outcome measures. If you do an Oswestry on a 25-year-old yoga instructor and then I do an Oswestry on a 65-year-old railroad worker that smokes every day and eats fast-food, those scores are irrelevant comparatively. The global picture for patient care isn’t as effective as looking at the individual patient using a larger cross-section of assessment tools outlined within the treatment record. 

Bombardier (2000) stated, “Overall, the SF-36 struck the best balance between length, reliability, validity, responsiveness and experience in large populations of people with back pain” (p. 3101). She continued, “Measures of ‘pain severity’ are distinct from measures of ‘pain affect’” (Bombardier, 2000, p. 3200).

Regarding the spine, when dealing with patients that have a pain syndrome from a muscle problem, a ligament problem, a fracture, a tumor, or a disc herniation, measuring the severity includes “pain severity” questions such as, “How are you today on a scale of 0 to 10?”  versus the “pain affect” which is what he/she can or can’t do.  Those are critically important and they’re very different measures and should be considered when considering MMI’ing (maximum medical improvement) your patient.

Bombardier (2000) continued: 

Pain severity is how much a person hurts, while pain affect is more complex and reflects a mental state triggered by the pain [like the pinky finger example above].  The measure of pain severity is relatively straightforward, while there are many unresolved questions about the construct of pain affect.  For these reasons, it is recommended as part of the core set, to use a brief measure of pain severity.  The bodily pain subscale of the SF-36 is the most recommended scale – it has strong psychometric support and extensive normative data.  This two-item scale measures pain intensity (six levels: none, very mild, mild, moderate, sever, and very severe) and interference with activities (five levels: not at all, a little bit, moderately quite a bit, extremely).  It is a generic pain scale since it asks about overall pain. (p. 3102)

The Patient Satisfaction Scale, (PSS), another outcome modality is a multi-item scale with 17 questions covering information, emotional support and assurance and the effectiveness of prescribed treatment…It, however, does not include issues of access to care, involvement in decision making, coordination of care among caregivers, or trust in one’s clinician, which are dimensions of importance to patients. (p. 3102)

Bombardier (2000) concluded by stating:

Finally, the most common reason for using patient-based outcome measures is to assess patients’ response to treatment. Is the patient better? How well do the measures described in this special focus issue detect patient improvement when it has occurred?  What is their smallest clinically relevant change?  There is no set answer to such questions…These are all different concepts of change.  No wonder then that the responsiveness of the RDQ [Roland-Morris Disability Questionnaire] found in the literature will range from 3 to 8 points on its 0 to 24 scale…[That’s up to a 33% error rate.] (p. 3103)

When you consider a more expansive subset of subjective complaints and then clinically correlate it to changes in orthopedic, neurological and biomechanical clinical/functional tests that show objective restoration of cervical or lumbar curvatures, decreased muscle spasm, increases in range of motion, increases in functional activity, it now renders a more complete clinical picture as compared to a simple form.  An individual “form” which is designed to only consider a portion of the entire spine is severely deficient in rendering any level of accuracy for a complete spinal organ.  Too many providers, unfortunately, utilize these forms as a “filler” for poor documentation and render an inaccurate diagnosis, prognosis and treatment plan as a result.  That is why complete clinical documentation is the only true way to monitor and assess the patient’s response to care.

One of the most important aspects in the functional care of the spine is the range of motion occurring throughout a specific region as well as the individual motor units.  In this paper, we purposefully omitted research and validity of ranges of motion as discussed in both the fifth and sixth editions of The Guides to the Evaluation of Permanent Impairment published by the American Medical Association. The AMA Guides clearly position ranges of motion as a valid tool for assessing clinical progress or the lack thereof. However, it should be mentioned that ranges of motion are just one tool and the astute clinician should never rely on just one assessment parameter when determining outcomes. It is the totality of all measures that lend a valid outcome assessment.

We have heard doctors and groups discussion labeling range of motion as invalid which even according to the AMA is an important tool in assessing disability and response to care.  To single out ranges of motion as an invalid tool for outcomes is “fodder” for carriers and defense lawyers to utilize against practitioners because the commentary is misleading. To denigrate ranges of motion as an outcome assessment tool is suggesting that it should not be utilized when Medicare, insurance carriers as well as every court in the nation consider it a valid analytical tool when used properly to determine biomechanical pathology.

Measuring outcomes in a patient with a spinal condition is a complex process, however it should not be a surprise. As the spine is one of the most complex systems in the body, chiropractic as a profession is in a perfect position to take a leadership position in the diagnosis, assessment, treatment and management of spinal biomechanical disorders.  Leadership requires an intellectual and forward thinking approach to the patient interview, objective documentation and reporting, there is no other way to properly care for a patient and tell their story.  We need to embrace the challenge and lead though both our daily clinical practices and teaching all who treat spine. 

References:

1. Feiss, R. (year). Why you should stop using ROM as an outcome measure. Institute of Evidence-Based Chiropractic. Retrieved November 11, 2017, from http://www. researchcapsule240.com/video-library/

2. Bombardier, C. (2000). Outcome assessments in the evaluation of treatment of spinal disorders: Summary and general recommendations. Spine25(24), 3100-3103.

3. Sackett, D. L., Rosenberg, W. M., Gray, J. A., Haynes, R. B., & Richardson, W. S. (1996). Evidence based medicine: What it is and what it isn't. British Medical Journal, 312(7023), 71-72.

4. RAND Medical Outcome Studies. (n.d.). 36-Item Short Form Survey (SF-36). RAND Health. Retrieved November 11, 2017, from https://www.rand.org/health/surveys _tools/mos/36-item-short-form.html

5. Scheer, J. K., Passias, P. G., Sorocean, A. M., Boniello, A. J., Mundis Jr, G. M., Klineberg, E.,...Shaffrey, C. I. (2016). Association between preoperative cervical sagittal deformity and inferior outcomes at 2-year follow-up in patients with adult thoracolumbar deformity: analysis of 182 patients: Presented at the 2015 AANS/CNS Joint Section on Disorders of the Spine and Peripheral Nerves. Journal of Neurosurgery: Spine24(1), 108-115.

6. American Chiropractic Association. (n.d.). Clinical documentation guidelines. Commentary on Centers for Medicare and Medicaid Services (CMS)/PART. Retrieved November 11, 2017, from http://www.chiro.org/ documentation/ABSTRACTS/Medicare_Documentation_ACA.pdf

7. Cocchiarella L., & Anderson G. (2008).  Guides to the evaluation of permanent impairment, 6th edition. Chicago, IL: American Medical Association Press.

Dr. Mark Studin is an Adjunct Associate Professor of Chiropractic at the University of Bridgeport College of Chiropractic, an Adjunct Professor of Clinical Sciences at Texas Chiropractic College and a clinical presenter for the State of New York at Buffalo, School of Medicine and Biomedical Sciences for post-doctoral education, teaching MRI spine interpretation, spinal biomechanical engineering and triaging trauma cases. He is also the president of the Academy of Chiropractic teaching doctors of chiropractic how to interface with the medical and legal communities (www.DoctorsPIProgram.com), teaches MRI interpretation and triaging trauma cases to doctors of all disciplines nationally and studies trends in healthcare on a national scale (www.TeachDoctors.com). He can be reached at This email address is being protected from spambots. You need JavaScript enabled to view it. or at 631-786-4253.

Dr. Bill Owens is presently in private practice in Buffalo and Rochester NY and generates the majority of his new patient referrals directly from the primary care medical community.  He is an Associate Adjunct Professor at the State University of New York at Buffalo School of Medicine and Biomedical Sciences as well as the University of Bridgeport, College of Chiropractic and an Adjunct Professor of Clinical Sciences at Texas Chiropractic College.  He also works directly with doctors of chiropractic to help them build relationships with medical providers in their community. He can be reached at This email address is being protected from spambots. You need JavaScript enabled to view it. or www.mdreferralprogram.com or 716-228-3847  

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Chiropractic and Cervical Arterial Dissection:

Causal Relationship or Medical Dogma?

By Mark Studin

William J. Owens

A report on the scientific literature and commentary

There has been much controversy over the last 2 decades about the perceived causal relationship between a chiropractic cervical adjustment and dissecting arterial aneurysm on the internet, in the literature and in the beliefs of some in the medical community. Prior to examining the published facts, lets first clarify what an arterial dissection is.

 

According to Haneline and Rosner (2007)

Arterial dissection is an uncommon vascular wall condition that typically involves a tear at some point in the artery's lining and the formation of an intimal flap, which allows blood to penetrate into the muscular portion of the vessel wall. Blood flowing between the layers of the torn blood vessel may cause the layers to separate from each other, resulting in arterial narrowing or even complete obstruction of the lumen (Fig 1). Moreover, pulsatile pressure damages the muscular layer, resulting in a splitting or dissection of the intimal and medial layers that may extend along the artery variable distances, usually in the direction of blood flow.Another way for dissection to occur involves a primary intramural hemorrhage of the vasa vasorum, which builds pressure between the intimal and medial layers and may eventually rupture into the vessel's true lumen. Occasionally, a double lumen (also known as false lumen) is formed when the subintimal hemorrhage ruptures back into the arterial lumen distally. (pgs. 113-114) 

 

 

Fig. 1

 

In addition, Haneline and Rosner (2007) wrote a decade ago:

Of special interest to chiropractors is the role cervical spine manipulation [CSM] plays, if any, in the pathogenesis of CAD [Cervical Artery Dissection]. Indeed, patients do experience CAD on rare occasions after CSM, making knowledge about the cervical arteries, the predisposing factors, and the pathogenesis of the condition important for chiropractors. (pg. 110)

 

This comment, early in the potential relationship between cervical adjusting and cervical arterial dissection [CAD] warranted a warning to healthcare provider about CAD and cervical adjusting making it important to understand the cervical arteries. This is underscored by the authors themselves being chiropractors and memorizing this “caveat” to the profession.

 

 

In a September 2017 presentation by Candice Perkins MD, Neurology, Vascular Neurology (an attending stroke neurologist and both an Associate and Assistant Professor of Clinical Neurology at the State University of New York at Stony Brook Hospital and Medical Center from 2001 - 2016) in New York, she stated that there is zero evidence for direct causal relationship between stroke and a chiropractic cervical adjustment performed by a licensed chiropractor in the appropriate clinical presentation. Dr. Perkins went on to explain that there are numerators and denominators. The denominator are strokes and the presence of a patient with a stroke. The numerator is the associated incidence. In her vast experience with stroke, there are an unlimited number of numerators with chiropractic being one, however if one uses that same equation, there are hundreds of other equally potential factors with primary care medical visits being of equal incidence. In addition, with her understanding chiropractic as a patient and from the literature, there is scant evidence that a chiropractic adjustment can be the causative factor of cervical dissecting aneurysm.

 

 

Researchers from the University of Pennsylvania Department of Neurosurgery came to the same conclusions. In a systematic and meta-analysis of chiropractic care and cervical arterial dissection, they concluded:

There is no convincing evidence to support a causal link between chiropractic manipulation and CAD. (pg. 1)

 

Church et. Al reviewed 253 published articles and scored them on a GRADE system with 4 variables, high, moderate, low and very low in reliability of the research available on CAD and chiropractic adjustments. They concluded:

Scrutiny of the quality of the body of data using the GRADE criteria revealed that it fell within the “very low” category. We found no evidence for a causal link between chiropractic care and CAD. This is a significant finding because belief in a causal link is not uncommon, and such a belief may have significant adverse effects such as numerous episodes of litigation.  (pg. 6)

 

 

Perhaps the greatest threat to the reliability of any conclusions drawn from these data is that together they describe a correlation but not a causal relationship, and any unmeasured variable is a potential confounder. The most likely potential confounder in this case is neck pain. Patients with neck pain are more likely to have CAD (80% of patients with CAD report neck pain or headache), and they are more likely to visit a chiropractor than patients without neck pain. (pg. 7)

 

This is the same opinion of Dr. Perkins as reported above, where the presence of CAD does not have a causal relationship simply because the neck pain brought them to a chiropractor. The CAD would have happened with or without the chiropractic adjustment as is concluded by medical experts and the literature.

 

 

To further the argument, Cassidy, Boyle, Cote`, He, Hogg-Johnson, Silver and Bondy (2008) reported:

There were 818 VBA [Vertebral Basilar Artery] strokes hospitalized in a population of more than 100 million person-years. In those aged 45 years, cases were about three times more likely to see a chiropractor or a PCP before their stroke than controls. Results were similar in the case control and case crossover analyses. There was no increased association between chiropractic visits and VBA stroke in those older than <45 years. Positive associations were found between PCP visits and VBA stroke in all age groups. (pg. S176)

 

Murphy (2010) reported,

Therefore, based upon the best current evidence, it appears that there is no strong foundation for a causal relationship between CMT [Chiropractic Manipulative Therapy] and VADs [Vertebral Artery Dissection]. The most plausible explanation for the association between CMT and VADs is that individuals who are experiencing a vertebral artery dissection seek care from a chiropractic physician or other manual practitioner for relief of the neck pain and headache that results from the dissection. Sometime after the visit the dissection proceeds along its natural course to produce arterial blockage, leading to stroke. This natural progression from dissection to stroke appears to occur independent of the application of CMT. (pg. 4)

 

Church, Sieg, Hussain, Glantz and Harbaugh (2016) concluded, and an opinion that appears to reflect the facts of the issue and in accordance with those in chiropractic and medical academia based upon the author’s strong agreement:

Our systematic review revealed that the quality of the published literature on the relationship between chiropractic manipulation and CAD is very low. A meta-analysis of available data shows a small association between chiropractic neck manipulation and CAD. We uncovered evidence for considerable risk of bias and confounding in the available studies. In particular, the known association of neck pain both with cervical artery dissection and with chiropractic manipulation may explain the relationship between manipulation and CAD. There is no convincing evidence to support a causal link, and unfounded belief in causation may have dire consequences. (pg. 10)

In spite of the very weak data supporting an association between chiropractic neck manipulation and CAD, and even more modest data supporting a causal association, such a relationship is assumed by many clinicians. In fact, this idea seems to enjoy the status of medical dogma. (pg. 9)

 

That is the final definitive opinion of the Neurosurgery Department at the University of Pennsylvania.

 

 

References:

  1. Haneline, M. T., & Rosner, A. L. (2007). The etiology of cervical artery dissection. Journal of chiropractic medicine6(3), 110-120.
  2. Church, E. W., Sieg, E. P., Zalatimo, O., Hussain, N. S., Glantz, M., & Harbaugh, R. E. (2016). Systematic review and meta-analysis of chiropractic care and cervical artery dissection: no evidence for causation. Cureus8(2).
  3. Murphy, D. R. (2010). Current understanding of the relationship between cervical manipulation and stroke: What does it mean for the chiropractic profession? Chiropractic & Osteopathy, 18

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The Mechanism of the Chiropractic

Spinal Adjustment/Manipulation:

Subluxation Degeneration

 

Effect of Sagittal Alignment on Kinematic Changes and Degree of Disc Degeneration in the Lumbar Spine

 

Part 4 of a 5 Part Series

 

William J Owens Jr   

Mark E. Studin  

 

A report on the scientific literature

 

More and more evidence is coming forward demonstrating both spinal stability and biomechanical balance as an important aspect of spine care.  The good news is this is well within chiropractic’s scope, however many doctors of chiropractic are missing the education to accurately evaluate and objectify these types of biomechanical lesions.  Our profession has spent most the last 122 years focused on TREATING these biomechanical lesions (Vertebral Subluxation, Joint Fixation, etc.) with little regard to the “assessment” component.  The reason that is a critical statement, is that too often we treat compensation vs. the unstable joint. 

 

Our founding doctors had used very specific techniques to analyze the spine from a functional perspective and most of our contemporary treatment techniques came out of these analysis, which are the basis for many of our most common techniques taught in today’s chiropractic academia.  It seems in hindsight, that the major discussions of the time [early chiropractic] were about “identification” of the lesion to adjust, then evolved into the best WAY to deliver the adjustment.  

Our roots and subsequently the true value and expertise of the doctor of chiropractic is in the assessment with treatment far secondary to an accurate diagnosis  The medical community that both the authors and the doctors we teach no longer confuse our delivering of chiropractic care with a physical therapy manipulation or mobilization.  The reason, our focus is on the diagnosis, prognosis and treatment plan BEFORE we render our treatment. 

With medical specialists who understand spine, our conversation centers on spinal biomechanics and how a specific chiropractic spinal adjustment will restore sagittal/coronal alignment and coupled motion balance the spine.  We discuss spinal biomechanics and have the literature and credentials to validate our diagnosis, prognosis and treatment plan.  Chiropractic has been the leader in this treatment for over a century, but since we had chosen to stay outside of the mainstream healthcare system we had no platform to take a leadership position or be heard. 

Medicine at both the academic and clinical levels are embracing chiropractic as the primary solution to mechanical spine issues (no fracture, tumor or infection) because as one primary care provider shared with us “traditional medical therapies inclusive of physical therapy has no basis in reality in how to treat these patients, which has led us in part, to the opiate crisis.” Part of the validation of what chiropractic offers in a biomechanical paradigm comes from surgical journals in the medical community. 

  Keorochana et al, (2011) published in Spine and out of UCLA, titled “To determine the effects of total sagittal lordosis on spinal kinematics and degree of disc degeneration in the lumbar spine. An analysis using positional MRI.”  Remember that this article was 8 years ago and as a concept has evolved considerably since it was first discussed in the late 1990s.  This is the clinical component of what Panjabi had successfully described and reproduced in the laboratory. It is now starting to become mainstream in clinical practice. 

Many people ask why would surgeons care about the biomechanics of the spine when they are looking simply for an anatomical lesion to stabilize [fracture, tumor, infection, cord compression]?  The authors answer this question by stating “It has also been a topic of great interest in the management of lumbar degenerative pathologies, especially when focusing on the role it may play in accelerating adjacent degeneration after spinal fusionand non-fusion procedures such as dynamic stabilization and total disc replacement.”  [pg. 893] 

They continue by stating “Alterations in the stress distribution may ultimately influence the occurrence of spinal degeneration. Moreover, changes in sagittal morphology may alter the mechanics of the lumbar spine, affecting mobility. Nevertheless, the relationships of sagittal alignment on lumbar degeneration and segmental motion have not been fully defined.” [pg. 893] This is precisely what our founding fathers called “Subluxation and Subluxation Degeneration!” 

Regarding the type and number of patients in the study, the authors reported the following, “pMRIs [positional MRI] of the lumbar spine were obtained for 430 consecutive patients (241 males and 189 females) from February 2007 to February 2008. All patients were referred for pMRI [positional MRI – which included compression in both flexion and extension with a particular focus on segmentation translation and angular motions] due to complaints of low back pain with or without leg pain.” [pg. 894] This is the part where they looked for hypermobility. 

In the first step in the analysis, the authors reviewed data regarding the global sagittal curvature as well as the individual angular segmental contributions to the curvature.  The next step involved the classification of the severity of lumbar disc degeneration using the Pfirrmann classification system. [See Appendix A if you are not familiar]. This is where they looked for segmental degeneration.  The patients were then classified based on the lordosis angle [T12-S1]. The groups were as follows: 

Group A – Straight Spine or Kyphosis – [lordosis angle <20°]  

Group B – Normal Lordosis – [lordosis angle 20° to < 50°]  

Group C – Hyperlordosis – [lordosis angle >50°] 

There is a structural categorization [lordosis] and a degenerative categorization [Pfirrmann] in this paper and the authors sought to see if there was a predictable relationship.

 

The results of this study were interesting and validated much of what the chiropractic profession has discussed relating to segmental “compensation” in the spine.  Meaning, when one segment is hypomobile, adjacent segments will increase motility to compensate.  The authors stated, “The sagittal lumbar spine curvature has been established as an important parameter when evaluating intervertebral disc loads and stresses in both clinical and cadaveric biomechanical investigations.” [pg. 896] They continue by stating “In vitro [in the laboratory or outside of the living organism] biomechanical tests do not take into account the influence of ligaments and musculature, and may not adequately address the complex biomechanics of the spine.” [pg. 896] 

When it comes to spinal balance and distribution of loads in the spine, the authors reported “Our results may indicate that the border segments of lordosis, especially in the upper lumbar spine (L1–L2, L2–L3, and L3–L4), have greater motion in straight or kyphotic spines, and less segmental motion in hyperlordotic patients.” [pg. 896] 

They continued by stating, A greater degree of rigidity is found at the apical portion of straight or kyphotic spines, and more mobility is seen at the apical portion of hyperlordotic spines.” [pg. 897]  Therefore, in both cases we see that changes in the sagittal configuration of the human spine has consequences for the individual segments involved. 

This raises the question, “how does this related to accelerated degeneration of the motion segments involved?” [Subluxation Degeneration] The authors reported, “Regarding the relationship between the degree of disc degeneration and posture, subjects with straight or kyphotic spines tended to have a greater degree of disc degeneration at border segments, with statistical significance in the lower spine (L5–S1). On the other hand, hyperlordotic spines had a significantly greater degree of disc degeneration at the apex and upper spine (L4–L5 and L1–L2). The severity of disc degeneration tended to increase with increased mobility at the segments predisposed to greater degeneration (border segments of straight or kyphotic spines and apical segments of hyperlordotic spines).” [pg. 897] 

The scientific literature and medicine is now validating (proving) what chiropractic has championed for 122+ years, that the human spine is a living neurobiomechanical entity, which responds to the changes in the external environment and compensates perpetually seeking a homeostatic equilibrium.  We can now have verification that changes or compensation within the spinal system as a result of a bio-neuro-mechanical lesion (vertebral subluxation) results in degeneration (subluxation degeneration) of individual motion segments. 

In conclusion, the authors state… 

“Changes in sagittal alignment may lead to kinematic changes and influence load bearing and the distribution of disc degeneration at each level.” [pg. 897] 

“Sagittal alignment may alter spinal load and mobility, possibly influencing segmental degeneration.” [pg. 897] 

“Motion and the segmental contribution to the total mobility tended to be lower at the border of lordosis, especially at the upper segments, and higher at the apex of lordosis in more lordotic spines, whereas the opposite was seen in straight or kyphotic spines.”  [pg. 897]

 

Although medicine is addressing this at the surgical level, as a profession they realize they have no conservative solutions, which has “opened the door” for the credentialed doctor of chiropractic to be in a leadership role in both teaching medicine about the role of the chiropractor as the primary spine care provider and the central focus of the care path for mechanical spine issues. 

When communicating with patients and medical professionals it is critically important to educate them on what “current research” is showing and why it is important that this chiropractic approach to spine care is the future of spine care in the United States. 

 

REFERENCE: 

1. Keorochana, G., Taghavi, C. E., Lee, K. B., Yoo, J. H., Liao, J. C., Fei, Z., & Wang, J. C. (2011). Effect of sagittal alignment on kinematic changes and degree of disc degeneration in the lumbar spine: an analysis using positional MRI. Spine36(11), 893-898. 

2. Teichtahl, A. J., Urquhart, D. M., Wang, Y., Wluka, A. E., Heritier, S. & Cicuttini, F. M. (2015). A dose-response relationship between severity of disc degeneration and intervertebral disc height in the lumbosacral spine. Arthritis Research & Therapy, 17(297). Retrieved from https://openi.nlm.nih.gov/detailedresult.php?img=PMC4619538_13075_2015_820_Fig1_HTML&req=4 

3. Teraguchi, M., Yoshimura, N., Hashizume, H., Muraki,S., Yamada, H.,Minamide, A., Oka, H., Ishimoto, Y., Nagata, K. Kagotani, R., Takiguchi, N., Akune, T., Kawaguchi,  H., Nakamura, K., & Yoshida, M. (2014). Prevalence and distribution of intervertebral disc degeneration over the entire spine in a population-based cohort: the Wakayama Spine Study. Osteoarthritis and Cartilage, 22(1). Retrieved from http://www.sciencedirect.com/science/article/pii/S1063458413010029 

4. Puertas, E.B., Yamashita, H., Manoel de Oliveira, V., & Satiro de Souza, P. (2009). Classification of intervertebral disc degeneration by magnetic resonance. Acta Ortopédica Brasileira, 17(1). Retrieved from http://www.scielo.br/scielo.php?pid=S1413-78522009000100009&script=sci_arttext&tlng=en

 

 

 

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Should Chiropractic Follow the

American Chiropractic Association

/ American Board of Internal Medicine’s

Recommendations on X-Ray?

 

By Mark Studin

William J. Owens

 

In reviewing the American Chiropractic Associations’ (ACA) position on x-ray and adopting the posture of the American Board of Internal Medicine’s (ABIM) initiative, “Choosing Wisely,” regarding x-ray, we must consider both the far-reaching effects of those recommendations as well as the education of the originators of the recommendations. In addition, the ACA in their 2017 published article Five Things Clinicians and Patients Should Question, they state, “The recommendations are not intended to prohibit any particular treatment in all scenarios or to dictate care decisions. They are also not intended to establish coverage decisions or exclusions” (https://www.acatoday.org/Patients-Choosing-Wisely?utm_campaign=sniply). 

The ACA, a highly-regarded chiropractic political organization that has done a great deal in advancing the profession, is adopting the ABIM’s current position and regardless of the wording of the policy which, in the form of a disclaimer, is opining and setting precedent that can be used against individual practitioners or the entire profession. Granted, the underlying tone is to prevent unnecessary exposure to ionizing radiation, but at what cost to patient care?   

The scientific evidence has shown, and continues to show, chiropractic as being highly effective for managing and treating non-specific or mechanical spine pain. 2-3-4-5-6-7 In this article, we are only considering acute low back pain treatment to meet the scope of the ACA/ABIM policy and are therefore excluding all other conditions treated within the lawful scope of chiropractic. Mechanical spine pain, pain of non-anatomical origin, is defined as spine pain not originating from fracture, tumor, infection or specifically co-related to an anatomical lesion such as degenerative intervertebral disc disease, intervertebral disc bulge or intervertebral disc herniation.  The ACA/ABIM states in the absence of “red flags,” imaging should not be considered for at least 6 weeks of care.  Some of these “red flags” are clearly present on physical examination, others may not reveal themselves without radiographic evidence. 

The definition of red flags by the American Chiropractic Association (2017): 

Red flags include history of cancer, fracture or suspected fracture based on clinical history, progressive neurologic symptoms and infection, as well as conditions that potentially preclude a dynamic thrust to the spine, such as osteopenia, osteoporosis, axial spondyloarthritis and tumors. (https://www.acatoday.org/Patients-Choosing-Wisely?utm_campaign=sniply) 

When considering the training of internal medicine physicians, we recognize they are focused on the diagnosis and management of systemic disease. However, when considering musculoskeletal diagnosis, basic medical training for internal medicine residency is quite the opposite.  Although it is understandable given the current climate of spine pain management in the United States that the American Board of Internal Medicine would take a stance on spine care, I would consider the opinion of an internal medicine board valuable, but less authoritative than a board comprised of practicing spine specialists that is trained in the diagnosis and management of mechanical spine pain with specific treatment designed to deliver high velocity-low amplitude thrusts (chiropractic spinal adjustments).  Interestingly, in this specific case, we have a chiropractic political organization agreeing with a medical board that is specifically trained on the diagnosis of internal medicine disorders with little or no training on the management of acute spine pain. 

In an article written by Humphreys, Sulkowski, McIntyre, Kasiban, and Patrick (2007), they stated:

In the United States, approximately 10% to 25% of all visits to primary care medical doctors are for MSK [musculoskeletal] complaints, making it one of the most common reasons for consulting a physician...Specifically, it has been estimated that less than 5% of the undergraduate and graduate medical curriculum in the United States and 2.26% in Canadian medical schools is devoted to MSK medicine. (p. 44)

It should be noted that primary care medical doctors are not spine specialists and are generally comprised of family or internal medicine physicians.  Medical school is lacking in musculoskeletal education, particularly in spine.  Graduate level medical education including residency and fellowship training, only provides spine specialty training in those boards that are focused on spine care, namely orthopedic surgery and neurosurgery.  It should also be noted that both orthopedic and neurosurgery disciplines are focused on the anatomical lesion in the spine as a primary method of determining the medical necessity of intervention. 

Research has shown musculoskeletal complaints have a major impact on the healthcare system. Many patients believe that traditional medical providers are highly trained in diagnosis and management of musculoskeletal conditions and trust the referrals they provide to physical therapy as the best care path. A recent publication relating to basic competency have shown otherwise. 

Humphreys et al. (2007) state:

A study by Childs et al on the physical therapists’ knowledge in managing MSK conditions found that only 21% of students working on their master’s degree in physical therapy and 25% of students working on their doctorate degree in physical therapy achieved a passing mark on the BCE [Basic Competency Examination]. (p. 45)

Humphreys et al. (2007) continued by reporting a comparative analysis:

The typical chiropractic curriculum consists of 4800 hours of education composed of courses in the biological sciences (i.e., anatomy, embryology, histology, microbiology, pathology, laboratory diagnosis, biochemistry, nutrition, and psychology), chiropractic sciences, and clinical sciences (i.e., clinical diagnosis, neurodiagnosis, orthorheumatology, radiology, and psychology).  As the diagnosis, treatment, and management of MSK [musculoskeletal] disorders are the primary focus of the undergraduate curriculum as well as future clinical practice, it seems logical that chiropractic graduates should possess competence in basic MSK medicine. The objective of this study was to examine the cognitive (knowledge) competency of final-year chiropractic students in MSK medicine. (p. 45).

The following results were published in the article by Humphreys et al. (2007) relating to the Basic Competency Examination and evaluating the various professions that are on the “front line” in the diagnosis and treatment of musculoskeletal conditions. Passing grades were attained by 22% of recent medical graduates, 20.7% of medical students, residents, and staff physicians, 33% of osteopathic students, 21% of MSc [masters] level physical therapy students, and 26 % of DPT [doctors of physical therapy] level physical therapy and chiropractic student 64.7%…

This indicates, that unless a “boarded internist” goes back for advanced education in physical medicine, neurology, orthopedics or neurosurgery, his/her basic competency is between 20% and 33% (if a DO) at best and it is the guidelines of that profession’s board that are being adopted by the ACA. In addition, no profession, inclusive of the ACA, is discussing the difference between a diagnosis, prognosis or treatment plan for mechanical spine pain. The only discussion is related to anatomical origins and anatomical spinal pathology. They are only considering the “red flags” of non-mechanical spine pain (to the detriment of the patient with mechanical spine pain), which only drives triage to medical specialists and ignores clinically necessary treatment plans focusing on the mechanical sources of pain found within chiropractic clinics globally.  

The ACA/ABIM guidelines are very specific to low back pain and refer to the “routine use of imaging,” which is understood to be x-ray as the article uses the term “ionizing imaging.” However, it is not clear if they are also including CAT scan imaging as well.   What their suggested “evidence-based recommendations” omits is the diagnosis of spinal biomechanical pathology and the osseous pathology that is discovered because of a complete clinical evaluation inclusive of spinal biomechanics, which ultimately protects our patients with an accurate spinal diagnosis. That consideration is something that board certified internal medicine practitioners do not have to be concerned with as it is outside of their focus of treatment. Typically, internal medicine physicians have less chance of causing harm to their patients in the short-term with a prescription pad (drug abuse is a topic for a different conversation) vs. a high velocity-low amplitude thrust, the primary treatment modality for the doctor of chiropractic. In this specific case it is the specific type of “treatment” that requires a specific level of diagnosis to be safe.

In the process of concluding an accurate diagnosis, prognosis and treatment plan, an assessment of the structural and biomechanical integrity of the spine is integral to specific treatment recommendations and visual assessment often fails.

Fedorak, Ashworth, Marshall and Paull (2003) reported:

This study has shown that the visual assessment of cervical and lumbar lordosis is unreliable. This tool only has fair intrarater reliability and poor interrater reliability. Visual assessment of spinal posture was previously shown to be inaccurate, and this study has demonstrated that is reliability is poor. (p. 1858)

In contrast, the reliability of x-ray in morphology, measurements and biomechanics has been determined accurate and reproducible.10-11-12-13-14-15-16-17-18-19 In addition, Ohara, Miyamoto, Naganawa, Matsumoto and Shimzu (2006) reported, “Assessment of the sagittal alignment of the spine is important in both clinical and research settings… and it is known that the alignment affects the distribution of the load on the intervertebral discs” (p. 2585).

Assessment of distribution or load of spinal biomechanics, if left aberrant, will result in the initiation of the piezoelectric effect and Wolff’s Law remodeling the spine. This is the basis for the subluxation degeneration theory which historically many have scoffed at as it is not considered to be based on scientific principles.  We have now verified it based upon the research, and it is now a current and verifiable event that must be taken into consideration when assigning prognosis to a biomechanically flawed spine.

A very recent and timely study by Scheer et al. (2016) takes the biomechanical assessment of the spine to an entirely different level.  This concept was originally presented at the 2015 American Academy of Neurosurgery symposium. 

Scheer et al. (2016) state:

Several recent studies have demonstrated that regional spinal alignment and pathology can affect other spinal regions. These studies highlight the importance of considering the entire spine when planning for the surgical correction of ASD [adult spinal deformity/scoliosis]. (p. 109)

Scheer et al. (2016) continue:

Furthermore, the cervical spine plays a pivotal role in influencing adjacent and global spinal alignment as compensatory changes occur to maintain horizontal gaze. (p. 109).

Scheer et al. (2016) also wrote:

There has been a shift from the regional view of the spine to a more global perspective, and recent work has found concomitant spinal deformities in patients. Specifically, there is a high prevalence of CD [cervical deformity/loss of cervical lordosis] among adult patients with thoracolumbar spinal deformity. (p. 109).

Finally, according to Scheer et al. (2016):

Concomitant cervical positive sagittal alignment [loss of cervical curve] in adult patients with thoracolumbar deformity is strongly associated with inferior outcomes and failure to reach MCID [minimal clinically important difference] at 2-year follow-up compared with patients without CD [cervical deformity]. (p. 114)

We are seeing that biomechanical assessment is a critical component of spine care and is a trending topic in spine research.  These topics are not addressed in the Board of Internal Medicine’s opinions and should be considered strongly prior to any chiropractic advocacy organization taking a position that would give doctors pause when attempting to fully diagnose their patients, no matter the disclaimers.  

When it comes to spinal assessment particularly with stress views, Hammouri, Haimes, Simpson, Alqaqa and Grauer (2007) reported, “A survey questionnaire study recently completed by our laboratory confirmed that 43% of practicing spine surgeons also obtain dynamic flexion-extension views in the initial evaluation of those patients” (p. 2361).  They later stated, “These findings led to no change in conservative management and no decision to go to surgery based solely from the dynamic flexion-extension radiographs” (p. 2363).

Hammouri et. al. (2007) also discussed the possible cumulative effects of small doses of radiation as another reason to avoid taking flexion-extension x-rays. This has been a position held by practitioners for years despite the evidence that diagnostic ionizing radiation has been proven to be non-carcinogenic. When examining the evidence, Tubiana, Feinendegen, Yang and Karminski (2009) reported:

Several studies in patients after x-ray–based examinations…have not detected any increase in leukemia or solid tumors. The only positive studies were in girls or young women after repeated chest fluoroscopic procedures for chronic tuberculosis…or scoliosis…Among these patients, excess breast cancer was detected only for cumulative doses greater than about 0.5 Gy. No other excess cancer appeared after cumulative doses up to 1 Gy. There was also no increased cancer after cardiac catheterization…

Several studies stressed the risk of cancer after diagnostic irradiation with x-rays by using the LNT [linear no-threshold] model…However, several investigators…have questioned these estimates because of their doubtful assumptions. An overestimate of the diagnostic radiology risk may deprive patients from adequate treatment. (p. 17)

When considering rendering a diagnosis, prognosis and treatment plan, Hammouri et al. (2007) concluded that flexion-extension x-rays are not a determining factor for spinal surgery. However, chiropractic renders disparate treatment compared to surgeons and medical primary care doctors (family practice and internal medicine).

The authors of this current article recently sent a survey to the chiropractic profession and asked a simple question: Does the clinical use of x-rays change either your diagnosis, prognosis or treatment plan? The question was posed with the understanding that “screening purposes” are not considered clinically necessary and all testing and treatment orders must be consistent with a patient’s presentation and physical examination. The results demonstrated that 98.42% of those surveyed, used x-rays in their clinical practices that changed either the diagnosis, prognosis and/or the treatment plan.  

The next question was when should an x-ray or any other type of imaging be considered? Clinically, if the patient has pain with limited range of motion in a spinal region upon either visual evaluation or dual inclinometry testing, the clinician should ask why is there biomechanical failure coupled with pain? In the absence of diagnosing anatomical (osseous or any other space occupying lesion) pathology, the aberrant verified biomechanics indicates failure at the connective tissue level (ligaments and tendons) and the mechanical source/rationale of the ensuing nociceptive, mechanoreceptive and proprioceptive neuro-pathological cascade. This in turn allows the practitioner to conclude an accurate diagnosis, prognosis and/or treatment plan based upon the pathological “listings” visualized. As reflected above with the 98.42% response, it is clear that when considering the biomechanical assessment of the human spine, x-ray analysis outside of simple anatomic pathology can change how a doctor of chiropractic manages and treats their patients.  

The following is from a small sampling of responses we received from another survey of doctors nationwide. The instructions were to send over examples of how x-ray had changed their diagnoses, prognoses and/or treatment plans within the last 2-3 months. These responses underscored why chiropractors utilize x-ray and often need it to determine accurate mechanical diagnoses, prognoses and treatment plans prior to rendering care. Please note, the clinical protocols presented and x-ray diagnoses are all taught in CCE accredited chiropractic colleges and underscore the quality of a chiropractic education.

Kentucky:

Male 70-year old.  Presented in my office for 2nd opinion after the prior doctor of chiropractic did not take films.  Focal sacral pain unchanged by position or movement.  Plain lumbar/pelvic films revealed large radiolucency in sacrum.  Patient referred out to MD/oncology for follow up.  Diagnosis: Metastatic in nature.  

North Carolina:

Here is an example of how x-ray helped save a life. I had a patient 6 weeks ago come in with lumbar pain.  The patient is 68yr old male with a history of lumbar pain but the pain recently became worse.  During the history the patient relayed that they had recently been to their cardiologist for his regular checkup.  I completed a thorough physical exam where the only positive findings were limited range of motion with pain in extension and left lateral flexion.  I took lumbar x-rays of the patient.  While reviewing the x-rays I noticed the outline of an Abdominal Aortic Aneurysm that measured 5cm on my lateral films.  I immediately told the patient to go to the emergency room and sent the films with him.  The patient stated he did not want to go and he just was at his cardiologist.  I insisted and the patient finally listened. The patient had immediate surgery to repair the aneurysm and I received a thank you call from the cardiologist!!  More important the patient thanked me for saving his life!! 

Abdominal Aortic Aneurysms have a symptom of back pain.  I will never touch a patient without being able to x-ray a patient.  Who would have been blamed if my patient's aneurysm ruptured??

Michigan:

We had female patient in her thirties present to our office complaining of severe and unrelenting neck pain, with bilateral pain into her shoulders. She did not want an x-ray, however one of the other associates that I worked with convinced her to have two films, AP and lateral cervical. Those films revealed a lyric metastasis of the C5 vertebra, with almost a complete destruction of the vertebral body.  Had she been adjusted without the images; the results would have been catastrophic.  

Georgia:

54-year old male post MVA, Primary complaint = Low back pain, examination findings revealed positive orthopedic tests in the cervical and lumbar spine with diminished reflexes, upper and lower muscle strength 5/5. Cervical spine x-rays revealed a 3.28 mm anteriorlisthesis of C4 on C5, flexion view revealed an increased displacement to 8.28 mm.  Extension view measured 5.48 mm.  

Imaging altered treatment plan: Without the x-ray study, the unstable C4 would go undetected and as a result of the x-ray findings the patient was recommended to wear a c-spine collar and have a c-spine MRI. The MRI revealed a 4 x 10 mm left paracentral herniated disc with annular tear compressing the cord by 75% with myelomalacia. It also leaked into the right neural canal compressing the right C4 nerve root. I called my neurosurgeon and he will be in surgery tomorrow. Given the fragmentation of the cord seen on MRI, I shudder to think what would have happened if a high velocity thrust was introduced to his neck!

New York:

A patient presented with mild to moderate low back pain. Images revealed a secondary spondylolesthesis and contraindicated in a lumbar side posture. This has happened many times before and once again, prevented me from hurting my patient.

Ohio

I had a patient that presented with low back pain. The lumbar film showed a 66mm aneurysm. I immediately sent him to the hospital where he was admitted and went into emergency surgery for repair. This could have ended very badly without those x-rays.

California:

36-year old female with acute neck pain, insidious, limited cervical ROM, positive cervical tests, pain worse at night, pain described as "deep, boring, nauseating".  AP and lateral cervical x-rays taken in my office revealed complete absence of C5 vertebral body. I immediately referred patient to the local ER with films in hand.

Florida:

Parents brought their 10-year old son for a second opinion to evaluate a mass on the side of his neck. Their pediatrician had sent them home and told them to check back in 3 days if it didn't resolve. I took AP and lateral cervical films. Both showed the mass but particularly concerning was the AP showed the laryngeal shadow deviated laterally from the pressure of the mass. I told them not to wait 3 days but to go directly to the local emergency department. The local hospital immediately put him in an ambulance and sent him to the children's hospital in Miami. Pediatricians at the children's hospital told the parents the next day, he wouldn't have survived the night had they not taken him to the E.D. on my recommendation, based on the x-ray findings.

Pennsylvania:

I had a 22-year old male present to my office complaining of bilateral low back pain and occasional mild numbness and tingling in his left leg for about 4 years following an injury at wrestling practice when he was 17 years old.  Even though the complaints were moderate and his injury was 4 years old, I decided to take lumbar x-rays including oblique views.  The x-rays revealed bilateral L3 and L4 pars fractures.  I then took lumbar flexion/extension views which revealed a 5mm anterior translation of L4 on L5.  His MRI evaluation was unremarkable and without these x-rays there would have seemed to be no contraindication to diversified adjustments including side posture.   Had I not taken these x-rays, I would likely have delivered a high velocity thrust into an unstable region of the patient’s spine, potentially injuring him further.  Instead, I sent him for an immediate surgical consultation.

New York:

Several days ago, a 30-year old female patient presented with a primary complaint of low back pain, neck stiffness and previous diagnosis of ocular migraines by her Neurologist.  Radiographs of her Cervical and Lumbar spine were taken to evaluate her spine.  A fracture of the vertebral body of C5 was found at the posterior and inferior aspect with an increase in spacing noted at the fracture site on flexion view. 

California:

I had a 15-year-old girl present to my office with severe neck pain. She stated that she had no injuries or trauma that she was aware of. She just "woke up with it". The examination revealed that she was not able to turn her head at all -literally zero range of motion in any direction. Something didn't seem right and I decided to take an x-ray. Her X-ray revealed a burst fracture of C1. It turns out that her mother who signed all the consent forms and dropped her off at my office gave her strict instructions not to tell me about the minor fender bender she was in the day before. Also, the daughter explained later that she had landed on the top of her head during volleyball about a year before. After the volleyball accident she had presented to the emergency room but they decided not to take an x-ray and told her she was fine. I sent her to the emergency room. They took an x-ray and sent her home saying there was no fracture. Later the radiologist called her back insisting she return to the hospital immediately. They confirmed the fracture. I think it is quite safe to assume what would've happened if I tried to adjust her.

New Jersey:

I had a patient who was having pain in the mid thoracic region between the spine and the scapula.  The patient had been to another chiropractor who did not take x-rays, and who did not get good clinical results. I examined and x-rayed the patient.  I saw an abnormal mass in the lung field. I sent the patient to a local radiology center and ordered a plain film chest x-ray, the radiologist confirmed a mass in the right lung.

Based upon the literature, radiation is not cumulative and has rendered no evidence of long term effects. Therefore, the doctor of chiropractic must weigh the risk of treating blindly in the presence of clear biomechanical markers. Treating blindly is often done at the expense of our patients and the malpractice carriers, especially in a scenario where little risk exists.  Our concern is the adoption of recommendations or guidelines that are deficient in the published and clinical evidence at hand.  There also needs to be a larger clinical and academic conversation interprofessionally, to educate organizations like the ABIM and others who access spine patients, where together we can collaboratively, across professional boundaries, devise care paths to better serve society.   

Dr. Mark Studin is an Adjunct Associate Professor of Chiropractic at the University of Bridgeport College of Chiropractic, an Adjunct Professor of Clinical Sciences at Texas Chiropractic College and a clinical presenter for the State of New York at Buffalo, School of Medicine and Biomedical Sciences for post-doctoral education, teaching MRI spine interpretation, spinal biomechanical engineering and triaging trauma cases. He is also the president of the Academy of Chiropractic teaching doctors of chiropractic how to interface with the medical and legal communities (www.DoctorsPIProgram.com), teaches MRI interpretation and triaging trauma cases to doctors of all disciplines nationally and studies trends in healthcare on a national scale (www.TeachDoctors.com). He can be reached at This email address is being protected from spambots. You need JavaScript enabled to view it. or at 631-786-4253.

Dr. Bill Owens is presently in private practice in Buffalo NY and generates the majority of his new patient referrals directly from the primary care medical community.  He is an Associate Adjunct Professor at the State University of New York at Buffalo School of Medicine and Biomedical Sciences, an Adjunct Assistant Professor of Clinical Sciences at the University of Bridgeport, College of Chiropractic and an Adjunct Professor of Clinical Sciences at Texas Chiropractic College.  He also works directly with doctors of chiropractic to help them build relationships with medical providers in their community. He can be reached at This email address is being protected from spambots. You need JavaScript enabled to view it. or www.mdreferralprogram.com or 716-228-3847  

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The Mechanism of the Chiropractic

Spinal Adjustment/Manipulation:

Bio-Neuro-Mechanical Effect

Part 3 of a 5 Part Series

By: Mark Studin

William J. Owens

 

 

A report on the scientific literature

Citation: Studin M., Owens W., (2017) The Mechanism of the Chiropractic Spinal Adjustment/Manipulation: Bio-Neuro-Mechanical Component Part 3 of 5, American Chiropractor 39 (7), pgs. 30,32,34, 36, 38, 40-41

 

In part 1 of this series, we discussed the osseous mechanisms of the chiropractic spinal adjustment (CSA) and in part 2 we discussed the mechanical and neurological functions of connective tissue. It is in this connective tissue as well as in other neurological components located in the osseous structures of the spine that the primary effector structures of a CSA are to be found. To fully understand the bio-neuro-mechanical mechanism of the CSA, we must explore the mechanical aspect of the chiropractic adjustment, what effect it has on the neurological effector organs, how the spine and brain are inter-related and finally, how the muscles and ligaments (intervertebral discs) working in tandem effectuate homeostasis.

 

HISTORICAL REPORTING

 

                Kent (1996) reported:

Dishman and Lantz developed and popularized the five component model of the “vertebral subluxation complex” attributed to Faye. However, the model was presented in a text by Flesia dated 1982, while the Faye notes bear a 1983 date.The original model has five components:

 

1. Spinal kinesiopathology

2. Neuropathology

3. Myopathology

4. Histopathology

5. Biochemical changes.

 

 

The “vertebral subluxation complex” model includes tissue specific manifestations described by Herfert which include:

 

 

1. Osseous component

2. Connective tissue involvement, including disc, other ligaments, fascia, and muscles

3.The neurological component, including nerve roots and spinal cord

4. Altered biomechanics

5. Advancing complications in the innervated tissues and/or the patient’s symptoms. This is sometimes termed the “end tissue phenomenon” of the vertebral subluxation complex.

 

Lantz has since revised and expanded the “vertebral sub- luxation complex” model to include nine components:

 

1. Kinesiology

2. Neurology

3. Myology

4. Connective tissue physiology

5. Angiology

6. Inflammatory response

7. Anatomy

8. Physiology

9. Biochemistry.

 

Lantz summarized his objectives in expanding the model: “The VSC allows for every aspect of chiropractic clinical management to be integrated into a single conceptual model, a sort of ‘unified field theory’ of chiropractic… (p.1)

 

However, like many theories, these concepts have proven close to accurate and this report of the literature, although not designed to prove or disprove the Vertebral Subluxation Complex, validated many of the previous “beliefs” based upon contemporary findings in the literature and personal clinical experience, which along with patient expectations, are the three key components to evidence-based medicine.

 

CONTEMPORARY FINDINGS      

 

In Part 1, we discussed specific biomechanical references in modern literature.

Evans (2002) reported:

 

…on flexion of the lumbar spine, the inferior articular process of a zygapophyseal joint moves upward, taking a meniscoid with it. On attempted extension, the inferior articular process returns toward its neutral position, but instead of re-entering the joint cavity, the meniscoid impacts against the edge of the articular cartilage and buckles, forming a space-occupying "lesion" under the capsule: a meniscoid entrapment…A large number of type III and type IV nerve fibers (nociceptors) have been observed within capsules of zygapophyseal joints. Pain occurs as distension of the joint capsule provides a sufficient stimulus for these nociceptors to depolarize. Muscle spasm would then occur to prevent impaction of the meniscoid. (p. 252-253)

 

This verifies that with a vertebrate out of position, there is a negative neurological sequella that causes a “cascade effect” bio-neuro-mechanically. Historically, this has been objectively identified and in chiropractic practices called a vertebral subluxation. This nomenclature has been accepted federally by the U.S. Department of Health and Human Services and by the Centers for Medicare and Medicaid Services as an identifiable lesion, for which the chiropractic profession has specific training in its diagnosis and management.   

 

To further clarify the modern literature, Panjabi (2006) stated:

 

The spinal column has two functions: structural and transducer. The structural function provides stiffness to the spine. The transducer function provides the information needed to precisely characterize the spinal posture, vertebral motions, spinal loads etc. to the neuromuscular control unit via innumerable mechanoreceptors present in the spinal column ligaments, facet capsules and the disc annulus. These mechanical transducers provide information to theneuromuscular control unit which helps to generate muscular spinal stability via the spinal muscle system and neuromuscular control unit. (p. 669)

 

Panjabi (2006) reported:

 

1. Single trauma or cumulative microtrauma causes subfailure injury of the spinal ligaments and injury to the mechanoreceptors [and nociceptors] embedded in the ligaments.

2. When the injured spine performs a task or it is challenged by an external load, the transducer signals generated by the mechanoreceptors [and nociceptors] are corrupted.

3. Neuromuscular control unit has difficulty in interpreting the corrupted transducer signals because there is spatial and temporal mismatch between the normally expected and the corrupted signals received.

4. The muscle response pattern generated by the neuromuscular control unit is corrupted, affecting the spatial and temporal coordination and activation of each spinal muscle.

5. The corrupted muscle response pattern leads to corrupted feedback to the control unit via tendon organs of muscles and injured mechanoreceptors [and nociceptors], further corrupting the muscle response pattern.

6. The corrupted muscle response pattern produces high stresses and strains in spinal components leading to further subfailure injury of the spinal ligaments, mechanoreceptors and muscles, and overload of facet joints.

7. The abnormal stresses and strains produce inflammation of spinal tissues, which have abundant supply of nociceptive sensors and neural structures. (p. 669-670)

 

This indicates that once there is a bio-neuro-mechanical lesion (aka vertebral subluxation), there is a “negative cascade” both structurally (biomechanically) and neurologically in the body’s attempt to create homeostasis. However, should the cause of the lesion not be “fixed,” the entire system will perpetually fail. Over time, due to the Piezoelectric effect and Wolff’s Law of remodeling, the skeletal structure is now permanently altered. Therefore, treatment goals then switch from curative to simply management and is a long-term process.  

 

In part 2, we discussed subfailure,and will examine it again as explained by Solomnow (2009).

 

Solomonow (2009): 

 

Inflammatory response in ligaments is initiated whenever the tissue is subjected to stresses which exceed its routine limits at a given time. For example, a sub-injury/failure load, well within the physiological limits of a ligament when applied to the ligament by an individual who does not do that type of physical activity routinely. (p. 143)

 

Jaumard, Welch and Winkelstein (2011) reported: 

 

In the capsular ligament under stretch, the collagen fiber structure and the nerve endings embedded in that network and cells (fibroblasts, macrophages) are all distorted and activated. Accordingly, capsular deformations of certain magnitudes can trigger a wide range of neuronal and inflammatory responses…Although most of the proprioceptive and nociceptive afferents have a low-strain threshold (~10%) for activation, a few receptors have a high-strain threshold (42%) for signal generation via neural discharge. In addition, capsular strains greater than 47% activate nociceptors with pain signals transmitted directly to the central nervous system. Among both the low- and high-strain threshold neural receptors in the capsular ligament a few sustain their firing even after the stretching of the capsular ligament is released. This persistent afterdischarge evident for strains above 45% constitutes a peripheral sensitization that may lead to central sensitization with long-term effects in some cases. (p. 12)

 

The cascade effect works in 2 directions, one to create a bio-neuro-mechanically failed spinal system and one to correct a bio-neuro-mechanically failed system.

 

Pickar (2002) reported:

 

The mechanical force introduced into the during a spinal manipulation (CSA) may directly alter segmental biomechanics by releasing trapped meniscoids, releasing adhesions or by reducing distortion of the annulus fibrosis. (p. 359)

 

This fact verifies that there is an osseous-neurological component that exists with the nociceptors at the facet level.

 

Pickar (2002) also stated:

 

In addition, the mechanical thrust could either stimulate or silence nonnociceptive, mechanosensitive receptive nerve endings in paraspinal tissue, including skin, muscle, tendons, ligaments, facet joints and intervertebral disc.  (p. 359)

 

CENTRAL NERVOUS SYSTEM MODULATION

 

When discussing central nervous system activity as a direct sequella to a CSA, we must divide our reporting into 2 components, reflexively at the area being adjusted and through higher cortical responses. When discussing local reflexive activity, we must also determine if it is critical to adjust the specific segment in question or if the adjustment will elicit neurological and end organ (muscle) responses to help create a compensatory action for the offending lesion.

 

Reed and Pickar (2015) reported in an animal study:

 

First, during clinically relevant spinal manipulative thrust durations (<=150 ms), unilateral intervertebral joint fixation significantly decreases paraspinal muscle spindle response compared with non-fixated conditions. Second and perhaps more importantly, this study shows that while L6 muscle spindle response decreases with L4 HVLA-SM, 60%-80% of an L6 HVLA-SM muscle spindle response is still elicited from an HVLA-SM delivered 2 segments away in both the absence and presence of intervertebral joint fixation. These findings may have clinical implications concerning specific (targeted) versus nonspecific (nontargeted) HVLA-SM. (p. E755-E756)

 

Reed and Pickar (2015) also reported:

 

The finding that nontarget HVLA-SM delivered 2 segments away elicited significantly less but yet a substantial percentage (60%–80%) of the neural response elicited during target HVLA-SM may have important clinical implications with regard to HVLA-SM thrust accuracy/specificity requirements. It may explain how target vs non-target site manual therapy interventions can show similar clinical efficacy. In a recent study using the same model as the current study, the increase in L6 muscle spindle response caused by an HVLA-SM is not different between 3 anatomical thrust contact sites (spinous process, lamina, and mammillary body) on the target L6 vertebra but is significantly less when the contact site is located 1 segment caudal at L7…The current study confirms that a nontarget HVLA-SM compared with a target HVLA-SM decreases spindle response but adds the caveat that a substantial percentage (60%–80%) of afferent response can be elicited from an HVLA-SM delivered 2 segments away irrespective of the absence or presence of intervertebral fixation. (p. E756)

 

Coronado, Gay, Bialosky, Carnaby, Bishop and George (2012) reported that:

 

 

Reductions in pain sensitivity, or hypoalgesia, following SMT [spinal manipulative therapy or the chiropractic adjustment] may be indicative of a mechanism related to the modulation of afferent input or central nervous system processing of pain…The authors theorized the observed effect related to modulation of pain primarily at the level of the spinal cord since 1.) these changes were seen within lumbar innervated areas and not cervical innervated areas and 2.) the findings were specific to a measure of pain sensitivity (temporal summation of pain), and not other measures of pain sensitivity, suggesting an effect related to attenuation of dorsal horn excitability and not a generalized change in pain sensitivity. (p. 752)

 

These findings indicate that a chiropractic spinal adjustment affects the central nervous system specifically at the interneuron level in the dorsal horn.  This is part of the cascade effect of the CSA where we now have objectively identified the mechanism of the central nervous system stimulation and its effects. 

 

Gay, Robinson, George, Perlstein and Bishop (2014)

 

 

…pain-free volunteers processed thermal stimuli applied to the hand before and after thoracic spinal manipulation (a form of MT [Manual Therapy]).  What they found was, after thoracic manipulation, several brain regions demonstrated a reduction in peak BOLD [blood-oxygen-level–dependent] activity. Those regions included the cingulate, insular, motor, amygdala and somatosensory cortices, and the PAG [periaqueductal gray regions].

 

 

The purpose of this study was to investigate the changes in FC [functional changes] between brain regions that process and modulate the pain experience after MT [manual therapy]. The primary outcome was to measure the immediate change in FC across brain regions involved in processing and modulating the pain experience and identify if there were reductions in experimentally induced myalgia and changes in local and remote pressure pain sensitivity. (p. 615)

 

Therefore, a thoracic CSA adjustment produced direct and measurable effects on the central nervous system across multiple regions, specifically the cingular cortex, insular cortex, motor cortex, amygdala cortex, somatosensory cortex and periaqueductal gray matter.  This could only occur if “higher centers,” also known as the central nervous system, were affected.

 

Gay, Robinson, George, Perlstein and Bishop (2014) went on to report:

 

Within the brain, the pain experience is subserved by an extended network of brain regions including the thalamus (THA), primary and secondary somatosensory, cingulate, and insular cortices. Collectively, these regions are referred to as thepain processing network(PPN) and encode the sensory discriminate and cognitive and emotional components of the pain experience. Perception of pain is dependent not merely on the neural activity within the PPN [pain processing network] but also on the flexible interactions of this network with other functional systems, including the descending pain modulatory system. (p. 617)

Daligadu, Haavik, Yielder, Baarbe, and Murphy (2013) reported that:

 

 

Numerous studies indicate that significant cortical plastic changes are present in various musculoskeletal pain syndromes. In particular, altered feed-forward postural adjustments have been demonstrated in a variety of musculoskeletal conditions including anterior knee pain, low back pain and idiopathic neck pain. Furthermore, alterations in trunk muscle recruitment patterns have been observed in patients with mechanical low back pain. (p. 527)

 

This concludes that there are observable changes in the function of the central nervous system seen in patients with musculoskeletal conditions and chronic pain.  Chiropractors have observed this clinically and it demonstrates the necessity for chiropractic care for both short and long-term management of biomechanical spinal conditions.

 

 

CONCLUSION

 

Although there is significantly more research verifying what occurs with a CSA, the above outlines the basics of how the adjustment works both biomechanically and neurologically from the connective tissue and peripheral nerves to the central nervous system both at the cord level and higher cortical regions. The final question is one of public safety.

 

Based on their study on 6,669,603 subjects after the unqualified subjects had been removed, Whedon, Mackenzie, Phillips, and Lurie (2015) concluded, “No mechanism by which SM [spinal manipulation] induces injury into normal healthy tissues has been identified” (p. 265).

 

Part 4 will be the evidence of subluxation degeneration and the literature verifying the mechanisms. Part 5, the final part of our series, will be an in-depth contemporary comparative analysis of the chiropractic spinal adjustment vs. physical therapy joint mobilization.

 

References:

 

1. Kent, C. (1996). Models of vertebral subluxation: A review. Journal of Vertebral Subluxation Research1(1), 1-7.

2. Evans, D. W. (2002). Mechanisms and effects of spinal high-velocity, low-amplitude thrust manipulation: Previous theories. Journal of Manipulative and Physiological Therapeutics, 25(4), 251-262.

3. Department of Health and Human Services, Centers for Medicare and Medicaid Services. (2017). Medicare coverage for chiropractic services – Medical record documentation requirements for initial and subsequent visits. MLN Matters, Retrieved from https://www.cms.gov/Outreach-and-Education/Medicare-Learning-Network-MLN/MLNMattersArticles/downloads/SE1601.pdf

4. Panjabi, M. M. (2006). A hypothesis of chronic back pain: Ligament subfailure injuries lead to muscle control dysfunction.European Spine Journal,15(5), 668-676.

5. Solomonow, M. (2009). Ligaments: A source of musculoskeletal disorders.Journal of Bodywork and Movement Therapies,13(2), 136-154.

6. Jaumard, N. V., Welch, W. C., & Winkelstein, B. A. (2011). Spinal facet joint biomechanics and mechanotransduction in normal, injury and degenerative conditions.Journal of Biomechanical Engineering,133(7), 071010.

7. Pickar, J. G. (2002). Neurophysiological effects of spinal manipulation.Spine,2(5), 357-371.

8. Reed, W. R., & Pickar, J. G. (2015). Paraspinal muscle spindle response to intervertebral fixation and segmental thrust level during spinal manipulation in an animal model.Spine,40(13), E752-E759.

9. Coronado, R. A., Gay, C. W., Bialosky, J. E., Carnaby, G. D., Bishop, M. D., & George, S. Z. (2012). Changes in pain sensitivity following spinal manipulation: A systematic review and meta-analysis. Journal of Electromyography Kinesiology, 22(5), 752-767.

10. Gay, C. W., Robinson, M. E., George, S. Z., Perlstein, W. M., & Bishop, M. D. (2014). Immediate changes after manual therapy in resting-state functional connectivity as measured by functional magnetic resonance imaging in participants with induced low back pain.Journal of Manipulative and Physiological Therapeutics, 37(9), 614-627.

11. Daligadu, J., Haavik, H., Yielder, P. C., Baarbe, J., & Murphy, B. (2013). Alterations in coritcal and cerebellar motor processing in subclinical neck pain patients following spinal manipulation.Journal of Manipulative and Physiological Therapeutics, 36(8), 527-537.

12. Whedon, J. M., Mackenzie, T. A., Phillips, R. B., & Lurie, J. D. (2015). Risk of traumatic injury associated with chiropractic spinal manipulation in Medicare Part B beneficiaries aged 66-69 years. Spine, 40(4), 264-270.

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Falls Chiropractic and Injury

6009 Falls of Neuse Road Raleigh, NC 27609

(919)876-9472 (919)876-9478 FAX

RE: Sample Patient

Date: 8/3/2017

RE: Age dating C4-C5 herniated disc in a low speed crash

To whom it may concern:

Specific to Sample Patient’ case, when looking at the images there is no infiltration of calcium at the area of the protrusion type herniation of the C4-C5 disc.  Wolfe law states that a bone will adapt to the loads upon which it is placed.  When there is a herniation of an intervertebral disc, there is abnormal mechanical shearing thus creating an increase in negative charge within the joint capsule as compared to the osseous structures above and below.  As a result, the trabecular bone will give a positive charge by means of calcium (Ca+) that infiltrates into the injured joint1.  This is called the piezoelectric effect1.  This can be usually visualized beginning at a minimum of 6 months’ post trauma2.  The osteophytic changes noted in other parts of the cervical spine as well as other aspects of the C4-C5 joint itself indicate previous injury.  However, the lack of calcium infiltration and osteophytic changes around the protrusion type herniation at C4-C5 indicates that this herniation is acute in nature, is causally related to the accident, and clinically correlates with the patient’s injury. A clear contrast of this can be seen in the C3-C4 old protrusion type herniation above.

In addition, there were Modic type 1 changes present on the inferior end plate of C4 and the superior end plate of C5.

 

According to Xiong, Huang, Cun, Aghdasi and Zhou (2012)3

Histologic studies have shown that Type 1 Modic changes are characterized by edema, vascularization, and inflammation… (pg. 1943)

 

The presence of Modic type 1 changes is a direct response to the trauma and indicates a recent injury due to the presence of inflammation still present in the bone.

Therefore, the herniation at C4-C5 is acute and is causally related to her accident on 5/20/2017.

Lastly, it is important to note that low impact motor vehicle collisions can and do cause serious injury to the cervical spine. It has been clearly shown in the literature that injury to the cervical spine can occur at speeds as little as 4km/h (2.49 miles per hour)4. To completely ascertain the amount of force that was invoked on Mrs. Patient, one needs to bring into account many factors of the dynamics of the crash. One obvious fact in Mrs. Patient case is that the bullet car’s mass was significantly greater than the target car’s mass; Mrs. Patient was in a Honda Sudan and the bullet car was a Ford SUV as documented by the crash report. This means that the bullet car’s mass was greater than the target car and thus increases the amount of force that was applied to the Mrs. Patient’s vehicle. In addition, the infrastructures of most vehicles are designed to bend and flex at higher speeds to create a crash zone. In Mrs. Patient’s accident, there was little damage to the vehicle infrastructure which affords no crash zone. This thus causes the occupants, such as Mrs. Patient, to receive more force and therefore, more injury with less speed.

 

References:

  1. Issacson, B. M., & Bloebaum, R. D. (2010). Bone electricity: What have we learned in the past 160 years? Journal of Biomedical Research, 95A(4), 1270-1279.
  2. He, G., & Xinghua, Z. (2006). The numerical simulation of osteophyte formation on the edge of the vertebral body using quantitative bone remodeling theory. Joint Bone Spine 73(1), 95-101.
  3. Xiong, C., Huang, B., Cun, Y., Aghdasi, B. G., & Zhou, Y. (2014). Migration inhibitory factor enhances inflammation via CD74 in cartilage end plates with Modic type 1 changes on MRI. Clinical Orthopaedics and Related Research®472(6), 1943-1954.
  4. Brault, J. R., Wheeler, J. B., Siegmund, G. P., & Brault, E. J. (1998). Clinical response of human subjects to rear-end automobile collisions. Archives of Physical Medicine and Rehabilitation, 79(1), 72-80.

 

 

Sincerely,

 

 

Richard A. Laviano, D.C. 

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The Mechanism of the Chiropractic

Spinal Adjustment/Manipulation:

Ligaments and the Bio-Neuro-Mechanical Component

Part 2 of a 5 Part Series

By: Mark Studin

William J. Owens

A report on the scientific literature

 

Citation: Studin M., Owens W., (2017) The Mechanism of the Chiropractic Spinal Adjustment/Manipulation: Ligaments and the Bio-Neuro-Mechanical Component, Part 2 of 5, American Chiropractor 39 (6), pgs. 22,24-26, 28-31

Introduction

 

When we consider the mechanism of the spinal adjustment/manipulation as discussed in part 1 of this series, for clarity for the chiropractic profession, it will be solely referred to as a chiropractic spinal adjustment (CSA) so as not to confuse chiropractic treatment with either physical therapy or osteopathy. In analyzing how the CSA works, we must go beyond the actual adjustment or thrust and look at the tissue and structures that “frame” the actions. Although there are osseous borders and boundaries, there is a significant network of connective tissue that plays a major role in the CSA. We will focus this discussion on the ligaments that both act as restraints to the human skeleton and also function as sensory organs, we will also examine the role of the muscles and tendons that interact with the ligaments. It is critical to realize that muscles act as active and amplified restraints in the spinal system.

 

The neurological innervations of the ligaments play a significant role in influencing the central nervous system, both reflexively and through brain pathways. Those innervations either support homeostasis in a balanced musculoskeletal environment or creates confusion in a system that has been impaired either post-traumatically or systemically. The human body does not discriminate the etiology of biomechanical failure, it only reacts to create a “low energy” or neutral state utilizing the lowest amount of energy to function.  This balanced or “low energy state” is considered the most optimal function state as nervous system function is not compromised by aberrant sensory input, this is why a “low energy state” is considered the highest function state.

 

 

With understanding the full functional and resultant role of the ligaments and other connective tissues in either macro or repetitive micro traumas, bio-neuro-mechanical failure (something we have historically called vertebral subluxation) occurs. This is the basis for chiropractic care and explains why immediate (pain management), intermediate (corrective) and long-term (wellness or health maintenance) care are necessary to reintegrate the bio-neuro-mechanical system of the human body. Often, the best we can accomplish as practitioners is to support compensation secondary to tissue failure to slow down the resultant joint remodeling and neurological corruption/compromise.

 

 

Ligamentous Function

 

Solomonow (2009) wrote:

 

The functional complexity of ligaments is amplified when considering their inherent viscoelastic properties such as creep, tension–relaxation, hysteresis and time or frequency-dependent length–tension behavior. As joints go through their range of motion, with or without external load, the ligaments ensure that the bones associated with the joint travel in their prescribed anatomical tracks, keep full and even contact pressure of the articular surfaces, prevent separation of the bones from each other by increasing their tension, as may be necessary, and ensuring stable motion. Joint stability, therefore, is the general role of ligaments without which the joint may subluxate, cause damage to the capsule, cartilage, tendons, nearby nerves and blood vessels, discs (if considering spinal joints) and to the ligaments themselves. Such injury may debilitate the individual by preventing or limiting his/her use of the joint and the loss of function…Dysfunctional or ruptured ligaments, therefore, result in a complex- syndrome, various sensory–motor disorders and other long-term consequences, which impact the individual’s well-being, his athletic activities, employer, skilled work force pool and national medical expenses. (p. 137)

 

Ligaments are closely packed collagen fibers that are helical at rest in a crimp pattern. This crimp pattern allows the ligament to recruit other fibers when stressed to support the joint and helps prevent ligamentous failure or subfailure (tearing of the ligament). They are comprised of collagen and elastin which give them both tensile strength and elasticity with no two joints being alike in composition.  Each joint has a specific biomechanical role and varies depending upon the needs of that joint.

 

Note. Ligaments and tendons,” by I. Ziv, (n.d.), [PowerPoint slides]. Retrieved from https://wings.buffalo.edu/eng/mae/courses/417-517/Orthopaedic%20Biomechanics/ Lecture%203u.pdf

 

Solomonow (2008) continued:

 

As axial stretching of a ligament is applied, fibers or bundles with a small helical wave appearance straighten first and begin to offer resistance (increased stiffness) to stretch. As the ligament is further elongated, fibers or fiber bundles of progressively larger helical wave straighten and contribute to the overall stiffness. Once all the fibers are straightened, a sharp increase in stiffness is observed. (p. 137)

 

Solomonow (2008) later stated:

 

Over all, the mostly collagen (75%), elastin and other substances structure of ligaments is custom tailored by long evolutionary processes to provide various degrees of stiffness at various loads and at various ranges of motion of a joint, while optimally fitting the anatomy inside (inter-capsular) or outside (extra-capsular) a given joint. The various degrees of helical shape of the different fibers allows generation of a wide range of tensile forces by the fiber recruitment process, whereas the overall geometry of the ligament allows selective recruitment of bundles such as to extend function over a wide range of motion. The large content of water (70%) and the cross weave of the long fibers by short fibers provides the necessary lubrication for bundles to slide relative to each other, yet to remain bundled together and generate stiffness in the transverse directions.(p. 137)

 

 

Solomonow (2008):

Length–tension and recruitment: The general length–tension (or strain–stress) behavior of a ligament is non-linear…The initial [reports] demonstrate rather large strain for very small increase in load. Once all the waves in the collagen fibers of the ligament have been straightened out, and all of the fibers were recruited, additional increase in strain is accompanied with a fast increase in tension…


Creep: When a constant load is applied to a ligament, it first elongates to a given length. If left at the same constant load, it will continue to elongate over time in an exponential fashion up to a finite maximum…


Tension–relaxation:When ligaments are subjected to a stretch and hold over time (or constant elongation) the tension–relaxation phenomena is observed. The tension in the ligament increases immediately upon the elongation to a given value. As time elapses, the tension decreases exponentially to a finite minimum while the length does not change…


Strain rate: The tension developed in a ligament also depends on the rate of elongation or strain rate (Peterson, 1986). In general, slow rates of elongation are associated with the development of relatively low tension, whereas higher rates of elongation result in the development of high tension. Fast stretch of ligaments, such as in high-frequency repetitive motion or in sports activities are known to result in high incidents of ligamentous damage or rupture…Fast rates of stretch, therefore, may exceed the physiological loads that could be sustained by a ligament safely, yet it may still be well within the physiological length range. Development of high tension in the ligaments may result in rupture and permanent sensory–motor deficit to the joint in addition to deficit in its structural functions. (p. 137-139)


Author’s note: A fast strain rate within the physiological limit may also cause ligamentous damage as the ligament hasn’t had enough time to adapt (stretch) to its new tensile demand and this is called a “sub-failure.”
“This phenomenon is associated with repetitive motion when a series of stretch-release cycles are performed over time (Solomnow, 1008, p. 140).


Ligament Reaction to Trauma and Healing


Solomnow (2008) stated:

Ligament Inflammation: Inflammatory response in ligaments is initiated whenever the tissue is subjected to stresses which exceed its routine limits at a given time. For example, a sub-injury/failure load, well within the physiological limits of a ligament when applied to the ligament by an individual who does not do that type of physical activity routinely. The normal homeostatic metabolic, cellular, circulatory and mechanical limits are therefore exceeded by the load, triggering an inflammatory response…


Another case where acute inflammation is present is when physical activities presenting sudden overload/stretch cause a distinct damage to the tissue which is felt immediately. Such cases, as a sudden loss of balance, a fall, collision with another person, exposure to unexpected load, etc., may result in what is called a sprain injury or a partial rupture of the ligament. Acute inflammation sets in within several hours and may last several weeks and up to 12 months. The healing process, however, does not result in full recovery of the functional properties of the tissue. Mostly, only up to 70% of the ligaments original structural and functional characteristics are attained by healing post-injury (Woo et al. 1990)...
Chronic inflammation is an extension of an acute inflammation when the tissue is not allowed to rest, recover and heal. Repetitive exposure to physical activity and reloading of the ligament over prolonged periods without sufficient rest and recovery represent cumulative micro-trauma. The resulting chronic inflammation is associated with atrophy and degeneration of the collagen matrix leaving a permanently damaged, weak and non-functional ligament (Leadbenter, 1990). The dangerous aspect of a chronic inflammation is the fact that it builds up silently over many weeks, months or years (dependent on a presently unknown dose-duration levels of the stressors) and appears one day as a permanent disability associated with pain, limited motion, weakness and other disorders (Safran, 1985). Rest and recovery of as much as 2 years allows only partial resolution of the disability (Woo and Buckwalter, 1988). Full recovery was never reported. (p. 143-144)


Hauser et al. (2013) reported that once a ligament is overloaded in either a failure or subfailure, then the tissue fails which results in partial or complete tears known as a sprain. When this occurs, the body “attempts” to repair the damaged ligament, but cannot completely.


Hauser et al. (2013) wrote:

With time, the tissue matrix starts to resemble normal ligament tissue; however, critical differences in matrix structure and function persist. In fact, evidence suggests that the injured ligament structure is replaced with tissue that is grossly, histologically, biochemically, and biomechanically similar to scar tissue. (p. 6)


Hauser et al. (2013) also stated:

The persisting abnormalities present in the remodeled ligament matrix can have profound implications on joint biomechanics, depending on the functional demands placed on the tissue. Since remodeled ligament tissue is morphologically and biomechanically inferior to normal ligament tissue, ligament laxity results, causing functional disability of the affected joint and predisposing other soft tissues in and around the joint to further damage. (p. 7)

Hauser et al. (2013) further said:
In fact, studies of healing ligaments have consistently shown that certain ligaments do not heal independently following rupture, and those that do heal, do so with characteristically inferior compositional properties compared with normal tissue. It is not uncommon for more than one ligament to undergo injury during a single traumatic event. (p. 8)

Author’s note: Ligaments are made with fibroblasts which produce collagen and elastin, and model the ligament throughout puberty. Once puberty is over, the fibroblasts stop producing any ligamentous tissue and remain dormant. Upon injury, the fibroblast activates, but now can only produce collagen, leaving the joint stiffer and in a biomechanically compromised functional environment. The above comment verifies that in the literature.

Hauser et al. (2013) explained:
Osteoarthritis [OA] or joint degeneration is one of the most common consequences of ligament laxity. Traditionally, the pathophysiology of OA was thought to be due to aging and wear and tear on a joint, but more recent studies have shown that ligaments play a crucial role in the development of OA. OA begins when one or more ligaments become unstable or lax, and the bones begin to track improperly and put pressure on different areas, resulting in the rubbing of bone on cartilage. This causes the breakdown of cartilage and ultimately leads to deterioration, whereby the joint is reduced to bone on bone, a mechanical problem of the joint that leads to abnormality of the joint’s mechanics.


Hypermobility and ligament laxity have become clear risk factors for the prevalence of OA. The results of spinal ligament injury show that over time the inability of the ligaments to heal causes an increase in the degeneration of disc and facet joints, which eventually leads to osteochondral degeneration. (p. 9)


Ligaments as Sensory Organs
Spinal pain and the effects of the chiropractic spinal adjustment is both central and peripheral in etiology. According to Studin and Owens (2016), the CSA also affects the central nervous system with systemic sequelae verifying that chiropractic supports systemic changes and is not comprised solely of “back pain providers.” Although chiropractic is not limited to pain, chiropractors do treat back pain, inclusive of all spinal regions. Regarding pain, much of the pain generators originate in the ligaments.


Solomonow (2009) wrote:While ligaments are primarily known for mechanical support for joint stability, they have equally important sensory functions. Anatomical studies demonstrate that ligaments in the extremity joints and the spine are endowed with mechanoreceptors consisting of: Pacinian, Golgi, Ruffini and bare nerve endings. (Burgess and Clark, 1969; Freeman and Wyke, 1967a,b; Gardner, 1944; Guanche et al., 1995; Halata et al., 1985; Jackson et al., 1966; Mountcastle, 1974; Petrie et al., 1988, Schulz et al. 1984, Sjölander, 1989; Skoglund, 1956; Solomonow et al., 1996; Wyke, 1981; Yahia and Newman, 1991; Zimney and Wink, 1991). The presence of such afferents in the ligaments confirms that they contribute to proprioception and kinesthesia and may also have a distinct role in reflex activation or inhibition of muscular activities.(p. 144)


Dougherty (n.d.) reported:
Pacinian corpusclesare found in subcutaneous tissue beneath the dermis…and in the connective tissues of bone [ligaments and tendons], the body wall and body cavity. Therefore, they can be cutaneous, proprioceptive or visceral receptors, depending on their location…


When a force is applied to the tissue overlying the Pacinian corpuscle…its outer laminar cells, which contain fluid, are displaced and distort the axon terminal membrane. If the pressure is sustained on the corpuscle, the fluid is displaced, which dissipates the applied force on the axon terminal. Consequently, a sustained force on the Pacinian corpuscle is transformed into a transient force on its axon terminal. The Pacinian corpuscle 1° afferent axon response is rapidly adapting and action potentials are only generated when the force is first applied. (http://neuroscience.uth.tmc.edu/ s2/chapter02.html)

Dougherty (n.d.) stated: 

TheRuffini corpusclesare found deep in the skin…as well as in joint ligaments and joint capsules and can function as cutaneous or proprioceptive receptors depending on their location. The Ruffini corpuscle…is cigar-shaped, encapsulated, and contains longitudinal strands of collagenous fibers that are continuous with the connective tissue of the skin or joint. Within the capsule, the 1° afferent fiber branches repeatedly and its branches are intertwined with the encapsulated collagenous fibers. (http://neuroscience.uth.tmc. edu/s2/chapter02.html) “Ruffini corpuscles in skin are considered to be skin stretch sensitive receptors of the discriminative touch system. They also work with the proprioceptors in joints and muscles to indicate the position and movement of body parts” (Dougherty, http://neuroscience.uth.tmc.edu/s2/chapter02.html).


Dougherty (n.d.) stated:
Golgi tendon organsare found in the tendons of striated extrafusal muscles near the muscle-tendon junction…Golgi tendon organs resemble Ruffini corpuscles. For example, they are encapsulated and contain intertwining collagen bundles, which are continuous with the muscle tendon, and fine branches of afferent fibers that weave between the collagen bundles…They are functionally "in series" with striated muscle. (http://neuroscience.uth.tmc.edu/s2/ chapter02.html)
“TheGolgi tendon organis a proprioceptor that monitors and signals muscle contraction against a force (muscle tension), whereas the muscle spindle is a proprioceptor that monitors and signals muscle stretch (muscle length)” (Dougherty, http://neuroscience.uth.tmc.edu/ s2/chapter02.html).


Dougherty (n.d.) stated:
…free nerve endings of 1° afferents are abundant in muscles, tendons, joints, and ligaments. These free nerve endings are considered to be the somatosensory receptors for pain resulting from muscle, tendon, joint, or ligament damage and are not considered to be part of the proprioceptive system. [These free nerve endings are called nociceptors.]


Solomonow (2009) commented:
The presence of such afferents in the ligaments confirms that they contribute to proprioception and kinesthesia and may also have a distinct role in reflex activation or inhibition of muscular activities…
Overall, the decrease or loss of function in a ligament due to rupture or damage does not only compromise its mechanical contributions to joint stability, but also sensory loss of proprioceptive and kinesthetic perception and fast reflexive activation of muscles and the forces they generate in order to enforce joint stability…


It was suggested, as far back as the turn of the last century, that a reflex may exist from sensory receptors in the ligaments to muscles that may directly or indirectly modify the load imposed on the ligament (Payr, 1900)…A clear demonstration of a reflex activation of muscles was finally provided in 1987 (Solomonow et al., 1987) and reconfirmed several times since then (beard et al., 1994; Dyhre-Poulsen and Krogsgard, 2000; Raunest et al., 1996; Johansson et al., 1989; Kim et al., 1995). It was further shown that such a ligamento-muscular reflex exists in most extremity joints (Freeman and Wyke, 1967b; Guanche et al., 1995, Knatt et al., 1995; Schaible and Schmidt, 1983; Schaible et al., 1986; Solomonow et al., 1996; Phillips et al., 1997; Solomonow and Lewis, 2002) and in the spine (Indahl et al., 1995, 1997; Stubbs et al., 1998; Solomonow et al., 1998). (p. 144).


“Ligamento-muscular reflexes, therefore, may be inhibitory or excitatory, as may be fit to preserve joint stability; inhibiting muscles that destabilize the joint or increased antagonist co-activation to stabilize the joint” (Solomonow, 2009, p. 145).
Spinal Stabilization and Destabilization


Panjabi (2006) reported:
1. Single trauma or cumulative microtrauma causes subfailure injury of the spinal ligaments and injury to the mechanoreceptors [and nociceptors] embedded in the ligaments.
2. When the injured spine performs a task or it is challenged by an external load, the transducer signals generated by the mechanoreceptors [and nociceptors] are corrupted.
3. Neuromuscular control unit has difficulty in interpreting the corrupted transducer signals because there is spatial and temporal mismatch between the normally expected and the corrupted signals received.
4. The muscle response pattern generated by the neuromuscular control unit is corrupted, affecting the spatial and temporal coordination and activation of each spinal muscle.
5. The corrupted muscle response pattern leads to corrupted feedback to the control unit via tendon organs of muscles and injured mechanoreceptors [and nociceptors], further corrupting the muscle response pattern. (p. 669)

The above stabilization-destabilization scenario is the foundation for why a CSA is clinically indicated for short, intermediate and long-term treatment (biomechanical stabilization) as clinically indicated. It also clearly outlines what the goal of the CSA is, to integrate the bio-neuro-mechanical system to bring the human body to utilize its lowest form of energy for homeostasis or as close to normal as tissue pathology allows.
This is part 2 of a 5-part series where part 1 covers the osseous mechanics of the chiropractic spinal adjustment. This part covered the ligamentous involvement from a supportive and neurological perspective. The topic of part 3 will be spinal biomechanics and their neurological components in addition to how the chiropractic spinal adjustment makes changes bio-neuro-mechanically. Part 4 will be an in-depth contemporary comparative analysis of the chiropractic spinal adjustment vs. physical therapy joint mobilization. The final part will be a concise overview of the chiropractic spinal adjustment.

References:

1. Solomonow, M. (2009). Ligaments: A source of musculoskeletal disorders.Journal of Bodywork and Movement Therapies,13(2), 136-154.

2. Ziv, I. (n.d.). Ligaments and tendons [PowerPoint slides]. Retrieved from https://wings.buffalo.edu/eng/mae/courses/417-517/Orthopaedic%20Biomechanics/Lecture%203u.pdf

3. Hauser, R. A., Dolan, E. E., Phillips, H. J., Newlin, A. C., Moore, R. E., & Woldin, B. A. (2013). Ligament injury and healing: A review of current clinical diagnostics and therapeutics.The Open Rehabilitation Journal,6, 1-20.

4. Solomonow, M. (2006). Sensory–motor control of ligaments and associated neuromuscular disorders.Journal of Electromyography and Kinesiology,16(6), 549-567.

5. Studin M., & Owens W. (2016). Chiropractic spinal adjustments and the effects on the neuroendocrine system and the central nervous system connection. The American Chiropractor, 38(1), 46-51.

6. Dougherty, P. (n.d.). Chapter 2: Somatosensory systems. Neuroscience Online. Retrieved from  http://neuroscience.uth.tmc.edu/s2/chapter02.html

7. Panjabi, M. M. (2006). A hypothesis of chronic back pain: Ligament subfailure injuries lead to muscle control dysfunction.European Spine Journal,15(5), 668-676.

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Chiropractic and Successful Outcomes with Chronic Obstructive Pulmonary Disease

 

By: Mark Studin

William J. Owens

 

A report on the scientific literature

 

Chronic Obstructive Pulmonary Disease (COPD) is a preventable and treatable disease that makes it difficult to empty air out of the lungs. This difficulty in emptying air out of the lungs (airflow obstruction) can lead to shortness of breath or feeling tired because you are working harder to breathe. COPD is a term that is used to include chronic bronchitis, emphysema, or a combination of both conditions. Asthma is also a disease where it is difficult to empty the air out of the lungs, but asthma is not included in the definition of COPD. It is not uncommon, however for a patient with COPD to also have some degree of asthma. Chronic bronchitis is a condition of increased swelling and mucus (phlegm or sputum) production in the breathing tubes (airways). Airway obstruction occurs in chronic bronchitis because the swelling and extra mucus causes the inside of the breathing tubes to be smaller than normal. The diagnosis of chronic bronchitis is made based on symptoms of a cough that produces mucus or phlegm on most days, for three months, for two or more years (after other causes for the cough have been excluded). Emphysema is a condition that involves damage to the walls of the air sacs (alveoli) of the lung. Normally there are more than 300 million alveoli in the lung. The alveoli are normally stretchy and springy, like little balloons. Like a balloon, it takes effort to blow up normal alveoli; however, it takes no energy to empty the alveoli because they spring back to their original size. In emphysema, the walls of some of the alveoli have been damaged. When this happens, the alveoli lose their stretchiness and trap air. Since it is difficult to push all of the air out of the lungs, the lungs do not empty efficiently and therefore contain more air than normal. This is called air trapping and causes hyperinflation in the lungs. The combination of constantly having extra air in the lungs and the extra effort needed to breathe results in a person feeling short of breath. Airway obstruction occurs in emphysema because the alveoli that normally support the airways open cannot do so during inhalation or exhalation. Without their support, the breathing tubes collapse, causing obstruction to the flow of air. (http://www.thoracic.org/patients/patient-resources/resources/copd-intro.pdf)

Wearing, Beaumont, Forbes, Brown and Engler (2016) reported:

 

Extrapulmonary effects, such as skeletal muscle dysfunction, affect the severity of the disease and provide a potential target for therapeutic intervention. An estimated 18%–36% of people with COPD experience skeletal muscle dysfunction at a level that affects exercise capacity and dyspnea levels, both predictors of mortality in COPD. Because exercise capacity is a measure of the amount of exercise that can be performed before the onset of leg fatigue or exercise-limiting dyspnea, a decrease in capacity has been associated with poorer quality of life and higher hospitalization rates. Nonpharmacologic interventions benefit people with COPD.  For example, pulmonary rehabilitation (PR) is considered to be a well-developed, multidisciplinary approach to managing many extrapulmonary effects associated with COPD.  However, PR has little clinical effect on lung function. Similarly, research into the effect of acupuncture has shown that this modality has little effect on long-term lung function despite helping improve dyspnea levels and exercise tolerance. (pgs. 108-109)

  

The authors have had long-term experience in treating COPD utilizing a portion of the "Evidence-based behavioral practice“ model in observing results from patients over the past 3 decades.

Evidence-based behavioral practice(EBBP) entails making decisions about how to promote health or provide care by integrating the best available evidence with practitioner expertise and other resources, and with the characteristics, state, needs, values and preferences of those who will be affected. This is done in a manner that is compatible with the environmental and organizational context. Evidence is comprised of research findings derived from the systematic collection of data through observation and experiment and the formulation of questions and testing of hypotheses (Evidence-Based Practice, http://en.wikipedia.org/wiki/Evidence-based_practice).

In the observation component of the evidence-based behavioral practice model, the authors have observed COPD patients realize increased tidal volumes, forced vital volume, forced expiratory volume and residual increased volumes performed on a Renaissance Spirometer by Puritan-Bennett in the 1990’s, post chiropractic spinal adjustment. These results (the printouts have since been discarded) were consistent with both acute and chronic emphysema patients with multiple etiologies and were verified both with the spirometer volumes and the patient’s feedback. Due to limited resources (and research inexperience) of the authors in the 1990’s, this information was limited to patients who had similar issues at the local clinical level. Nonetheless, the results were consistent and reproducible, however the was no literature to corroborate or validate these findings at the time.

In contemporary literature, there is now a basis to support the authors previous findings. Wearing, Beaumont, Forbes, Brown and Engler (2016) continued:

 

This systematic review updates the results from a previous review and is the first to focus on evidence of the effect of administering SMT (spinal manual treatment of the chiropractic spinal adjustment) in conjunction with other interventions in the management of COPD. Improvements in lung function (increases in forced expiratory and forced vital volume; decrease in residual volume) and exercise capacity (increase in 6-minute walking test) were reported in three random clinical trials following a combination of SMT and exercise. While these findings were recorded in pilot and preliminary trials, they represent preliminary evidence that the combination of SMT with exercise may be more beneficial to people with COPD than exercise or SMT alone. Furthermore, the results provide additional information to the review by Heneghan and colleagues; however, the findings of this review contrast with the earlier conclusion that no evidence supported or refuted the use of MT on patients with COPD.

 

In conclusion, this appears to be the first systematic review to investigate the evidence for administering SMT in conjunction with other modalities, such as exercise, on people with COPD. The exclusion of such combinations may explain the disparity in findings between this review and the review by Heneghan et al., who found no evidence to support or refute the use of MT in the management of COPD. The importance of increasing exercise capacity, even by indirect methods such as increasing thoracic mobility should not be underestimated because exercise capacity is a predictor of mortality in COPD. As pulmonary rehabilitation does not improve lung function, the current findings may have wider implications if repeated in a larger cohort. (pg. 113)

 

Although Wearing et. Al (2016) acknowledged that this study was very limited in numbers and acknowledged that there could be benefit through co-management with exercise, the results mimicked the findings realized by the authors in the 1990’s.  In addition, Wearing et. Al.  reported no significant adverse effects of chiropractic care and is consistent with previous reports that chiropractic is one of the safest treatments currently available in healthcare and when there is a treatment where the potential for benefits far outweighs any risk, it deserves serious consideration. Whedon, Mackenzie, Phillips, and Lurie (2015) based their study on 6,669,603 subjects after the unqualified subjects had been removed from the study and accounted for 24,068,808 office visits. They concluded, “No mechanism by which SM [spinal manipulation] induces injury into normal healthy tissues has been identified (Whedon et al., 2015, p. 5).

 

References:

  1. American Thoracic Society (2017) Retrieved from: http://www.thoracic.org/patients/patient-resources/resources/copd-intro.pdf
  2. Wearing, J., Beaumont, S., Forbes, D., Brown, B., & Engel, R. (2016). The use of spinal manipulative therapy in the management of chronic obstructive pulmonary disease: a systematic review.The Journal of Alternative and Complementary Medicine,22(2), 108-114.
  3. Evidence-Based Practice. (n.d.). In Wikipedia. Retrieved January 3, 2012, from http://en.wikipedia.org/wiki/Evidence-based_practice
  1. Whedon, J. M., Mackenzie, T. A., Phillips, R. B., & Lurie, J. D. (2015). Risk of traumatic injury associated with chiropractic spinal manipulation in Medicare Part B beneficiaries aged 66-69 years. Spine, 40(4), 264-270.

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A Chiropractic Adjustment Has a Direct Effect of the Pre-Frontal Cortex of the Brain

 

Verifying a positive effect of the chiropractic spinal adjustment on reflexes, memory, coordination and decision making

 

By: Mark Studin

William J. Owens

 

A report on the scientific literature

For most of the 20th century, based upon results in individual chiropractic offices, the profession’s success was founded on a patient-based model. This model drove utilization at predominantly a “grass roots” level and over the last 10-20 years, research has started to give reasons to why patients not only get out of pain, but executive functions such as decision making, anxiety, managing tasks and being able to focus at a higher level are improving. It is these types of results that have driven many patients to appreciate chiropractic as a “miracle cure” while others, mostly from organized medicine and insurers, who in the past have considered it an "invalid claim” because of the lack of credible evidence despite mounting feedback from patients over the last century. Factually, their arguments had merit on many issues in the past, but as research has been published through the years, those arguments are outdated and incorrect.

"Evidence-based behavioral practice (EBBP) entails making decisions about how to promote health or provide care by integrating the best available evidence with practitioner expertise and other resources, and with the characteristics, state, needs, values and preferences of those who will be affected. This is done in a manner that is compatible with the environmental and organizational context. Evidence is comprised of research findings derived from the systematic collection of data through observation and experiment and the formulation of questions and testing of hypotheses" (Evidence-Based Practice, http://en.wikipedia.org/wiki/Evidence-based_practice).

When considering a purely “evidenced-based” approach, it often precludes advances through a doctor’s immediate experiences in “breakthroughs” that has historically saved lives and then set up the research to render the evidence of what doctors have found on an “experiential level.” This is formally termed best medical practice.

“Abest practice is a method or technique that has consistently shown results superior to those achieved with other means and that is used as a benchmark. In addition, a "best" practice can evolve to become better as improvements are discovered. Best practice is considered by some as a business buzzword, used to describe the process of developing and following a standard way of doing things that multiple organizations can use" (Best Practice, http://en.wikipedia.org/ wiki/Best_practice).

Sackett, Rosenberg, Gray, Haynes and Richardson (1996) stated, 

 “Criticism has ranged from evidence based medicine being old hat to it being a dangerous innovation, perpetrated by the arrogant to serve cost cutters and suppress clinical freedom (p. 71)."  They go on to comment “Good doctors use both individual clinical expertise and the best available external evidence, and neither alone is enough. Without clinical expertise, practice risks becoming tyrannized by evidence, for even excellent external evidence may be inapplicable to or inappropriate for an individual patient. Without current best evidence, practice risks becoming rapidly out of date, to the detriment of patients" (Sackett et al, 1996, p. 72).  The point is that the provider plays a huge role and ultimately is the check and balance of this process. Without the provider, the payor becomes the determining factor in the delivery of healthcare by "tying the doctor's hands" with the limitation of evidence. 

They further stated:

“External clinical evidence can inform, but can never replace, individual clinical expertise, and it is this expertise that decides whether the external evidence applies to the individual patient at all and, if so, how it should be integrated into a clinical decision" (Sackett et al, 1996, p. 73).  Lastly, they state, “Evidence based medicine is not restricted to randomized trials and meta-analyses. It involves tracking down the best external evidence with which to answer our clinical questions" (Sackett et al, 1996, p. 73). This is often a process that takes years, preventing the final papers from being published in a timely enough fashion to meet the ever-changing advancement of medicine and the technologies that support the current needs of the patients.  

When considering executive function at the central (brain) level, based upon contemporary literature, we can now go beyond the “best medical practice” model of purely patient feedback and as Sackett et. Al. suggested, add the evidence as verification. In order to better understand how chiropractic plays a role in executive function, we must start at neural plasticity. According to Leung et. Al (2015) Neural plasticity refers to the capacity of our brain to change in response to internal demand and/or external experience. Burgeoning research has corroborated that the neural plastic changes induced in our brains and behaviors are specific to the experiences. [pg. 1] 

Neuroplasticity, also known as brain plasticity or neural plasticity, is an umbrella term that describes lasting change to the brain throughout an individual's life course. The term gained prominence in the latter half of the 20th century, when new research showed that many aspects of the brain can be altered (or are "plastic”) even into adulthood. (https://en.wikipedia.org/wiki/Neuroplasticity) 

This article focuses on the actions and effects of neuroplasticity on the pre-frontal cortex of the brain. According to Lelic et. Al (2016) 

The prefrontal cortex is known to play a vital role in SMI and is also responsible for a number of other functions. The prefrontal cortex is known to be a key structure responsible for the performance of what is known as “executive functions.” Executive function is the mechanism by which the brain integrates and coordinates the operations of multiple neural systems to solve problems and achieve goals based on the ever-changing environment around us. Executive function is considered to be a product of the coordinated operation of various neural systems and is essential for achieving any particular goal. The prefrontal cortex is believed to be the main brain structure responsible for enabling this coordination and control. It requires planning a sequence of subtasks to accomplish a goal, focusing attention on relevant information as well as inhibiting irrelevant distractors, being able to switch attention between tasks monitoring memory, initiation of activity, and responding to stimuli. [pg. 7] 

Lelic et. Al.’s study resulted in two major findings. Firstly, the study reproduced previous findings of somatosensory evoked potential (SEPs) studies that have shown that chiropractic spinal adjusting of dysfunctional spinal segments alters early sensorimotor integration (SMI) of input from the upper limb. The second major finding of this study was that we were able to show, using dipole source localization, that this change in SMI that occurs after spinal manipulation predominantly happens in the prefrontal cortex. The SEP peak showed multiple neural generators including primary sensory cortex, basal ganglia, thalamus, premotor areas, and primary motor cortex. The frontal N30 peak is therefore thought to reflect early SMI.

The current study adds to previous work by not only confirming that spinal manipulation [chiropractic spinal adjustment] of dysfunctional joints decreases the N30 SEP peak amplitude but also demonstrating that this decrease occurs predominantly in one of the known neural generators of N30, that is, the prefrontal cortex. This suggests that, at least in part, the mechanisms by which spinal manipulation improves performance are due to a change in function at the prefrontal cortex.

Lelic et. Al (2016) continued,

The prefrontal cortex is known to play a vital role in SMI and is also responsible for a number of other functions. The prefrontal cortex is known to be a key structure responsible for the performance of what is known as “executive functions.” Executive function is considered to be a product of the coordinated operation of various neural systems and is essential for achieving any particular goal. The prefrontal cortex is believed to be the main brain structure responsible for enabling this coordination and control. It requires planning a sequence of subtasks to accomplish a goal, focusing attention on relevant information as well as inhibiting irrelevant distractors, being able to switch attention between tasks, monitoring memory, initiation of activity, and responding to stimuli. A change in prefrontal activity following chiropractic care may therefore explain and/or link some of the varied improvements in neural function previously observed in the literature, such as improved joint position sense error, reaction time, cortical processing, cortical sensorimotor integration, reflex excitability, motor control, and lower limb muscle strength.

To accomplish the coordinated operations of multiple neural systems and structures, the prefrontal cortex must monitor the activities in other cortical and subcortical structures and control and integrate their operations by sending command signals in a so-called “top-down” manner. This is a complex operation, and the importance of this monitoring, integration, and coordination is highlighted in studies where damage to the prefrontal cortex has been shown to impair the ability to create new and adaptive action programs or choose the best among several equally probable alternatives, despite such individuals displaying normal IQs in most psychological tests, having normal long-term memory functions, and exhibiting normal perceptual, motor, and language skills

 To accomplish the coordinated operations of multiple neural systems and structures, the prefrontal cortex must monitor the activities in other cortical and subcortical structures and control and integrate their operations by sending command signals in a so-called “top-down” manner. This is a complex operation, and the importance of this monitoring, integration, and coordination is highlighted in studies where damage to the prefrontal cortex has been shown to impair the ability to create new and adaptive action programs or choose the best among several equally probable alternatives, despite such individuals displaying normal IQs in most psychological tests, having normal long-term memory functions, and exhibiting normal perceptual, motor, and language skills [43].The change in prefrontal cortex as seen in this study therefore suggests that the altered input from dysfunctional joints that leads to altered processing of somatosensory inputs can influence processing of somatosensory information by the prefrontal cortex.

Chiropractic care, by treating the joint dysfunction, appears to change processing by the prefrontal cortex. This suggests that chiropractic care may as well have benefits that exceed simply reducing pain or improving muscle function and may explain some claims regarding this made by chiropractors.

Although the change in N30 due to chiropractic treatment is an important finding, it is not clear how long this finding lasts. To date, some of the authors of this study have shown that the N30 changes on average are present for at least 20–30 minutes after spinal manipulation. For some subjects, the changes were still evident at 30 minutes after spinal manipulation and we have not yet followed up for longer than 30 minutes, due to the length of the study as is.

The literature has clearly suggested that a chiropractic spinal adjustment has a clear and reproducible effect on brain physiology and function and is consistent with reports from Reed, Pickjar, Sozio and Long (2014) and Gay, Robinson, George, Peristen and Bishop (2014) on a chiropractic spinal adjustment effecting brain function. These results, in addition to chiropractic patient’s feedback since 1895, have combined both “best practice” and evidenced based” models and start to explain through science, why people are experiencing so much more than their beck or neck pain resolving.

References:

  1. Best Practice. (n.d.). In Wikipedia. Retrieved January 3, 2012, fromhttp://en.wikipedia.org/wiki/Best_practice
  2. Evidence-Based Practice. (n.d.). In Wikipedia. Retrieved January 3, 2012, fromhttp://en.wikipedia.org/wiki/Evidence-based_practice
  3. Leung, N. T., Tam, H. M., Chu, L. W., Kwok, T. C., Chan, F., Lam, L. C., ... & Lee, T. (2015). Neural plastic effects of cognitive training on aging brain.Neural plasticity,2015.
  4. Neuroplasticity (2017), Retrieved from: https://en.wikipedia.org/wiki/Neuroplasticity
  5. Lelic, D., Niazi, I. K., Holt, K., Jochumsen, M., Dremstrup, K., Yielder, P., ... & Haavik, H. (2016). Manipulation of dysfunctional spinal joints affects sensorimotor integration in the prefrontal cortex: A brain source localization study.Neural plasticity,2016
  6. Reed, W. R., Pickar, J. G., Sozio, R. S., & Long, C. R. (2014). Effect of spinal manipulation thrust magnitude on trunk mechanical activation thresholds of lateral thalamic neurons.Journal of Manipulative and Physiological Therapeutics, 37(5), 277-286.
  7. Gay, C. W., Robinson, M. E., George, S. Z., Perlstein, W. M., & Bishop, M. D. (2014). Immediate changes after manual therapy in resting-state functional connectivity as measured by functional magnetic resonance imaging in participants with induced low back pain. Journal of Manipulative and Physiological Therapeutics, 37(9), 614-627..

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Traumatic Ligament Laxity of the Spine and

Associated Physical Impairment

Lawrence Lefcort, DC

 

Author Note

            Correspondence concerning this article should be addressed to Lawrence Lefcort, DC at

Bayside Physical Therapy, Chiropractic, and Acupuncture, PLLC, 213-15 33rd Road Bayside,

NY 11361

 

TRAUMATIC LIGAMENT LAXITY OF THE SPINE

Abstract

This paper explores the relationship between traumatic ligament laxity of the spine and the

resultant instability that may occur. Within, there is a discussion of the various spinal

ligamentous structures that may be affected by both macro and micro traumatic events, as

well as the neurologic and musculoskeletal effects of instability. There is detailed discussion of

the diagnosis, quantification, and documentation as well.

            Keywords: ligament laxity, instability

 

                                                              

TRAUMATIC LIGAMENT LAXITY OF THE SPINE

Traumatic Ligament Laxity of the Spine and

Associated Physical Impairment

            Soft tissue cervical and lumbar sprain/strains are the most common injury in motor vehicle collisions, with 28% to 53% of collision victims sustaining this type of injury (Galasko et al., 1993; Quinlan et al., 2000). The annual societal costs of these injuries in the United States are estimated to be between 4.5 and 8 billion dollars (Kleinberger et al., 2000; Zuby et al., 2010). Soft tissue injuries of the spinal column very often become chronic, with the development of long-term symptoms, which can inevitably adversely affect the victim’s quality of life. Research has indicated that 24% of motor vehicle collision victims have symptoms 1 year after an accident and 18% after 2 years (Quinlan et al., 2004). Additionally, it has been found that between 38% and 52% of motor vehicle collision cases involved rear-impact scenarios

( Kleinberger et al.,2000; Galasko et al., 1993).

            It is well known that the major cause of chronic pain due to these injuries is directly related to the laxity of spinal ligamentous structures (Ivancic, et al., 2008). One must fully understand the structure and function of ligaments in order to realize the effects of traumatic ligament laxity. Ligaments are fibrous bands or sheets of connective tissue which link two or more bones, cartilages, or structures together. We know that one or more ligaments provide stability to a joint during rest as well as movement. Excessive movements such as hyper-extension or hyper-flexion, which occur during a traumatic event such as a motor vehicle collision, may be restricted by ligaments, unless these forces are beyond the tensile-strength of these structures; this will be discussed later in this paper.

TRAUMATIC LIGAMENT LAXITY OF THE SPINE

            Three of the more important ligaments in the spine are the ligamentum flavum, the anterior longitudinal ligament, and the posterior longitudinal ligament (Gray’s Anatomy, 40th Edition). The ligamentum flavum forms a cover over the dura mater, which is a layer of tissue that protects the spinal cord. This ligament connects under the facet joints to create a small curtain, so to speak, over the posterior openings between vertebrae (Gray’s Anatomy, 40th edition). The anterior longitudinal ligament attaches to the front (anterior) of each vertebra and runs vertical or longitudinal (Gray’s Anatomy, 40th edition). The posterior longitudinal ligament also runs vertically or longitudinally behind (posterior) the spine and inside the spinal canal (Gray’s Anatomy, 40th Edition). Additional ligaments include facet capsular ligaments, interspinous ligaments, supraspinous ligaments, and intertransverse ligaments. The aforementioned ligaments limit flexion and extension, with the exception of the ligament, which limits lateral flexion. The ligamentum nuchae, which is a fibrous membrane, limits flexion of the cervical spine (Gray’s Anatomy, 40th Edition). The four ligaments of the sacroiliac joints

(iliolumbar, sacroiliac, sacrospinus, sacrotuberous), provide stability and some motion. The upper cervical spine has its own ligamentous structures or systems; occipitoatlantal ligament complex, occipitoaxial ligament complex, atlantoaxial ligament complex, and the cruciate ligament complex (Gray’s Anatomy, 40th Edition). The upper cervical ligament system is especially important in stabilizing the upper cervical spine from the skull to C2 (axis) (Stanley Hoppenfeld, 1976). It is important to note, that although the cervical vertebrae are the smallest, the neck has the greatest range of motion.

TRAUMATIC LIGAMENT LAXITY OF THE SPINE

            Ligament laxity may happen as a result of a ‘macro trauma”, such as a motor vehicle collision, or may develop overtime as a result of repetitive use injuries, or work-related injuries. The cause of this laxity develops through similar mechanisms, which leads to excessive motion of the facet joints, and will cause various degrees of physical impairment. When ligament laxity develops over time, it is defined as “creep” and refers to the elongation of a ligament under a constant or repetitive stress (Frank CB, 2004). Low-level ligament injuries, or those where the ligaments are simply elongated, represent the vast majority of cases and can potentially incapacitate a patient due to disabling pain, vertigo, tinnitus, etc.. Unfortunately, these types of strains may progress to sub-failure tears of ligament fibers, which will lead to instability at the level of facet joints (Chen HB et al., 2009). Traumatic or repetitive causes of ligament laxity will ultimately produce abnormal motion and function between vertebrae under normal physiological loads, inducing irritation to nerves, possible structural deformation, and/or incapacitating pain.

            Patients’, who have suffered a motor vehicle collision or perhaps a work-related injury, very often have chronic pain syndromes due to ligament laxity. The ligaments surrounding the facet joints of the spinal column, known as capsular ligaments, are highly innervated mechanoreceptive and nociceptive free nerve endings. Therefore, the facet joint is thought of as the primary source of chronic spinal pain (Boswell MV et al., 2007; Barnsley L et al., 1995). When the mechanoreceptors and nociceptors are injured or even simply irritated the overall joint function of the facet joints are altered (McLain RF, 1993).

TRAUMATIC LIGAMENT LAXITY OF THE SPINE

            One must realize that instability is not similar to hyper-mobility. Instability, in the clinical context, implies a pathological condition with associated symptomatology, whereas joint hypermobility alone, does not. Ligament laxity which produces instability refers to a loss of “motion stiffness”, so to speak, in a particular spinal segment when a force is applied to this segment, which produces a greater displacement than would be observed in a normal motion segment. When instability is present, pain and muscular spasm can be experienced within the patient’s range of motion and not just at the joint’s end-point. In Chiropractic, we understand that there is a “guarding mechanism”, which is triggered after an injury, which is the muscle spasm. These muscle spasms can cause intense pain and are the body’s response to instability, since the spinal supporting structures, the ligamentous structures, act as sensory organs, which initiate a ligament-muscular reflex. This reflex is a “protective reflex” or “guarding mechanism”, produced by the mechanoreceptors of the joint capsule and these nerve impulses are ultimately transmitted to the muscles. Activation of surrounding musculature, or guarding, will help to maintain or preserve joint stability, either directly by muscles crossing the joint or indirectly by muscles that do not cross the joint, but limit joint motion (Hauser RA et al., 2013). This reflex is fundamental to the understanding of traumatic injuries.

            This reflex is designed to prevent further injury. However, the continued feedback and reinforcement of pain and muscle spasm, will delay the healing process. The ‘perpetual loop” may continue for a long period of time, making further injury more likely due to muscle contraction. Disrupting this cycle of pain and inflammation is key to resolution.

TRAUMATIC LIGAMENT LAXITY OF THE SPINE

            When traumatic ligament laxity produces joint instability, with neurologic compromise, it is understood that the joint has sustained considerable damage to its stabilizing structures, which could include the vertebrae themselves. However, research indicates that joints that are hypermobile demonstrate increased segmental mobility, but are still able to maintain their stability and function normally under physiological loads (Bergmann TF et al., 1993).

            Clinicians classify instability into 3 categories, mild, moderate, and severe. Severe instability is associated with a catastrophic injury, such as a motor vehicle collision. Mild or moderate clinical instability is usually without neurologic injury and is most commonly due to cumulative micro-trauma, such as those associated with repetitive use injuries; prolonged sitting, standing, flexed postures, etc..

            In a motor vehicle collision, up to 10 times more force is absorbed in the capsular ligaments versus the intervertebral disc (Ivancic PC et al., 2007). This is true, because unlike the disc, the facet joint has a much smaller area in which to disperse this force. Ultimately, as previously discussed, the capsular ligaments become elongated, resulting in abnormal motion in the affected spinal segments (Ivancic PC et al., 2007; Tominaga Y et al., 2006). This sequence has been clearly documented with both in vitro and in vivo studies of segmental motion characteristics after torsional loads and resultant disc degeneration (Stokes IA et al., 1987; Veres SP et al., 2010). Injury to the facet joints and capsular ligaments has been further confirmed during simulated whiplash traumas (Winkelstein BA et al., 2000).

TRAUMATIC LIGAMENT LAXITY OF THE SPINE

            Maximum ligament strains occur during shear forces, such as when a force is applied while the head is rotated (axial rotation). While capsular ligament injury in the upper cervical spine region can occur from compressive forces alone, exertion from a combination of shear, compression and bending forces is more likely and usually involves much lower loads to causes injury (Siegmund GP et al., 2001). If the head is turned during whiplash trauma, the peak strain on the cervical facet joints and capsular ligaments can increase by 34% (Siegmund GP et al., 2008). One research study reported that during an automobile rear-impact simulation, the magnitude of the joint capsule strain was 47% to 196% higher in instances when the head was rotated 60 degrees during impact compared with those when the head was forward facing (Storvik SG et al., 2011). Head rotation to 60 degrees is similar to an individual turning his/her head to one side while checking for on-coming traffic and suddenly experiences a rear-end collision. The impact was greatest in the ipsilateral facet joints, such that head rotation to the left caused higher ligament strain at the left facet joint capsule.

            Other research has illustrated that motor vehicle collision trauma has been shown to reduce ligament strength (i.e., failure force and average energy absorption capacity) compared with controls or computational models (Ivancic PC et al., 2007; Tominaga Y et al., 2006). We know that this is particularly true in the case of capsular ligaments, since this type of trauma causes capsular ligament laxity. Interestingly, one research study conclusively demonstrated that whiplash injury to the capsular ligaments resulted in an 85% to 275% increase in ligament elongation (laxity), compared to that of controls (Ivancic PC et al., 2007).

TRAUMATIC LIGAMENT LAXITY OF THE SPINE

The study also reported evidence that tension of the capsular ligaments due to trauma, requisite for producing pain from the facet joint. Whiplash injuries cause compression injuries to the posterior facet cartilage. This injury also results in trauma to the synovial folds, bleeding, inflammation, and of course pain. Simply stated, this stretching injury to the facet capsular ligaments will result in joint laxity and instability.

            Traumatic ligament laxity resulting in instability is a diagnosis based primarily on a patient’s history (symptoms) and physical examination. Subjective findings are the patient’s complaints in their own words, or their perception of pain, sensory changes, motor changes, or range of motion alterations. After the patient presents their subjective complaints to the clinician, these subjective findings, must be correlated and confirmed through a proper and thorough physical examination, including the utilization of imaging diagnostics that explain a particular symptom, pattern, or area of complaint objectively. Without some sort of concrete evidence that explains a patient’s condition, we merely have symptoms with no forensic evidence. Documentation is key, as well as quantifying the patient’s injuries objectively.

            In order to adequately quantify the presence of instability due to ligament laxity, the clinician could utilize functional computerized tomography, functional magnetic resonance imaging scans, as well as digital motion x-ray (Radcliff K et al., 2012; Hino H et al., 1999). Studies using functional CT for diagnosing ligamentous injuries have demonstrated the ability of this technique to shoe excess movement during axial rotation of the cervical spine (Dvorak J et al., 1988; Antinnes J et al., 1994).             

TRAUMATIC LIGAMENT LAXITY OF THE SPINE

This is important to realize when patients have the signs and symptoms of instability, but have normal MRI findings in the neutral position. Functional imaging technology, as opposed to static standard films, is necessary for the adequate radiologic depiction of instability because they provide dynamic imaging during movement and are extremely helpful for evaluating the presence and degree of instability.

            Although functional imaging maybe superior plain-film radiography is still a powerful diagnostic tool for the evaluation of instability due to ligament laxity. When a patient presents status-post motor vehicle collision, it is common practice to perform a “Davis Series” of the cervical spine. This x-ray series consists of 7 views: anterior-posterior open mouth, anterior-posterior, lateral, oblique views, and flexion-extension views. The lumbar spine is treated in similar fashion. X-ray views will include: anterior-posterior, lateral, oblique views, and flexion-extension views. The flexion-extension views are key in the diagnosis of instability. It is well known, that the dominant motion of the cervical and lumbar spine, where most pathological changes occur, is flexion-extension. Translation of one vertebral segment in relation to the one above and/or below will be most evident on these views. Translation is the total anterior-posterior movement of vertebral segments. After the appropriate views are taken, the images may be evaluated utilizing CRMA or Computed Radiographic Mensuration Analysis. These measurements are taken to determine the presence of ligament laxity. In the cervical spine, a 3.5mm or greater translation of one vertebra on another is an abnormal and ratable finding, indicative of instability (AMA Guides to the Evaluation of Permanent Impairment, 6th Edition).

TRAUMATIC LIGAMENT LAXITY OF THE SPINE

            Alteration of Motion Segment Integrity (AOMSI) is extremely crucial as it relates to ligament laxity. The AMA Guides to the Evaluation of Permanent Impairment 6th Edition, recognize linear stress views of radiographs, as the best form of diagnosing George’s Line

(Yochum & Rowe’s Essentials of Radiology, page 149), which states that if there is a break in George’s Line on a radiograph, this could be a radiographic sign of instability due to ligament laxity.

            Our discussion of ligament laxity and instability continues with the “Criteria for Rating Impairment Due to Cervical and Lumbar Disorders”, as described in the AMA Guides to the Evaluation of Permanent Impairment, 6th Edition. According to the guidelines, a DRE (Diagnosed Related Estimate) Cervical Category IV is considered to be a 25% to 28% impairment of the whole person. Category IV is described as, “alteration of motion segment integrity or bilateral or multilevel radiculopathy; alteration of motion segment integrity is defined from flexion and extension radiographs, as at least 3.5mm of translation of one vertebra on another, or angular motion of more than 11 degrees greater than at each adjacent level; alternatively, the individual may have loss of motion of a motion segment due to a developmental fusion or successful or unsuccessful attempt at surgical arthrodesis; radiculopathy as defined in Cervical Category III need not be present if there is alteration of motion segment integrity; or fractures: (1) more than 50% compression of one vertebral body without residual neural compromise. One can compare a 25% to 28% cervical impairment of the whole person to the 22% to 23% whole person impairment due to an amputation at the level of the thumb at or near the carpometacarpal joint or the distal third of the first metacarpal.

TRAUMATIC LIGAMENT LAXITY OF THE SPINE

            Additionally, according to the guidelines, a DRE (Diagnosed Related Estimate) Lumbar Category IV is considered to be a 20% to 23% impairment of the whole person. Category IV is described as, “loss of motion segment integrity defined from flexion and extension radiographs as at least 4.5mm of translation of one vertebra on another or angular motion greater than 15 degrees at L1-2, L2-3, and L3-4, greater than 20 degrees at L4-5, and greater than 25 degrees at L5-S1; may have complete or near complete loss of motion of a motion segment due to developmental fusion, or successful or unsuccessful attempt at surgical arthrodesis or fractures: (1) greater than 50% compression of one vertebral body without residual neurologic compromise. One can compare a 20% to 23% Lumbar Impairment of the whole person to the 20% whole person impairment due to an amputation of the first metatarsal bone.  

Conclusions

            After careful interpretation of the AMA Guides to the Evaluation of Permanent Impairment, 6th Edition, regarding whole person impairment due to ligament laxity/instability of the cervical and lumbar spine, one can certainly see the severity and degree of disability that occurs. Once ligament laxity is correctly diagnosed, it will objectively quantify a patient’s spinal injury regardless of symptoms, disc lesions, range of motion, reflexes, etc. When we quantify the presence of ligament laxity, we also provide a crucial element with which to demonstrate instabilities in a specific region. Overall, clarification and quantification of traumatic ligament laxity will help the patient legally, objectively, and most importantly, clinically.  

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