The Chiropractic Impact Report

May 2012

admin — Tue, 01 May 2012 23:59:07 +0000

Chiropractic For Neck Pain?

…An Update

On October 12, 2009, Mercer Health and Benefits released a study titled:

Do Chiropractic Services for the Treatment of Low Back and Neck Pain Improve the Value of Health Benefits Plans?

An Evidence-Based Assessment of Incremental Impact on Population Health and Total Health Care Spending

A Google Internet search of Mercer states:

“Mercer is a leading global provider of consulting, outsourcing and investment services. Mercer works with clients to solve their most complex benefit and human capital issues, designing and helping manage health, retirement and other benefits. It is a leader in benefit outsourcing. Mercer’s investment services include investment consulting and multi-manager investment management. Mercer’s 18,000 employees are based in more than 40 countries. The company is a wholly owned subsidiary of Marsh & McLennan Companies, Inc., which lists its stock on the New York, Chicago and London stock exchanges.”

PhysiciansNiteesh Choudhry,MD, PhD, and Arnold Milstein, MD, MPH, author this Mercer report.

Dr. Niteesh Choudhry is fromHarvardMedicalSchoolwhere he is an Assistant Professor of Medicine and an Associate Physician in the Division of Pharmaco-epidemiology and Pharmaco-economics. He is also associated with the Hospital Program at Brigham and Women’s Hospital where he practices inpatient general internal medicine and is actively involved in resident education.

Dr. Arnold Milstein is from Mercer Health and Benefits inSan Francisco,Californiawhere he is the Medical Director at Pacific Business Group on Health, the largest employer health care purchasing coalition in theUS. At Pacific Business Group he is the National Health Care Thought Leader. His work focuses on improving managed care programs for large purchasers and for the government.

Dr. Milstein’s 40 book chapters and published articles have centered on managed care program design. Dr. Milstein is Mercer’s chief physician and national thought leader, and he earned the Elliott M. Stone Award of Excellence in Health Data Leadership from the National Association of Health Data Organizations (NAHDO) at its annual meeting inAlexandria,VA, on October 15, 2009. The NAHDO stated:

“Through this award, NAHDO honors Dr. Milstein’s strong advocacy of public comparative health care provider performance and public reporting. Dr. Milstein has successfully advocated for quality and pay-for-performance initiatives at the Centers for Medicare and Medicaid Services. As a national thought leader, his support of the state health care data reporting programs and their missions to provide health care data for policy and market purposes has been, and will continue to be, essential to the success and advancement of these databases.”

The National Association of Health Data Organizations (NAHDO) is a national, not-for-profit membership organization dedicated to improving health care through the collection, analysis, dissemination, public availability, and use of health data. NAHDO provides leadership in health care information management and analysis, promotes the availability of and access to health data, and encourages the use of these data to make informed decisions and guide the development of health policy. NAHDO provides information on current issues and strategies to develop a nationwide, comprehensive, integrated health information system, sponsors educational programs, provides assistance, and serves as a forum to foster collaboration and the exchange of ideas and experiences among collectors and users of health data.

Business Insurance magazine selected Dr. Milstein as “one of the 20 people who has made a difference in employee benefits management in the past 20 years.” Last year’s New England Journal of Medicine’s series on employer sponsored health insurance described him as a “pioneer” in employer efforts to advance quality.

In October 2006 Dr. Milstein was elected to theInstituteofMedicine. He is a member of the Medicare Payment Advisory Commission. Since January 2002, Dr. Milstein has also served on the Strategic Advisory Council of the National Quality Forum.

Dr. Milstein’s work focuses on health care purchasing strategy, the psychology of clinical performance improvement and clinical innovations that reduce total health care spending. Among his many accomplishments in the quality field have been co-founding both the Leapfrog Group and the Consumer-Purchaser Disclosure Project. He heads performance measurement activities for both initiatives and is a Congressional MedPAC Commissioner.

Dr. Milstein holds a medical degree fromTuftsUniversityand a master’s degree in health services planning from theUniversityofCalifornia,Berkeley. He received a bachelor’s degree in economics fromHarvardUniversity. He is an Associate Clinical Professor at theUniversityofCalifornia,San FranciscoMedicalCenterand a Worldwide Partner at Mercer.

Tom Elliott, president of Mercer’s global health and benefits business and a member of the firm’s global executive committee made these comments pertaining to Dr. Milstein:

“As the leader in providing innovative health care solutions to employers, Mercer takes great pride in celebrating the accomplishments of Arnie Milstein, who has had such a profound impact on how health care is delivered in the US. At a time when there is greater pressure than ever to deliver quality health care and at the same time control costs, we need innovative leaders who challenge employers, providers, health plans and policy makers to change their business models. Accurate and transparent data is essential in order to improve the delivery and efficacy of health care. Dr. Milstein has been a driving force behind improving the efficiency of the delivery system and his work has certainly influenced the national initiative to bridge the quality gap.”

The New England Journal of Medicine’s series on employer-sponsored health insurance described Dr. Milstein as a “pioneer” in national efforts to advance quality of care. He was selected for the highest annual award of the National Business Group on Health for distinguished innovation in health care cost reduction and quality gains. He was elected to theInstituteofMedicineof the National Academy of Sciences and is a faculty member atUniversityofCalifornia,San Francisco, Institute for Health Policy Studies.

This biographical information on Dr. Niteesh Choudhry and Dr. Arnold Milstein shows that there are none more qualified to present an evidence-based assessment on the value to Health Benefits Plans of chiropractic services.

This report (Mercer) by Drs. Choudhry and Milstein is twelve pages in length and cites 18 references from the National Library of Medicine PubMed database. A complete copy of the report can be accessed at www.f4cp.org.

The Executive Summary of the report makes the following points:

1) “Low back and neck pain are extremely common conditions that consume large amounts of health care resources.”

2) “Chiropractic care, including spinal manipulation and mobilization, are used by almost half of theUSpatients with persistent back-pain seeking out this modality of treatment.”

[This is an important point. It indicates that patients seek chiropractic treatment primarily for the management of chronic spinal musculoskeletal conditions. It is established that these chronic problems are both expensive and problematic because they do not spontaneously resolve and those suffering from these chronic complaints tend to seek the help from multiple healthcare providers].

3) “The peer-reviewed scientific literature evaluating the effectiveness ofUSchiropractic treatment for patients with back and neck pain suggest that these treatments are at least as effective as other widely used treatments.”

4) “Chiropractic care is more effective than other modalities for treating low back and neck pain.”

5) Pertaining to the total cost of care per year:

“For neck pain, chiropractic physician care reduces total

annual per patient spending by $302 compared to medical

physician care.”

Importantly, these authors indicate that chiropractic care

is known to reduce the need for drug treatment.

Additionally, the cost of medical physician care noted above

did not include the cost of drug spending. Consequently, the

authors state:

“Because we were unable to incorporate savings in drug spending commonly associated with US chiropractic care, our estimate of its comparative cost effectiveness is likely to be understated.”

“When considering effectiveness and costs together, chiropractic physician care for low back and neck pain is highly cost-effective, represents a good value in comparison to medical physician care and to widely accepted cost- effectiveness thresholds.”

6) “Our findings in combination with existingUSstudies published in peer-reviewed scientific journals suggests that chiropractic care for the treatment of low back and neck pain is likely to achieve equal or better health outcomes at a cost that compares very favorably to most therapies that are routinely covered inUShealth benefit plans.”

7) “The addition of chiropractic coverage for the treatment of low back and neck pain at prices typically payable in US employer-sponsored health benefit plans will likely increase value-for-dollar by improving clinical outcomes and either reducing total spending (neck pain) or increasing total spending (low back pain) by a smaller percentage than clinical outcomes improve.”

••••••••••

In their paper, Drs. Choudhry and Milstein note that neck pain is extremely common in theUnited States, and it consumes large amounts of health care resources. They note:

About 14% of theUSadult population report neck pain in a year.

TheUnited Statesannual spending for spine-related problems is about $85 billion.

Drs. Choudhry and Milstein note that vast scientific

literature has evaluated the cost effectiveness of chiropractic treatment for patients with common types of back and neck pain, which support these conclusions:

“Chiropractic care is at least as effective as other widely used therapies for low back pain.”

“Chiropractic care when combined with other modalities, such as exercise, appears to be more effective than other treatments for patients with neck pain.”

In this study, Drs. Choudhry and Milstein assessed whether chiropractic care was cost-effective by applying the widely-accepted standard “quality-adjusted life years,” or QALYs to existing studies that compared chiropractic services to medical physical services and physical therapy services. “Quality-adjusted life years,” or QALYs are “a standard means assessing both the length and quality of a patient’s life.” Studies show that treatments with cost-effectiveness ratios below $50,000 to $100,000 per QALY are considered to be cost effective.

RESULTS FOR NECK PAIN:

Patients who received chiropractic care for neck pain “achieved better clinical outcomes at lower costs than medical physician care.”
The cost of medical physician care for neck pain was $579 per patient. The cost of chiropractic care for neck pain was $277 per patient, $302 less than medical care.
Compared to medical physician care for neck pain, chiropractic care would save $6,035 per QALY (-$6,035). If chiropractic care cost $100 per visit, the savings per QALY would still be $5,875 per patient.
Exercise-only care for neck pain costs $952 per case, which is $373 more than medical-only care and $677 more than chiropractic-only care. Yet, exercise only care was less effective than chiropractic, costing $18,665 per QALY, or about 4 times more than chiropractic-only care (at -$6035).
“If exercise therapy were provided by chiropractors instead of physical therapists, one-year costs would fall to $464, resulting in savings of $114 per [insurance] beneficiary.” As attractive as this is, the combination of exercise plus chiropractic manipulation was less effective and more costly than chiropractic-only care.

Drs. Choudhry and Milstein make the following concluding remarks:

“Using data from high-quality randomized controlled European trials and contemporary Unites States based average unit prices payable by commercial insures, we project that insurance coverage for chiropractic coverage for chiropractic physician care for low back and neck pain for conditions other than fracture and malignancy is likely to drive improved cost-effectiveness of United States care.”

“For neck pain it is also likely to reduce total United States health care spending.”

“These favorable results would likely occur within a 12-month timeframe.”

“In combination with the existing United States-based literature, our findings support the value of health insurance coverage of chiropractic care for low back and neck pain at average fees currently payable by Unites States commercial insurers.”

The article by Mercer Health and Benefits is a unique analysis of the costs and effectiveness of chiropractic in the management of low back and neck pain as compared to medical care and physiotherapy-led exercise. The standard used by the authors was the cost per quality-adjusted life year, or QALY. The analysis showed chiropractic care to be extremely effective for the cost of the service. In the case of low back pain, the cost of chiropractic per quality-adjusted life year was $1,837, which the authors labeled as “extremely favorable.” In the case of neck pain, chiropractic care was the most cost effective service, and its improvement in the quality-adjusted life year showed that if chiropractic care is used in the management of neck pain there would be a savings of $6,035 per person per year.

When insurance companies evaluate the cost effectiveness of various benefits they cover, it seems prudent that they include chiropractic in the management of both low back and neck pain.

••••••••••

Two additional studies have added to the support for spinal manipulation in the management of neck pain this year (2012). Both of these studies are reviewed here:

Spinal Manipulation, Medication, or Home Exercise With Advice for Acute and Subacute Neck Pain

A Randomized Trial

Annals of Internal Medicine

January 3, 2012; Vol. 156; pp. 1-10

Gert Bronfort, DC, PhD; Roni Evans, DC, MS; Alfred V. Anderson, DC, MD; Kenneth H. Svendsen, MS; Yiscah Bracha, MS; and Richard H. Grimm, MD, MPH, PhD

Dr. Gert Bronfort, the lead author of this study, had 54 articles in the PubMed database search of the National Library of Medicine. Dr. Bronfort was awarded the Researcher of the Year by the Foundation For Chiropractic Education in 2009. Dr. Bronfort is fromNorthwesternHealthScienceUniversity inMinneapolis,MN.

This study was funded by theNationalCenterfor Complementary and Alternative Medicine of the National Institutes of Health of theUnited States. The authors note that mechanical neck pain is a common condition that affects an estimated 70% of persons at some point in their lives. This study sought to determine the relative efficacy of chiropractic spinal manipulation therapy (SMT), medication, and home exercise with advice (HEA) for acute and subacute neck pain in both the short and long term. This is a randomized, controlled trial using 272 subjects aged 18 to 65 years who had nonspecific neck pain for 2 to 12 weeks. The intervention was 12 weeks of SMT, medication, or HEA.

The primary measurement outcome was participant-rated pain, measured at 2, 4, 8, 12, 26, and 52 weeks after randomization. Secondary measures were self-reported disability, global improvement, medication use, satisfaction, general health status (Short Form-36 Health Survey physical and mental health scales), and adverse events. Neck motion was performed at 4 and 12 weeks.

Results: For neck pain, chiropractic spinal manipulation had a statistically significant advantage over medication after 8, 12, 26, and 52 weeks, and HEA was superior to medication at 26 weeks.

The authors concluded that for participants with acute and subacute neck pain, chiropractic spinal manipulation was more effective than medication in both the short and long term.

The chiropractic spinal manipulation focused on manipulation of areas of the spine with segmental hypomobility. The specific number of manipulations over the 12 weeks was left to the discretion of the chiropractor, based on manual palpation of the spine and associated musculature and the participant’s response to treatment.

The home exercise was advice that was provided in two 1-hour sessions. The therapists provided instruction, primarily focusing on simple self-mobilization exercise (gentle controlled movement) of the neck and shoulder joints, including neck retraction, extension, flexion, rotation, lateral bending motions, and scapular retraction, with no resistance. Participants were instructed to do 5 to 10 repetitions of each exercise up to 6 to 8 times per day. A booklet (McKenzie R. Treat Your Own Neck. 3rd ed.Waikanae,New Zealand: Spinal Publications; 2002) of prescribed exercises was provided.

The medication group was provided by a licensed medical physician, with the focus of treatment on prescription medication. The first line of therapy was nonsteroidal anti-inflammatory drugs, acetaminophen, or both.

Participants who did not respond to or could not tolerate first-line therapy received narcotic medications. Muscle relaxants were also used.

The authors made these comments:

“Spinal manipulation therapy was superior to medication at the end of treatment and during follow-up in terms of global improvement, participant satisfaction, and SF-36 –assessed physical function; SMT was also superior to medication in measures of long-term medication use.”

“The SMT and HEA groups performed similarly on most of the secondary outcomes, although SMT performed better than HEA for satisfaction with care in both the short and long term.”

“Spinal manipulation therapy and HEA led to similar short- and long-term outcomes, but participants who received medication seemed to fare worse, with a consistently higher use of pain medication for neck pain throughout the trial’s observation period.”

“Our results suggest that SMT and HEA both constitute viable treatment options for managing acute and subacute mechanical neck pain.”

Additional findings include, 40% of the chiropractic adjustment patients and 46% of the home exercise/advice patients experienced an adverse event; 100% of these adverse events were musculoskeletal in nature and of short duration. In contrast, 60% of the drug patients experienced an adverse event, and 100% of these were of a more serious nature; they included:

1% increased blood pressure

1% stress incontinence

5% disturbed sleep

6% nausea

7% congestion

8% rash

12% cognitive symptoms

12% dry mouth

20% gastrointestinal symptoms

21% drowsiness

Thus, the mechanical approaches to acute/subacute neck pain management were shown not only to be significantly more effective than medication, but also significantly safer.

Although the printed words in the article suggest that chiropractic spinal adjusting and home exercise/advice are essentially equal in the management of acute and subacute neck pain, a careful review of the measured markers presented in the article show that chiropractic adjustments were nearly always superior to those from home exercise/advice. As examples:

9 markers are listed for “Portion With Absolute Reduction In Pain“:

Spinal adjusting was superior in 8 of 9 of the listed markers.

6 markers are listed for “Pain Score“:

Spinal adjusting was superior in 5 of the 6 markers listed.

Additionally, a careful review of the charts presented in the article show that during the randomization, nearly twice as many of the chiropractic group (29.7%) had trauma initiated neck pain compared to the home exercise/advice group (16.5%). My clinical experience, which is extensive, has been that trauma triggered neck pain is always more difficult to manage in both the short and long term as compared to non-trauma triggered neck pain. It appears to me that the chiropractors had a tougher patient draw as compared to the home exercise /advice group. This finding was not discussed in the text of the article.

Although the article states several times that the chiropractic adjustments were given over a period of 12 weeks, the actual range of adjustments was 2-23 with a mean of 15.3. This is slightly more than 1 adjustment per week for 12 weeks. In my experience, acute neck pain responds best to daily treatment or at a minimum 3 times per week for a period of 2-3 weeks. I believe that an increase in the frequency of treatment by the chiropractors, as is commonly prescribed by many chiropractors, would have increased the chiropractic advantage over home exercise/advice.

Additionally, this article does not represent typical chiropractic clinical practice, which would usually include a greater range of management than spinal adjusting alone, often further improving clinical outcomes. Typical chiropractic clinical approaches to the management of pain syndromes would also include anti-inflammatory nutrition, low level laser therapy, traction, as well as home exercise/advice.

In contrast, the home exercise/advice group was seen only 1 or 2 times, but instructed to do neck exercises at home daily. The exercises consisted of 7 isolated maneuvers that required 3 different positions: sitting, supine head supported, and supine head unsupported. Each maneuver required 10 repetitions, and the patient was instructed to repeat all of the maneuvers 6-8 times per day. I performed the exercise maneuvers as prescribed and found that a session takes approximately 10 minutes.

Consequently, the authors are advocating that patients with acute/subacute neck pain exercise 60-80 minutes per day. I find this to be both impractical and unrealistic.

Consequently, I believe that for all of these reasons, chiropractic spinal manipulation (and chiropractic commonly employed adjuncts, including exercise/advice) is the most practical and effective management for acute/subacute neck pain.

••••••••••

Upper Cervical and Upper Thoracic Thrust Manipulation Versus Nonthrust Mobilization in Patients With Mechanical Neck Pain:

A Multicenter Randomized Clinical Trial

Journal of Orthopaedic & Sports Physical Therapy

January 2012; Volume 42; Number 1; pp. 5-18

James R. Dunning, Joshua A. Cleland, Mark A. Waldrop, Cathy Arnot, Ian Young, Michael Turner, Gisli Sigurdsson

Although there are significant differences between the various techniques employed by clinical chiropractic, chiropractic is best known for the inclusion of thrust manipulation of dysfunctional spinal joints resulting in audible joint cavitation. This study is a randomized clinical trial to compare the short-term effects of upper cervical and upper thoracic high-velocity low-amplitude (HVLA) thrust manipulation to nonthrust mobilization in patients with neck pain. Although upper cervical and upper thoracic HVLA thrust manipulation and nonthrust mobilization are common interventions for the management of neck pain, no studies have directly compared the effects of both upper cervical and upper thoracic HVLA thrust manipulation to nonthrust mobilization in patients with neck pain.

In this study, 107 neck pain participants were evaluated subjectively and objectively, and then randomized to receive either HVLA thrust manipulation or nonthrust mobilization to the upper cervical (C1-2) and upper thoracic (T1-2) spines (n = 56) or nonthrust mobilization (n = 51).

The participants were reexamined 48-hours after the initial examination/treatment and again completed the outcome measures. The effects of treatment on disability, pain, C1-2 passive rotation range of motion, and motor performance of the deep cervical flexors were examined.

The patients with mechanical neck pain who received the combination of upper cervical and upper thoracic HVLA thrust manipulation experienced significantly greater reductions in disability (50.5%) and pain (58.5%) than those of the nonthrust mobilization group (12.8% and 12.6%, respectively) following treatment. In addition, the HVLA thrust manipulation group had significantly greater improvement in both passive C1-2 rotation range of motion and motor performance of the deep cervical flexor muscles as compared to the group that received nonthrust mobilization.

The authors concluded that the combination of upper cervical and upper thoracic HVLA thrust manipulation is appreciably more effective in the short term than nonthrust mobilization in patients with mechanical neck pain.

The authors note that a bout 54% of individuals have experienced neck pain within the last 6 months. The economic burden associated with the management of patients with neck pain is high, second only to low back pain in annual workers’ compensation costs in theUnited States.

The C1-2 articulation has a high frequency of involvement in patients with neck pain and headaches. Disturbances in joint mobility in the upper thoracic spine may be an underlying contributor to musculoskeletal disorders in the cervical spine. Decreased mobility in the cervicothoracic junction (C7-T2) is associated with mechanical neck pain.

The primary outcome measure used in this study was the patient’s perceived level of disability as measured by the Neck Disability Index (NDI). The NDI is the most widely used condition-specific disability scale for patients with neck pain. The NDI has been demonstrated to be a reliable and valid outcome measure for patients with neck pain.

The authors state:

“A single session of HVLA thrust manipulation directed to both the upper cervical and upper thoracic spines results in greater improvements in disability, pain, atlantoaxial joint ROM, and motor performance of the deep cervical flexor muscles than nonthrust mobilization directed to the same regions.”

“We directed treatment to the atlantoaxial joints, because the C1-2 articulation has been found to have a high frequency of symptomatic involvement in patients with neck pain and headaches and previous studies have demonstrated that this articulation is where the majority of cervical rotation occurs.”

“The results of the current study demonstrated that patients with mechanical neck pain who received the combination of upper cervical and upper thoracic HVLA thrust manipulation, experienced greater reduction in pain and disability, showed greater improvement in passive C1-2 rotation range of motion, and had greater increases in motor performance of the deep cervical flexor muscles, as compared to the group that received nonthrust mobilization at a 48-hour follow-up visit.”

“The combination of HVLA thrust manipulation procedures directed to both the upper cervical and upper thoracic articulations may enhance the overall outcomes of patients with mechanical neck pain.”

Nonthrust mobilization is not worthless; it clearly helped the patients in this study. However, thrust/cavitation manipulations of the same spinal regions (upper cervical and upper thoracic spines) were significantly superior to mobilization in:

1) Overall successful outcomes

2) Disability reduction

3) Pain reduction

4) Increased cervical range of motion

5) Improvements in motor performance of the deep cervical flexors

Also, this study indicates that upper cervical and upper thoracic spines are biomechanically functionally linked and that the superior results achieved in this study as compared to other studies is as a consequence of adjusting both regions.

•••••

The purpose of The Chiropractic Impact Report™ is to keep you updated as to relevant academic concepts pertaining to whiplash-injured patients. The hope is that the information is useful in terms of enhanced understanding, as well as helping the personal injury attorney deal with insurance claim adjusters and adverse medical experts.

The chiropractor sending you this Report is well versed and trained in these concepts, and can be a valuable asset in personal injury cases in terms of both academics and treatment. Additionally, these expert chiropractors have access to a monthly phone consultation with me to discuss any pertinent issues that they may be facing on a particular case. I hope that you find this Report and the referring chiropractor a valuable resource.

Sincerely,

Daniel J. Murphy DC, DABCO

April 2012

admin — Mon, 16 Apr 2012 15:35:49 +0000

The “Connective Tissue – Cytoskeleton” Matrix
The “Tissue – Tensegrity” Matrix
And Chronic Low Back Pain

Chiropractors primarily look at patient’s problems from a mechanical perspective. A classic chiropractic mechanical analogy is a pinched nerve (compressive neuropathology). Although chiropractors occasionally do treat compressive neuropathology, most chiropractors are aware that there are patients with compressive neuropathology that require a surgical decompression. Overall, compressive neuropathology is a rare clinical syndrome in chiropractic clinical practice. Most of the mechanical approach of chiropractic is not to “unpinch a pinched nerve.” Rather, the primary mechanical approach of chiropractic patient management is the improvement of the Tensegrity Matrix.

The human body is composed of four tissue types: epithelium, muscle, connective, and nerve. Everything in the body is made from these four basic tissues.

The connective tissue is found throughout the body. The great Canadian histologist, Arthur Ham (d.1992 at age 90), states (1):

“Connective tissue was given its name because it connects, and thus holds, the other tissues together.”

Connective tissue includes tissues that produce blood cells (hemopoietic tissue), the blood cells themselves, and the strong supporting types of connective tissue. The strong supporting types of connective tissues include, bone, cartilage, ligaments, tendons, fascia, etc.

The strong supporting types of connective tissues have two components:

The living cells (like osteocytes, chondrocytes, fibroblasts, etc.).

A non-living intercellular substance; this non-living intercellular substance is produced by the living cells.

The chief role of these living cells is to produce and maintain the intercellular substances.

Collagen is a protein. It is the primary protein produced as intercellular substance by the living cells of the strong supporting types of connective tissues. Collagen is the most abundant protein in our bodies. Most of the collagen in our bodies is produced by the fibroblasts.

•••••

Rene Cailliet, MD, has had an accomplished life. Born in 1917 and still living at age 95, he helped pioneer the specialty of Physical Medicine and Rehabilitation during World War II. Dr. Cailliet served as a chairman of the Department of Physical Medicine and Rehabilitation at theUniversityofSouthern California. He is currently an emeritus professor of Physical Medicine and Rehabilitation at the medical school at theUniversityofCalifornia,Los Angeles(UCLA). Dr. Cailliet has authored more than a dozen medical texts, and he has 49 articles in a PubMed database search of the National Library of Medicine (March 2012). Interestingly, his most recent PubMed indexed article was published in 2008, and is co-authored by chiropractors Deed and Don (d. 2011) Harrison (2).

In his 1987 book The Rejuvenation Strategies, Dr. Cailliet notes that, under a microscope, collagen produces a whole body lattice of fibers that appear as a grid (3):

Dr. Cailliet notes that ideally, at the contact points between these fibers they remain independent and glide on one another when moving. However, as a consequence of inflammation, trauma, or even inactivity, the points of intersection become fibrotic and “stick together,” resulting in “loss of flexibility.”

•••••

In his 2000 book Energy Medicine, The Scientific Basis (4), James Oschman, PhD, notes that the cytoskeletons of all of the cells in the body are physically and mechanically linked to a collagenous connective tissue extracellular matrix. Proteins called “integrins” do this trans-cellular linking. The molecules that link the cell interior with the extracellular collagenous matrix are these integrins. Likewise, there is a physical mechanical link between the cellular cytoplasmic matrix and the nuclear envelope, nuclear matrix, and the DNA of the genes/chromosomes. This physical continuum, beginning with the skin and extending to the genetic material, can be affected physically as a consequence of postural distortions, injury, physical stress and scar tissue, resulting in alterations in expression of our genetic material. Dr. Oschman notes that this entire interconnected system is called the:

“connective tissue – cytoskeleton” matrix
or
the “tissue – tensegrity” matrix.

Our bodies behave as a tensegrity system. A tensegrity system is characterized by a series of continuous tensional networks. This means that the entire body is physically interconnected. A stress on one part of the system will spread to other parts of the system. This includes to the genome and its genetic expression. One can change the genomic expression of DNA by alterations of physical stress. All the components of our bodies, from the skin to the genome are physically and mechanically interlinked by a connective tissue collagenous matrix and integrins. Again, this is often referred to as the “tensegrity matrix.”

Dr. Oschman explains how progressive changes in the function of the tensegrity matrix takes place because of the ways in which individuals use their bodies in relation to gravity, because of habits or injuries. These soft tissue changes provide a basis for the mechanically based restorative measures by chiropractors and others.

Dr. Oschman argues that the tensegrity matrix best serves physiology when it is flexible and balanced. This serves to reduce injury and enhance healing. He states:

“Tensegrity accounts for the ability of the body to absorb impacts without being damaged. Mechanical energy flows away from a site of impact through the tensegrous living matrix. The more flexible and balanced the network (the better the tensional network), the more readily it absorbs shocks and converts them to information rather than damage.”

“Tensegrity accounts for the fact that inflexibility or shortening in one tissue influences structure and movement in other parts.”

Dr. Oschman explains that the most significant influence on the tensegrity matrix is our alignment in the gravity field. He notes that gravity is the most potent physical influence in any human life. Simple mechanical calculations reveal that gravity gives rise to surprisingly large forces within the body as a consequence of levers that amplify the forces exerted on joints and other tissues.

The gravity system connects, via integrins, to the cytoskeleton of cells throughout the body. Therefore, an imbalance in one part of the body will affect the whole body.

Dr. Oschman states:

“Gravity pervades our bodies and our environment and affects our every activity. All of the structures around us – our homes, furniture, buildings, machinery, plant, and animal, – and our own bodies, are designed to function in a world dominated by gravity. The form of each bone, muscle, and sinew tells a story of its particular role in maintaining and moving the body in the gravitational field. Many of the injuries faced in the therapeutic setting are consequences of falling down, or of habitual movement patterns that strain tissues. Hence therapists of virtually every tradition can benefit from an appreciation of the ways in which gravity interacts with structures, energy flows, and emotions, and the clinical approaches that remedy ‘gravitational traumas.’”

“To introduce the therapeutic significance of gravity, we summarize the work of Joel E. Goldthwait and his colleagues at Harvard Medical School.”

“A surgeon in Boston and founder of the orthopaedic clinic at the General Hospital, Goldthwait developed a successful therapeutic approach to chronic disorders. The aim of his therapies was to get his patients to sit, stand, and move with their bodies in a more appropriate relationship with the vertical. After years of treating patients with chronic problems, he concluded that many of these problems arise because parts of the body become misaligned with respect to the vertical, and organ functions therefore become compromised.”

“Goldthwait’s therapeutic approach was based in part on observations made while performing surgery on such patients. He noticed that abdominal nerves and blood vessels are under tension in individuals whose bodies are out of alignment. He also reported ‘stretching and kinking’ of the cerebral arteries and veins in those whose necks were bent. Various cardiac problems were correlated with ‘faulty body mechanics’ that distorted the chest cavity in a way that impaired circulatory efficiency. Goldthwait also documented with X-rays a build-up of calcium deposits around the vertebrae of individuals with chronic arthritis, and observed that these deposits can diminish when the individual acquires a more vertical stance. His therapeutic approach corrected many difficult problems without the use of drugs. He viewed the human body from a mechanical engineering perspective, in which alignment of parts is essential to reduce wear and stress. He pleaded with physicians to recognize and correct misalignments to prevent long-term harmful effects.”

Dr. Goldthwait pleaded for everyone to pay more attention to the way in which they hold and move their bodies in relation to the gravity field. He noted that misalignment of any part will affect the whole system, and that restoration of verticality is a way to address a wide variety of clinical problems. Optimal performance in a gravity field occurs only at a narrow peak of balance, and the slightest deviation reduces optimum efficiency. Altered posture in our gravity environment affects the tensegrity matrix continuum. This in turn influences physiology, pain perception, and health.

•••••

Another champion of the concepts of the importance of mechanical influence on the physiology of the living matrix is Harvard’s Donald Ingber, MD, PhD. Dr. Ingber is from the Vascular Biology Program, Departments of Surgery and Pathology, Children’s Hospital andHarvardMedicalSchool. A check of the National Library of Medicine using the PubMed search engine finds 211 articles that have included Dr. Ingber as author (March 2012).

A relevant article by Dr. Ingber was published in the Annals of Medicine in 2003, and titled (5):

Mechanobiology and Diseases of Mechanotransduction

In this article, Dr. Ingber expresses his concern that contemporary medical practice focuses primarily on molecular genetics while largely ignoring the physical basis of disease. He notes that many of the problems that lead to pain and morbidity, and bring patients to the doctor’s office, result from changes in tissue structure or mechanics. He stresses that mechanics should be integrated into understanding the molecular basis of disease.

In agreement with Dr. Oschman above, Dr. Ingber describes the key roles that physical forces, extracellular matrix and cell structure play in the control of normal development, as well as in the maintenance of tissue form and function.

Dr. Ingber defines cellular mechanotransduction as the molecular mechanism by which cells sense and respond to mechanical stress. He notes that a wide range of diseases included within virtually all fields of medicine and surgery share a common feature: “their etiology or clinical presentation results from abnormal mechanotransduction.”

A central theme in Dr. Ingber’s discussion is that there are “mechanisms by which cells sense mechanical signals and convert them into a chemical or electrical response.” The molecules that mediate mechanotransduction are the extracellular matrix molecules, trans-membrane integrin receptors. The function of these molecules is modifiable with appropriate mechanical therapeutic intervention. This is relevant and important in chiropractic clinical practice.

Dr. Ingber makes these important points:

“Mechanical forces are critical regulators of cellular biochemistry.”
“There is a huge disconnect between ‘genome-age’ technologies and the reality of how diseases manifest themselves. From the time the first human looked, listened and felt for what is wrong with a sick friend, caregivers have recognized the undeniable physical basis of disease.”
“In the current genome euphoria, there appears to be no place for ‘physicality’. This is especially worrisome given that abnormal cell and tissue responses to mechanical stress contribute to the etiology and clinical presentation of many important diseases, including asthma, osteoporosis, atherosclerosis, diabetes, stroke and heart failure.”
There is a “strong mechanical basis for many generalized medical disabilities, such as lower back pain and irritable bowel syndrome, which are responsible for a major share of healthcare costs world-wide.”
“In biology and medicine, we tend to focus on the importance of genes and chemical factors for control of tissue physiology and the development of disease, whereas we commonly ignore physical factors. This is interesting because it was common knowledge at the turn of the last century that mechanical forces are critical regulators in biology.”
“These new insights into mechanobiology suggest that many ostensibly unrelated diseases may share a common dependence on abnormal mechanotransduction for their development or clinical presentation.”
“Understanding of the relation between structure and function in living tissues and of fundamental mechanisms of cellular mechanotransduction may therefore lead to entirely new modes of therapeutic intervention.”
“The therapeutic value of physical therapy, massage, and muscle stimulation is also well known.”

Dr. Ingber restates that tissues are composed of groups of living cells held together by an extracellular matrix which is primarily composed of a network of collagens. A summary of his article states:

“The current focus in medicine is on the genetic basis of disease. However, it is not necessary to correct the underlying genetic defect in order to treat clinically relevant symptoms or relieve the pain and morbidity of disease. Moreover, most of the clinical problems that bring a patient to the doctor’s office result from changes in tissue structure and mechanics. Although these physical alterations have been commonly viewed as the end-result of the disease process, recent advances in mechanobiology suggest that abnormal cell and tissue responses to mechanical stress may actively contribute to the development of many diseases and ailments. Thus, it might be wise to search for a physical cause when chemical or molecular forms of investigation do not suffice.”

•••••

Helene M. Langevin, MD, is a neurologist from the Department of Neurology, University of Vermont College of Medicine. In 2006 she published an article in the journal Medical Hypothesis, titled (6):

Connective tissue: A body-wide signaling network?

In this article, Dr. Langevin notes that connective tissue forms an anatomical network throughout the body that functions as a body-wide mechanosensitive signaling network. This connective tissue signaling network is affected by changes in movement and posture, and may be altered in pathological conditions (e.g. local decreased mobility due to injury or pain). Connective tissue thus functions as a whole body communication system. Since connective tissue is intimately associated with all other tissues (e.g. lung, intestine), connective tissue signaling may coherently influence (and be influenced by) the normal or pathological function of a wide variety of organ systems.

Dr. Langevin notes that the musculoskeletal system does not physiologically function in isolation from the rest of the body, and that the musculoskeletal tissues (bones, muscles, cartilage, tendons) are strongly associated with posture and movement. Dr. Langevin makes these important points:

“Connective tissue not only forms a continuous network surrounding and infiltrating all muscles, but also permeates all other tissues and organs.”
“Since connective tissue plays an intimate role in the function of all other tissues, a complex connective tissue network system integrating whole body mechanical forces may coherently influence the function of all other physiological systems.”
Local connective tissue fibrosis following an injury may affect both electrical conductivity as well as fibroblast-to-fibroblast communication. Therefore, local pathology can affect whole-body connective tissue signaling.
“Understanding the temporal and spatial dynamics of connective tissue bioelectrical, cellular and tissue plasticity responses, as well as their interactions with other tissues, may be key to understanding how pathological changes in one part of the body may cause a cascade of “remote” effects in seemingly unrelated areas and organ systems.”

Importantly, Dr. Langevin describes how the connective tissue matrix will adversely remodel when subjected to chronic stresses, postural distortions, injury, etc. Similarly, therapeutic improvements in posture, motion and fibrosis will improve the structure of the connective tissue matrix, improving whole body physiology. This therapeutic remodeling can take place over a period of days, weeks or months.

•••••

Dr. Langevin added to her 2006 article in Medical Hypothesis the following year, 2007, with an article titled (7):

Pathophysiological Model for Chronic Low Back Pain
Integrating Connective Tissue and Nervous System Mechanisms

In this article, Dr. Langevin and colleague propose an etiology for chronic low back pain, and a plausible biological clinical approach that should improve clinical outcomes. Their model stems from Dr. Langevin’s prior work (2006) which indicated that adverse connective tissue remodeling leads to inflammation, nervous system sensitization and further decreased mobility. The decrease in movement leads to an increase in chronic low back pain. Specifically, she states:

“The integration of connective tissue and nervous system plasticity into the model of chronic LBP will potentially illuminate the mechanisms of a variety of treatments that may reverse these abnormalities by applying mechanical forces to soft tissues (e.g. physical therapy, massage, chiropractic manipulation, acupuncture), by changing specific movement patterns (e.g. movement therapies, yoga) or more generally by increasing activity levels (e.g. recreational exercise).”

Chronic low back pain may be caused by pathological connective tissue fibrosis, which causes adverse changes in movement. This is well documented in ligaments and joint capsules. This pathological connective tissue fibrosis is plastic and can therefore be remodeled. However, the remodeling must take place over time. Non-invasive measures of connective tissue remodeling may eventually become important tools to evaluate and follow patients with chronic LBP in clinical practice.

In this study, Dr. Langevin notes that adverse connective tissue remodeling cannot be imaged with X-ray, CT, MRI. She claims that this is why the association between such imaging and patient symptoms “has been consistently weak, and up to 85% of patients with low back pain cannot be given a precise pathoanatomical diagnosis using these methods.”

One of the proven strategies to successfully improve the clinical outcomes in those with chronic low back pain is to avoid rest and to resume physical activity as soon as possible. Dr. Langevin notes that this approach would facilitate the remodeling of the connective tissue matrix. Specifically, Dr. Langevin makes these comments:

“We hypothesize that connective tissue remodeling occurs in chronic LBP as a result of emotional, behavioral and motor dysfunction.”

“We further hypothesize that increased connective tissue stiffness due to fibrosis is an important link in the pathogenic mechanism leading to chronicity of pain, fear-avoidance and further movement impairment.”

“Abnormal movement patterns can have important influences on the connective tissues that surround and infiltrate muscles.”

“A hallmark of connective tissue is its plasticity or ‘remodeling’ in response to varying levels of mechanical stress.”

“Both increased stress due to overuse, repetitive movement and/or hypermobility, and decreased stress due to immobilization or hypomobility can cause changes in connective tissue.”

“A consistent absence of stress, on the other hand, leads to connective tissue atrophy, architectural disorganization, fibrosis, adhesions and contractures.”

“Fibrosis can be the direct result of hypomobility or the indirect result of hypermobility via injury and inflammation.”

“Connective tissue fibrosis is detrimental, as it leads to increased tissue stiffness and further movement impairment.”

Therapeutically, Dr. Langevin makes a number of suggestions that are consistent with chiropractic clinical practice, including:

“In addition to its role in the pathological consequences of immobility and injury, the dynamic and potentially reversible nature of connective tissue plasticity may be key to the beneficial effects of widely used physical therapy techniques as well as ‘alternative’ treatments involving external application of mechanical forces (e.g. massage, chiropractic manipulation, acupuncture), changes in specific movement patterns (e.g. movement therapies, tai chi, yoga) or more general changes in activity levels (e.g. increased recreational exercise).”

“Manual or movement-based treatments have the advantage of not causing drug-induced side effects (e.g. gastritis, sedation).”

A “carefully applied direct tissue stretch may be necessary in cases of long standing hypomobility with pronounced fibrosis and stiffness.”

“The model presented in this paper predicts that beneficial connective tissue remodeling can result from a variety of therapeutic interventions.”

•••••

Summary

Dr. Arthur Ham notes that collagenous connective tissue is found throughout the body.

Dr. Rene Cailliet notes that the collagenous connective tissue matrix is arranged in a grid-like pattern. When functioning normally, the fibers of the grid slide over each other during stress and motion. However, when chronically stressed, inflamed or traumatized the collagenous matrix becomes fibrotic, which impairs motion.

Dr. James Oschman refers to the collagenous connective tissue matrix as the tensegrity matrix. He notes that the matrix confers optimum physiology when it is flexible and balanced. He notes that the matrix becomes pathological as a consequence of alterations of the manner in which we live, exist and function in a gravity environment. He further notes that our physiology and function is improved when we improve our alignment with respects to gravity.

Dr. Donald Ingber, like Dr. James Oschman, refers to the collagenous connective tissue matrix as the tensegrity matrix. Dr. Ingber notes that abnormal mechanical stresses in the matrix are linked to a wide range of diseases included within virtually all fields of healthcare. He notes that there are mechanisms by which cells sense mechanical signals and convert them into a chemical or electrical response that influence function and health. He stresses that there is a physical basis for many diseases and symptoms, and that applied mechanics should not be forgotten by mainstream medical practice.

Dr. Helene Langevin notes that the collagenous soft tissue matrix functions as a body-wide mechanosensitive signaling network. This body-wide mechanosensitive signaling network is capable of influencing the normal or pathological function of a wide variety of musculoskeletal organ systems. She notes that many things can adversely influence the integrity of the matrix, including postural stresses, emotional stresses, inflammation, trauma, etc. Long-standing mechanical problems cause a remodeling of the matrix which in turn further adversely influences function and physiology. Dr. Langevin notes that applied mechanical forces can reverse and remodel the matrix, improving function, physiology, and associated symptoms. The mechanical approaches she advocates for this purpose include physical therapy, massage, chiropractic manipulation, acupuncture, movement therapies, yoga, and exercise. Each of these are commonly used in today’s chiropractic clinical practice.

Chiropractic is not primarily the “unpinching” of a nerve. Rather it involves a series of techniques, exercises, tissue work, ergonomics, etc. that are designed to improve the way in which our patients live, exist, and function in a gravity environment. This in turn remodels adverse changes in the collagenous connective matrix, improving many aspects of function, physiology, and pain. Because this remodeling occurs over a period of time, it is not uncommon for the chiropractor to recommend a program of treatment that extends for a period of weeks to months.

•••••

Sincerely,

Daniel J. Murphy DC, DABCO

REFERENCES:

Ham AW; Histology; seventh edition; Lippincott; 1974.
Harrison DE, Janik TJ, Cailliet R, Harrison DD, Normand MC, Perron DL, Oalkey PA; Upright static pelvic posture as rotations and translations in 3-dimensional from three 2-dimensional digital images: validation of a computerized analysis. Journal of Manipulative and Physiological Therapeutics; February 2008; 31(2):137-45.
Cailliet R, Gross L, The Rejuvenation Strategy, Pocket Books, 1987.
Oschman J; Energy Medicine, The Scientific Basis, Churchill Livingstone, 2000.
IngberDE; Mechanobiology and Diseases of Mechanotransduction; Annals of Medicine; 2003;35(8), pp.564-77.
Langevin HM; Connective tissue: A body-wide signaling network?; Medical Hypotheses; Volume 66, Issue 6, June 2006, pp. 1074-1077.
Langevin HM, Sherman KJ; Pathophysiological Model for Chronic Low Back Pain: Integrating Connective Tissue and Nervous System Mechanisms; Medical Hypotheses; Volume 68, Issue 1, January 2007, pp. 74-80.

March 2012

admin — Mon, 05 Mar 2012 18:27:10 +0000

Spinal Joint Mechanoreceptors, Proprioception, and The Pain Gate

William H. Kirkaldy-Willis, MD, had an accomplished professional career. Dr. Kirkaldy-Willis was trained as an orthopedic surgeon. From 1965 to 1988 he was associated with the University Hospital in Saskatoon, Canada where he became Emeritus Professor of Orthopedic Surgery and Head of the Department in 1967. He was President of the East African Association of Surgeons (1959-1960); President of the Canadian Orthopedic Research Society (1971-1972); President of the International Society for Study of the Lumbar Spine (1982-1983); President of the North American Spine Society (1986-1987); and President of the American Back Society (1988-1991).

In his career, Dr. Kirkaldy-Willis published 71 articles that are indexed in the National Library of Medicine, and he was the primary author of the universally accepted gold standard reference text Managing Low Back Pain, which published four editions between 1983 and 1999.

Dr. Kirkaldy-Willis died in 2006 at the age of 93.

The August 15, 2006 issue of the journal Spine printed a tribute to Dr. Kirkaldy-Willis, which included these words (1):

Kirkaldy-Willis was one of the very few spine surgeons who recognized, at the very beginning, the important role of exercise in maintaining a healthy spine. An important special interest of his was in promoting cooperation between physicians and chiropractors to the benefit of both.

In 1985, Dr. Kirkaldy-Willis was the lead author of a study published in the journal Canadian Family Physician (2), titled:

“Spinal Manipulation in the Treatment of Low back Pain”

In this study, Dr. Kirkaldy-Willis notes that spinal manipulation is one of the oldest forms of therapy for back pain, and that it has mostly been practiced outside of the medical profession. He further notes that there has been an escalation of clinical and basic science research on manipulative therapy, which has shown that there is a scientific basis for the treatment of back pain by manipulation.

In this study, Dr. Kirkaldy-Willis discusses that a specific diagnosis and pathology is not evident in most cases of low back pain, but that compressive neuropathology is extremely rare. Specifically, he states:

“Most causes of low back pain lack objective clinical signs and overt pathological changes.”

“Less than 10% of low back pain is due to herniation of the intervertebral disc or entrapment of spinal nerves by degenerative disc disease.”

Dr. Kirkalady-Willis discusses how the key to successfully managing chronic low back pain is through the utilization of applied motion. He categorizes applied motion into three groups:

1) Active Range of Motion
This range is achieved through active exercise.

2) Passive Range of Motion
Beyond the end of the Active Range of Motion of any synovial joint, there is a small passive range of mobility. A joint can only move into this zone with passive assistance. Going into this Passive Range of Motion constitutes mobilization. This is not manipulation.

3) Paraphysiological Range of Motion
At the end of the passive range of motion, an elastic barrier of resistance is encountered. This barrier has a “spring-like end-feel.” When motion separates the articular surfaces of a synovial joint beyond this elastic barrier, the joint surfaces suddenly move apart with a cracking noise. This additional motion can only be achieved after cracking the joint and has been labeled the Paraphysiological Range of Motion. This constitutes manipulation. Spinal manipulation is an assisted passive motion applied to the spinal facet joints that creates motion into the Paraphysiological Range.

The cracking sound on entering the Paraphysiological Range of Motion is the result of sudden liberation of synovial gases—a phenomenon known to physicists as cavitation.

At the end of the Paraphysiological Range of Motion, the limit of anatomical integrity is encountered. The facet joint capsular ligaments create the limit of anatomical integrity.

•••••

In this study, Dr. Kirkaldy-Willis presents the results of a prospective observational study of spinal manipulation in 283 patients with chronic low back and leg pain. All 283 patients in this study had failed prior conservative and/or operative treatment, and they were all totally disabled (“Constant severe pain; disability unaffected by treatment.”)

These patients were given a two or three week regimen of daily spinal manipulations by an experienced chiropractor. No patients were made worse by the manipulation, yet many experienced an increase in pain during the first week of treatment. Even with this initial increase in pain, Dr. Kirkaldy-Willis emphasized the importance of continuing with manipulative treatment and not stopping treatment. He states:

“In most cases of chronic low back pain, there is an initial increase in symptoms after the first few manipulations. In almost all cases, however, this increase in pain is temporary and can be easily controlled by local application of ice.”

“Patients undergoing manipulative treatment must therefore be reassured that the initial discomfort is only temporary.”

In this study, Dr. Kirkaldy-Willis considered a good clinical outcome from manipulation to be:

1) “Symptom-free with no restrictions for work or other activities.”

2) “Mild intermittent pain with no restrictions for work or other activities.”

81% of the patients with referred pain syndromes subsequent to joint dysfunctions achieved the “good” result.

48% of the patients with nerve compression syndromes, primarily subsequent to disc lesions and/or central canal spinal stenosis, achieved the “good” result.

These results are impressive, especially considering that all of the patients were chronic, disabled and had failed prior conservative and surgical approaches to their problems.

•••••

To explain the impressive outcomes from this study, Dr. Kirkaldy-Willis used the Gate Theory of Pain. Ronald Melzack and Patrick Wall first proposed the Gate Theory of Pain in 1965 (3). In discussing Melzack and Wall’s Gate Theory of Pain, Dr. Kirkaldy-Willis states that this theory has “withstood rigorous scientific scrutiny.” He specifically makes these additional observations:

“The central transmission of pain can be blocked by increased proprioceptive input.” Pain is facilitated by “lack of proprioceptive input.” This is why it is important for “early mobilization to control pain after musculoskeletal injury.”

The facet capsules are densely populated with mechanoreceptors. “Increased proprioceptive input in the form of spinal mobility tends to decrease the central transmission of pain from adjacent spinal structures by closing the gate. Any therapy which induces motion into articular structures will help inhibit pain transmission by this means.”

Importantly, Dr. Kirkaldy-Willis pioneered the concept of the “three joint complex.” This concept stresses that the function of the two facet joints are always linked to the function of the intervertebral disc. In other words, the facets and the disc are mechanically linked.

•••••

As noted, Dr. Kirkaldy-Willis’ discussion of the Gate Theory of Pain involved the “closing” of the pain gate through the enhancement of proprioception. This was done by increasing the firing of mechanoreceptors of the facet joints, which occurred as a consequence of moving the facet joints into the Paraphysiological Range of Motion via spinal manipulation.

Many other authors make similar claims concerning the Gate Theory of Pain, including the following:

Remember: Pain afferents are small diameter neurons.
Mechanoreceptors are large diameter neurons.

The perception of pain is dependent upon the balance of activity in large [mechanoreceptor] and small [nociceptive] afferents. (4)
If large myelinated fibers (mechanoreceptors) were selectively stimulated, then normal “balance” of activity between large [mechanoreceptor] and small [nociceptive] fibers would be restored and the pain would be relieved. (5)
“Pain is not simply a direct product of the activity of nociceptive afferent fibers but is regulated by activity in other myelinated afferents that are not directly concerned with the transmission of nociceptive information.” (6)
“The idea that pain results from the balance of activity in nociceptive and non-nociceptive afferents was formulated in the 1960s and was called the gate control theory.” (6)
“Simply put, non-nociceptive afferents ‘close’ and nociceptive afferents ‘open’ a gate to the central transmission of noxious input.” (6)
“The balance of activity in small- and large-diameter fibers is important in pain transmission…” (7)

In 2002, the British Journal of Anaesthesia published a study reaffirming the validity of the Gate Theory of Pain in an article titled (8):

“Gate Control Theory of Pain Stands the Test of Time”

•••••

Proprioception is the sense of the relative position of neighboring parts of the body. Proprioception can be either conscious or unconscious, and both types aid in “closing” the pain gate. Proprioception includes both position sense and motion sense (kinesthesia).

It is proprioception that allows people to drive without having to look at one’s feet, to type without having to look at one’s fingers, and to run and catch a ball without having to look at one’s feet or hands.

Proprioceptive sense is composed of information from sensory neurons of the vestibular apparatus of the inner ear and from mechanoreceptors located in the muscles and joint tissues. Proprioception is awareness of position and/or movement derived from muscular, tendon, and articular sources. The awareness is derived from mechanoreceptive nerve endings that transmit data from joint capsules and muscles. Joint and muscle mechanoreceptors drive an important component of proprioception. Occasionally, joint mechanoreceptors are called “proprioceptors.”

In 1975, Princeton educated physiologist Irvin Korr, PhD, published a study titled (9):

Proprioceptors and Somatic Dysfunction

In this study, Dr. Korr notes that proprioceptors “from countless thousands of reporting stations and articular components, entering the cord via the dorsal roots, is essential to the moment-to-moment control and fine adjustment of posture and locomotion.”

Dr. Korr discusses the feedback loop that exists between these proprioceptors and the muscle system. He notes that adverse or inappropriate mechanical events can create a mismatch of communication within the feedback loop, which is deleterious [opens the pain gate]. He also notes how the adverse loop can be corrected through spinal manipulation.

•••••

The Mechanoreceptors

Melzack and Wall’s Gate Theory of Pain was published in 1965. Dr. Korr’s article on proprioceptors was published in 1975. Dr. Kirkaldy-Willis’ article on manipulation and the Gate Theory of Pain was published in 1985. Since 1985, a number of studies have investigated the anatomy and physiology of joint mechanoreceptors, often using human subjects. Several of these are listed below:

In 1992, the journal Spine published a study titled (10):

“Neural Elements in Human Cervical Intervertebral Discs”

The authors document that the human cervical intervertebral disc is innervated with mechanoreceptors. They state:

“The presence of neural elements within the intervertebral disc indicates that the mechanical status of the disc is monitored by the central nervous system.”

“The location of the mechanoreceptors may enable the intervertebral disc to sense peripheral compression or deformation as well as alignment.”

Key points from this study include:

The intervertebral disc is innervated with mechanoreceptors, perhaps as deep as to the nucleus pulposus.
These mechanoreceptors communicate to the central nervous system.
These mechanoreceptors provide basic proprioceptive function, specifically the sense of compression, deformation, and alignment.

•••

In 1994, the journal Spine published a study titled (11):

“Mechanoreceptor endings in human cervical facet joints”

These authors state:

“Encapsulated mechanoreceptors are a consistent finding in normal human cervical facets.”

“The presence of these receptors in the facet capsule indicate that the mechanical state of the capsule (position, tension, pressure, etc.) is under the surveillance of the central nervous system.”

“The presence of mechanoreceptive and nociceptive nerve endings in cervical facet capsules proves that these tissues are monitored by the central nervous system and implies that neural input from the facets is important to proprioception and pain sensation in the cervical spine.”

Key points from this study include:

The cervical facet joints are innervated with mechanoreceptors.
These mechanoreceptors communicate to the central nervous system.
These mechanoreceptors provide basic proprioceptive function, specifically the sense of tension, pressure, and position.

•••

In 1998, the same primary author and colleague investigated the presence of mechanoreceptors in the facets joints of the thoracic and lumbar spines. They published their findings in Spine in an article titled (12):

“Mechanoreceptor endings in human thoracic
and lumbar facet joints”

These authors state:

“Ongoing studies of spinal innervation have shown that human facet tissues contain mechanoreceptive endings capable of detecting motion and tissue distortion.”

“Encapsulated nerve endings are believed to be primarily mechanosensitive and may provide proprioceptive and protective information to the central nervous system regarding joint function and position.”

Key points from this study include:

The thoracic and lumbar facet joints are innervated with mechanoreceptors.
These mechanoreceptors communicate to the central nervous system.
These mechanoreceptors provide basic proprioceptive function, specifically the sense of motion, tissue distortion, and position.

•••

In 1995, the journal Spine published a study titled (13):

“Mechanoreceptors in intervertebral discs:
Morphology, distribution, and neuropeptides”

The authors documented the occurrence and morphology of mechanoreceptors in human and bovine intervertebral discs and longitudinal ligaments. They note that:

“Physiologically, these mechanoreceptors “provide the individual with sensation of posture and movement.”

“In addition to providing proprioception, mechanoreceptors are thought to have roles in maintaining muscle tone and reflexes.”

“Their presence in the intervertebral disc and longitudinal ligament can have physiologic and clinical implications.”

Key points from this study include:

The lumbar intervertebral discs are innervated with mechanoreceptors.
These mechanoreceptors provide basic proprioceptive function, including the maintenance of muscle tone and muscular reflexes.

•••

More recently, in 2010, the Journal of Clinical Neuroscience published a study titled (14):

“An immunohistochemical study of mechanoreceptors
in lumbar spine intervertebral discs”

The study used twenty-five lumbar (L4–5 and L5–S1) fresh human intervertebral discs. These authors state:

“These receptors have a key role in the perception of joint position and adjustment of the muscle tone of the vertebral column.”

“An important component of low back pain is an intense muscle spasm of the vertebral musculature, elicited through reflex arches mediated by specialized nerve endings.”

“During axial loading of a motion segment, compressive stresses in the nucleus will generate tensile stresses in the peripheral annulus, which is rich in neural receptors.”

“In conclusion, this study confirms the existence of an abundant network of encapsulated and non-encapsulated receptors in the intervertebral discs of the lower lumbar spine in normal human subjects. The principal role of encapsulated structures is assumed to be the continuous monitoring of position, velocity and acceleration (kinesthesia).”

Key points from this study include:

The lumbar intervertebral disc is innervated with mechanoreceptors.
These mechanoreceptors are important in maintaining proper muscle tone and when dysfunctional can create intense muscle spasms.
These mechanoreceptors provide basic proprioceptive function, specifically the sense of compression, deformation, kinesthesia, and alignment.

•••••

SUMMARY

Spine pain is extremely common in our society. Chemical (pharmaceutical) approaches to the management of spinal pain syndromes are also common and popular. Chemical (pharmaceutical) approaches for pain management are marketed on television, radio, internet, and printed media, etc. These chemical (pharmaceutical) products are both over the counter and prescription.

When a patient presents with spinal pain syndrome to a chiropractic office, history usually reveals that a chemical (pharmaceutical) solution has been tried or is concurrently being tried, often with unacceptable results. In these cases, chiropractors primarily look for mechanical problems.

The basic premise, as supported above, is that physical stresses and/or trauma result in mechanical problems. These mechanical problems impair the appropriate function of articular mechanoreceptors. These articular mechanoreceptors are proven to exist, as noted above. These articular mechanoreceptors have three primary functions:

Control, through neurological reflexes, the tone in the related musculature. This enhances spinal function and protects the spinal joints against additional injury and future degenerative processes.
Provide proprioceptive senses to the central nervous system. This includes information on alignment, position, compression, deformation, and motion. Once again, this enhances spinal function and protects the spinal joints against additional injury and future degenerative processes.
The quality of the mechanoreceptive input and proprioception are a significant factor in the state of the Pain Gate. Simply put, improved mechanoreception and proprioception close the Pain Gate.

According to low back pain pioneer, Dr. Kirkaldy-Willis, spinal adjusting (manipulation) influences and benefits the back pain patient through two mechanisms:

1) Stretching of facet joint capsules will fire capsular mechanoreceptors which will reflexly “inhibit facilitated motoneuron pools” which are responsible for the muscle spasms that commonly accompany low back pain. Not only does spasm relief improve a patient’s pain, it also improves spinal motion, improves spinal mechanoreception, improves proprioception, and further inhibits pain by closing the Pain Gate.

2) In chronic cases, there is a shortening of periarticular connective tissues and intra-articular adhesions may form. Orthopedically trained chiropractors refer to these soft tissue changes as the “Fibrosis of Repair.” Dr. Kirkaldy-Willis suggests that spinal adjusting (specific line-of-drive manipulation) will stretch or break these adhesions, and enhance remodeling of other fibrotic tissue changes. These also give the patient long-term improvement in joint function, mechanoreception, proprioception, neuromuscular controls and Pain Gate closure.

Importantly, Dr. Kirkaldy-Willis notes that once an adjustment breaks the adhesion, they will often reform to create the same degree of adverse joint mechanical function. His solution, as documented in his 1985 study above (2), is that the patient be adjusted daily for two to three weeks, at a minimum. His study included prior chiropractic failures, and he attributed the success of the new chiropractic intervention to daily spinal adjusting for two to three weeks. Dr. Kirkalady-Willis states:

“However, the gain in mobility must be maintained during this period to prevent further adhesion formation.”

“In our experience, anything less than two weeks of daily manipulation is inadequate for chronic low back pain patients.”

It is chiropractically important to understand that the intervertebral disc and facet capsules (and other tissues) are innervated with mechanically sensitive nerves that communicate with the central nervous system. These nerves tell the CNS about the mechanical status of spinal function and alignment of the spine, as well as controlling local neuromuscular reflexes and the Pain Gate. Undoubtedly, chiropractic adjustments influence these nerves both during an adjustment and afterwards as a consequence of improved biomechanical function and posture.

•••••

The Chiropractic Impact Report™ is a monthly publication by myself, Dan Murphy, DC. I am a 1978 graduate of Western States Chiropractic College in Portland, OR. I have managed about 10,000 whiplash-injury cases. In the past 32 years, I have taught more than 500 12-hour post graduate continuing education classes pertaining to whiplash and spinal trauma, including 21 years of coordinating a year-long certification program in spine trauma, certified through the International Chiropractic Association. Additionally, I am board certified in chiropractic orthopedics (DABCO), and I am on the faculty at Life Chiropractic College West in Hayward, CA (28 years).

The purpose of The Chiropractic Impact Report™ is to keep you updated as to relevant academic concepts pertaining to whiplash-injured patients. The hope is that the information is useful in terms of enhanced understanding, as well as helping the personal injury attorney deal with insurance claim adjusters and adverse medical experts.

The chiropractor sending you this Report is well versed and trained in these concepts, and can be a valuable asset in personal injury cases in terms of both academics and treatment. Additionally, these expert chiropractors have access to a monthly phone consultation with me to discuss any pertinent issues that they may be facing on a particular case. I hope that you find this Report and the referring chiropractor a valuable resource.

Sincerely,

Daniel J. Murphy DC, DABCO

REFERENCES:

1) In Memoriam, A Tribute to William Kirkaldy-Willis; Spine; Vol. 31; No. 18; Aug. 15, 2006; pp. 2034-2035.

2) Kirkaldy-Willis WH and Cassidy JD; Spinal Manipulation in the Treatment of Low back Pain; Canadian Family Physician; March 1985, Vol. 31, pp. 535-540.

3) Melzack R, Wall P; Pain mechanisms: a new theory; Science; November 19, 1965;150(3699); pp. 971-979.

4) John Nolte, The Human Brain, Mosby Year Book, 1993, p. 139.

5) John Nolte, The Human Brain, Mosby Year Book, 1999, p. 203.

6) Eric Kandel, James Schwartz, Thomas Jessell, Principles of Neural Science. McGraw-Hill, 2000, pp. 482-3.

7) Eric Kandel, James Schwartz, Thomas Jessell, Principles of Neural Science, McGraw-Hill, 2000, pp. 490.

Dickenson AH; Gate Control Theory of Pain Stands the Test of Time; British Journal of Anaesthesia; June 2002; Vol. 88; No. 6; pp. 755-757.

9) Korr IM; Proprioceptors and somatic dysfunction; Journal of the American Osteopathic Association; March 1975; Vol. 74; No. 6; pp. 683-650.

10) Mendel T, Wink CS, Zimny ML; Neural elements in human cervical intervertebral discs; Spine; February 1992;17(2):pp. 132-5.

11) McLain RF; Mechanoreceptor endings in human cervical facet joints; Spine; March 1, 1994;19(5):495-501.

12) McLain RE, Pickar JG; Mechanoreceptor endings in human thoracic and lumbar facet joints; Spine; January 15, 1998;23(2):168-73.

13) Roberts S, Eisenstein SM, Menage J, Evans EH, Ashton IK; Mechanoreceptors in intervertebral discs: Morphology, distribution, and neuropeptides; Spine; December 15, 1995;20(24): pp. 2645-51.

14) Dimitroulias A, Tsonidis C, Natsis K, Venizelos I, Djau SN. Tsitsopoulos P; An immunohistochemical study of mechanoreceptors in lumbar spine intervertebral discs; Journal of Clinical Neuroscience; Volume 17, Issue 6, June 2010, Pages 742-745.

February 2012

admin — Wed, 01 Feb 2012 00:01:56 +0000

Whiplash Injuries Review
and Update on Facet Joint Trauma

For 34 years, my academic and clinical interests have primarily centered around whiplash trauma, its understanding and management. I have often heard that the pathology for both acute and chronic whiplash pain are unknown and undiagnosable. It is commonplace to label the pathology of whiplash syndrome as unknown, self limiting, psychometric, secondary gain, biosocial, etc. However, all of this is largely not true.

Perhaps, the most accomplished clinical anatomist of our time is Nikolai Bogduk, MD, PhD, from Australia. Dr. Bogduk is a professor of Pain Medicine at the Universityof Newcastleand the Head of the Department of Clinical Research at the RoyalNewcastleHospitalin Newcastle, Australia. He was the Director of the National Musculoskeletal Medicine Initiative in Australia(from 1997 to 2001) and is currently a member on the Executive Group of the Guidelines for Acute Musculoskeletal Pain in Australia. Dr. Bogduk is on the Editorial Board for many publications including Spine, The Spine Journal, Clinical Biomechanics, Pain Medicine and Cephalalgia.

Dr. Bogduk began researching the anatomical basis of various spinal syndromes 40 years ago (1972). A PubMed search of the National Library of Medicine using “bogduk n” brings up 216 citations (January 10, 2012). Dr. Bogduk has authored 9 books on various aspects of clinical anatomy (the most recent being this year, 2012), and many chapters in others books. Dr. Bogduk has been the single most published person in history on the anatomical basis of acute and chronic whiplash pain syndrome.

The understanding of whiplash biomechanics was forever changed when an experimental study appeared in the journal Spine in November 1997 (1). In this study, Grauer and associates from the Department of Orthopaedics and Rehabilitation at Yale University School of Medicine performed a series of rear-end collisions on human cadavers. Because the subjects in this series were cadavers, exposure to ionizing radiation was moot, allowing the team to view cervical spine dynamics during the collision using cineradiography. This unique method of assessment brought forth the following conclusions and opinions:

1) In the earliest phase of the cervical spine dynamics following a rear-end collision, the cervical spine forms an “S” shaped configuration, with flexion of the upper cervical spine and simultaneous significant hyperextension of the lower cervical spine.

2) The tissue distortion noted during this “S” configuration of the cervical spine was of a magnitude that is injurious.

3) This injurious “S” configuration of the cervical spine occurs very quickly, between 50 – 75 milliseconds following impact.

4) The quickness of this “S” configuration of the cervical spine is shorter than the time required by the stretched muscles to react and to afford meaningful protection of the cervical spine joints. Therefore, the injury is primarily imparted to the joints of the cervical spine.

5) In most cases, this quick injurious “S” configuration of the cervical spine occurs before the head contacts the head restraint, meaning the head restraint often does not offer adequate protection.

Several other cadaver studies confirmed this “S” configuration of the cervical spine in the initial phase of whiplash injury. In 1999, similar cineradiography studies were performed on live human volunteers by Kaneoka and colleagues (2), and the results were the same as those of the cadaver studies. This 1999 live human volunteer study generated this following official (invited) Point of View, published in Spine:

POINT OF VIEW

Nikolai Bogduk,MD, PhD, DSc, FAFRM
Department of Anatomy and Musculoskeletal Medicine
UniversityofNewcastle
NewcastleBone and Joint Institute
RoyalNewcastleHospital
Newcastle,New South Wales,Australia

“The study of Kaneoka et al now fills a critical gap in the story of cervical facet pain. It provides the missing biomechanical link. Their’s is the most significant advance in the biomechanics of whiplash since the pioneering studies of Severy et al in 1955.”

“As a result of this study, we no longer rely on inference or speculation; we have a direct demonstration of the mechanism of injury in whiplash.”

Essentially all articles published regarding whiplash biomechanics since 1997 – 1999 cite these studies that agree the pathology of whiplash primarily occurs during this “S” configuration very early on (50–75 ms) following the collision. As an example, last fall (October 2007), a review article by Schofferman and colleagues (3) titled:

Chronic whiplash and whiplash-associated disorders
An evidence-based approach
Journal of the American Academy of Orthopedic Surgeons
October 2007;15(10):596-606

makes the following comments:

“In a typical rear-end motor vehicle collision, the injury is caused by the abnormal biomechanics of neck motion resulting from the forward and upward motion of the torso while the head lags behind as the result of inertia.”

“Whiplash injury is any structural damage sustained because of the whiplash forces.”

“The forward acceleration of the torso deforms the cervical spine into a nonphysiologic S-shaped curve, with extension developing between the lower segments and flexion developing between the uppermost segments. Most of the whiplash injury occurs during this deformation phase.”

“The cervical facet joint is the most common source of chronic neck pain after whiplash injury, followed by disk pain. Some patients experience pain from both structures.”

“The facet joints are the most common source [more than half of the cases] of chronic neck pain after whiplash injury.”

“Some patients have pain that arises from a disk, and some have a combination of facet joint pain and discogenic pain.”

••••••••••

Importantly, the 1999 live human cineradiography cervical spine biomechanical study by Kaneoka and colleagues (2) showed that the primary injury from whiplash trauma was to the facet joints and to the intervertebral disc. Their article makes the following points:

“The zygapophysial joint is the suspected origin of neck pain after rear-end car collision.”

The facet joint collision that occurs during the first phase of whiplash trauma creates a bending moment. “If this bending moment is large enough, this motion is likely to cause the disruption of the disc from the vertebral rim (rim lesion) or to cause a zygapophysial joint injury.”

“Most whiplash injuries occur during low-speed rear-end collisions and rarely produce morphologic changes such as fracture of the joint. The zygapophysial joint is a synovial joint and has a synovial fold (meniscus), between the articular facets that is innervated with nociceptive receptors. Thus, we hypothesize that facet collisions are likely to impinge on and inflame the synovial folds in the zygapophysial joints, causing neck pain (facet synovial fold impingement syndrome).”

Once again, in the official, invited POINT OF VIEW by Dr. Bogduk of the Kaneoka study, the following comments are found:

“The critical observation is that in whiplash the lower cervical segments undergo sagittal rotation about an abnormally high instantaneous axis of rotation. As a result, there is no translation; there is only rotation. As the vertebra spins, its anterior elements separate from, while the posterior elements crunch into, the vertebra below. This mechanism predicts that the resultant lesions should be tears of the anterior annulus and fractures of the zygapophysial joints or contusions of their meniscoids. These are the very lesions seen at postmortem.”

In 2002, additional evidence for whiplash trauma causing injury to the facet joints and intervertebral disc of the lower cervical spine was presented by Lars Uhrenholt and colleagues from the Instituteof Sports Scienceand Clinical Biomechanics, Universityof Southern Denmark, Odense, Denmark(4). Their study, published in Spine, was titled:

Cervical spine lesions after road traffic accidents:
a systematic review

The authors concluded that occult pathoanatomical lesions in the cervical intervertebral disc and zygapophysial joints were possible in survivors of motor vehicle collisions. This article was also well summarized in the Point Of View from Dr. Nikoli Bogduk, as follows:

Point of View

Nikolai Bogduk, MD

This study has “harvested the best available evidence concerning the possible pathology of whiplash.”

The injuries documented include:

(1) Articular fractures

(2) Intra-articular contusions

(3) Tears of the anterior annulus

The credibility of these injuries is enhanced because different lines of investigation, using totally independent methods, point to the same conclusion. “This constitutes convergent validity.”

“In the case of whiplash, postmortem studies, biomechanics studies, and clinical studies converge.”

“Postmortem studies point to lesions in the zygapophysial joints.”

“Biomechanical studies show how these joints can be injured to produce the lesions seen at mortem.”

“Clinical studies have shown that zygapophysial joint pain is common in patients with chronic neck pain after whiplash.”

“All three lines of investigation point to the same culprit,” the facet joint.

Two years later, in 2004, Pearson and colleagues from the Biomechanics Research Laboratory, Department of Orthopaedics and Rehabilitation, Yale University School of Medicine, published in the journal Spine the most detailed evidence to date showing the biomechanics of facet joint injury during whiplash mechanism (5). Their article is titled:

Facet joint kinematics and injury mechanisms during simulated whiplash

••••••••••

In 1993, Drs. Nikoli Bogduk and Charles Aprill published primary research in the journal Pain (6) pertaining to the sources of chronic neck pain by using both provocation discography and cervical zygapophysial joint blocks. Comments found in their study include:

“Both a symptomatic disc and a symptomatic zygapophysial joint were identified in the same segment in 41% of the patients.”

“Discs alone were symptomatic in only 20% of the sample.”

“Zygapophysial joints were symptomatic but discs were asymptomatic in 23%.”

“Only 17% of the patients had neither a symptomatic disc nor a symptomatic zygapophysial joint at the segments studied.”

Neck muscle injury “does not provide a satisfying model for persistent or chronic neck pain” because extremity muscle injuries heal rapidly, “in a matter of days or weeks.”

Persistent neck pain suggests injury to tissues that heal poorly or slowly, such as the intervertebral disc and the facet joints. “However, painful disorders of these structures are not demonstrable by plain radiography, computed tomography or magnetic resonance images.”

No findings on plain radiography, computed tomography or magnetic resonance images are correlated with pain.

The most frequent finding was “both a symptomatic disc and a symptomatic zygapophysial joint at the same segment,” seen in 41%.

The second most frequent finding was a symptomatic zygapophysial joint, alone, with no disc involvement, which was found in 23%.

“This indicated that 64% of the sample had a symptomatic zygapophysial joint.” [41% + 23% = 64%]

The third most frequent finding was a symptomatic disc alone, with no zygapophysial joint involvement, found at 20%.

This indicated that 61% of the sample had a symptomatic disc.

[41% + 20% = 61%]

“If cervical segments are fully investigated, it emerges that cervical discs are not the most common, primary source of neck pain.”

“A large proportion, if not the majority, of patients with post-traumatic neck pain have symptomatic zygapophysial joints.”

••••••••••

In the following few years, Dr. Bogduk ad colleagues continued to engage in primary research pertaining to the clinical sources of chronic whiplash pain. In 1995, they published a study in the journal Spine titled (7):

The prevalence of chronic cervical
zygapophysial joint pain after whiplash

In this study, the authors note and conclude:

“In a significant proportion of patients with whiplash, chronic, refractory neck pain develops.”

“Painful joints were identified in 54% of the patients.”

“In this population, cervical zygapophysial joint pain was the most common source of chronic neck pain after whiplash.”

The following year in 1996 the same authors publish a follow-up article in Spine titled (8):

Chronic cervical zygapophysial joint pain after whiplash:
A placebo-controlled prevalence study

Their findings and conclusions include:

“Overall, the prevalence of cervical zygapophysial joint pain (C2-C3 or below) was 60%.”

“Cervical zygapophysial joint pain is common among patients with chronic neck pain after whiplash.”

••••••••••

The entire December 1, 2011 supplement of the journal Spine is dedicated to whiplash trauma. The issue contains 27 articles by the world’s foremost authorities on whiplash biomechanics, pathology and outcomes. Importantly, and as appropriately expected, Dr. Bogduk is a co-author for two of the articles and a solo author for one study. Dr. Bogduk’s solo article pertains to the facet joint, and is titled (9):

On Cervical Zygapophysial Joint Pain After Whiplash

In this article, Dr. Bogduk cites 72 references while summarizing the evidence that implicates the cervical zygapophysial joints as the leading source of chronic neck pain after whiplash trauma. He states that the patho-anatomic basis for neck pain after whiplash is not elusive, but rather well documented and well known. Dr. Bogduk notes that there is convergent validity from (1) whiplash postmortem studies, (2) whiplash biomechanics studies, and (3) whiplash clinical studies indicating that the primary source of chronic whiplash pain is injury to the cervical zygapophysial joints. He sumarizes by noting that in whiplash, four convergent lines of evidence “implicate the cervical zygapophysial joints as the leading source of pain in patients with chronic whiplash-associated disorder:”

1) Postmortem studies show that a spectrum of injuries occur in the facet joints in motor vehicle accidents.

2) Biomechanics studies of normal volunteers and of cadavers reveal the mechanisms by which the facet joints sustain injury during whiplash.

3) Whiplash studies in cadavers and laboratory animals have produced facet joints injuries.

4) Clinical studies have shown that facet joint pain is very common among patients with chronic neck pain after whiplash.

•••••

The postmortem studies identified a variety of nonlethal injuries:

Nerve-root lesions
Rim-lesions to the intervertebral discs (the disc is traumatically separated from the cartilaginous end-plate of the vertebral body)
Intraarticular hemorrhages
Fractures of the facet articular cartilage
Fractures of the facet subchondral bone
Fractures of the entire facet articular processes

Importantly, virtually none of these lesions were seen on postmortem radiography. Dr. Bogduk states:

“Medical imaging in vivo may fail to identify lesions that are definitely present at postmortem. Consequently, in the context of whiplash injury, normal radiographs, or even normal magnetic resonance imaging, do not mean that the patient has no lesion.”

•••••

The human biomechanics studies identified these injurious mechanisms:

a) The cervical spine undergoes a “highly abnormal” “S” shaped deformation with extension of the lower cervical spine and flexion of the upper cervical spine.

b) During the extension of the lower cervical spine, the anterior margins of the vertebral bodies are widely separated, resulting in an avulsion of the annulus fibrosus from the vertebral endplate (a rim lesion).

c) Also during the extension of the lower cervical spine the inferior facet articular process chisels into the superior facet articular surface of the vertebra below, allowing for a spectrum of lesions to the facet joints.

The intraarticular meniscoids could be contused or ruptured

Impaction fractures of the articular processes could occur

Cadaver studies during whiplash show that the facet joints undergo compression that exceeds physiological limits and the capsules undergo strains beyond normal limits.

Strains in the annulus fibrosus can exceed normal limits.

Dr. Bogduk states:

“Collectively, these various biomechanics studies, in normal volunteers and in cadavers, predict or produce the same spectrum of lesions as that identified in postmortem studies. In particular, they indicate that the zygapophysial joints can be injured.”

Dr. Bogduk lists the following proven non-lethal pain producing injuries caused by whiplash trauma

Intra-articular Hemorrhage [causes organization, adhesions, fibrosis]

Facet Capsular Tear

Meniscoid Contusion [can result in joint motion block, spasm, torticollis]

Articular Subchondral Fracture [acceleration of cartilage arthritis]

Fracture of the Articular Pillar

Disc Tear or Torn From the Vertebral Rim [acceleration of disc degenerative disease, these injuries do not heal (reattach)]

Overall, Dr. Bogduk indicates that the prevalence of neck pain stemming from a facet joint is just over 50%, indicating the facet joint is a very common source for neck pain. Dr. Bodguk cites 7 studies showing a prevalence of cervical facet joint pain between 36-67%.

Year	Journal	Prevalence
1995	Spine	54%
1996	Spine	60%
2001	Medical Journal ofAustralia	36%
2002	Pain Physician	67%
2007	Journal of Spinal Disorders and Techniques	39%
2008	Pain Medicine	46%
2008	Pain Physician	39%

Dr. Bogduk concludes:

“The zygapophysial joints are the single, most common source of pain in patients with chronic neck pain after whiplash.”

There is an extensive amount of evidence indicating that post-whiplash pain syndrome is attributed to injury to the cervical facet joints; no other explanation for whiplash pain has more evidence.

••••••••••

Dr. Bogduk notes that chronic cervical facet joint pain can be treated with radiofrequency neurotomy (the ablation of the nerves that transmit pain from the injured facet joints). However, he also qualifies the statement with:

a) Radiofrequency Neurotomy only treats cervical facet pain, which afflicts about 50% of those suffering from chronic whiplash pain. The other 50% of chronic whiplash pain sufferers are not amenable to the Radiofrequency Neurotomy procedure.

b) Inclusion criteria for the Radiofrequency Neurotomy procedure requires successful pain relief with diagnostic blocks of the medial branch of the posterior primary rami performed on two separate occasions.

c) Successful Radiofrequency Neurotomy on appropriately selected patients is about 70%, and the pain relief lasts for a medium of about 400 days. This would mean that the procedure works on about 35% of chronic whiplash patients [50% X .7 = 35%] for about 400 days on average. Dr. Bogduk notes that if/when the pain returns, the procedure can be repeated.

d) “Medial branch blocks and radiofrequency neurotomy cannot be performed other than by specially trained, medical practitioners,” and there are very few medical practitioners who are properly trained and qualified to do these procedures. He states:

“Few practitioners around the world are skilled in these procedures; and among those who purport to be skilled, there is no guarantee that they perform the procedures properly.” “The available evidence indicates that good outcomes can only be expected if those guidelines are followed.”

e) Some medical practitioners that claim do to these procedures do not follow the proper guidelines, performing it “irresponsibly if not fraudulently.”

f) Radiofrequency neurotomy outcomes in patients pursuing litigation are about the same as in patients not involved in litigation.

Whiplash injures the facet joint.

The facet joint has nociceptors “R” which are connected to the brain through the medial branches of the posterior primary rami.

If diagnostic anesthetic blocking of the medial branch of the posterior primary rami eliminates pain, it indicates the facet is the source of the pain.

Radiofrequency neurotomy of the facet joint capsules coagulates the neurofiliment proteins, giving 70% of the patients longer relief of their whiplash pain.

This study by Dr. Bogduk reiterates:

Many involved in a whiplash injury develop chronic neck pain.
This chronic whiplash-generated neck pain does not seem to be associated with litigation status.
The primary injury and source of pain in the chronic whiplash patient is the facet joint.
It is highly unlikely that the pain producing facet joint injury, including fractures, are discernable with either radiography or MR imaging.
For facet joint pain to be definitely ruled-in or ruled-out, the patient must undergo, on two separate occasions, medial branch blocks of the posterior primary rami.

Although Dr. Bogduk is advocating radiofrequency neurotomy ablation of the facet joint nerves as the best treatment option in the management of chronic whiplash pain, it should be understood that:

1) only about 50% of chronic whiplash patients are appropriate for this procedure

2) it only works on about 70% of those judged to be appropriate candidates for the technique, and

3) the effective pain relief is for about 400 days

Chiropractic adjusting affects many tissues but primarily the facet joints. There are several studies indicating that chiropractic spinal adjusting is more effective that radiofrequency neurotomy ablation in the treatment of the chronic whiplash patient (10, 11). The Woodward study was 93% effective (10). The Khan study was 74% effective (11). We have reviewed both studies several times before. Consequently, I believe that chiropractic spinal adjusting should be performed on all chronic whiplash patients prior to having the patient undergo medial branch blocks of the posterior primary rami and radiofrequency neurotomy ablation of the facet joints.

OTHER CONCERNS

Radiofrequency ablation of the facet joints not only stops nociception but also stops mechanoreception. Many chiropractors, including myself, and other providers, are concerned that ablation of the mechanoreceptors may adversely affect local neuromuscular reflexes controlling stability and therefore the incidence of future joint degeneration, as well as adversely affecting central summation and central neurological function. These concerns could have critical long-term implications for whiplash patients treated with radiofrequency neurotomy. Consequently, I reiterate that radiofrequency neurotomy should only be performed if Chiropractic and other conservative approaches have not delivered acceptable clinical outcomes.

•••••

Sincerely,

Daniel J. Murphy DC, DABCO

REFERENCES:

1) Grauer JN, Panjabi MM, Cholewicki J, Nibu K, Dvorak J. Whiplash produces an S-shaped curvature of the neck with hyperextension at lower levels. Spine. 1997 Nov 1;22(21):2489-94.

2) Kaneoka K, Ono K, Inami S, Hayashi K. Motion analysis of cervical vertebrae during whiplash loading. Spine. 1999 Apr 15;24(8):763-9.

3) Schofferman J, Bogduk N, Slosar P. Chronic whiplash and whiplash-associated disorders: An evidence-based approach; Journal of the AmericanAcademyofOrthopedic Surgeons; October 2007;15(10):596-606.

4) Uhrenholt L, Grunnet-Nilsson N, Hartvigsen J. Spine. Cervical spine lesions after road traffic accidents: a systematic review; 2002 Sep 1;27(17):1934-41.

5) Pearson AM, Ivancic PC, Ito S, Panjabi MM. Facet joint kinematics and injury mechanisms during simulated whiplash; Spine; 2004 Feb. 15; 29(4):390-7.

6) Bogduk N, Aprill C. On the nature of neck pain, discography and cervical zygapophysial joint blocks; Pain; August 1993;54(2):213-7.

7) Barnsley L, Lord SM, Wallis BJ, Bogduk N. The prevalence of chronic cervical zygapophysial joint pain after whiplash. Spine. 1995 Jan 1;20(1):20-5.

8) Lord SM, Barnsley L, Wallis BJ, Bogduk N. Chronic cervical zygapophysial joint pain after whiplash. A placebo-controlled prevalence study. Spine. 1996 Aug 1;21(15):1737-44.

9) Bogduk N; On Cervical Zygapophysial Joint Pain After Whiplash; Spine

December 1, 2011; Volume 36, Number 25S, pp S194–S199.

10) Woodward MN, Cook JCH, Gargan MF, and Bannister GC. Chiropractic treatment of chronic ‘whiplash’ injuries; Injury; Volume 27, Issue 9, November 1996, pp 643-645.

11) Khan S, Cook J, Gargan M, Bannister G. A symptomatic classification of whiplash injury and the implications for treatment; The Journal of Orthopaedic Medicine 21(1) 1999, 22-25.

January 2012

admin — Tue, 03 Jan 2012 20:07:08 +0000

Osteoarthritis

Another Look

Our government (United States of America) collects and owns what experts consider to be reputable biomedical healthcare literature. This literature is catalogued in a library that is physically located in Bethesda, Maryland. The name of the library is The National Library of Medicine. The biomedical journals of the entire world can be found in our National Library of Medicine.

Our National Library of Medicine has collected and catalogued more than 20 million citations, and thousands more are added every day. One can access this database of citations by using a search engine that is commonly referred to as PubMed (www.pubmed.gov). Anyone with Internet access can use PubMed to search the biomedical contents of our National Library of Medicine by simply typing in any health topic into the search bar such as “whiplash” or “vitamin D” or “fibromyalgia” or thousands of other topics. The literature that is pulled up from searching the National Library of Medicine is always the most technical in the world, meaning that it is geared for health care professional and researchers, not for introductory knowledge that may appeal to lay people (even though anyone can access this information).

•••••

Electrons are negatively charged particles that spin around the nucleus of atoms. The different orbits of these spinning electrons are called shells. The biochemistry and physiology of life is often linked to events occurring with the electrons in the outer shells of atoms. The donation or sharing of these outer shell electrons expedites the efficiency of most human physiological processes.

The spinning electrons like to exist in pairs. Atoms and/or molecules are stable when the outer shell electrons are in even numbers. If something happens to the outer shell electrons (like adding or subtracting an electron) so that an odd number of electrons exist, the atom/molecule becomes unstable, and in general, this is not good. This unstable atom/molecule is called a Free Radical. Free Radicals can damage adjacent atoms/molecules by disrupting their compliment of outer shell electrons, creating deleterious things such as mutations and toxic substances.

The most notorious of the Free Radicals are Oxygen Free Radicals. This is because Oxygen Free Radicals are produced as a normal byproduct of respiration, the creation of ATP energy molecules from glucose and oxygen in the inner membrane of the mitochondria. All of us make these Oxygen Free Radicals continually throughout our life, from birth until death. The only way to stop the production of these Oxygen Free Radicals is to stop breathing.

Healthy people make more ATP Energy than Oxygen Free Radicals. However, the damage caused by Oxygen Free Radicals accumulates throughout our lives. This accumulated damage includes damage to the mitochondrial machinery. As the mitochondria are progressively damaged by Oxygen Free Radicals, they produce less and less ATP Energy and more and more Oxygen Free Radicals, thus a vicious cycle of damage ensues.

This example is that of a relatively healthy person; 95% of the oxygen and glucose is converted into ATP Energy, while 5% is converted into Oxygen Free Radicals:

Oxygen Free Radicals are technically called Reactive Oxygen Species and are commonly abbreviated ROS. When a tissue is damaged by a Free Radical, that tissue is declared to be Oxidized or to have sustained Oxidative Injury or Oxidative Stress.

•••••

One of the best-documented concepts in health care is the Free Radical Theory of Aging. The vicious cycle of,

Mitochondria produce Oxygen Free Radicals

Oxygen Free Radicals damage the mitochondria

(Oxidized mitochondria)

Oxidized mitochondria produce more Oxygen Free Radicals and simultaneously produce less ATP energy, accelerating the aging process

accounts for the deleterious nature of Free Radicals and ageing.

When researching the Free Radical Theory of Aging, using the technical words “Reactive Oxygen Species” is a good way to start. Typing the words “reactive oxygen species” into the PubMed search bar (12/07/11) called up 116,200 articles from the National Library of Medicine. The words “reactive oxygen species AND ageing” in the PubMed search bar produced 7,662 articles. The words “reactive oxygen species AND osteoarthritis” in the PubMed search bar produced 175 articles.

The consensus among these articles is that Free Radical damage is an important contributor to osteoarthritis. A few examples of this include:

In December 2009, the Journal of the Medical Association of Thailand published an article titled (Sutipornpalangkul):

Free Radicals in Primary Knee Osteoarthritis

The abstract of this article includes:

“Free radicals have an important role in the pathogenesis of knee osteoarthritis. Reactive oxygen species (ROS) produced by abnormal chondrocyte metabolism exceeds the physiological buffering capacity and results in oxidative stress. The excessive production of ROS can damage proteins, lipids, nucleic acids, and matrix components. They also serve as important intracellular signaling molecules that amplify the inflammatory response. An understanding of oxidative stress involved in this disease might allow the use of antioxidant therapies in the prevention and/or treatment of knee osteoarthritis.”

In September 2010, the journal Orthopedic Reviews published an article titled (Ziskoven):

Oxidative stress in secondary osteoarthritis:
from cartilage destruction to clinical presentation?

The abstract of this article includes:

“Due to an increasing life expectance, osteoarthritis (OA) is one of the most common chronic diseases.”

“The dysbalance between free radical burden and cellular scavenging mechanisms defined as oxidative stress is a relevant part of OA pathogenesis.”

“Free radical exposure is known to promote cellular senescence and apoptosis. Radical oxygen species (ROS) involvement in inflammation, fibrosis control and pain nociception has been proven. The data from literature indicates a link between free radical burden and OA pathogenesis mediating local tissue reactions between the joint compartments. Hence, oxidative stress is likely not only to promote cartilage destruction but also to be involved in inflammative transformation, promoting the transition from clinically silent cartilage destruction to apparent OA.”

“ROS induced by exogenous factors such as overload, trauma, local intra-articular lesion and consecutive synovial inflammation cause cartilage degradation. In the affected joint, free radicals mediate disease progression. The interrelationship between oxidative stress and OA etiology might provide a novel approach to the comprehension and therefore modification of disease progression and symptom control.”

In September 2011, the journal Current Opinion in Rheumatology published an article titled (Loeser):

Aging and Osteoarthritis

The abstract of this article includes:

“Osteoarthritis is strongly linked to aging but the mechanisms for this link are incompletely understood.”

“Cell stress or cell damage response contributes to chronic inflammation that promotes age-related diseases. This cellular response results in the senescence-associated secretory phenotype which has many of the characteristics of an osteoarthritic chondrocyte in terms of the cytokines, chemokines, and proteases produced. Oxidative stress can promote cell senescence and studies have shown a role for oxidative stress in altering cell signaling pathways in chondrocytes that can disrupt the response to growth factors. Mitochondria are an important source of reactive oxygen species and studies continue to support a role for the mitochondria in osteoarthritis, including work suggesting changes in energy production.”

My favorite article pertaining to osteoarthritis and free radical damage was published in the American Journal of Physical Medicine and Rehabilitation in 2006, titled (Garstang):

Osteoarthritis
Epidemiology, Risk Factors, and Pathophysiology

The authors, Susan V Garstang, MD and Todd P Stitik, MD, are from theUniversityofMedicineand Dentistry of New Jersey. In this article, Drs. Garstang and Stitik note that osteoarthritis is:

“the clinical and pathologic outcome of a range of disorders that results in structural and functional failure of synovial joints. Osteoarthritis occurs when the dynamic equilibrium between the breakdown and repair of joint tissues is overwhelmed.”

Drs. Garstang and Stitik note that osteoarthritis is the most prevalent form of arthritis and a major cause of disability in people aged 65 and older. Osteoarthritis affects the majority of adults over age 55.

Garstang and Stitik note that the incidence of osteoarthritis is influenced by both systemic and local factors. Important to this discussion, Drs. Garstang and Stitik note that pertaining to systemic factors, that there is evidence that osteoarthritis is linked to free radicals, and that high dietary antioxidants (especially vitamins C and D) are protective against the development of osteoarthritis. They state: “Chondrocyte senescence is thought to be the result of chronic oxidative stress.”

Garstang and Stitik note that if elevated oxidative stress systemic factors are present, the joints are vulnerable, and thus local biomechanical factors will have more of an impact on joint degeneration and osteoarthritis. Historically, traditional chiropractic patient management emphasizes the treatment and resolution of the local biomechanical factors which are undoubtedly factors in the genesis and progression of joint osteoarthritis. Considering the impact of Free Radicals and Oxidative Stress as systemic influences on joint degeneration and osteoarthritis is an important addition to the management of these patients.

•••••

Turning our discussion to Free Radicals and Oxidative Stress, an authoritative text on the subject is the book:

Oxidative Stress, Disease and Cancer

This book is edited by Keshav K. Singh of the Roswell Park Cancer Institute inNew York. This 2006 reference book has more than 1,000 pages of information.

A central theme of this book is that free radicals and inflammation are intimately linked: free radicals drive inflammation and inflammation drives free radicals. This book lists six (6) primary drivers of the production of Reactive Oxygen Species (ROS). They are:

1) The arachidonic acid cascade to inflammatory prostaglandins and leukotrienes.

2) The glutamate cascade.

3) Low antioxidant defenses.

4) Excessively high metabolic activities.

5) High levels of metal toxins, such as iron and copper.

6) Increased production and release of catecholamines.

Discussing aspects of each of these six drivers of Reactive Oxygen Species is relevant to his discussion:

1) The arachidonic acid cascade to inflammatory prostaglandins and leukotrienes.

Arachidonic acid is a 20-carbon long omega-6 fatty acid. It is a metabolic precursor to the powerfully pro-inflammatory eicosanoid prostaglandin (PGE2) and leukotriene (LTB4) hormones. Dr. Singh describes how these pro-inflammatory eicosanoid arachidonic acid derivatives increase the production Oxygen Free Radicals which would systemically contribute to joint osteoarthritis.

The biochemical anti-inflammatory nemesis of arachidonic acid is the omega-3 fatty acid eicosapentaenoic acid. Eicosapentaenoic acid produces anti-inflammatory eicosanoid hormones, stopping cartilage degradation and osteoarthritis (Curtis).

Cyclo-oxygenase (COX)/Lipo-oxygenase (LOX) Pathways

The 2006 book Weiner’s Pain Management, A Practical Guide for Clinicians (Boswell) notes that Paleolithic humans evolved with a ratio of omega-6/omega-3 of about 1/1, but that contemporary ratios are often as high as 25/1. This ratio is pro-inflammatory and drives the production of Free Radicals, leading to osteoarthritis.

2)The glutamate cascade.

Glutamic acid (glutamate) is an amino acid. It is also the primary excitatory neurotransmitter for the nervous system. Recently retired neurosurgeon Russell Blaylock, MD, describes in his 1997 book Excitotoxins, The Taste That Kills, how glutamate excites pain, excites the production of Free Radicals, and also excites taste. As a consequence of its taste enhancing qualities, glutamate is added to nearly all processed and packaged foods. It is classically labeled as monosodium glutamate or MSG, but Dr. Blaylock notes that manufacturers usually change the name to literally a few dozen different words, such as hydrolyzed vegetable protein. A more complete list of these other names appears in the back of Dr. Blaylock’s book, and I have included a list from the webpage www.truthinlabeling.org at the end of this article.

There are studies on chronic pain patients who abstain from all sources of free glutamic acid for four months becoming completely cured of their pain complaints (Smith).

Once again, Dr. Singh describes how the glutamate cascade increases the production of Oxygen Free Radicals which would systemically contribute to joint osteoarthritis.

3)Low antioxidant defenses.

Free Radicals damage many tissues, including joint cartilage, leading to and accelerating osteoarthritis. Yet, these Free Radicals can be neutralized prior to causing tissue damage. Molecules termed Antioxidants do this neutralization. Our exogenous antioxidant defenses are dependent upon the quality of our habitual eating habits. Fruits and vegetables are particularly rich in antioxidants. Their ability to neutralize Free Radicals could reduce the oxidative damage to the joint, preventing or minimizing osteoarthritis.

Sadly, a 2009 study by the United States Centers for Disease Control (Anderson) found that only 14% of US adults and 9.5% of high school students consumed the daily-recommended portion of fruits and vegetables. This suggests that anti-oxidant supplementation may be necessary for a large portion of theUSpopulation.

4)Excessively high metabolic activities.

Although most Americans do not exercise regularly, most Americans do believe that exercise is good for health. However, exercise is a paradox.

Aerobics began in 1968 by cardiologist Kenneth Cooper, MD. Yet, in 1994, Dr. Cooper wrote the book Dr. Kenneth Cooper’s Antioxidant Revolution. In this book, Dr. Cooper notes that excessive exercise produces excessive Free Radicals, damaging tissues, and the greater the exercise level the greater the need for supplemental anti-oxidants. His book notes:

Free radicals—or unstable oxygen molecules, also known as reactive oxygen species—are implicated in more than 50 diseases including cancer, heart disease, premature aging, cataracts and AIDS.

Free radicals are central actors in most human disease.

Too much exercise may actually increase the risk of developing medical problems.

I strongly recommend the use of antioxidants on a regular basis, regardless of the level of physical activity.

“The more the body is exposed to free radicals, the shorter the life span will be.”

The body’s increased need for oxygen during exercise increases the production of free radicals which oxidize the fats in muscle cell membranes, making muscle cells susceptible to aging and other damage.

“To build strong protection against free radicals, you need to take far larger amounts of antioxidants than the official RDA provides.”

The degenerative changes associated with aging are caused by an accumulation of free radical damage.

An antioxidant is any substance that protects tissues from oxidative damage.

“It is absolutely necessary that you fortify your body’s natural defenses with exogenous antioxidants.”

The bottom line is that excessive exercise increases the genesis of destructive Oxygen Free Radicals, and this problem is magnified if one has poor anti-oxidant defenses.

5) High levels of metal toxins, such as iron and copper.

Excessive metal ions are toxic to our bodies because they increase the production of Free Radicals. The sources of these toxic metals are too many to list (Cranor). Although complete avoidance is impossible, common sense and knowledge can reduce our exposures to metal toxins, reduce the genesis of Oxygen Free Radicals, and reduce their impact on our bodies, including osteoarthritis.

Some of these common sense and knowledge strategies include:

Arsenic in chicken (The Meat You Eat, Midkiff, 2004)

Mercury in fish (Diagnosis Mercury, Jane Hightower, 2009)

Copper in municipal water and in supplements (Brewer, Journal of theAmericanCollegeof Nutrition, 2009)

Strategies to reduce adverse toxic metal ions include avoidance and detoxification (briefly described below).

6)Increased production and release of catecholamines.

Catecholamines are our stress hormones such as epinephrine and norepinephrine. Dr. Singh describes how the chronic increase production and release of catecholamines drives the production of Oxygen Free Radicals.

In 1953, Leonard Hayflick, PhD, anatomy professor at the Universityof California, San Francisco, discovered that human cells divided about 50 times, and then die. This is known as the Hayflick limit. Dr. Hayflick continues to research and publish on human aging and longevity.

About 30 years ago, scientists discovered the reason for the Hayflick limit was telomeres. Telomeres are short caps of DNA on the ends of chromosomes. Each time the cell divides, the telomere shortens a little. When most of the telomere disappears, the cell dies. Consequently, telomere length has been proposed as a marker of biological aging.

In 2004, the Proceedings of the National Academy of Sciences of theUnited States of America(Epel) published a study indication that chronic stress significantly shortens the telomeres. Elizabeth Blackburn, the second author of the study, was awarded the 2009 Nobel Prize in medicine/physiology for her work on telomeres.

In 2009, a study published in the American Journal of Clinical Nutrition noted that daily supplementation with a quality antioxidant multi-vitamin/mineral resulted in significantly longer telomeres (Xu). This suggests that quality antioxidant multi-vitamin/mineral supplementation counteracts the effects of chronic stress and catecholamines.

In 2010, a study published in the Journal of the American Medical Association noted that omega-3 fatty acid consumption also resulted in significantly longer telomeres (Farzaneh-Far). This is consistent with the arachidonic acid cascade from #1 above, suggesting that the anti-inflammatory benefit of omega-3 fatty acids also counteracts the effects of chronic stress and catecholamines.

•••••

Summary and Conclusions

The core of chiropractic management of patients suffering from osteoarthritis will continue to emphasize mechanical aspects of the condition. This includes addressing problems with articular alignment, problems with motion/movement patterns, and problems with joint mechanoreception/proprioception.

However, the information presented here indicates that patients with these joint mechanical problems have greater vulnerability to develop osteoarthritis in the presence of increased Oxidative Stress. Following the lead of Singh, our total management of these patients should include approaches to minimize the generation of Reactive Oxygen Species and its consequent Oxidative Stress. These strategies would include:

Balancing the omega-6/omega-3 fatty acid ratio through diet or supplementation.

Minimizing dietary consumption of glutamate (MSG) from processed and packaged foods. This would include becoming familiar with the many hidden names for free glutamic acid on food labeling (see the list at the end of this article from www.truthinlabeling.org).

Eat a minimum of 5 servings of fruits and vegetables daily (2 fruits, 3 vegetables. Use a quality anti-oxidant multi-vitamin/mineral supplement daily (just be sure that it has no more than 100 micrograms of copper).

Do not over exercise. Regular moderate exercise is good and acceptable. The more one exercises, the more one needs to rely on anti-oxidant supplements.

Avoid well-published sources of metal ion toxins, such as some fish (mercury), chicken (arsenic), municipal water (copper), and many multi-vitamin/mineral supplements (copper). Read the book Legally Poisoned, How the Law Puts Us at Risk of Toxicants by Carl Cranor, 2011.

Detoxify by elevating levels of glutathione and using infra-red saunas. Read Glutathione, Your Body’s Most Powerful Healing Agent by Jimmy Gutman, MD, 2008. Read Detoxify or Die by Sherry Rodgers, MD, 2002.

Minimize both physical and emotional stress.

Sincerely,
Daniel J. Murphy DC, DABCO

REFERENCES:

Sutipornpalangkul W, Morales NP, Harnroongroj T; Free radicals in primary knee osteoarthritis; Journal of the Medical Association of Thailand; December 2009 Dec; Vol. 92; Supplemental 6:S268-74.

Ziskoven C, Jager N, Zilkens C, Bloch W, Brixius K, Krauspe R; Oxidative stress in secondary osteoarthritis: from cartilage destruction to clinical presentation? Orthopedic Reviews; September 23, 2010;Vol. 2; No. 2; pp. e23.

Loeser RF; Aging and osteoarthritis; Current Opinion in Rheumatology; September 2011; Vol. 32; No. 5; PP. 492-496.

Garstang SV, Stitik, TP; Osteoarthritis: Epidemiology, Risk Factors, and Pathophysiology; American Journal of Physical Medicine and Rehabilitation; November 2006, Vol. 85, No. 11, pp. S2-S11.

Singh KK; Oxidative Stress, Disease and Cancer;ImperialCollege Press; 2006.

Curtis CL, Rees SG, Little CB, Flannery CR, CHughes CE, Wilson C, Dent CM, Otterness IG, Harwood JL, Caterson B; Pathologic indicators of degradation and inflammation in human osteoarthritic cartilage are abrogated by exposure to n-3 fatty acids; Arthritis & Rheumatism; Volume 46, Issue 6, 2002, pp 1544-1553.

Boswell M and Cole BE; Weiner’s Pain Management; A Practical Guide for Clinicians; American Academy of Pain Management; Seventh Edition, 2006, pp.584-585.

Blaylock R; Excitotoxins, The Taste That Kills, Health Press, 1997.

Smith JD, Terpening CM, Schmidt SOF, Gums JG; Relief of Fibromyalgia Symptoms Following Discontinuation of Dietary Excitotoxins; The Annals of Pharmacotherapy: Vol. 35, No. 6, pp. 702–706; June 2001.

AndersonL; US Diets Fall Short on Fruit, Vegetables;USAToday; September 30, 2009.

Cooper K; Dr. Kenneth Cooper’s Antioxidant Revolution; Thomas Nelson Publishers; 1994.

Midkiff K; The Meat You Eat: How Corporate Farming Has Endangered America’s Food Supply;St. Martin’s Press, 2004

Hightower J; Diagnosis Mercury: Money, Politics, and Poison;Island Press, 2009.

Cranor C; Legally Poisoned, How the law Puts Us at Risk of Toxicants; Harvard University Press; 2011.

Brewer GJ; The Risks of Copper Toxicity Contributing to Cognitive Decline in the Aging Population and to Alzheimer’s Disease; Journal of the American College of Nutrition; June 2009, Vol. 28. No. 3, pp. 238-242.

Epel ES, Blackburn EH, Lin J, Dhabhar FS, Alder NE, Morrow JD, Cawthon RM; Accelerated telomere shortening in response to life stress; Proceedings of the National Academy of Sciences of the United States of America (PNAS); December 7, 2004, Vol. 101, No. 49 17312-17315.

Qun Xu, Christine G Parks, Lisa A DeRoo, Richard M Cawthon, Dale P Sandler and Honglei Chen; Multivitamin use and telomere length in women; American Journal of Clinical Nutrition; Vol. 89, No. 6, 1857-1863, June 2009, pp. 1857-1863.

Ramin Farzaneh-Far, MD, Jue Lin, PhD, Elissa S. Epel, PhD, William S. Harris, PhD, Elizabeth H. Blackburn, PhD, and Mary A. Whooley, MD; Association of Marine Omega-3 Fatty Acid Levels With Telomeric Aging in Patients With Coronary Heart Disease; Journal of the American Medical Association; January 20, 2010; Vol. 303 No. 3.

www.truthinlabeling.org

HIDDEN SOURCES OF PROCESSED FREE GLUTAMIC ACID (MSG)

Autolyzed, hydrolyzed, glutamate, glutamic acid, hydrolyzed, autolyzed

NAMES OF INGREDIENTS THAT CONTAIN ENOUGH MSG TO SERVE AS COMMON MSG-REACTION TRIGGERS

These ALWAYS contain MSG

GlutamateGlutamic acid

Gelatin

Monosodium glutamate

Calcium caseinate

Textured protein

Monopotassium glutamateSodium caseinate

Yeast nutrient

Yeast extract

Yeast food

Autolyzed yeast

Hydrolyzed corn glutenHydrolyzed protein (any protein that is hydrolyzed)

These OFTEN contain MSG or create MSG during processing

CarrageenanMaltodextrin

Malt extract

Natural pork flavoring

Citric acid

Malt flavoring

Bouillon and Broth

Natural chicken flavoring

Soy protein

Soy protein isolate

Anything fermented

Whey proteinNatural beef flavoring

Ultra-pasteurized

Soy sauce

Stock Barley malt

Soy sauce extract

Whey protein concentrate

Pectin

Natural flavor & flavoring

Protease

Soy protein concentrate Whey protein isolate

Anything enzyme modified

Enzymes Anything protein fortified Flavors(s) & Flavoring(s)

Enzymes anything Seasonings (the word “seasonings”)

The new game is to label hydrolyzed proteins as pea protein, whey protein, corn protein, etc.

If a pea, for example, were whole, it would be identified as a pea.

Calling an ingredient pea protein indicates that the pea has been hydrolyzed, at least in part, and that processed free glutamic acid (MSG) is present.

Relatively new to the list are wheat protein and soy protein.

December 2011

admin — Thu, 01 Dec 2011 21:58:02 +0000

Chronic Pain Syndrome And Vitamin D

Humans evolved outdoors, in the sunshine. Exposure to the sun’s ultraviolet radiation produces a hormone known as “vitamin D”. Vitamin D is critical for human health. The nucleus of all of our cells have vitamin D receptors. There is evidence that vitamin D influences the expression of about 10% of human genes.With very rare exceptions, humans cannot achieve optimal levels of vitamin D through diet alone. Although some foods are fortified with vitamin D, consumption of large amounts of such foods will not achieve optimal levels. To achieve and maintain optimal levels of vitamin D, we must either use vitamin D supplements or use the sun.The sun showers onto earth a large range of radiation, including ultraviolet radiation (UV). UV radiation has three wavelengths, as follows:Ultraviolet A (UVA): 320-400 nm

UVA has the longest wavelength and therefore it penetrates deepest into the skin. The most superficial layer of skin cells is the squamous cells. Deeper to the squamous cells are the basal cells. Below the basal cells are the melanocytes. Because UVA penetrates deepest into the skin, it is the primary UV influence on the melanocytes. Melanocytes produce the dark colored skin pigment melanin. This means that it is UVA that is primarily responsible for skin tanning. Sadly, damage to these same melanocytes increases the risk of the deadly skin cancer melanoma. UVA radiation is also primarily responsible for skin wrinkles.Ultraviolet B (UVB): 280-319 nm

UVB should be subcategorized: 280-289 nm and 290-319 nm

280-289 nm UVB radiation is absorbed by the atmosphere and therefore does not influence human physiology, neither positively nor negatively.

290-319 UV radiation is most important. This range of UVB is primarily responsible for burning of the skin with excess sun exposure. Because of its shorter wavelength (as compared to UVA), it is less likely to affect the deeper melanocytes, and therefore is less associated with deadly melanoma. Older sunscreens (UVB blockers only) and contemporary non-broad-spectrum sunscreens (UVB and UVA blockers) only blocked the skin burning UVB radiation, allowing the user to spend more time in the sun without burning. Ironically, this increased the sunscreen user’s exposure to the dangerous wrinkle and melanoma producing UVA radiation.

To add to the irony, it is UVB radiation in the 290-319 nm wavelength that starts the production of vitamin D, as detailed below.Consequently, older sunscreens (UVB blockers only) reduced skin burning, reduce the skin production of vitamin D, increase skin wrinkles, and increase deadly melanomas.Ultraviolet C (UVC): 200-280 nm

UVC has the shortest wavelength and therefore it does not penetrate well. In fact, it is unable to penetrate the earth’s atmosphere, where it is 100% absorbed.

•••••

James Dowd, MD, is an Associate Professor of Medicine atMichiganStateUniversity. He is also the founder and director of both the Arthritis Institute of Michigan and theMichiganArthritisResearchCenter. He is board certified in internal medicine, adult rheumatology and pediatric rheumatology.In 2008, Dr. Dowd published a book titled The Vitamin D Cure: Five Steps to Heal Your Pain and Improve Your Mood.Dr. Down states that the optimal level of vitamin D is between 50-70 ng/ml.

PAIN

In his book, Dr. Dowd states:“Research tells us that a lack of vitamin D makes us ache. Symptoms that point to vitamin D deficiency are muscle spasms, bone pain, and joint pain.”

“Doctors often mistake vitamin D deficiencies for fibromyalgia, rheumatoid arthritis, and lupus.”

“Because I’m a rheumatologist, people come to me because they want solutions for the pain they’re experiencing in their joints, tendons, ligaments, muscles, and bones. They typically have at least one disease involving muscles, ligaments, joints, and bones, but all of the aches and pains they have are actually connected to their vitamin D levels and what they eat.”Dr. Dowd explains how joint cartilage integrity is dependent upon the quality of the bone the cartilage sits upon, stating:“The bone that lies under the joint cartilage keeps the cartilage stable, functioning, and durable.” “You will speed up the rate of your cartilage breaking down when anything destabilizes the bone below the cartilage, such as poor bone development or increased bone turnover caused by vitamin D deficiency.”

Dr. Dowd notes that there is a 2-3 fold faster rate of osteoarthritis progression in those with the lowest 20% of vitamin D levels compared to those with the highest levels.Dr. Dowd notes that adequate vitamin D supplementation can eliminate chronic back pain symptoms in nearly all patients, stating:“Those who took vitamin D supplements saw dramatic resolution of pain, muscle fatigue and muscle cramps.”

MAGNESIUM

Dr. Dowd emphasizes that there is an important relationship between vitamin D and magnesium, stating:1) Magnesium is critical for one’s body to produce the active form of vitamin D.2) The receptor that vitamin D uses in the nuclear membrane is poorly expressed when one is magnesium deficient.3) Magnesium is required for vitamin D to function properly.Dr. Dowd further explains that magnesium is low when the body becomes acidic. He notes that the two main causes of an acidic body are the consumption of grains and dairy products, so he discourages both. He states that the most abundant and absorbable source for magnesium is the consumption of green leafy vegetables.

•••••

The world’s leading authority on vitamin D is Michael F. Holick, PhD, MD. Dr. Holick is a professor atBostonUniversityMedicalCenterand the director of the university’s General Clinical Research Unit, Bone Health Clinic, and the Heliotherapy, Light, and Skin Research Laboratory. A search of the National Library of Medicine

using the PubMed search engine identified 345 articles using the key words “holick mf AND vitamin d”.Dr. Holick is the discoverer of the active form of vitamin D (1,25, dihydroxy vitamin D). In his 2010 book titled The Vitamin D Solution; A 3-Step Strategy to Cure Our Most Common Health Problems, Dr. Holick details these steps to the formation of the active form of vitamin D:

STEP #1

Our skin cells contain a molecule called

7-dehydrocholesterol = provitamin D3

which absorbs ultraviolet light B (UVB, wavelength 290-319 nm)

STEP #2

The absorption of UVB by provitamin D3

produces

pre-vitamin D3

within the skin cells

STEP #3

Our body heat

converts

pre-vitamin D3

into

vitamin D3

within the skin cell

(this is the same molecule as supplemental vitamin D3)

STEP #4

Vitamin D3

exits the skin cell into the blood stream

and

travels to the liver

where

25-hydroxy vitamin D (calcidrol) is produced

STEP #5

25-hydroxy vitamin D

leaves the liver

into the blood stream

to the kidney

STEP #6

The kidney makes the active form of vitamin D

1, 25 dihydroxy vitamin D

(this is the active form of vitamin D that was discovered by Dr. Holick)

STEP #7

This active form of vitamin D (1, 25 dihydroxy vitamin D)

circulates throughout the body

binding to receptors in the nucleus of the cell

influencing gene expression

Dr. Holick discusses the following FACTSpertaining to vitamin D:1) Humans evolved in a manner as to be dependent upon sunshine for life and health.2) There has been a 22% reduction of vitamin D levels in theUSpopulation in the last 10 years.3) In theUnited Statesvitamin D insufficiency occurs in:

70% of Whites
90% of Hispanics
97% of Blacks

4) The activated form of vitamin D that is found in your blood is produced in the kidneys. However, some other tissues also make the activated form of vitamin D. These include the prostate, breast, lungs, colon and brain. The activated vitamin D formed in these tissues does not enter the blood stream, but remains in those specific tissues.5) “You could easily consume 5,000 IU of vitamin D a day, probably forever,” without overdosing.6) The assay for 25-vitamin D is the most ordered assay in theUnited States. This is the form of vitamin D that exists after the liver but before the kidney.7) It is more difficult to synthesize the active form of vitamin D as one ages. A 70-year old person is 75% less efficient in synthesizing vitamin D as compared to a 20-year old person.8) Neither calcium levels nor activated vitamin D levels (1, 25 dihydroxy vitamin D) levels are indicative of one being vitamin D deficient or not. The only acceptable measure for vitamin D deficiency is 25-vitamin D (made in the liver). Dr. Holick states:

“Do not accept any other marker

no matter what your doctor tells you.”

Dr. Holick discusses the following MYTHS pertaining to vitamin D:1) It is a myth that one can wash vitamin D off from the skin shortly after being in the sun. Dr. Holick says this is not true because vitamin D3 is actually produced inside the skin cell itself, and therefore cannot be washed off.2) Vitamin D2 does not work or is inferior to vitamin D3. Dr. Holick says it is now proven and understood that vitamin D2 works just as well as vitamin D3.3) One can obtain adequate activated vitamin D from eating a good diet. Dr. Holick disagrees with this. He is adamant that one can only achieve adequate levels of vitamin D by being exposed to sufficient sunshine or by supplementation. He further notes that one cannot obtain optimal levels of vitamin D by consuming vitamin D fortified foods or by taking a multiple vitamin supplement, as the levels of vitamin D are too low.

PAIN

In 2007, Dr. Sota Omoigui states:“The origin of all pain is inflammation and the inflammatory response.”

“Irrespective of the type of pain, whether it is acute or chronic pain, peripheral or central pain, nociceptive or neuropathic pain, the underlying origin is inflammation and the inflammatory response.”

“Activation of pain receptors, transmission and modulation of pain signals, neuroplasticity and central sensitization are all one continuum of inflammation and the inflammatory response.”

“Irrespective of the characteristic of the pain, whether it is sharp, dull, aching, burning, stabbing, numbing or tingling, all pain arises from inflammation and the inflammatory response.”Dr. Holick details how vitamin D has substantial anti-inflammatory properties.

•••••

Dr. Holick notes that osteomalacia is a known widespread chronic pain syndrome that is caused by vitamin D deficiency. Dr. Holick states:“Osteomalacia is characterized by vague but often intense bone and muscle aches and is frequently misdiagnosed as fibromyalgia, chronic fatigue syndrome, or arthritis.”

Dr. Holick estimates that 40 – 60% of those diagnosed with fibromyalgia or chronic fatigue syndrome are actually suffering from osteomalacia subsequent to a massive vitamin D deficiency.Dr. Holick notes that when a patient has a deficiency of vitamin D, there also exists a deficiency of calcium mineralization in the bones. Poorly mineralized bones consist of a “Jell-O-like” collagen matrix that expands with pressure, abnormally stretching the highly innervated periosteal coverings. The result is a throbbing, aching bone pain. Dr. Holick states:“When people are sitting with aches in their hips or lying in bed with throbbing aches in their bones, it can be very hard for physicians to immediately think of vitamin D deficiency. But often that’s exactly what’s causing the problem.”

•••••

Dr. Holick notes that 93% of those suffering from nonspecific muscular and skeletal aches and pains are shown to be vitamin D deficient.

RECENT SUPPORTIVE STUDIES

In 2009, Gerry Schwalfenberg, MD from the Department of Family Medicine, University of Alberta, Canada, published an article in the Journal of the American Board of Family Medicine, titled:

Improvement of Chronic Back Pain or

Failed Back Surgery with Vitamin D Repletion: A Case Series

In this study, Dr. Schwalfenberg describes 6 cases of improvement/resolution of chronic back pain or failed back surgery after vitamin D repletion in a Canadian family practice. He notes that vitamin D insufficiency is common; repletion of vitamin D to normal levels in patients who have chronic low back pain or have had failed back surgery may improve quality of life or, in some cases, result in complete resolution of symptoms. In this report, there were 4 patients who had chronic back pain for more than a year and 2 patients who suffered for more than 3 years from failed back surgery.In this study, Dr. Schwalfenberg makes the following key points:“Back pain is the most common neurological complaint in North America, second only to headache.”

“Low back pain (LBP) and proximal myopathy are common symptoms of vitamin D deficiency and osteomalacia.”

“Vitamin D is required for the differentiation, proliferation, and maturation of cartilage cells and for the production of proteoglycan synthesis in articular chondrocytes.”

”Patients who have chronic, nonspecific LBP or have had failed back surgery may have an underlying vitamin D insufficiency/deficiency.”

“All patients had tried various pain treatments, including physiotherapy, visiting a chiropractor, acupuncture, or visit to a pain management clinic, all without much benefit.”

“Repletion of inadequate vitamin D levels demonstrated significant improvement or complete resolution of chronic LBP symptoms in these patients.”

Physicians should have a high index of suspicion for low vitamin D levels in patients with LBP.

“The patients in this study who responded best used between 4000 and 5000 IU of vitamin D3/day.”

“This case series supports information that has recently become apparent in the literature about vitamin D deficiency and its influence on back pain, muscle pain, and failed back surgery. Doses in the range of 4000 to 5000 IU of vitamin D3/day may be needed for an adequate response.”

•••••

In 2009, (Straube) a study was published in the journal Pain, titled:

Vitamin D and Chronic Pain

The authors reviewed 22 studies that indicated a strong association between vitamin D deficiency and chronic pain.

•••••

In 2010, JoAnn Manson, MD from the Division of Preventive Medicine, Brigham and Women’s Hospital, HarvardMedicalSchool, published an article in the journal Metabolism, titled:

Pain: sex differences and implications for treatment

In this study, Dr. Manson found that women have a higher prevalence than men of several clinical pain conditions and of inflammation-mediated disorders. Given the important role of inflammation in mediating pain, nutritional factors that modulate the inflammatory response offer a promising and exciting new avenue for the prevention and treatment of chronic pain disorders. Of particular interest is the potential role of moderate- to high-dose vitamin D and omega-3 fatty acid supplements, both of which have powerful anti-inflammatory effects. These nutritional interventions, which influence cytokine, leukotriene, and prostaglandin pathways, may be of particular benefit to women due to their higher prevalence of inflammatory chronic pain disorders.In this study, Dr. Manson makes the following key points:Inflammation increases the incidence of pain. Both vitamin D and omega-3 fatty acids “have powerful anti-inflammatory effects.”

“Women tend to have a heightened inflammatory response compared with men. This enhanced inflammatory response may contribute to the substantially higher risk of painful inflammatory autoimmune conditions in women compared with men, including rheumatoid arthritis, lupus and other collagen vascular disorders, and osteoarthritis.”

Two very promising nutritional interventions for pain management are moderate- to high-dose vitamin D and the marine omega-3 fatty acids (eicosapentaenoic acid + docosahexaenoic acid).

Vitamin D and omega-3 fatty acids “reduce levels of circulating pro-inflammatory cytokines, decrease chronic joint pain, and may reduce the risk of autoimmune diseases.”

“Vitamin D, in addition to its role in calcium homeostasis, has powerful effects on the immune system, inhibiting proinflammatory cytokines such as interleukin-6 and tumor necrosis factor–alpha and reducing C-reactive protein.”

Vitamin D deficiency increases chronic widespread pain and/or fibromyalgia, especially in women.

A high level of vitamin D reduces knee and hip osteoarthritis and pain.

Given the important role of inflammation and cytokines in mediating and modulating pain, there is a “promising role of moderate- to high-dose vitamin D and omega-3 fatty acid supplementation in preventing and treating inflammation and chronic pain disorders. These nutritional interventions may be of particular benefit to women due to their higher prevalence of inflammatory chronic pain disorders.”

•••••

In October 2010, (Heidari) a study was published in the journal International Journal of Rheumatic Disease, titled:

Association between nonspecific

skeletal pain and vitamin D deficiency

The authors detail the evidence on how deficiency of vitamin D is reported in patients in many types of musculoskeletal pain. Their study evaluated 276 chronic skeletal pain sufferers and 202 control subjects to add to the evidence that vitamin D deficiency is associated with chronic nonspecific skeletal pain.

•••••

In November 2010 (Bhatty) a study published in the journal Journal of the Pakistan Medical Association, titled:

Vitamin D Deficiency in Fibromyalgia

The authors assessed 40 female patients diagnosed with fibromyalgia fromKarachi,Pakistan. They found that 100% of these woman had suboptimal levels of vitamin D. Specifically, they found that 80% had vitamin deficiency (averaging about 15 ng/ml) and 20% had vitamin D insufficiency (below 30 ng/ml). The authors concluded that vitamin D deficiency is frequently seen in patients with fibromyalgia and nonspecific musculoskeletal pain syndromes.

•••••

In April 2011, (Arnson) an editorial appeared in the journal Israeli Medical Association Journal, titled:

Is Vitamin D a New Therapeutic Agent in

Auto-inflammatory and Pain Syndromes?

The authors note that “hypovitaminosis D is a worldwide epidemic, due to insufficient intake and inadequate sunlight exposure,” estimating that worldwide 40-90% of older persons are vitamin insufficient. They recommend that all chronic pain persons be assessed for vitamin D levels.

•••••

In September 2011, Tague and colleagues from the University of Kansas Medical Center published a study in the Journal of Neuroscience, titled:

Vitamin D deficiency Promotes Skeletal

Muscle Hypersensitivity and Sensory Hyperinnervation

The authors note that “musculoskeletal pain affects nearly half of all adults and most of them are vitamin D deficient.” They also know that nociceptors express vitamin D receptors, and that a lack of vitamin D can cause nociceptive hyperinnervation of skeletal muscles, contributing to muscular hypersensitivity and pain.

•••••

In 2011, the editorial of the Scandinavian Journal of Primary Health Care (Kragstrup) is titled:

Vitamin D Supplementation for Patients with Chronic Pain

In this editorial Dr. Kragstrup reviews the epidemiological studies that link low levels of vitamin D to chronic pain. He advocates both testing for and supplementing of vitamin D in chronic pain sufferers.

•••••

Also in 2010, Joseph Pizzorno, ND, the Editor in Chief of the journal Integrative Medicine, published an editorial in his journal titled:

What We Have Learned About Vitamin D Dosing?

In this article, Dr. Pizzorno makes the following key points:1) “Over the past several years, the surprising prevalence of vitamin D deficiency has become broadly recognized.”2) Vitamin D deficiency is linked to:

Osteoporosis
Cardiovascular disease
Cancer
Autoimmune diseases
Multiple sclerosis
Pain
Loss of cognitive function
Decreased strength
Increased rate of all-cause mortality

3) “Deficiency of vitamin D is now recognized as a pandemic, with more than half of the world’s population at risk.”4) Approximately 50% of the healthy North American population and more than 80% of those with chronic diseases are vitamin D deficient.5) 80% of healthy Caucasian infants are vitamin D deficient. [And the rate of vitamin D deficiency tends to be greater in African American and Hispanic children].6) Those with vitamin D deficiency experience 39% higher annual healthcare costs than those with normal levels of vitamin D.7) The minimum blood levels of vitamin D [25(OH)D3] is 32 ng/ml; the optimal level is 50-70 ng/ml.8) Prolonged intake of 10,000 IU of supplemental vitamin D3 “is likely to pose no risk of adverse effects in almost all individuals.”9) The recommended loading dose of supplemental vitamin D3 should be about 20,000 IU/day for 3 – 6 months with a maintenance dose of 5,000 IU/day. Those taking this amount of supplemental vitamin D3 should periodically have their serum 25(OH)D3 levels measured.

SUMMARY POINTS FROM DAN MURPHY:

All chronic pain patients should have their 25 hydroxy vitamin D levels checked.

If a patient’s 25 hydroxy vitamin D levels are below 50 ng/ml, and especially if they are below 30 mg/ml, the patient needs more UVB sun exposure without sunscreen, or they need to supplement with 5,000 IU of vitamin D3 per day until optimal levels are achieved.

•••••

Personal Injury Cases and the Chiropractor

Chiropractic education instills that personal injury cases have two components:

An injury component. This component requires healthcare, treatment to the injured patient.

A legal component. This component involves the protection of the injured patient’s legal rights.

Chiropractors who treat personal injury patients understand that their clinical protocols can influence the legal component of a personal injury case. Specifically, there is no substitute for:

Taking a good case history
Doing a thorough orthopedic and neurological examination
Taking good quality and adequate radiographs
Creating an accurate diagnosis that can be supported by history, complaints and examination findings
Doing standard and thorough daily charting
Using standard measurement outcomes, such as pain drawings, Oswestry, Roland Morris, Neck Disability Index, SF-36, algometer, visual analogue scale, etc.
Doing periodic (monthly) thorough subjective and objective re-evaluations with a follow-up written report of findings
Having referred the patient out for needed diagnostic procedures that are not done in the chiropractic office (MRI, EMG, SEP, SPECT, etc.)
Having referred to other health care providers and/or colleagues for verifying or additional opinions
Being able to determine when the patient has reached a point of maximum improvement, and consequently ending regularly scheduled treatment so that the case can proceed towards settlement of claim
Being knowledgeable and conversant in the academic concepts of soft tissue injury, such as the phases of injured tissue healing, the relationship of vehicle damage to patient injury, the influence of pre-accident degenerative joint disease, and the influence of variables such as pre-accident awareness or head rotation

The Chiropractic Impact Report™ is a monthly publication by myself, Dan Murphy, DC. I am a 1978 graduate ofWesternStatesChiropracticCollege inPortland,OR. I have managed about 10,000 whiplash-injury cases. In the past 32 years, I have taught more than 500 12-hour post graduate continuing education classes pertaining to whiplash and spinal trauma, including 21 years of coordinating a year-long certification program in spine trauma, certified through the International Chiropractic Association. Additionally, I am board certified in chiropractic orthopedics (DABCO), and I am on the faculty at Life Chiropractic College West inHayward,CA (28 years).The purpose of The Chiropractic Impact Report™ is to keep you updated as to relevant academic concepts pertaining to whiplash-injured patients. The hope is that the information is useful in terms of enhanced understanding, as well as helping the personal injury attorney deal with insurance claim adjusters and adverse medical experts.The chiropractor sending you this Report is well versed and trained in these concepts, and can be a valuable asset in personal injury cases in terms of both academics and treatment. Additionally, these expert chiropractors have access to a monthly phone consultation with me to discuss any pertinent issues that they may be facing on a particular case. I hope that you find this Report and the referring chiropractor a valuable resource.Sincerely,Daniel J. Murphy DC, DABCO

REFERENCES

Arnson Y, Amital H; Is Vitamin D a New Therapeutic Agent in Auto-inflammatory and Pain Syndromes?; Israeli Medical Association Journal; Vol. 13, April 2011; pp. 234-235.Bhatty SA, Shaikh NA, Irfan M, Kashif SM, Vaswani AS, Sumbhai A, Gunpat; Vitamin D Deficiency in Fibromyalgia; Journal of the Pakistan Medical Association; November 2010; Vol. 60; No. 11; pp. 949-951.Cedric F. Garland, Christine B. French, Leo L. Baggerly and Robert P. Heaney; Vitamin D Supplement Doses and Serum 25-Hydroxyvitamin D in the Range Associated with Cancer Prevention; Anticancer Research; February 2011; Vol. 31; No. 2; pp. 617-622.Heidari B, Shirvani JS, Firouzjahi A, Heidari P, Hajian-Tilaki KO; Association between nonspecific skeletal pain and vitamin D deficiency; International Journal of Rheumatic Disease; October 2010; Vol. 13. No. 4; pp. 340-346.Kragstrup TW; Vitamin D Supplementation for Patients with Chronic Pain; Scandinavian Journal of Primary Health Care; 2011, 29: pp. 4-5.Manson JE; Pain: sex differences and implications for treatment; Metabolism; October 2010, Volume 59, Supplement 1, pp. S16-S20.Omoigui S; The biochemical origin of pain: The origin of all pain is inflammation and the inflammatory response: Inflammatory profile of pain syndromes; Medical Hypothesis; 2007, Vol. 69, pp. 1169–1178.Pizzorno J; What We Have Learned About Vitamin D Dosing?; Integrative Medicine; Vol. 9, No. 1, Feb/Mar 2010.Schwalfenberg G; Improvement of Chronic Back Pain or Failed Back Surgery with Vitamin D Repletion: A Case Series; Journal of the American Board of Family Medicine; January–February 2009; Vol. 22; No. 1; pp. 69 –74.Straube S, Andrew Moor R, Derry S, McQuay HJ, Thomas A; Vitamin D and chronic pain; Pain; 2009; 141: pp. 10-13.Tague SE, Clarke GL, Winter MK, McCarson KE, Wright DE, Smith PG; Vitamin D deficiency Promotes Skeletal Muscle Hypersensitivity and Sensory Hyperinnervation; Journal of Neuroscience; September 2011; Vol. 31; No. 39; pp. 13728-38.

November 2011

admin — Tue, 01 Nov 2011 19:33:49 +0000

Children In Motor Vehicle Collisions

In the legal cases I have consulted in, often it is claimed that children cannot be injured in motor vehicle collisions, and therefore they do not require any treatment. To escalate this perspective, I have consulted in cases where the chiropractor treating such a child is accused of committing fraud, a crime. Occasionally, these cases will even progress to courtroom trial.

Pertaining to the causes of death of our children, the following statistics were compiled from the United States Centers for Disease Control (CDC) National Center for Health Statistics (NCHS).

Age Group	Most Prevalent Cause of Death	Most Prevalent Cause of Accidental Death
<1	Birth Defects
1 – 4	Accidental	Motor Vehicle Accident
5 – 9	Accidental	Motor Vehicle Accident
10 – 14	Accidental	Motor Vehicle Accident
15 – 24	Accidental	Motor Vehicle Accident

In addition, the second leading cause for accidental death in children < 1 year of age was motor vehicle accident.

Based upon these statistics, it seems ludicrous to claim that children cannot be injured in motor vehicle crashes.

•••••

Recently, a new-graduate chiropractor asked my advice regarding the management of an infant who had been injured in a motor vehicle collision. The insurance adjuster controlling the case stated: “our chiropractic consultant informs us that it is unlikely that an infant can be injured in a motor vehicle collision and therefore treatment of an infant after a motor vehicle collision is not likely to be reasonable or necessary.” Chiropractors that treat motor vehicle collision injuries, including those to children, are probably familiar with this attitude.

More than a decade ago, I had the opportunity to testify in a case in which a 7-year-old child and a 22-month-old toddler were injured in a motor vehicle collision. The children were treated successfully by a chiropractor. The mother of the children was adamant that the chiropractic care her children received was necessary for the improvement of their condition caused by the motor vehicle collision. Yet the case went to trial because of the attitude by the insurance company and their chiropractic paper reviewer that the children did not need the amount of care they received; or that the treating chiropractor’s records could not justify the care that he gave to the children.

One of the consequences of this trial was my generation of a chapter in a book, Pediatric Chiropractic, edited by Claudia Anrig and Greg Plaugher, Williams and Wilkins, 1998. The second edition of this book is due out later this year (2011). I did an extensive review of the literature pertaining to injuries to children from motor vehicle collisions, using more than 200 references. This article is a summary of some of the main principles of child injuries from motor vehicle collisions.

•••••

Many of the concepts that pertain to adults in motor vehicle collisions also apply to children, including the basic principles of inertial acceleration/deceleration injuries, patient preparedness prior to impact, and rotation of the head or trunk prior to impact. Overall, studies indicate that the pattern of injury among children in motor vehicle collisions is similar to those of the general population.

However, injuries to children in motor vehicle collisions can be unique as a consequence of the following reasons:

Child safety seats.
The increased size of the child’s head as a proportion of the overall body mass.
The child’s ability to be restrained while facing rearward.
The use of seat belts that are designed for adults.
The use of lap belts without shoulder harnesses.
The reduced height of the developing pediatric pelvis.
The underdevelopment of the pediatric anterior superior iliac spine.
The higher center of gravity for the pediatric body.
The diminished development and strength of various spinal musculoskeletal components.
The ability to sit on the lap of adults when traveling in a vehicle.
The probability that a child injured in a motor vehicle collision is unprepared for the collision, or caught by surprise.
The more unfavorable head diameter to neck diameter ratio, as compared to adults.

I believe that each aspect (above) of this uniqueness regarding children injury during motor vehicle collisions should be understood by the health care provider so that he/she can better explain the appropriateness of treatment given to these injured children. Specifically, I believe that the health care provider should:

1. Understand the biomechanical uniqueness of injury for each age group of children involved in a motor vehicle collision.

2. Learn how to examine and document pediatric trauma, including daily charting.

3. Become proficient at the treatment management of injuries in such small bodies.

I will briefly review these concepts below. A more detailed explanation with graphics and references is available in the next edition of Chiropractic Pediatrics, edited by Anrig and Plaugher, 2011.

•••••

Anthropometric Variables For Children

Head Size

The increased size of the pediatric head as a proportion of the overall body mass influences the location and type of injuries sustained by children involved in a motor vehicle collision. At birth the head is proportionately larger and accounts for approximately 25% of the body length as compared with 15% in the adult. Consequently in motor vehicle collisions it is the head and cervical spine of the newborn that is most likely to be injured in a motor vehicle collision.

Toddlers up to 3 years of age continue to have disproportionately large head size and higher centers of gravity, and, therefore, also tend to sustain head injuries. Rear facing child safety seats tend to restrict forward head movement and prevent young heads from striking the interior of the vehicle.

Pelvic Height

The reduced height of the developing pediatric pelvis predisposes children to unique injury. Every anatomical part of children is reduced in size as compared to the adult, including the height of their pelvis. This reduced height increases the probability for a lap belt to slip over the top of the brim of the pelvis during a motor vehicle collision, resulting in more serious abdominal visceral and lumbar spine fulcrum injuries.

Anterior Superior Iliac Spine

The underdevelopment of the pediatric anterior superior iliac spine increases the probability for unique injury for young patients. Children younger than 10 years of age have less development of the anterior superior iliac spine as compared to the adult. This increases the probability for a lap belt to slip over the top of the brim of the pelvis during a motor vehicle collision, resulting in more serious abdominal visceral and lumbar spine fulcrum injuries.

Center of Gravity

The higher center of gravity for the pediatric body changes the nature and location of injury. Children have a relatively higher center of gravity and a greater tendency for the lap belt to ride cephalad to across the abdomen as compared to adults. This elevated position allows the child to submarine forward under the belt, increasing injury to the abdomen and/or the spine.

4-9 year olds have a relatively lower center of gravity in contrast to infants and toddlers, closer to the umbilicus but still above the lap belt. Yet the iliac crests are underdeveloped in this age group and the lap belt tends to slip up over the bony pelvis and onto the abdomen. With a rapid deceleration event, with a greater proportion of body mass above the lap belt and with the lap belt already in contact with the abdomen, “jackknifing” occurs with compression and injury of abdominal viscera. The hallmark indicator of abdominal viscera and mid-lumbar spine injury is abdominal or flank ecchymosis.

Tissue Strength

The diminished development and strength of various spinal musculoskeletal components increases the probability of significant tissue injury in children. Children have less well developed muscle and connective tissue, which increases probabilities for spinal joint and neurological injury.

Submarining:

Primarily because of the shortness of their pelvis and under development of their anterior superior iliac spine, children, especially those between ages 4-9, have a higher probability of having their torso slip under the lap belt during a motor vehicle collision thus sustaining associated injuries. This is termed submarining. 10-14 year olds have a better developed anterior superior iliac spine, a “taller” pelvis, and consequently experience submarining less often.

Child on Adult Lap

A parent should never hold an infant or child on their lap while riding in a motor vehicle. In a front-end collision at 25 miles per hour at impact, the forces on the baby may reach 20 G. If the weight of the baby is 7.5 pounds its effective weight raises to 150 pounds (7.5 lb X 20 G = 150 lb). If the weight of the child is 25 pounds its effective weight raises to 500 pounds (25 lb X 20 G = 500 lb). It is impossible for the adult to hold the baby under those circumstances. To hold a 10-pound infant at 30 mph the adult strength required would be roughly that needed to lift 300 pounds one foot off the ground.

If the adult holder is also unrestrained, their body may crush the baby against the dashboard or the back of the front seat. When the adult is not restrained, the infant is crushed by a force equal to the mass of the adult multiplied by the square of the speed and divided by two. When the child is held in the arms of an adult and both are not using belt restraints, the weight of the adult is added to the child’s weight as they are thrown forward. The adult will crush the child with an incredible force.

Studies indicate that many infants under the age of one travel in cars while being carried on adult laps.

Unrestrained Children

Careful observation of anthropomorphic video graphically shows that even though the principles of inertia apply to children, they are different, especially when the child is less than 40 lbs. When young children are unrestrained, their entire body functions as a single piece of inertial mass, and will fly through the air during motor vehicle collisions, becoming “human projectiles.” Injuries include crashing through the glass and being thrown from the vehicle, as well as colliding with the inside of the vehicle. In a moving vehicle that is stopped suddenly by an impact, an unrestrained smaller child will continue to move at the original vehicle speed until stopped by the interior of the vehicle. Even in low speed collisions an unrestrained child becomes a human projectile.

Studies indicate that children run more risk of injury or death traveling unrestrained in a vehicle than by being hit by a vehicle as a pedestrian. It is estimated that disabling to fatal injuries to these children would decrease by 78-91% if the child was using a restraint system during motor vehicle collisions. It is estimated that 49% of child passenger deaths from motor vehicle collisions could have been prevented with appropriate child restraint use. Children not in safety restraint devices are 11 times more likely to die in a motor vehicle collision than children placed in restraints. Unrestrained children are three times more likely to sustain a brain injury than restrained children.

Children in Restraints

Reduction In Injuries:

The April 2011 edition of the journal Pediatrics published the policy recommendations of the Committee on Injury, Violence, and Poison Prevention pertaining to Child Passenger Safety in motor vehicle collisions. This project used twenty-two expert collaborators. The abstract of their work project includes:

Child passenger safety has dramatically evolved over the past decade; however, motor vehicle crashes continue to be the leading cause of death of children 4 years and older.

This policy statement provides 4 evidence-based recommendations for best practices in the choice of a child restraint system to optimize safety in passenger vehicles for children from birth through adolescence:

Rear-facing car safety seats for most infants up to 2 years of age.
Forward-facing car safety seats for most children through 4 years of age.
Belt-positioning booster seats for most children through 8 years of age.
Lap-and-shoulder seat belts for all who have outgrown booster seats.

In addition, a fifth evidence-based recommendation is for all children younger than 13 years to ride in the rear seats of vehicles.

It is important to note that every transition is associated with some decrease in protection; therefore, parents should be encouraged to delay these transitions for as long as possible.

The American Academy of Pediatrics urges all pediatricians to know and promote these recommendations as part of child passenger safety anticipatory guidance at every health-supervision visit.

Injuries from Restraints

The leading cause of morbidity and mortality in children is trauma and the most frequent mechanism is motor vehicle collisions. Restraining children decreases their chance of injury or death. Seat belts prevent ejections and reduce impact between the child and the interior of the vehicle. Yet serious injury can still occur even when restraining belts are used because the belts themselves can cause harm and injury. The belt systems have their own unique pattern of injury as they change the distribution of forces, especially to the abdominal viscera in a deceleration event. Violent hyperflexion of the child’s torso over the lap belt applies flexion-distraction forces to the spine. Submarining, or slipping of the child underneath the lap belt can occur and predispose the child to additional abdominal trauma. Children at maximum risk are those too large to be in a safety seat yet too small for the available restraint belt system which are designed for adults (transition age from above). In spite of the drawbacks, adult seat belts are recommended over no restraint at all as they reduce injury and death.

Seat belts may cause injuries from the neck to the pelvis. The probability of seat belt induced injuries increases when the restraint device is not used properly. Common errors in restraint use include:

The child is placed in a restraint not designed for his/her size or weight.
The child restraint is not properly anchored to the vehicle.
The restraint is not properly applied to the child.

Children and Lap Belt Injuries

Lap belt injuries are usually associated with children between ages 4-9, as these children are too large to use restraint seats and are too small to safely use adult lap belts. Children in this age group have special and unique anatomical characteristics that increase their vulnerability to lap belt injuries. Children have relatively larger heads and less well developed spinal musculature than adults, putting children at greater risk of hyperflexion injuries. The immature pelvis is more likely to slip below the seat belt creating fulcrum load injuries to the abdomen.

Conventional lap restraints do not properly restrain or protect children because the anterior superior iliac spine is under developed in this population. The belt rides up onto the abdomen and chest and may itself cause significant injury. If the vehicle rapidly decelerates the child may whip forward with increased force than an adult because of the child’s higher center of gravity and greater body mass above the waist. Children have greater probability of lap belt induced abdominal and spinal injuries because of their greater percentage of body mass above the umbilicus, the poorly developed anterior superior iliac spine, and the frequent lack or misuse of the shoulder harness for children. Children lap belt syndrome injuries typically have an abrasion or contusion across the abdomen, created by the lap belt. These children may suffer from fracture, dislocations, neurologic damage, and significant intra-abdominal injuries.

A 1986 report from the National Transportation Safety Board suggested that the use of rear seat lap belts may be more harmful than no seat belt use at all for children, stating: “In many cases, the lap belts induced severe to fatal injuries that probably would not have occurred if the lap belts had not been worn.” Although rear seat lap belts do not meet the special needs of children, most agree that restraining a child with a lap belt is preferable to having no restraint at all.

Children and Shoulder Harness Injury

Children between ages 4-9 are generally too large to use a restraint seat and yet are too small to safely use an adult shoulder harness restraint. If such children use an improperly fitting adult shoulder harness across their neck or face, serious and fatal injuries have been reported. As the neck / face position for the shoulder harness is uncomfortable for these children, they often will modify its placement by putting the shoulder harness behind their back or under their arm.

Infants and Air Bags

The deployment of air bags occurs at high velocity and creates a serious hazard for children as a result of “bag slap.” The air bag mushrooms out in a fraction of a second, reaching speeds up to 200 mph. Because the rear of the infant child restraint seat is close to the air bag compartment, it will receive a tremendous force from air bag deployment, resulting in serious head injuries to the child. Therefore, rear-facing infant seats should be used only in the back seat of vehicles that have front passenger air bags.

Types of Injuries to Children

As noted, both injury and death are frequently reported in children who are involved in motor vehicle crashes. Injury risk and seriousness is greatest when the child is unrestrained or improperly restrained. However, serious injury and death routinely occurs in properly restrained children. The injuries best documented in the literature include:

Brain Injury
Facial Fractures
Cervical Spine Injuries
Upper Cervical Injury
Cervical Disc Injury
Apophysis (growth center)Injury
Cervical Spinal Cord Injury
The Gamete of Soft Tissue Injuries
Seat Belt Syndrome Abdominal Injuries
Psychological Injury

Summary

Children are injured in motor vehicle collisions, and it is not a small problem; rather, it is a huge problem. Motor vehicle collisions have consistently proven to be the number one reason for both mortality and morbidity in children younger than 25 years of age.

The bodies of children younger than one year of age function as a single piece of inertial mass during motor vehicle collisions. Children in this age group have a proportionately larger head size as compared to overall body mass. Consequently, when they are unrestrained during a motor vehicle collision, they tend to “lead” with their head. Their heads and bodies will collide with the interior of the vehicle, and ejections of their bodies are known to occur. Such unrestrained children sustain serious head, brain, and cervical spinal cord injuries, leading to death and significant lifelong disabilities.

When children younger than one year of age are restrained in a child restraint seat and that child restraint seat is not securely attached to the vehicle seat with the appropriate adult restraint belt, the child’s body and the restraint seat together will function as a single piece of inertial mass. Once again the child will sustain serious head and brain injuries. Not securing the child safety seat to the vehicle is considered to be misuse of the safety device.

When children younger than one year of age are properly restrained in a forward facing child safety seat, and that child safety seat is properly secured to the vehicle with the adult restraint belt, serious head, brain, and cervical spinal cord injuries are largely avoided. Yet, in this forward facing position the properly restrained child has increased vulnerability to cervical spine injury, especially in frontal impacts. This is because the restraints immobilize the child’s body, yet their head remains moveable. With this young child’s proportionately larger head size as compared to overall body mass, and with the child’s poorly developed strength of the cervical spine musculoskeletal tissues, significant cervical spine soft tissues occur.

Most serious injuries to restrained children younger than one year of age occur during a frontal impact collision. These serious injuries can be reduced by placing the child restraint seat in a rearward facing direction, and then properly securing this child restraint seat to the vehicle using the adult restraint belts. Serious injuries are reduced as the forces of the frontal impact are dispersed over a broader surface area of the child; over the back of the skull, the thoracic cage, and the pelvis. There is no doubt that a child of this age group who is properly restrained in the rearward facing position has the best chance of avoiding injury in a motor vehicle collision, and especially in serious frontal impact collisions.

When children younger than one year of age are restrained in a child safety seat that is properly secured to the vehicle by the adult belt, but the crotch strap of the child safety seat is not properly attached, the child’s body will “submarine” under the waist strap, catching the child under the chin. The results are serious cervical spine injury, including fracture of the odontoid process or a bipedicular (hangman’s) fracture of C2. An adult must always properly secure the crotch strap portion of the child restraint seat for children in this age group.

Children younger than one year of age should not be restrained in a child safety seat in the rearward facing position in the front seat of a vehicle that has a passenger side air bag. In this position, the closeness of the child to a rapidly outwardly exploding air bag can launch the safety seat and child at an extremely high velocity, resulting in serious head and brain injury.

Children between 1 – 4 years of age are similar to children younger than age one in that their heads are proportionately larger as compared to overall body mass, the strength of their musculoskeletal spinal tissues are not as developed as those of the adult. When they are unrestrained they tend to “lead” with their heads sustaining serious head, brain, and cervical spinal cord injuries after colliding with the interior of the vehicle, and are at risk of ejection. Recent retrospective statistical studies show that the children in this age group are least injured when they are properly restrained in a child safety seat facing the rearward direction. When children in this age group are properly restrained and facing the forward direction, they sustain significant cervical spine soft tissue injury during frontal collisions. Contrary to common practice, it is recommended that children remain in child restraint seats facing the rearward position for a long as possible as they age, ideally to approximately age 4.

Caution should be used when restraining children between 1- 4 years of age in an adult lap belt. The pelvis of children in this age group is much shorter in height, and the anterior superior iliac spine is grossly underdeveloped as compared to that of the adult, increasing the tendency for the lap belt to slip up over the top of the pelvis rim and to be in contact with the abdomen and its contents. Because of the shorter stature of these children, in a frontal impact their face or chest will not collide with the dashboard or with the seat in front of them. This results in a serious rapid flexion of the child’s torso around the adult lap belt, or “jackknifing.” Serious and fatal abdominal viscera and mid lumbar spinal injuries result.

Children between ages 4 – 9 years have the greatest difficulty with motor vehicle collision safety. Children in this age group face forward nearly always and are restrained in the adult seat belt. Unfortunately, adult seat belts do not meet the special needs of this group of children. Often they are riding in the rear seat of the vehicle, and there are still many vehicles that do not have shoulder harness restraints available for rear seat passengers. As the developing pelvis remains short in height with an underdeveloped anterior superior iliac spine in this age group, it is once again common for the adult lap belt restraint to slip over the rim of the pelvis and to come into contact with the abdomen and its contents. The center of gravity for these children is higher as compared to that of the adult, superior to the lap belt. This proportionately increases the fulcrum stress above the lap belt in a frontal impact or during a rebound flexion following a rear impact. Again, this results in serious injuries to the abdominal viscera and mid lumbar spine, including Chance fractures. Depending on the stature of these children, their face/head may impact the dashboard or the seat in front of them, resulting in significant face, head, brain, and cervical spinal cord injuries. It is, therefore, recommended that whenever possible, children of this age group should be restrained in a lap belt shoulder belt combination.

Children between ages 4 – 9 years also have unique problems when using the recommended adult lap belt with shoulder harness combination. Because of their short stature, the shoulder harness does not fit their body adequately. For many children in this age group, the shoulder harness will cut across their cervical spine or face rather than their chest. When left in this position, the shoulder harness can cause serious and fatal cervical spine and facial injuries. Also, because of the uncomfortable annoyance of the shoulder belt crossing the neck or face, many children of this age group will simply place the shoulder strap behind their back, rendering them susceptible to the lap belt injuries noted above. Other children will place the shoulder harness under the arm. This position is also quite dangerous, as the thoracic cage is not capable of handling the forces of a frontal collision during this age of skeletal maturation that are generated by the shoulder harness. The stresses imparted to the child can seriously injure the thoracic cage, including imparting cardiac and pulmonary trauma. The proper shoulder harness placement for this age is across the chest, over the clavicle, but remaining off the cervical spine and face. This is best accomplished by using a booster seat that effectively increases the height of the child, or by using a device that lowers the shoulder harness away from the face and neck and into the proper position and secures it in place by attaching to the lap belt.

Very young children cannot communicate to their parents or health care providers the location or nature of their injuries. Even non-life threatening injuries in children should be documented and properly managed. I have created a useful form to help me evaluate very young children with a history of being involved in a motor vehicle collision. (From Biedermann, attached separately)

Personal Injury Cases and the Chiropractor

Chiropractic education instills that personal injury cases have two components:

An injury component. This component requires healthcare, treatment to the injured patient.

A legal component. This component involves the protection of the injured patient’s legal rights.

Chiropractors who treat personal injury patients understand that their clinical protocols can influence the legal component of a personal injury case. Specifically, there is no substitute for:

Taking a good case history
Doing a thorough orthopedic and neurological examination
Taking good quality and adequate radiographs
Creating an accurate diagnosis that can be supported by history, complaints and examination findings
Doing standard and thorough daily charting
Using standard measurement outcomes, such as pain drawings, Oswestry, Roland Morris, Neck Disability Index, SF-36, algometer, visual analogue scale, etc.
Doing periodic (monthly) thorough subjective and objective re-evaluations with a follow-up written report of findings
Having referred the patient out for needed diagnostic procedures that are not done in the chiropractic office (MRI, EMG, SEP, SPECT, etc.)
Having referred to other health care providers and/or colleagues for verifying or additional opinions
Being able to determine when the patient has reached a point of maximum improvement, and consequently ending regularly scheduled treatment so that the case can proceed towards settlement of claim
Being knowledgeable and conversant in the academic concepts of soft tissue injury, such as the phases of injured tissue healing, the relationship of vehicle damage to patient injury, the influence of pre-accident degenerative joint disease, and the influence of variables such as pre-accident awareness or head rotation

Sincerely,

Daniel J. Murphy DC, DABCO

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Cyriax, James, M.D., Orthopaedic Medicine, Diagnosis of Soft Tissue Lesions, Bailliere Tindall, Vol. 1, (1982).

Fischgrund, Jeffrey S, Neck Pain, monograph 27, American Academy of Orthopaedic Surgeons, 2004.

Gargan, MF, Bannister, GC, Long-Term Prognosis of Soft-Tissue Injuries of the Neck, Journal of Bone and Joint Surgery, September, 1990.

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Hodgson, S.P. and Grundy, M., Whiplash Injuries: Their Long-term Prognosis and Its Relationship to Compensation, Neuro-Orthopedics, (1989), 7.88-91.

Jonsson H, Cesarini K, Sahlstedt B, Rauschning W, Findings and Outcome in Whiplash-Type Neck Distortions; Spine, Vol. 19, No. 24, December 15, 1994, pp. 2733-2743.

Kannus P, Immobilization or Early Mobilization After an Acute Soft-Tissue Injury?; The Physician And Sports Medicine; March, 2000; Vol. 26 No 3, pp. 55-63.

Kellett J; Acute soft tissue injuries-a review of the literature; Medicine and Science of Sports and Exercise, American College of Sports Medicine, Vol. 18 No.5, (1986), pp. 489-500.

Kirkaldy-Willis, W.H., M.D., Managing Low Back Pain, Churchill Livingston, (1983 & 1988).

Kirkaldy-Willis, W.H., M.D., & Cassidy, J.D.,”Spinal Manipulation in the Treatment of Low-Back Pain,” Can Fam Physician, (1985), 31:535-40.

Majno, Guido and Joris, Isabelle, Cells, Tissues, and Disease: Principles of General Pathology,OxfordUniversity Press, 2004.

Mealy K, Brennan H, Fenelon GCC; Early Mobilization of Acute Whiplash Injuries; British Medical Journal, March 8, 1986, 292(6521): 656-657.

Oakes BW. Acute soft tissue injuries. Australian Family Physician. 1982; 10 (7): 3-16.

Omoigui S; The biochemical origin of pain: The origin of all pain is inflammation and the inflammatory response: Inflammatory profile of pain syndromes; Medical Hypothesis; 2007, Vol. 69, pp. 1169-1178.

Oschman, James L, Energy Medicine: The Scientific Basis, Churchill Livingstone, 2000.

Rogier M. van Rijn, Anton G. van Os, Roos M.D. Bernsen, Pim A. Luijsterburg, Bart W. Koes, Professor, Sita M.A. Bierma-Zeinstra; What Is the Clinical Course of Acute Ankle Sprains? A Systematic Literature Review; The American Journal of Medicine; April 2008, Vol. 121, No. 4, pp. 324-331.

Rosenfeld M, Gunnarsson R, Borenstein P, Early Intervention in Whiplash-Associated Disorders, A Comparison of Two Treatment Protocols; Spine, 2000;25:1782-1787.

Roy, Steven, M.D., and Irvin, Richard, Sports Medicine: Prevention, Evaluation, Management, and Rehabilitation, Prentice-Hall, Inc. (1983).

Salter R, Continuous Passive Motion, A Biological Concept for the Healing and Regeneration of Articular Cartilage, Ligaments, and Tendons; From Origination to Research to Clinical Applications, Williams and Wilkins, 1993.

Seletz E; Whiplash Injuries; Neurophysiological Basis for Pain and Methods Used for Rehabilitation; Journal of the American Medical Association; November 29, 1958, pp. 1750-1755.

Schofferman J, Bogduk N, Slosar P; Chronic whiplash and whiplash-associated disorders: An evidence-based approach; Journal of the AmericanAcademyofOrthopedic Surgeons; October 2007;15(10):596-606.

Stonebrink, R.D., D.C., “Physiotherapy Guidelines for the Chiropractic Profession,” ACA Journal of Chiropractic, (June1975), Vol. IX, p.65-75.

Stearns, ML, Studies on development of connective tissue in transparent chambers in rabbit’s ear; American Journal of Anatomy, vol. 67, 1940, p. 55.

Sturzenegger M, DiStefano G, Radanov BP, Schnidrig A. Presenting symptoms and signs after whiplash injury: the influence of accident mechanisms. Neurology. April 1994;44(4):688-93.

Sturzenegger M, Radanov BP, Di Stefano G. The effect of accident mechanisms and initial findings on the long-term course of whiplash injury. Journal of Neurology. July 1995;242(7):443-9.

Wyke, B.D., Articular neurology and manipulative therapy, Aspects of Manipulative Therapy, Churchill Livingstone, 1980, pp.72-77.

Woo, Savio L.-Y.,(ed.), Injury and Repair of the Musculoskeletal Soft Tissues, American Academy of Orthopaedic Surgeons,(1988), p.18-21; 106-117; 151-7; 199-200; 245-6; 300-19; 436-7; 451-2; 474-6.

October 2011

admin — Mon, 03 Oct 2011 21:34:38 +0000

Soft Tissue Injury and Repair

HISTORY: Mandy, a 50-year-old female, was injured in a motor vehicle collision.

Her stationary vehicle was struck from the rear by a vehicle of similar mass that was traveling at a speed of approximately 20 miles per hour at the time of collision. Damage to her vehicle was judged to be $6,600.

The collision caught Mandy by surprise, and she was looking left at the moment of impact. This is important because there is good evidence (Sturzenegger 1994, Sturzenegger 1995) that factors associated with greater initial injury and a worse outcome one year after injury are (in descending order):

Being involved in a collision in which the patient is caught by surprise.
Being involved in a collision in which the patient’s head is rotated.
Being involved in a collision in which the impact is from a rear-end direction.

Although dazed, Mandy did not lose consciousness. An ambulance did take her to the emergency department of her own HMO, which was geographically close by.

At the hospital, Mandy was evaluated and radiographs were taken. There were no broken bones, signs of instability, congenital anomalies, or degenerative disease. She was told she had suffered a soft tissue injury and that it would get better in a few days to a few weeks.

For treatment, Mandy’s doctors put her into a soft cervical spine collar, she was prescribed a nonsteroidal anti-inflammatory drug, and given a heat pack for home use. She was advised to return for a follow-up visit if she was having continuing problems. Mandy was advised to continue to work in her usual occupation as a real estate agent.

Mandy began wearing her cervical spine soft collar most of the time. Although the anti-inflammatory medicines and the hot pack seemed to help her (this seems paradoxical), she did not seem to be making overall relevant improvement. She continued to have significant neck pain and stiffness with an occasional headache.

Mandy did continue to work and actually missed no work at all. However, her neck was sore and stiff making her grumpy, and she became fatigued easily.

Mandy wore her cervical collar nearly constantly for about two weeks, then she reduced its usage to only when she was engaging in more strenuous activities, such as driving or shopping, and during certain activities at work. She liked her hot pack and she used it on average 3-4 times per day. She still needed her pain medicine, taking them a few times daily.

After about two months of being essentially unchanged, Mandy returned to her HMO physician and asked him if there was anything else she could do for her neck pain with occasional headaches. Her doctor authorized for Mandy to see one of the HMO’s physical therapists. She was prescribed one physical therapy session per week for the next four weeks.

Mandy’s physical therapist talked to her about her posture and gave her some exercises. He evaluated the ergonomics of her desk, primarily as related to when she was doing work on her computer.

After her four physical therapy visits, Mandy had incorporated his advice and exercises into her routine. Yet, she continued to suffer from neck pain and stiffness with occasional headaches.

Nine months after being injured, Mandy was still suffering and she could not go a full day without taking pain medications. Mandy needed to do something different.

Mandy became my patient nine months after being injured.

•••••

There is a common misconception that injured soft tissues will heal in a period of time between four and eight weeks. It is frequently claimed that injured soft tissues will heal spontaneously, leaving no long-term residuals, and that treatment is not required. This type of information is misleading and confusing because it is not true. As an example, in 2008, The American Journal of Medicine published a systemic review of the literature evaluating the clinical course of acute ankle sprain (Rijn 2008). The authors conducted a database search in MEDLINE, CINAHL, PEDro, EMBASE, and the Cochrane Controlled trial register. They found 31 studies that met their inclusion criteria. Their findings include:

5% to 33% of patients still experienced ankle pain after 1 year.
The studies reported an incidence of subjective instability of their injured ankle in up to 53% patients.
15% to 64% had not fully recovered at 3 years.
The incidence of re-sprains ranged from 3% to 34% of the patients.

Most of my med-legal experience is with whiplash injury. Often, insurance defense personnel and their chiropractic/medical experts make an analogy between the whiplash-injured neck and a sprained ankle. Their classic claim is that a sprained ankle will heal spontaneously (without any treatment) and quickly (weeks), and there are no long-term residuals.

This article by Rijn presents a much different reality pertaining to the healing of the sprained ankle: at 3 years up to 64% have not fully recovered, up to 33% have residual pain, up to 53% suffer from residual instability, and up to 34% suffer from re-injury. It appears that 15% to 64% have some degree of permanent injury. Additionally, the severity of ankle injury is not a strong predictor for the ultimate clinical outcome. It appears that trauma from ankle sprain and whiplash have a number of shared characteristics: significant residual pain, instability, re-injury rates, permanent injury residuals, and the severity of injury not being a predictor for the ultimate clinical outcome.

Consequently, I believe that the most important question is:

Is there an approach to the management of injured soft tissues that improves the timing and quality of the healing outcome?

•••••

Published articles and books concerning the healing of injured soft tissues (Oakes 1982; Roy and Irving 1983; Kellett 1986; Buckwalter/Woo 1988, Majno 2004) indicate that the time frame for soft healing is approximately one year.

The healing of injured soft tissues takes place in three specific phases. The first phase is called the acute inflammatory phase. This phase will last approximately 72 hours. During this phase, after the initial injury, an electrical current is generated at the wound, called the “current of injury.” This “current of injury” attracts fibroblasts to the wound (Oschman, 2000). During this phase there is also initial bleeding and continual associated inflammation of the injured tissues. Because of the increasing inflammatory cascade during this period of time, it is not uncommon for the patient to feel worse for each of the first three days following injury. Because there is disruption of local vascular supplies, there is insufficient availability of substrate (glucose, oxygen, etc.) to produce large enough quantities of ATP energy to initiate collagen protein synthesis to repair the wound.

Experience and published studies (Kellett 1996) indicate that the best management of soft tissue injuries during the acute inflammatory phase is ice therapy. Ice therapy during the first 72 hours following injury reduces pain and swelling, and minimizes the formation of scar tissue that often causes prolonged disability (Seletz 1958). [Unfortunately for Mandy, during this phase of soft tissue healing, she was prescribed and used heat].

After 72 hours following injury, the damaged blood vessels have mended. The resulting increased availability of glucose and oxygen elevates local ATP levels and collagen repair begins by the fibroblasts that accumulated during the acute inflammatory phase. This second phase of healing is called the phase of regeneration. During the regeneration phase the disruption in the injured muscles and ligaments is bridged. Some references call the regeneration phase the phase of repair, which creates confusion about the timing of healing (Jackson, 1977). “Repair” connotation is that the process has completed, which, as we will see, is not the case. The fibroblasts manufacture and secrete collagen protein glues that bridge the gap in the torn tissues. This phase will last approximately 6-8 weeks (Jackson, 1977). At the end of 6-8 weeks, the gap in the torn tissues is more than 90% bridged; more than 90% of the collagen that is laid down in the breach occurs during this second phase of healing. Consequently, many will erroneously claim this to be the end of healing. However, it clearly is not.

Experience and published studies (Stearns 1940, Seletz 1958, Cyriax 1982, Roy 1983, Kellett 1986, Mealy 1986, Cohen 1992, Salter 1993, Jonsson 1994, Buckwalter 1996, Kannus 2000, Rosenfeld 2000) document that the best management of soft tissue injuries during the second phase of healing is early, persistent, controlled mobilization. In contrast, immobilization is harmful, leading to increased risk of slowed healing and chronicity (Stearns 1940, Mealy 1986, Cohen 1992, Salter 1993, Jonsson 1994, Kannus 2000, Rosenfeld 2000, Schofferman 2007). [Unfortunately for Mandy, during this second phase of soft tissue healing, she was prescribed and used a cervical collar].

There is a third and final phase of healing. This phase is called the phase of remodeling.

The phase of remodeling starts near the end of the phase of regeneration. During the phase of remodeling the collagen protein glues that have been laid down for repair are remodeled in the direction of stress and strain. This means that the fibers in the tissue will become stronger, and will change their orientation from an irregular pattern to a more regular pattern, a pattern more like the original undamaged tissues. Proper treatment during this remodeling phase is very necessary if the tissues are to get the best end product of healing. It is during this remodeling phase that the tissues regain strength and alignment. Remodeling takes approximately one year from the date of injury. It is established that remodeling takes place as a direct byproduct of motion. Chiropractic healthcare puts motion into the tissues in an effort at getting them to line up along the directions of stress and strain, thereby giving a stronger, more elastic end product of healing.

Traditional chiropractic joint manipulation healthcare is directed towards putting motion into the periarticular paraphysiological space. The concept of paraphysiological joint motion was first described by Sandoz in 1976, and is explained well by Kirkaldy-Willis 1983 and 1988, by Kirkaldy-Willis/Cassidy 1985, and in the 2004 monograph on Neck Pain (edited by Fischgrund) published by the American Academy of Orthopedic Surgeons (see picture). These discussions clearly show that there is a component of motion that cannot be properly addressed by exercise, massage, etc., and that this component of motion can be properly addressed by osseous joint manipulation. Therefore, traditional chiropractic osseous joint manipulation adds a unique aspect to the treatment and the remodeling of periarticular soft tissues that have sustained an injury.

During this third phase of healing, the phase of remodeling, Mandy continued to wear a cervical collar, especially during high-demand activities. Although she did add some exercises to her management, which is helpful, she employed no management aspects that would have introduced motion into the periarticular paraphysiological space. As Schofferman and Bogduk state in their 2007 article titled: Chronic whiplash and whiplash-associated disorders: An evidence-based approach,

“exercise alone is rarely curative”

Additionally, Drs. Schofferman and Bogduk suggest there is value in spinal manipulation in the management of chronic whiplash patients (Schofferman, 2007).

•••••

Mandy’s whiplash soft tissue injury management that included heat, immobilization and limited exercises did not result in an acceptable clinical outcome. Nine months after being injured, she was suffering from chronic neck pain, weakness, and occasional headaches.

My approach to her management included:

Regular and strenuous resistive effort exercises of the muscles of her cervical and thoracic spines.

No more use of a cervical collar.

Transverse friction myotherapy to reduce the adverseness of post-traumatic muscular adhesions and fibrosis (Cyriax, 1982).

Specific osseous joint manipulation to the joints that were reduced in the symmetry and/or magnitude of normal motion. Such manipulations will reduce articular adhesions, remodel periarticular fibrosis, reduce muscle hypertonicity and spasm, and close the “pain gate” (Kirkaldy-Willis, 1983, 1985, 1988).

Specific chiropractic postural correctional techniques. Improved posture reduces stresses in both soft tissues, muscles, and articulations.

Mandy remained under my care for a period of 4 months, and she was seen a total of 32 visits at our clinic. Her progress was steady and progressive. When she was released from additional regularly scheduled treatment, she was instructed to continue to do her prescribed exercises. Mandy’s symptoms were not completely resolved, but she judged her clinical status to be 85% improved as compared to when she first entered our clinic.

•••••

There are some problems associated with the healing of injured soft tissues. Microscopic histological studies show that the repaired tissue is different than the original, adjacent, undamaged tissues. During the initial acute inflammatory phase there is bleeding from the damaged tissues and consequent local inflammation. This progressive bleeding releases increased numbers of fibroblasts into the surrounding tissues. Chemicals that are released trigger the inflammation response that is noted in cases of trauma. Subsequent to the inflammatory response and to the number of fibrocytes that are released into the tissues, the healing process is really a process of fibrosis. In 1975, Stonebrink addresses that the last phase of the pathophysiological response to trauma is tissue fibrosis. Boyd in 1953, Cyriax in 1983, and Majno/Joris in 2004 note that there is tissue fibrosis subsequent to trauma. This fibrosis of repair subsequent to soft tissue trauma creates problems that can adversely affect the tissues and the patient for years, decades, or even forever.

Fibrosed tissues are functionally different from the adjacent normal tissues. The differences fall into two main categories:

Category 1: The repaired tissue is weaker and less strong than the undamaged tissues. This is because the diameter of the healing collagen fibers are smaller, and the end product of healing is deficient in the number of crossed linkages within the collagen repair.

Category 2: The repaired tissue is stiffer or less elastic than the original, undamaged tissues. This is because the healing fibers are not aligned identically to that of the original. Examination range of motion studies will indicate that there are areas of decrease of the normal joint ranges of motion.

In addition, Cyriax notes “fibrous tissue is capable of maintaining an inflammatory response long after the initial cause has ceased to operate.” Since inflammation alters the thresholds of the nociceptive afferent system (Omoigui 2007), physical examinations in these cases will show these fibrotic areas display increased sensitivity, and digital pressure may show hypertonicity and spasm. This increased sensitivity can be documented with the use of an algometer, which is a device that uses pressure to determine the initiating threshold of pain.

Because the fibrotic residuals have rendered the tissues weaker, less elastic, and more sensitive, the patient will have a history of flare-ups of pain and/or spasm at times of increased use or stress. These episodes of pain and/or spasm at times of increased use or stress of the once damaged soft tissues is the rule rather than the exception, and a problem that the patient will have to learn to live with. It is likely that the patient will continue to have episodes of pain and/or spasm for an indefinite period of time in the future. It is probable that the patient will have a need for continuing care subsequent to these episodes of pain and/or spasm.

Consistent with these concepts, a study by Hodgson in 1989 indicated that 62% of those injured in automobile accidents still have significant symptoms caused by the accident 12 1/2 years after being injured; and that of the symptomatic 62%, 62.5% had to permanently alter their work activities and 44% had to permanently alter their leisure activities in order to avoid exacerbation of symptoms. One of the conclusions of the article is that these long-term residuals were most likely the result of post-traumatic alterations in the once damaged tissues.

A study by Gargan in 1990 indicated that only 12% of those sustaining a soft tissue neck injury had achieved a complete recovery more than ten years after the date of the accident. One of the conclusions of this study is that the patient’s symptoms would not improve after a period of two years following the injury.

It is established neurologically (Wyke 1985, Kirkaldy-Willis and Cassidy 1985) that when a chiropractor adjusts (specific directional spinal manipulation) the joints in the region of pain and/or spasm, that there is a depolarization of the mechanoreceptors that are located in the facet joint capsular ligaments, and that the cycle of pain and/or spasm can be neurologically aborted. This is why many patients feel better after they receive specific joint manipulation from a chiropractor following an episode of increased pain and/or spasm.

What is the basis for the chronic post-trauma pain syndromes that so many patients suffer from? A good explanation is found from Gunn (1978, 1980, 1989). He refers to this type of pain as supersensitivity. The supersensitivity type pain is a residual of the scarring or the fibrosis that was created by the injuries sustained in this accident. The treatment that we give to the patient for the injuries sustained in an accident is really not designed to heal the sprain or strain but rather, to change the fibrotic nature of the reparative process that has left the patient with residuals that are weaker, stiffer, and more sore. The actual diagnosis for this type of problem is initial sprain/strain injuries of the paraspinal soft tissues with fibrotic residuals subsequent to the fibrosis of repair of once damaged soft tissues that have left these tissues weaker, stiffer, and more sensitive as compared to the original tissues. The majority of our efforts in the treatment of post-traumatic chronic pain syndrome patients is in dealing with the residual fibrosis of repair and its associated mechanical and neurological consequences. These residuals to some degree are most probably permanent. The patient will have to learn to deal with the long-term residuals and the occasional episodes of pain and/or spasm. However, as noted above, occasional specific joint manipulation in the involved areas can neurologically inhibit muscle tone, improve ranges of motion, disperse accumulated inflammatory exudates, and the patient will have less pain and improved function.

The concepts briefly discussed above are frequently not understood or appreciated. There is a tendency for healthcare providers to not properly examine the patient in order to document these regions of tissue fibrosis and its consequent mechanical and neurological consequences and, therefore, to quote Stonebrink, the real problem is missed.

•••••

I believe that for Mandy, her poor early management resulted in excessive tissue fibrosis, and as noted above, that was the basis for her chronicity. Our management of her problems reduced the magnitude of her fibrotic residuals and their adverseness. Her cervical spine range of motion increased, her posture improved, her muscle strength increased and her musculoskeletal fatigue resolved. She no longer used her cervical collar and she did not need any pain medications. Her residual symptoms were manageable and tolerable with continuing cervical spine exercise. It is probable that some of her fibrotic residuals were not reducible, creating the pathoanatomical basis for her residual symptoms (Josson 1994).

Addendum

Three months after Mandy was released from treatment, she was involved in another similar motor vehicle collision. She sustained significant soft tissue injuries of her cervical and thoracic spines, essentially in the exact locations of the collision she had sustained approximately nineteen months prior.

The day of this second injury, Mandy presented herself to our clinic for management.

Our acute care protocol included recumbent traction (for 20 minutes) with a cervical pillow and ice pack. This was done four times per day, once in the office and three times at home. She was initially seen in our office daily for the first three weeks following her injury. Low-level laser therapy was applied for 20 minutes daily to her injured spinal regions in an effort to elevate ATP levels, accelerating the healing process.

On the fourth day, we added to her management a passive motion protocol to the joints of the cervical and thoracic spines; each of her joints were carefully pushed into the passive range of motion (see picture below) while using the laser with an anti-inflammatory setting. This is done in an effort to disperse inflammation and thereby reduce long-term scarring (fibrosis). It also puts tension in the developing granulation tissue, improving alignment and strength. This is a benefit that cannot be achieved by exercise alone.

At two weeks, we began to provide specific joint manipulation (adjustments) to the articulations that showed reduced and/or altered motion patterns. Simultaneously, postural corrections, transverse friction myotherapy and resistive effort exercises were initiated.

Mandy’s entire trauma management program lasted eighteen weeks; she was seen in our office a total of 34 times. When she was released from additional regularly scheduled treatment, she reported to be 100% resolved of all signs and symptoms. This means that the residuals she had from her prior accident had completely resolved. I believe that the second accident had re-torn the fibrotic residuals she retained from her prior collision. The magnitude of the second collision was such that it reduced fibrotic residuals that I was unable to reduce therapeutically. But I now had the opportunity to manage her new acute injuries with a different, superior approach. The results were gratifying for both Mandy and myself.

Personal Injury Cases and the Chiropractor

Chiropractic education instills that personal injury cases have two components:

An injury component. This component requires healthcare, treatment to the injured patient.

A legal component. This component involves the protection of the injured patient’s legal rights.

Chiropractors who treat personal injury patients understand that their clinical protocols can influence the legal component of a personal injury case. Specifically, there is no substitute for:

Taking a good case history
Doing a thorough orthopedic and neurological examination
Taking good quality and adequate radiographs
Creating an accurate diagnosis that can be supported by history, complaints and examination findings
Doing standard and thorough daily charting
Using standard measurement outcomes, such as pain drawings, Oswestry, Roland Morris, Neck Disability Index, SF-36, algometer, visual analogue scale, etc.
Doing periodic (monthly) thorough subjective and objective re-evaluations with a follow-up written report of findings
Having referred the patient out for needed diagnostic procedures that are not done in the chiropractic office (MRI, EMG, SEP, SPECT, etc.)
Having referred to other health care providers and/or colleagues for verifying or additional opinions
Being able to determine when the patient has reached a point of maximum improvement, and consequently ending regularly scheduled treatment so that the case can proceed towards settlement of claim
Being knowledgeable and conversant in the academic concepts of soft tissue injury, such as the phases of injured tissue healing, the relationship of vehicle damage to patient injury, the influence of pre-accident degenerative joint disease, and the influence of variables such as pre-accident awareness or head rotation

Sincerely,

Daniel J. Murphy DC, DABCO

REFERENCES

Boyd, William, M.D., Pathology, Lea & Febiger, (1952).

Buckwalter J, Effects of Early Motion on Healing of Musculoskeletal Tissues, Hand Clinics, Volume 12, Number 1, February 1996.

Cohen, I. Kelman; Diegelmann, Robert F; Lindbald, William J; Wound Healing, Biochemical & Clinical Aspects, WB Saunders, 1992.

Cyriax, James, M.D., Orthopaedic Medicine, Diagnosis of Soft Tissue Lesions, Bailliere Tindall, Vol. 1, (1982).

Fischgrund, Jeffrey S, Neck Pain, monograph 27, American Academy of Orthopaedic Surgeons, 2004.

Gargan, MF, Bannister, GC, Long-Term Prognosis of Soft-Tissue Injuries of the Neck, Journal of Bone and Joint Surgery, September, 1990.

Gunn, C. Chan, Pain, Acupuncture & Related Subjects, C. Chan Gunn, (1985).

Gunn, C. Chan, Treating Myofascial Pain: Intramuscular Stimulation (IMS) for Myofascial Pain Syndromes of Neuropathic Origin, University of Washington, 1989.

Hodgson, S.P. and Grundy, M., Whiplash Injuries: Their Long-term Prognosis and Its Relationship to Compensation, Neuro-Orthopedics, (1989), 7.88-91.

Jonsson H, Cesarini K, Sahlstedt B, Rauschning W, Findings and Outcome in Whiplash-Type Neck Distortions; Spine, Vol. 19, No. 24, December 15, 1994, pp. 2733-2743.

Kannus P, Immobilization or Early Mobilization After an Acute Soft-Tissue Injury?; The Physician And Sports Medicine; March, 2000; Vol. 26 No 3, pp. 55-63.

Kellett J; Acute soft tissue injuries-a review of the literature; Medicine and Science of Sports and Exercise, American College of Sports Medicine, Vol. 18 No.5, (1986), pp. 489-500.

Kirkaldy-Willis, W.H., M.D., Managing Low Back Pain, Churchill Livingston, (1983 & 1988).

Kirkaldy-Willis, W.H., M.D., & Cassidy, J.D.,”Spinal Manipulation in the Treatment of Low-Back Pain,” Can Fam Physician, (1985), 31:535-40.

Majno, Guido and Joris, Isabelle, Cells, Tissues, and Disease: Principles of General Pathology, Oxford University Press, 2004.

Mealy K, Brennan H, Fenelon GCC; Early Mobilization of Acute Whiplash Injuries; British Medical Journal, March 8, 1986, 292(6521): 656-657.

Oakes BW. Acute soft tissue injuries. Australian Family Physician. 1982; 10 (7): 3-16.

Oschman, James L, Energy Medicine: The Scientific Basis, Churchill Livingstone, 2000.

Rosenfeld M, Gunnarsson R, Borenstein P, Early Intervention in Whiplash-Associated Disorders, A Comparison of Two Treatment Protocols; Spine, 2000;25:1782-1787.

Roy, Steven, M.D., and Irvin, Richard, Sports Medicine: Prevention, Evaluation, Management, and Rehabilitation, Prentice-Hall, Inc. (1983).

Seletz E; Whiplash Injuries; Neurophysiological Basis for Pain and Methods Used for Rehabilitation; Journal of the American Medical Association; November 29, 1958, pp. 1750-1755.

Schofferman J, Bogduk N, Slosar P; Chronic whiplash and whiplash-associated disorders: An evidence-based approach; Journal of the American Academy of Orthopedic Surgeons; October 2007;15(10):596-606.

Stonebrink, R.D., D.C., “Physiotherapy Guidelines for the Chiropractic Profession,” ACA Journal of Chiropractic, (June1975), Vol. IX, p.65-75.

Stearns, ML, Studies on development of connective tissue in transparent chambers in rabbit’s ear; American Journal of Anatomy, vol. 67, 1940, p. 55.

Sturzenegger M, DiStefano G, Radanov BP, Schnidrig A. Presenting symptoms and signs after whiplash injury: the influence of accident mechanisms. Neurology. April 1994;44(4):688-93.

Sturzenegger M, Radanov BP, Di Stefano G. The effect of accident mechanisms and initial findings on the long-term course of whiplash injury. Journal of Neurology. July 1995;242(7):443-9.

Wyke, B.D., Articular neurology and manipulative therapy, Aspects of Manipulative Therapy, Churchill Livingstone, 1980, pp.72-77.

Woo, Savio L.-Y.,(ed.), Injury and Repair of the Musculoskeletal Soft Tissues, American Academy of Orthopaedic Surgeons,(1988), p.18-21; 106-117; 151-7; 199-200; 245-6; 300-19; 436-7; 451-2; 474-6.

September 2011

admin — Thu, 01 Sep 2011 21:47:28 +0000

Whiplash Update Two Important New Studies And Their Clinical Applications

BACKGROUND INFORMATION FROM DAN MURPHY

All pain has an inflammatory component. In his 2007 article, Omoigui, concludes:

“The origin of all pain is inflammation and the inflammatory response.”

“Irrespective of the type of pain, whether it is acute or chronic pain, peripheral or central pain, nociceptive or neuropathic pain, the underlying origin is inflammation and the inflammatory response.”

“Activation of pain receptors, transmission and modulation of pain signals, neuroplasticity and central sensitization are all one continuum of inflammation and the inflammatory response.”

“Irrespective of the characteristic of the pain, whether it is sharp, dull, aching, burning, stabbing, numbing or tingling, all pain arises from inflammation and the inflammatory response.”

Post-traumatic inflammation is often the consequence of the membrane release of arachidonic acid fat cascading into the pro-inflammatory hormone prostaglandin E2 (PGE2). In his 2010 article, Maroon states:

“A major component of the inflammatory pathway is called the arachidonic acid pathway because arachidonic acid is immediately released from traumatized cellular membranes.”

Cell membrane trauma releases arachidonic acid. Arachidonic acid is then transformed into the pro-inflammatory hormones prostaglandins and thromboxanes through the enzymatic action of cyclooxygenase.

This is why omega-6/omega-3 fatty acid balancing is an important clinical strategy in the management of patients suffering from pain syndromes (Boswell, 2006).

Inflammation alters the pain threshold and increases pain perception (Omoigui, 2007; Boswell, 2006; Maroon, 2006; Cleland, 2006; Goldberg 2007; Maroon, 2010). In 2007, Omoigui states:

The unifying Law of Pain indicates that there is an inflammatory soup of biochemical mediators that are present in all pain syndromes.

The resolution of inflammation is fibrosis or scar tissue (Manjo, 2004). In 2004, Manjo states:

“After a day or two of acute inflammation, the connective tissue—in which the inflammatory reaction is unfolding—begins to react, producing more fibroblasts, more capillaries, more cells—more tissue. In other words, granulation tissue arises from normal connective tissue, but it cannot be mistaken for normal connective tissue, because its fibroblasts are plump and activated.”

“Fibrosis means an excess of fibrous connective tissue. It implies an excess of collagen fibers, with a varying mixture of other matrix components. It can be a local phenomenon, as an end result to chronic inflammation and of wound healing.”

“When fibrosis develops in the course of inflammation it may contribute to the healing process.” “By contrast, an excessive or inappropriate stimulus can produce severe fibrosis and impair function.”

“Why does fibrosis develop? In most cases the beginning clearly involves chronic inflammation. Fibrosis is largely secondary to inflammation.”

Fibrotic granulation tissue is capable of maintaining an inflammatory response long after the completion of the healing process, a component of chronic pain (Cyriax, 1982). In 1982, Cyriax states:

“Fibrous tissue appears capable of maintaining an inflammation, originally traumatic, as the result of a habit continuing long after the cause has ceased to operate.”

“It seems that the inflammatory reaction at the injured fibers continues, not nearly during the period of healing, but for an indefinite period of time afterwards, maintained by the normal stresses to which such tissues are subject.”

Tension within the scar granulation tissue initiates remodeling, reducing inflammation. [Supports the need for early persistent mobilization and chiropractic adjustments]. Once again, in 1982 Cyriax states:

“Tension within the granulation tissue lines the cells up along the direction of stress. Hence, during the healing of mobile tissues, excessive immobilization is harmful. It prevents the formation of a scar strong in the important direction by avoiding the strains leading to due orientation of fibrous tissue and also allows the scar to become unduly adherent, e.g. to bone.”

•••••••••

Americans eat a lot of fat. This is important in a trauma clinical practice because one particular type of fat is linked to both acute and chronic pain. In fact, this fat was the central theme of the 1982 Nobel Prize in Medicine/Physiology, which pertained to pain.

Our bodies have somewhere around 75 trillion cells. The cell membranes are composed primarily of fat, and it is the fat that we habitually eat. Trauma/injury to tissues disrupts the cell membranes, releasing the fat and activating enzymes that metabolize those fats (Maroon, 2010).

There is a type of dietary fat that is linked to inflammation and pain. If people eat this pro-inflammatory pain producing fat, then it is that fat that is released as a consequence of trauma/injury. This fat is not a saturated fat. It is a poly-unsaturated fatty acid called arachidonic acid. Arachidonic acid is an omega-6 fat. Our bodies have enzymes that convert arachidonic acid into pro-inflammatory hormones (leukotrienes, thromboxanes, prostaglandins); and these pro-inflammatory hormones are linked to pain (Omoigui, 2007; Boswell, 2006; Maroon, 2006; Cleland, 2006; Goldberg 2007; Maroon, 2010).

The primary American source of dietary arachidonic acid is eating meat. Meat is not bad per se. Meat becomes bad when the animal is fed junk food that makes it fat and sick. Economically, our food animals are fed the food that is most fattening. That’s because they are sold by the pound. Fatter animals are worth more in the marketplace. Our food animals are proven to become really fat on a diet of corn and/or soybeans.

Of course, fattening animal feed is a poor economic choice unless it is also cheap feed. In today’s political environment, the cheapest feed is the food that is subsidized by the taxpayers; and it makes so much sense: lobbying our politicians to use taxpayer dollars to grow corn and soybeans creates a win-win situation for all, cheap meat (this is sarcasm, as noted below).

Meat, a source of complete proteins, historically was an expensive and therefore rare commodity (at least since the Agricultural Revolution, beginning about 10,000 years ago). Animals become big and fat on a corn/soybean diet, and if the taxpayers subsidize these crops, the corn and soybeans also become much cheaper. By extension, the taxpayers (and the Chinese, or whoever is buying our debt) are subsidizing the cost of meat, making it so that nearly all Americans can afford to eat meat daily (if they choose to do so).

Recent evidence suggests that nearly 100% of our chickens and 93% of our cows are exclusively fed corn (USA Today, 2008). A major source of feed for our farmed fish is soybeans (Greenberg, 2010). Sadly, when these food animals are fed corn and/or soybeans, they have enzymes that convert the fat found in these crops (linoleic acid) into the pro-inflammatory hormone precursor fat, arachidonic acid.

These pro-inflammatory fats are in the omega-6 family. One hundred years ago, the amount of omega-6 fats consumed by Americans was about 2 pounds per year. Today, as a consequence of politics and economics, consumption of omega-6 fats has increased to about 25 pounds (Boswell, 2006). In contrast, the quantity of anti-inflammatory omega-3 fats in our diets had decreased substantially.

Paleolithic humans evolved with a ratio of omega-6/omega-3 fats of about 1/1; the average modern ratio is about 25/1 (Boswell, 2006). This means that the average American is prone to pain syndromes as a consequence of dietary choices and habits. At any given moment, 28% of Americans are suffering from pain (Krueger, 2008); the omega-6/omega-3 ratio is critical. The sarcastic downside from the win-win of cheap fat meat is that it predisposes the consumers, Americans, to pain syndromes. This has resulted in Americans consuming more than 70 million nonsteroidal anti-inflammatory drug (NSAID) prescriptions every year; and 30 billion over-the-counter NSAID tablets are sold annually (Maroon, 2006). The cost is $17 billion per year (Krueger, 2008). Michael Pollan states in his 2008 book In Defense of Food “The billions we spend on anti-inflammatory drugs such as aspirin, ibuprofen, and acetaminophen is money spent to undo the effects of too much omega-6 in the diet.”

Dietary strategies to rebalance the omega-6/omega-3 ratio have proven to prevent an/or reverse many of these pathological syndromes. Such strategies have proven to be more effective than pain medications about 88% of the time (Maroon, 2006).

••••••••••

This month (August 2011), primary research from the Department of Bioengineering and the Department of Neurosurgery, University of Pennsylvania, provides some of the most important insights into the patho-biomechanics of chronic whiplash injury to date. The study was published in the journal Annals of Biomedical Engineering, and titled (Quinn, 2011):

Detection of Altered Collagen Fiber Alignment in the
Cervical Facet Capsule After Whiplash-Like Joint Retraction

The authors review that the cervical facet joint is the primary source of pain in patients with whiplash-associated disorders; yet, most clinical studies show no radiographic or MRI evidence of tissue injury. To evaluate this puzzle, these authors used quantitative polarized light imaging to assess the potential for altered collagen fiber alignment in human cadaveric cervical facet capsule specimens during and after a joint retraction simulating whiplash exposure.

The authors document that the whiplash mechanism involves a retraction event to the facet joint capsular ligaments. Although no evidence of ligament damage was detected during whiplash-like retraction, mechanical and microstructural changes of the facet joint capsular ligaments were identified following these whiplash loadings. The retraction experience produced significant decreases in ligament stiffness and increases in ligament laxity. The strained capsule regions showed altered fiber alignment, “suggesting the altered mechanical function may relate to a change in the tissue’s fiber organization.” The altered capsular ligament fiber alignment occurred without any tears that would classically be identified with diagnostic imaging, including radiographs and/or MRI. Consequently, the authors indicate that whiplash kinematics is a potential cause of microstructural damage that is not detectable using standard clinical imaging techniques.

The authors make these key points:

1) This is the first study that has assessed changes in tissue microstructural organization of the facet capsule following whiplash-like loading.

2) “Whiplash is a common cause of chronic neck pain, and the cervical facet joint has been identified as the site of pain in the majority of these cases.”

3) “Up to 62% of people affected by whiplash injuries report pain lasting 2 years or more after injury.”

4) Facet joint injuries cannot be imaged in most whiplash patients with x-rays or magnetic resonance imaging (MRI).

5) “The lack of any definitive evidence of facet capsular ligament damage following whiplash, despite the high incidence of facet-mediated pain, suggests radiographic and MRI techniques may lack the resolution or contrast to identify these subtle injuries.”

6) Low-speed rear-end impact collision causes the lower cervical spine to undergo a combination of compression, posterior shear, and extension. “This combination of forces and moments primarily induces a retraction of each vertebra in the posterior direction relative to its adjacent inferior vertebra in the lower cervical spine prior to head-headrest contact.” The facet capsular ligaments are at risk for excessive motion during this vertebral retraction, creating subfailure injuries to the facet capsule. “The facet capsular ligament may sustain partial failures and/or unrecovered deformation during whiplash.”

7) Facet joint injury causes altered collagen fiber organization and facet capsular ligament laxity that may produce persistent pain. “Neither partial failure nor capsule rupture is required to initiate facet-mediated pain, suggesting painful facet joint injuries cannot be identified through traditional load-based or medical imaging techniques.”

8) Prior to ligament visible rupture or mechanical failure, there is an anomalous fiber realignment, which may be used as a marker for subfailure capsule injury.

9) The retraction caused permanent deformation of ground substance materials of the ligament, leading to altered collagen fiber organization. This tissue damage may be sufficient to induce an inflammatory response or nociceptor firing in the ligament.

10) “These findings would suggest that radiographic or MRI diagnostic approaches may lack the resolution to detect the microstructural changes that can occur in the facet capsule without overt capsule rupture after a whiplash exposure.”

11) “Facet joint displacements that produce persistent pain symptoms also induce laxity in the capsular ligament and collagen fiber disorganization.”

12) “The detection of altered fiber alignment and unrecovered strain observed after facet retraction in the current study would suggest that whiplash-like loading may be sufficient to generate facet-mediated pain.”

This study indicates that whiplash injury causes microstructural changes, anomalous fiber realignment and laxity of the facet capsular ligaments. These injuries may cause permanent deformation of ground substance of the ligament, leading to altered collagen fiber organization. These injuries are subfailure in magnitude, but are capable of causing pain and permanent alterations in capsular mechanics. These injuries are not identifiable clinically, with x-ray, or MRI imaging. The tissue damage may be sufficient to induce an inflammatory response and/or nociceptor firing.

The anomalous fiber realignment noted in this study is probably

analogous to the writings of Cyriax when he stated that fibrotic granulation tissue is capable of maintaining an inflammatory response long after the completion of the healing process. This inflammatory granulation tissue becomes a factor in the initiation of chronic pain perception. Consequently, Cyriax also states “…that the scar tissue remains painful whenever tension is put upon it, perhaps for decades.”

This is an important study advancing the understanding of whiplash injury pathoanatomy, yet I believe there is still a missing piece. The authors document post-traumatic anomalous fiber realignment, but they only speculate that it is associated with pain producing inflammation. They offer no evidence for the existence of an actual inflammatory process. Fortunately, the next study does just that.

••••••••••

Clas Linnman (from Harvard Medical School) and an international team of colleagues published a study in April of this year (2011) titled:

Elevated [11C]-D-Deprenyl Uptake in Chronic Whiplash Associated Disorder Suggests Persistent Musculoskeletal Inflammation

These authors note that there are few diagnostic tools for chronic musculoskeletal pain, and especially for whiplash injury. In agreement with Quinn above, they note that structural imaging methods seldom reveal pathological alterations that can account for a patient’s ongoing pain. Therefore, they sought to visualize inflammatory processes in the neck region by means of Positron Emission Tomography (PET) using an inflammatory marker, 11C-D-deprenyl, or DDE. They evaluated 22 patients with chronic pain after a rear impact car accident and 14 healthy controls. The whiplash-injured subjects had pain and reduced motion but no neurological signs.

The whiplash-injured patients displayed significantly elevated inflammatory tracer uptake in the neck, suggesting that whiplash patients have signs of local persistent peripheral tissue inflammation. The authors concluded that inflammation and its associated pain in the periphery could be objectively visualized and quantified with PET using the inflammatory tracer DDE. Key points from this study include:

1) “Chronic musculoskeletal pain syndromes are common, cause extensive individual suffering and place a large burden on health care in society. Yet, pain remains notoriously difficult to visualize and diagnose objectively.”

2) “The pathophysiology of persistent pain is elusive and there is a great need for ways to visualize and quantify pain mechanisms.”

3) In a sub-portion of the population, “whiplash injuries proceed to chronic debilitating pain.”

4) “Structural imaging does not capture on-going biological processes; where as molecular imaging with positron emission tomography (PET) has the potential to visualize such mechanisms.”

5) The authors present evidence that shows “DDE can be used to visualize chronic inflammatory processes.”

6) The site of inflammation “appeared to be localized to adipose tissue surrounding deep cervical muscles.” “The tracer retention observed in fatty regions surrounding deep cervical muscle may indicate that adipose tissue is actively involved in the inflammatory process.”

7) Patients displayed elevated DDE retention in cervical soft tissue, suggesting that localized chronic inflammation is apparent in many chronic pain whiplash patients.

8) “A large subset of patients with chronic pain after a whiplash injury displayed elevated DDE retention, suggestive of persistent peripheral tissue inflammation.”

9) “The possibility to visualize and quantify sites of inflammation in chronic pain may be very useful in diagnosis and treatment monitoring.”

SUMMARY POINTS:

All pain has an inflammatory component.

Post-traumatic inflammation is often the consequence of the membrane release of the arachidonic acid fat cascading into pro-inflammatory hormones, including prostaglandin E2 (PGE2). [Therefore omega-6/-3 balancing is an important clinical strategy].

Inflammation alters the pain threshold and increases pain perception.

The resolution of inflammation is granulation, fibrosis, or scar tissue.

Fibrotic granulation tissue is capable of maintaining an inflammatory response long after the completion of the healing process, a component of chronic pain.

Whiplash trauma can create anomalous fiber alignment and granulation tissue.

From whiplash, granulation tissue and inflammation occurs as a consequence of subfailure injuries. Therefore, these injuries cannot be visualized with either x-rays or MRI.

Persistent post-traumatic inflammation has been linked to chronic pain syndrome. This inflammation can be documented with PET using the inflammatory tracer DDE.

Tension within the scar granulation tissue initiates remodeling, reducing inflammation. This supports the need for early persistent mobilization, exercise, and chiropractic adjustments.

I believe that anti-inflammatory omega-6/omega-3 balancing is critical in chronic pain management.

Personal Injury Cases and the Chiropractor

Chiropractic education instills that personal injury cases have two components:

An injury component. This component requires healthcare, treatment to the injured patient.A legal component. This component involves the protection of the injured patient’s legal rights.

Chiropractors who treat personal injury patients understand that their clinical protocols can influence the legal component of a personal injury case. Specifically, there is no substitute for:

Taking a good case history
Doing a thorough orthopedic and neurological examination
Taking good quality and adequate radiographs
Creating an accurate diagnosis that can be supported by history, complaints and examination findings
Doing standard and thorough daily charting
Using standard measurement outcomes, such as pain drawings, Oswestry, Roland Morris, Neck Disability Index, SF-36, algometer, visual analogue scale, etc.
Doing periodic (monthly) thorough subjective and objective re-evaluations with a follow-up written report of findings
Having referred the patient out for needed diagnostic procedures that are not done in the chiropractic office (MRI, EMG, SEP, SPECT, etc.)
Having referred to other health care providers and/or colleagues for verifying or additional opinions
Being able to determine when the patient has reached a point of maximum improvement, and consequently ending regularly scheduled treatment so that the case can proceed towards settlement of claim
Being knowledgeable and conversant in the academic concepts of soft tissue injury, such as the phases of injured tissue healing, the relationship of vehicle damage to patient injury, the influence of pre-accident degenerative joint disease, and the influence of variables such as pre-accident awareness or head rotation

Sincerely,

Daniel J. Murphy DC, DABCO

REFERENCES

Maroon J, Bost JW, Maroon A; Natural anti-inflammatory agents for pain relief; Surgical Neurological International; December 2010.

Boswell M, Cole EB; American Academy of Pain Management; Weiner’s Pain Management: A Practical Guide for Clinicians; Seventh Edition, 2006, pp.584-585.

Maroon JC, Bost JW; Omega-3 Fatty acids (fish oil) as an anti-inflammatory: an alternative to nonsteroidal anti-inflammatory drugs for discogenic pain; Surgical Neurology; 65 (April 2006) 326– 331.

Cleland LG, James MJ, Proudman SM; Fish oil: what the prescriber needs to know; Arthritis Research & Therapy; Volume 8, Issue 1, 2006, pp. 402.

Goldberg RJ, Katz J; A meta-analysis of the analgesic effects of omega-3 polyunsaturated fatty acid supplementation for inflammatory joint pain; Pain; May 2007, 129(1-2), pp. 210-223.

Manjo G, Joris I; Cells, Tissues, and Disease, Principles of General Pathology; Second Edition; Chapter 13: “Chronic Inflammation: Defense at a Price”; Oxford University Press; 2004.

Cyriax, James, M.D., Orthopaedic Medicine, Diagnosis of Soft Tissue Lesions, Bailliere Tindall, Vol. 1, (1982).

USA Today, November 12, 2008, quoting Proceedings of the National Academy of Sciences.

Greenberg P; Four Fish, The Future of the Last Wild Food; The Penguin Press, New York, 2010.

Krueger AB, Stone AA; Assessment of pain: a community-based diary survey in the USA; Lancet; 2008 May 3;371(9623):1519-25.

Pollan, M; In Defense of Food; 2008, pg. 131.

Quinn KP, Winkelstein BA; Detection of Altered Collagen Fiber Alignment in the Cervical Facet Capsule After Whiplash-Like Joint Retraction; Annals of Biomedical Engineering; August 2011, Vol. 39, No. 8, pp. 2163–2173.

Linnman C, Appel L, Fredrikson M, Gordh T, Soderlund A, Langstrom B, Engler H; Elevated [11C]-D-Deprenyl Uptake in Chronic Whiplash Associated Disorder Suggests Persistent Musculoskeletal Inflammation; Public Library of Medicine (PLoS) ONE; April 6, 2011, Vol. 6 No. 4, pp. e19182.

August 2011

admin — Tue, 02 Aug 2011 22:01:13 +0000

Diagnosis

Format

Clinical Features

Connecting The Dots

Personal injury cases have two components: a healthcare component and a legal component. Much of the legal component of a personal injury case is hinged upon the records of the healthcare provider. The healthcare records are often thoroughly reviewed. Accurate and complete healthcare records will protect the legal component of a personal injury claim. In contrast, healthcare records that are inaccurate will hurt the legal component of the case.

What is the patient’s diagnosis?

A diagnosis is a guess as to what is wrong with the patient. It is the treating doctor’s best guess as to the root causes of the patient’s symptoms and signs. As more information is obtained, the diagnosis will often change or be confirmed. For example, the doctor will probably suspect a discogenic L5 nerve root radiculopathy when a patient presents with low back and unilateral leg pain that extends below the knee, and examination shows a positive straight-leg-raising test at 35°, weakness of the extensor hallicus longus muscle, and hypoesthesia in an L5 dermatomal pattern. The diagnosis is confirmed when an exposed MRI shows a posterolateral L4 disc herniation compressing the L5 nerve root.

Also, for the legally defined expert treating doctor, the diagnosis falls under the standard of reasonable probability. As an example, it is often claimed that the cause of back pain is actually unknown or unproven in 85% of cases (Chou). Yet, essentially no healthcare providers list the diagnosis as “unknown.” Therefore, doctors often list a diagnosis based on reasonable probability.Seattlepersonal injury attorney Richard Adler (Adler) often defines reasonable probability as a 51% or greater chance of accuracy. I have heard him say often that the personal injury-treating doctor who has qualified as an expert to testify should be 100% certain that their opinion is at least 51% accurate. As an example, published studies (Kuslich) indicate that the tissue origin of pain in chronic low back pain patients is the annulus of the disc is more than half of the cases. This constitutes a reasonable probability. Another example is that published studies (Bogduk) indicate that the tissue origin of pain in chronic whiplash-injured patients is the facet joints in more than half of the cases. This also constitutes reasonable probability. A third example indicates that if a whiplash-injured patient had pre-accident degenerative joint disease of the cervical spine, follow-up x-rays taken 7 years later indicate that 55% developed degenerative disc disease at adjacent levels (Hohl); one could state that patients with pre-accident degenerative joint disease of the cervical spine who sustain a motor vehicle collision injury, will have a reasonable probability of developing disc degeneration at an adjacent level within the next seven years.

An actual example is a court case I testified in with an experienced personal injury attorney. This attorney thoroughly explored my opinions during my direct examination. After direct examination comes cross-examination by the insurance company attorney. His attempt to discredit me proceeded as follows:

QUESTION:
What is in your hand?

ANSWER:
A cup.

QUESTION:
What is in the cup?

ANSWER:
Water.

QUESTION:
Are you certain?

ANSWER:
Yes.

QUESTION:

Can you state with the same degree of certainty that you have a cup of water in your hand that the testimony you gave during your direct examination is accurate?

OBJECTION (by the plaintiff attorney who had just completed my direct examination):

[He] is holding the doctor to a standard that is not the law. The standard is to a reasonable probability, a 51% chance or greater, not to 100% certainty.

JUDGE:
Sustained.

ANSWER:

I state with the same degree of certainty that I have a cup of water in my hand that the testimony I gave is reasonably probable.

It is not below the standard for a diagnosis to be incorrect, as long as it is consistent with the evidence presented in a particular case. The classic evidence collected in a whiplash injury (or in most musculoskeletal cases) includes the history, the complaints, the examination findings, and imaging, such as x-rays, stress radiographs, videofluoroscopy, MRI, CT scan, etc.

Because treatment is designed to improve the pathophysiological process expressed in the diagnosis, appropriate treatment should improve the patient’s symptoms and signs. When expected improvement does not present, it is possible that the diagnosis was incorrect. Additional diagnostic investigations or possible referral to another provider is warranted.

In our electronic age, the clinical diagnosis is a numerical code or codes. Statisticians, policy makers, politicians, governmental agencies, reimbursement assessment personnel, electronic billing services, etc., like and even demand, these numerical diagnostic codes. It makes it much easier to evaluate and control the health care provider and the case. It makes it much easier to create policy and establish “outcome evidence.” These codes create simplicity.

However, what if the simple code is purposefully or inadvertently inaccurate? What if the health care provider used codes that have historically proven to generate better reimbursement rather than codes that more accurately represent the patient’s true clinical status? What if the health care provider had some educational gaps or lack of educational understanding of certain physiological processes and consequently used an incorrect diagnostic code? Then statistics, policies, and “outcome evidence” would all be erroneous.

In addition, and quite importantly, the convenience and simplicity of diagnostic codes may over simplify the true extent or uniqueness of a particular patient’s injuries. This scenario is particularly adverse for a patient with a personal injury because it could influence aspects of the legal component of the patient’s casee.

I have a friend who is both a chiropractor and a personal injury attorney. As a personal injury attorney, he has worked for both the plaintiff (for our injured patient) and for the defense (for the insurance company of the person who caused the injury to our patient). He has repeatedly expressed to me that the most prevalent “weak link” in a personal injury case treated by health care providers is the diagnosis. It is his position that as a rule, the diagnosis in the file or in the insurance billing forms is not supported by the history, complaint, examination findings and/or imaging studies. My friend has often expressed to me that he can discredit most health care providers by officially asking them a handful of questions pertaining to their diagnosis. In fact, my friend says that when discrediting the expertise of the treating doctor, probing the details and accuracy of the diagnosis is so simple and effective, that it is his standard starting point, and often the only process the doctor will have to endure before loss of credibility is assured.

Most health care providers use multiple diagnoses on every patient. Consequently, for a whiplash-injured patient, words (or codes) such as sprain, strain, myofascial pain syndrome, intervertebral disc syndrome, facet syndrome, radiculitis, radiculopathy, neuritis, neuropathy, nerve compression syndrome, headache, cervicogenic headache, subluxation, instability, carpal tunnel syndrome, thoracic outlet syndrome, double crush syndrome, myelopathy, cauda equina syndrome, fibromyalgia, etc., are commonly found.

For each and every word used in the diagnosis, the health care provider should be able to do the following:

Define the word. The dictionary denotation is not always necessary. Often, a layperson’s connotation will suffice, and may be preferred.

Know the history that is consistent with the word. As an example, are there historic facts that might distinguish a sprain injury from a strain injury? Is the diagnostic word used consistent with the given history?

Know the clinical features for the word. What examination findings (clinical features) support the diagnosis? As an example, what are the examination findings that support the diagnosis of strain; or, what are the examination findings that support the diagnosis of sprain?

Knowing what the clinical features are is important, but is not enough. The clinical features must be found in the records. A diagnosis not supported by the records is problematic and probably will be challenged on occasion.

EXAMPLE 1, Strain:

QUESTION:
Your diagnosis includes strain injury to the posterior cervical-thoracic spine. What is a strain injury?

ANSWER:
The soft tissue that moves bones are muscles. Muscles are attached to the bone by tendons. A strain is an injury to a muscle or to a tendon. A strain injury is considered to be a soft tissue injury because it does not involve injury to the bone.

QUESTION:
What history is consistent with a strain injury?

ANSWER:
There are three classic historic mechanisms for a strain injury:

A mechanism of overstretching. The injury occurs at the extreme of motion.
A mechanism of muscle contracting against a load that is too great for the muscle. The injury occurs in the middle of the range of motion.
Unaccustomed repetitive contracting of a muscle. The injury occurs in the middle of the range of motion.

QUESTION:
In this case, was one or more of these mechanisms documented through the taking of the patient’s history?

ANSWER:

Yes. The history is that of a whiplash mechanism, which is a classic example of muscle overstretching.

QUESTION:

What are the clinical features of a strain injury?

ANSWER:

Pain on resistive efforts.
Pain on stretching.
Pain on moderate digital pressure.
Alterations of muscle tone (usually it is increased).
Alterations of normal palpatory textures (such as swelling, edema).

QUESTION:
Can you please show me where these clinical findings are documented in your records?

ANSWER:

[You had better be able to do this, show him/her where the clinical features are documented in the records].

EXAMPLE 2, Sprain:

QUESTION:

Your diagnosis includes sprain injury to the facet capsular ligaments of the lower cervical spine. What is a sprain injury?

ANSWER:

The soft tissue that stops the movement of a bone at the joint is the ligament. Ligaments attach bones to bones at the joint. If the joint is moved too far, the ligament is injured. This injury to the ligament is called a sprain. A sprain injury is also considered to be a soft tissue injury because it does not involve injury to the bone.

QUESTION: What history is consistent with is a sprain injury?

ANSWER:

Ligaments are not injured in the middle of the range of motion. Rather, ligaments are only injured after the end of the range of motion is reached, and then motion exceeds the normal end of the range of motion. A history of exceeding the normal magnitude of range of motion is necessary for a sprain injury.

QUESTION:

In this case, is there a history of exceeding the normal magnitude of the range of motion?

ANSWER:

Yes. The history is that of a whiplash mechanism, which is a classic example of exceeding the normal range of motion of the facet joints of the cervical spine. Whiplash injury is proven to exceed the range of motion of the cervical spine facet joints, injuring the facet joint capsular ligaments. This constitutes a sprain injury.

QUESTION:
What are the clinical features of a sprain injury?

ANSWER:

Pain at the end of the passive range of motion.
Associated protective muscle spasm at the end of the passive range of motion.
Point tenderness with digital pressure over the injured ligament.
Palpable or visible swelling.
The diagnosis is confirmed if stress radiographs show signs of clinical instability or segmental hypermobility.

QUESTION:
Can you please show me where these clinical findings are documented in your records?

ANSWER:

[Once again, you had better be able to do this, show him/her where the clinical features are documented in the records].

EXAMPLE 3, Right C7 discogenic radiculopathy:

QUESTION:

Your diagnosis includes right C7 discogenic radiculopathy. What is a C7 radiculopathy?

ANSWER:

The bones of the spine are called vertebrae. Between every two adjacent vertebrae exits two nerves, one from the right side and the other from the left side. Because these nerves are attached to the spinal cord, they are called nerve roots. Radiculopathy means that a nerve root is injured and is not functioning properly. C7 indicates that the nerve root in question is exiting from between the sixth and seventh cervical vertebrae.

QUESTION:

What does discogenic radiculopathy mean?

ANSWER:

It means that the cause of the injury and dysfunction to the C7 nerve root is the C6-C7 intervertebral disc. The C6-C7 disc is irritating or pressing upon the C7 nerve root, causing its dysfunction. The disc is causing the radiculopathy, or discogenic radiculopathy.

QUESTION:

What history is consistent with a discogenic radiculopathy?

ANSWER:

There are two classic historic mechanisms for a discogenic radiculopathy:

1) As a consequence of injury.

2) As a consequence of degenerative disease.

QUESTION:

In this case, was one of these mechanisms documented through the taking of the patient’s history?

ANSWER:

Yes. The history is that of a whiplash mechanism, which can injure the intervertebral disc, causing irritation and dysfunction of the adjacent nerve root.

QUESTION:
Could the discogenic radiculopathy in this case be as a consequence of degenerative disease?

ANSWER:

No. The initial x-rays, which were taken the day following the whiplash injury, showed no signs of pre-accident degenerative disease. In addition, the symptoms and signs of discogenic radiculopathy developed acutely, immediately after being involved in this motor vehicle collision. It is therefore reasonably probable that the C7 discogenic radiculopathy was caused by the forces produced during this collision, the causation is post-traumatic. The cause is not degenerative.

QUESTION:
What are the clinical features of a C7 discogenic radiculopathy?

ANSWER:

Symptoms include pain radiating from the neck and into the arm, and often into the hand.

The symptoms are aggravated by performing the shoulder depression test.

The symptoms are aggravated upon compressing the head into the spine (foramina compression test), especially if the neck is slightly laterally flexed to the right, and even more likely if the neck is both laterally flexed to the right with simultaneous right side rotation (Spurling’s test).

A diminished right triceps deep tendon reflex.

Weakness in the C7 myotomes (triceps [elbow extension], wrist flexors, finger extensors), possibly accompanied with atrophy of the associated muscles.

Altered superficial sensation in a C7 dermatomal pattern, classically the anterior surface of the third digit.

QUESTION:
Can you please show me where these clinical findings are documented in your records?

ANSWER:
Again, you had better be able to do this, show him/her where the clinical features are documented in the records; not all of the clinical features need to be present to diagnose a suspected C7 radiculopathy, but having over half positive would argue in favor of the reasonable probability of such a diagnosis].

QUESTION:
Are there any imaging tests that confirm your diagnosis?

ANSWER:
Yes. To confirm my diagnosis, I ordered an MRI which was taken one week following the injury. The results show a right-sided herniation of the C6-C7 disc putting pressure on the right C7 nerve root.

The treating doctor should be able to answer this format of questions for every word that is used in the diagnosis.

Diagnostic Format

The patient’s diagnosis will and often should change (become updated) as the patient’s clinical status changes as a consequence of time and/or treatment. Spasm, radiculopathy, headache, etc., can resolve. Acute problems can become subacute or chronic. Post-traumatic scar tissue or fibrosis may develop.

To adequately describe a patient’s biological uniqueness subsequent to an injury, for more than 30 years I have advocated the three-point diagnostic format. This format also helps organize the doctor’s thoughts as to updating the diagnosis. The three components are:

1) List the mechanism of injury. The mechanism of injury never changes from the beginning of a case though the end of the case. The initial mechanism of injury is always the same throughout the case. A typical example would be:

Hyperextension strain and sprain injury to the lower cervical and upper thoracic paraspinal soft tissues.

2) List things that occurred as a consequence of the mechanism of injury. These resulting problems can change or resolve as a consequence of time and/or treatment. Therefore, updated diagnoses will often reflect these changes in the second part of the diagnostic format. I tend to list these resulting problems into four categories.

Examples include:

The second part of the diagnostic format may also include multifaceted syndromes, such as intervertebral disc syndrome, fibromyalgia syndrome, carpal tunnel syndrome, cervicogenic headache, temporomandibular joint dysfunction, vertigo, canalithiasis, BPPV (benign paroxysmal positional vertigo), thoracic outlet syndrome, etc.

The typical example would continue:

Hyperextension strain and sprain injury to the lower cervical and upper thoracic paraspinal soft tissues; with resulting myalgia and spasm of the affected muscles, altered instantaneous axis of rotation of the occiput-atlas-axis (subluxation complex), and right C7 motor and sensory radiculopathy

3) The third component of the diagnostic format is a listing of factors that makes a particular case more difficult or complicated than the usual case. It is important to list these factors not as being caused by the mechanism of the injury, but rather as factors that pre-existed the injury. Consequently, they complicate the recovery of those things that were caused by the injury.

Examples include:

Degenerative joint disease

Discogenic spondylosis

Facet joint arthrosis

Central canal stenosis

Cervical rib(s)

Hemi or Demi vertebrae

Scoliosis

Tropism

Lumbosacral transitional segment

Spondylolisthesis

Old spinal fractures

Osteoporosis

Rheumatoid arthritis

ETC.

As a rule, the third (complicating) component of the diagnosis does not change as a function of time or treatment. The typical diagnosis example would continue:

I advocate performing a complete reevaluation of the patient every 12 visits. At that time, depending on symptoms, signs, and examination findings, the second part of the diagnosis should be updated. Regardless of the billing diagnosis, the three point diagnostic format should be found in the file with as much detail as possible to truly represent the uniqueness of the patient’s injuries and unique complicating factors to recovery. This approach will help protect the legal component of the patient’s injury claim.

Personal Injury Cases and the Chiropractor

Chiropractic education instills that personal injury cases have two components:

An injury component. This component requires healthcare, treatment to the injured patient.

A legal component. This component involves the protection of the injured patient’s legal rights.

Chiropractors who treat personal injury patients understand that their clinical protocols can influence the legal component of a personal injury case. Specifically, there is no substitute for:

Taking a good case history
Doing a thorough orthopedic and neurological examination
Taking good quality and adequate radiographs
Creating an accurate diagnosis that can be supported by history, complaints and examination findings
Doing standard and thorough daily charting
Using standard measurement outcomes, such as pain drawings, Oswestry, Roland Morris, Neck Disability Index, SF-36, algometer, visual analogue scale, etc.
Doing periodic (monthly) thorough subjective and objective re-evaluations with a follow-up written report of findings
Having referred the patient out for needed diagnostic procedures that are not done in the chiropractic office (MRI, EMG, SEP, SPECT, etc.)
Having referred to other health care providers and/or colleagues for verifying or additional opinions
Being able to determine when the patient has reached a point of maximum improvement, and consequently ending regularly scheduled treatment so that the case can proceed towards settlement of claim
Being knowledgeable and conversant in the academic concepts of soft tissue injury, such as the phases of injured tissue healing, the relationship of vehicle damage to patient injury, the influence of pre-accident degenerative joint disease, and the influence of variables such as pre-accident awareness or head rotation

Sincerely,

Daniel J. Murphy DC, DABCO

REFERENCES

Chou R, Qaseem A, Snow V, Casey D, Cross JT, Shekelle P, Owens DK, for the Clinical Efficacy Assessment Subcommittee of the American College of Physicians and the American College of Physicians/American Pain Society Low Back Pain Guidelines Panel; Diagnosis and Treatment of Low Back Pain: A Joint Clinical Practice Guideline from the American College of Physicians (ACP) and the American Pain Society (APS); Annals of Internal Medicine; Volume 147, Number 7, October 2007, pp. 478-491.

Adler R; From Injury to Action: Navigating Your Personal Injury Claim; AdlerGiersch; 2011.

Hohl M; The Cervical Spine; The Cervical Spine Research Society; Lippincott, 1989; page 440.

Kuslich S, Ulstrom C, Michael C; The Tissue Origin of Low Back Pain and Sciatica: A Report of Pain Response to Tissue Stimulation During Operations on the Lumbar Spine Using Local Anesthesia; Orthopedic Clinics of North America, Vol. 22, No. 2, April 1991, pp.181-7.

Bogduk N, Aprill C; On the nature of neck pain, discography and cervical zygapophysial joint blocks; Pain. August 1993;54(2):213-7.

The Chiropractic Impact Report

May 2012

April 2012

March 2012

Spinal Joint Mechanoreceptors, Proprioception, and The Pain Gate

The Mechanoreceptors

February 2012

Whiplash Injuries Review and Update on Facet Joint Trauma

POINT OF VIEW

Point of View

January 2012

December 2011

Chronic Pain Syndrome And Vitamin D

November 2011

Children In Motor Vehicle Collisions

October 2011

Soft Tissue Injury and Repair

September 2011

Whiplash Update Two Important New Studies And Their Clinical Applications

August 2011

Whiplash Injuries Review
and Update on Facet Joint Trauma