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Anky Losing

The Use of Matrix Repatterning® on a Case of Ankylosing Spondylitis: A Case Report

by Dr. George B. Roth, B.Sc., D.C., N.D.

 

Abstract

Purpose: To investigate the effect of Matrix Repatterning® techniques in a case of a long-standing, moderately severe case of ankylosing spondylitis.

Methods: Matrix Repatterning uses a manual scanning procedure to determine the location of primary restrictions, followed by mechanical testing to determine specific vectors of fascial tension. Treatment is applied manually with light force directed into the resistance barriers. Four treatments were administered over a period of three months. Measurements included occiput-to-door (OTD) for determination changes in general range of spinal extension, and fingers-to-floor (FTF) to determine changes in range of spinal flexion. X-ray studies were also compared before and after the treatment regime.

Results: OTD measurements were 28 cm. before treatment regime and 12.7 cm. after the completion of treatment. FTF measurements were 22.2 cm. before treatment and 12.7 cm. after the completion of the treatment regime.

Conclusions: These findings suggest that Matrix Repatterning procedures may be beneficial in the management of ankylosing spondylitis, and suggest that a randomized controlled trial within a broader population base would be indicated.

Key Words: Matrix Repatterning, primary restriction, indicator, resistance barrier, induction, directional recoil


 

INTRODUCTION

Ankylosing spondylitis (AS) is a chronic inflammatory form of arthritis that affects the spinal joints with the onset of symptoms in the late teens to mid-twenties. The hallmark feature of AS is the involvement of the joints at the base of the spine where the spine joins the pelvis - the sacroiliac (SI) joints. Radiographic findings include sacroiliac joint sclerosis and fibro-calcific hyperproliferation of spinal joints. Laboratory findings include an elevation of HLA-B27. The disease course is highly variable, and while some individuals have episodes of transient back pain only, others have more chronic severe back pain that leads to differing degrees of spinal stiffness over time. In almost all cases the disease is characterized by acute painful episodes and remissions (periods where the problem settles). AS is three times more common in men than in women. It typically affects young people, beginning between the ages of 15 and 30. It may affect younger people also, although in very young people it may take a slightly different form, causing pain around the heels, knees, and hips rather than beginning with the spine. Onset after age 40 is uncommon.

Indications for a diagnosis of Ankylosing Spondylitis:

  • Frequent low back pain
  • Back stiffness that lasts longer than 30 minutes first thing in the morning or after a long period of rest.
  • Pain and tenderness in the ribs, shoulder blades, hips, thighs, shins, heels and along the bony points of the spine.
  • In the early stages, there may be mild fever, loss of appetite and general discomfort.
  • The eyes can also be affected and symptoms can include eye pain, watery eyes, red eyes, blurred vision, and feeling sensitive to bright light.

Various mechanisms have been postulated for its etiology, including genetic predisposition (Masi AT, King JR, Burgos-Vargas R 2001). The condition is considered progressive, with increasing severity of articular involvement, loss of mobility and the need for surgical intervention in more severe cases. AS tends to run in families. The tissue typing system is the Human Lymphocyte Antigen (HLA) system. One of the tissue types, HLA-B27, is found in only 6% of the broad population but occurs in approximately 93% of individuals with AS. The HLA-B27 tissue type, while not causing AS, does predispose individuals with the B27 tissue type to developing AS. Having the tissue type itself does not necessarily indicate the presence of AS, it simply increases a predisposition. Identifying the activating agent, that later triggers AS, is the focus of much current research. This case study suggests that altered biomechanics, due to a history of significant trauma, may be one mechanism for the expression of this genotypic pattern.

Matrix Repatterning® and The Tensegrity Matrix

Matrix Repatterning® is based on a revolutionary, new model of the underlying structure of organic tissue – the Tensegrity Matrix – that may explain the complex interrelationship of all the structural components of the body. It extends the basic concept of the tissue response to injury, beyond the level of joint, muscle and ligament, to include all structures of the body as potential sources of dysfunction.

According to a leading researcher in the field of cellular mechanics and structure:

Re-evaluation of human pathophysiology in this context reveals 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. This process may be altered by changes in cell mechanics, variations in extracellular matrix structure, or by deregulation of the molecular mechanisms by which cells sense mechanical signals and convert them into a chemical or electrical response. Molecules that mediate mechanotransduction, including extracellular matrix molecules, transmembrane integrin receptors, cytoskeletal structures and associated signal transduction components, may therefore represent targets for therapeutic intervention in a variety of diseases. (Ingber 2003)

Dr. Ingber goes on to state:

Mechanical forces are critical regulators of cellular biochemistry and gene expression as well as tissue development.

Mechanotransduction – the process by which cells sense and respond to mechanical signals – is mediated by extracellular matrix, transmembrane integrin receptors, cytoskeletal structures and associated signaling molecules.
Many ostensibly unrelated diseases share a common feature that their etiology or clinical presentation results from abnormal mechanotransduction. Mechanotransduction may be altered through changes in cell mechanics, extracellular matrix structures or by deregulation fo the molecular mechanisms by which cells sense mechanical signals or convert them into a chemical response.

Molecules that mediate mechanotransduction may represent future targets for therapeutic intervention in a variety of diseases. Insights into the mechanical basis of tissue regulation also may lead to development of improved medical devices, engineered tissues, and biomimetic materials for tissue repair and reconstruction.

Masi (2003) also implicates axial muscular dysfunction in the development of the joint pathology in ankylosing spondylitis. These factors may play a role in the transmission of excessive force directly to the spinal articular structures, leading to some the local pathophysiology (Hatfaludy, Hannsky, Vandenburgh 1989; Lewitt 1985).

METHODS

Subject

A 51-year-old male presented to our clinic with a long-standing history of back, hip and neck pain as well as severe loss of spinal and pelvic mobility and significant hyperkyphosis of the thoracic spine. His history included a fall from a cliff from a height of 30-40 feet at the age of 10, with multiple injuries, and a fall off a ladder onto his back at the age of 15. He developed progressive pain and limitation of motion during his mid to late teens. He was formally diagnosed with AS at the age of seventeen.

The patient was assessed posturally and orthopedically in order to determine the extent of functional biomechanical limitation. All ranges of spinal and pelvic motion were severely restricted as well as global hip movement, especially on the right. Overall height was measured at 5 feet 9 inches (175 cm.). Occiput-to-door (OTD) was measured at 28 cm. Fingers-to-floor (FTF) was measured at 22.2 cm. Right hip movement was measured using visual references, at 10 degrees of flexion, 5 degrees of external rotation, 0 degrees of internal rotation and 5 degrees of abduction. Neck range of motion, other than flexion and extension, was 0 degrees of right rotation, 3 degrees of left rotation, 3 degrees of right lateral flexion and 0 degrees of left lateral flexion.

Procedures

The Matrix Repatterning assessment involves the use of touch or pressure (induction or recoil) on various parts of the body to elicit a response in another standardized area of the body (the indicator), in order to determine the site of the primary sites of tissue pathophysiology (primary restrictions). This process is based on the premise of the fascial continuity of the tensegrity matrix, as postulated by Ingber, Levin and others (Levin 2002).

From this assessment procedure, certain areas of primary involvement were determined as potential treatment sites. These included the spine, the pelvic bones (ilium, pubis, ischium) and the fascial structures associated with several internal organs, namely the heart, liver, kidneys and spleen.

These areas were treated using a minimal application of manual force into the areas found from the assessment, using vectors determined by the use of the indicator response. The mechanism of conversion of the pathophysiological state to one of more normal tone due to the application of manual methods has been speculated on several researchers (Marsland, Brown 1942; Tanaka 1981; Oschman 2000). A total of four treatments were applied over a three-month period. The protracted nature of the clinical course was mainly the result of the patient’s rather busy work schedule.

RESULTS

OTD measurements were 28 cm. before treatment regime and 12.7 cm. after the completion of treatment. FTF measurements were 22.2 cm. before treatment and 12.7 cm. after the completion of the treatment regime. Right hip movement was 30 degrees of flexion, 10 degrees of external rotation, 10 degrees of internal rotation and 20 degrees of abduction. Neck range of motion, other than flexion and extension, was 10 degrees of right rotation, 10 degrees of left rotation, 10 degrees of right lateral flexion and 10 degrees of left lateral flexion. The patient’s overall height was remeasured following the course of treatment at 5 feet 11 inches (180.34 cm.). No data analysis was carried out at the time of this report.

The patient has also subjectively reported an increase in the level of comfort in the activities of daily living as well as in his rather demanding work as a finish carpenter. One of his early indications of subjective improvement was that he was able to see the top of the door-frame (see photographs below; this is an 8 foot high door seen in these photographs) he was working on for the first time in many years. He also stated that he no longer needed to support himself using his hand against the mirror, in order to shave in the mornings.

Posture before treatment Posture after treatment
Posture before treatment
Posture after treatment

DISCUSSION

Symptoms, especially in chronic musculoskeletal conditions, may often be the result of compensatory patterns of tension created within the body in response to primary sites of tissue injury in other locations within the kinetic chain (Ingber 2003). These same mechanisms have been postulated in the use of other therapeutic models (D’Ambrogio, Roth 1997). The primary lesion may often be asymptomatic after the acute phase, as the brain adapts to the continuing background stimulation from local pain receptors (Wall 2000). The resulting alteration in range of motion may create patterns of strain in secondary sites, resulting in painful movement and inflammation.

Matrix Repatterning is a manual approach, aimed at addressing the primary sources of tension in the connective tissue-fascial system. It incorporates a novel approach to the determination of the location of primary tissue response to injury (primary restrictions). This approach is based on the application of the principal of fascial continuity inherent in a new, proven model of structure at the microscopic and macroscopic levels (Wang, Butler, Ingber 1993; Ingber 1998; Levin 2002). Treatment is gentle and painless, and can often result in global reorganization and postural stabilization, encouraging the body towards normal, pain-free function. It is currently in use by physical therapists, chiropractors, physicians, osteopaths, athletic trainers, massage therapists and veterinarians on five continents and ten countries around the world. Matrix Repatterning courses are currently available through The Matrix Institute.

The present discussion is limited to a case report on one case of ankylosing spondylitis. In this current report, we have attempted to apply the basic principles of Matrix Repatterning to a moderately severe, long-standing case of ankylosing spondylitis. It has been the author’s experience with other spinal and articular conditions that joints are often under abnormal mechanical stress due to primary restrictions exerting their influence throughout the body. He has speculated that part of the compensatory mechanisms inherent in the body include the ability of joints to tolerate these disturbed mechanical forces through what has been described as non-physiologic motion, sometimes referred to as joint play (Zohn, Mennel 1976). It has been speculated that this feature of joint function does indeed serve the role of maintaining a degree of functional capacity, thereby allowing the organism the ability to ambulate and pursue the necessities of life, despite significant loss of function or mobility in other structures. This could be viewed as a compensatory mechanism, which up to a certain tolerance level, is capable of substituting additional range in ancillary structures in order to complete desired tasks, such as ambulation, manipulation of the environment and other necessary functions. The fact that some of these aberrant functional ranges result in strain to certain tissues, as well as pain, is secondary to the fact that they may serve, in certain instances to preserve life. It may also be conjectured that the price of compromised or aberrant motion may result in abnormal stresses on these secondary areas, thus resulting in the types of cellular changes alluded to by Ingber and others.

It is this latter premise that is considered one of the possible mechanisms in the development of ankylosing spondylitis. The fact that the spinal and pelvis joints may be responding to local and non-local sources of restriction within the overall continuous fascial fabric (the matrix) of the body, may explain the cellular and ultimately the physiological mechanisms, including genetic expression prevalent in this disorder (Ingber 2003).

CONCLUSIONS

Our clinical experience has suggested that visceral sources of primary restriction are often the sequelae to impact trauma. It has been postulated that the fluid contained in these organs responds by absorbing the energy of impact, thus leading to a hydrostatic expansion exerted against the internal parenchyma and fascial containment of these structures. The resultant force is therefore presumed to exert a strong mechanical influence on the cellular structure of these components, resulting in the development of cellular/molecular mechanical distortion to the linearly-stiffened status of the protein scaffold within the cells (Ingber 1998). By this same mechanism, it has been speculated that bone, increased in density relative to other tissues due to the deposition of high concentration of mineral salts within and throughout its collagen reinforcing elements, may also respond by absorbing a significant amount of the energy of an impact into its cellular/molecular structure (Duncan 1995). Certain other mechanisms of mechanical stress on tissue may also be factors in the development this and related conditions. Namely the hyperproliferative tendency of the articular structures, may be associated with the aberrant mechanical forces created the excessive mechanical stress placed across them (Ingber 2000; Ko, Arora, McCulloch 2001).

This case demonstrates a possible link to the effects of injury (impact and/or strain) to the musculoskeletal system and possible internal injuries linked to the effects of impact, as mechanisms in the etiology of the development of AS. The result of Matrix Repatterning intervention appears to demonstrate a possible resource in alleviating some of the mechanical effects of injury as they may relate to the expression of ankylosing spondylitis. Future studies may include specified controls and a more extensive subject base.

References:

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Ingber DE. 1998. The architecture of life. Scientific American 278:48-57.

Ingber DE. 2002. Mechanical signaling and the cellular response to extracellular matrix in angiogenesis and cardiovascular physiology. Circulatory Research 91:877-887.

Ingber DE. 2003. Mechanobiology and diseases of mechanotransduction. Annals of Medicine 35:1-14.

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

Roth, George B. 2000. A New Approach to Frozen Shoulder: A Pilot Study Using Matrix Repatterning®. Presented at the Conference of Canadian Chiropractic Research Centers.

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Wall, Patrick. 2000. The Science of Pain and Suffering. London: Weidenfeld and Nicholson.

Wang N, Butler JP, Ingber DE. 1993. Mechanotransduction across the cell surface and through the cytoskeleton. Science 260:1124-1127.

Waylonis GW; Perkins RH. 1994. Post-traumatic fibromyalgia. A long-term follow-up. American Journal of Physical Medicine and Rehabilitation 73(6):403-12.

Zimmerman J. 1990. Laying-on-of-hands healing and therapeutic touch: a testable theory. BEMI Currents, Journal of the Bio-Electro-Magnetics Institute 2:8-17.

Zohn DA, Mennell JM, 1976, Musculoskeletal Pain: Diagnosis and Physical Treatment, Little Brown, Boston, pp 3-12.

Dr. George Roth, D.C., N.D. is a practitioner with over 25 years experience in the field of energy medicine. He has developed a number of leading-edge technologies to assist individuals in the achievement of optimal wellness. He lectures extensively to various groups and educational institutions and is a published author.

For more information, or to make an appointment, please contact

Dr. George B. Roth,
Matrix Wellness Solutions,
67 Prospect St., Newmarket, Ontario, Canada, L4G 1R1
Phone: 905 836-WELL (9355)
1-877-905-7684
Fax: 905 726-8575
Email: info@matrixrepatterning.com
Web site: www.MatrixRepatterning.com

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