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Joint Motion’s Influence On…

Tissue Response, Infection, Inflammation, Trauma & Healing…

And The Potential Pitfalls Of Clinical Joint Immobilization

Back in 1984, orthopedic surgeon Sir James Cyriax, MD, reviewed The Concept Of Motion in his Textbook of Orthopaedic Medicine, Diagnosis of Soft Tissue Lesions (1). In this text, Dr. Cyriax carefully noted that harmful infections create tissue destruction, resulting in inflammation.

A current prevailing concept in explaining this observation is the body recognizes this inflammation and attempts to “wall off” the infectious pathogens by creating a fibrous response.

This is in fact in agreement with Dr. William Boyd who states in his pathology text (2):

“The inflammatory reaction tends to prevent the dissemination of infection. Speaking generally, the more intense the reaction, the more likely the infection to be localized.”

Physiologist and physician Arthur Guyton (3) provides support for this concept as well in his statement:

“One of the first results of inflammation is to ‘wall off’ the area of injury from the remaining tissues. This walling-off process delays the spread of bacteria or toxic products.”

Some interpret this type of response to mean that (in a world prior to the availability of antibiotics, inflammation, with reactive walling-off fibrosis to contain pathogens) it is desirable because it increases survivability of the host.

As explained by three vaunted researchers Cyriax, Boyd, and Guyton above, the trigger to the walling-off fibrosis response of the body is inflammation.

Problems appear to only seriously arise when the inflammatory trigger is non-infectious inflammation.

In such cases, excessive tissue fibrosis creates local impairments in biomechanical function.

This impairment in local biomechanical function affects performance, can generate pain, and accelerate degenerative changes. These impairments can adversely affect the patient for years or even decades.

Fortunately, abnormal tissue fibrosis can be minimized with early, persistent, controlled motion. Once established, abnormal tissue fibrosis can be improved with the use of a variety of motion applications.

Cyriax’s text (1) states the following:

“The excessive reaction of tissues to an injury is conditioned by the overriding needs of a process designed to limit bacterial invasion.

If there is to be only one pattern of response, it must be suited to the graver of the two possible traumas. However, elaborate preparation for preventing the spread of bacteria is not only pointless after an aseptic injury, but is so excessive as to prove harmful in itself. The principle on which the treatment of post-traumatic inflammation is based is that the reaction of the body to an injury unaccompanied by infection is always too great.” (Cyriax, p.14)

Cyriax finds support in the sports trauma text authored by physicians Steven Roy and Richard Irvin (4), who state:

“It is important to realize that the body’s initial reaction to an injury is similar to its reaction to an infection. The reaction is termed inflammation and may manifest macroscopically (such as after an acute injury) or at a microscopic level, with the latter occurring particularly in chronic overuse conditions.” (Roy, p. 125)

Additional support for these concepts from Cyriax and Roy/Irvin are the writings of

physician I. Kelman Cohen and associates (5). In their 1992 text Wound Healing, these authors note:

“There are two important consequences of being a warm-blooded animal. One is that body fluids make optimal culture media for bacteria. It is to the animal’s advantage, therefore, to heal wounds with alacrity in order to reduce chances of infection.”

“The prompt development of granulation tissue forecasts the repair of the interrupted dermal tissue to produce a scar.” In addition to providing tensile strength, scars are believed to be a barrier to infectious migration.

The chronic nature of this scar tissue or fibrosis is expressed in the 1998 article by Thomas Melham and associates (6).

These authors note that post-traumatic scar tissue can cause pain with activity, pain on palpation, decreased range of motion, and loss of function, and that these problems are resistant to surgery and to conventional physical.

Excessive scar tissue contributes to chronic soft tissue dysfunction that cause significant disabilities and time lost from work or training activities, and these problems are often difficult to successfully treat. The authors extensively elaborate on the mechanical and neurological adverseness caused by connective tissue fibrosis, noting:

“Many athletes develop excessive connective tissue fibrosis (scar tissue) or poorly organized scar tissue in and around muscles, tendons, ligaments, joints, and myofascial planes as a result of acute trauma, recurrent microtrauma, immobilization, or as a complication of surgical intervention.”

“This can lead to soft tissue adhesions, tendonitis, tendonosis, fascial restrictions, and chronic inflammation or dysfunction which in many cases responds poorly to conventional treatments.”

These authors present an argument that carefully and precisely applied external forces “appear to stimulate connective tissue remodeling through resorption of fibrosis, along with inducing repair and regeneration of collagen secondary to fibroblast recruitment.”

Pain, Healing, and MOTION…

As noted above, abnormal tissue fibrosis can be minimized with early, persistent, controlled motion.

Once established, abnormal tissue fibrosis can be improved with the use of a variety of motion applications.

Support for the value in using motion to treat soft-tissue injuries has been throughout the literature for decades.

As an example, Beverly Hills neurosurgeon Emil Seletz, associated with the medical school at the University of California, Los Angeles (UCLA), noted in the Journal of the American Medical Association in 1958, the following, with respects to the management of whiplash soft-tissue injuries (7):

“During injury, hemorrhage within the capsular ligaments gives rise to swelling of the nerves and eventually adhesions between the dural sleeve and the nerve root; these factors give rise to symptoms that may be prolonged for months or even years after the injury.”

“In reviewing the types of treatment with a number of specialists in this field, it is found that, while therapy naturally varies to suit the individual need, it consists primarily of local heat in the form of hot wet packs and cervical traction, followed by very gentile massage and manual rotations.”

“The importance of a carefully planned scheme of treatment must be emphasized to the patient, and treatments must be religiously carried out daily during the first two or three weeks (and then about three times weekly), depending, of course, on the individual case.”

“Delay or faulty treatment leads to adhesions about the facets and scarring about the capsular ligaments, persistent spasm, congestive lymph edema, and fibrosis of muscles, swelling, and eventual adhesions of nerves within the nerve root canals.”

“The resultant faulty posture in neglected cases enhances the degeneration of the intervertebral disks, as well as spur formation in the lateral co-vertebral articulations, which on the roentgenogram has come to be known as traumatic arthritis.”

“I cannot too strongly emphasize the urgency of early and persistent therapy, always by a specialist in this field.”

“Occasionally, a patient is seen with persistent complaints of head, neck, and shoulder pain, who has had on surgical exposure persistent swelling and adhesions of several nerve roots within the dural sleeve of exit. It is most likely that early, persistent, and adequate therapy by those expertly trained in physical medicine will prevent most patients from developing a surgical condition.”

On this very same topic, Cyriax’s comments include a review of the 1940 primary research by ML Stearns (8), stating:

“Her (Stearns) main conclusion on the mechanics of the formation of scar tissue was that external mechanical factors, were responsible for the development of the fibrillary network into orderly layers.

Within four hours of applying a stimulus, an extensive network of fibrils was already visible around the fibroblasts; during the course of 48 hours this became dense enough to hide the cells almost completely: and in 12 days a heavy layer of fibrils had appeared.

At first the fibrils developed at random, but later they acquired a definite arrangement, apparently as a direct result of the mechanical factors.

Of these factors, movement is obviously the most important and equally obvious it is most effective and least likely to cause pain before the fibrils have developed an abnormal firm attachment to neighboring structures.

When free mobility was encouraged from the onset, the fibers in the scar were arranged lengthwise as in a normal ligament.

Gentle passive movements do not detach fibrils from their proper formation at the healing breach but prevent their continued adherence at normal sites.

The fact that the fibrils rapidly spread in all directions provides sufficient reason for beginning movements at the earliest possible moment; otherwise they develop into strong fibrous scars (adhesions) that so often cause prolonged disability after a sprain.” (Cyriax, p. 15)

Cyriax notes further:

“When pain is due to bacterial inflammation, Hilton’s advocacy of rest remains unchallenged and is today one of the main principles of medical treatment.

When, however somatic pain is caused by inflammation due to trauma, his ideas require modification.

When non-bacterial inflammation attacks the soft tissues that move, treatment by rest has been found to result in chronic disability, later, although the symptoms may temporarily diminish.

Hence, during the present century, treatment by rest has given way to therapeutic movement in many soft tissue lesions.

Movement may be applied in various ways: the three main categories are:

(a) active and resistive exercises:

(b) passive, especially forced movement: and

(c) deep massage.” (Cyriax, p.14)

“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.” (Cyriax, p.15)

In 1983, sports physicians Steven Roy and Richard Irvin also note (4):

“The trauma, or initial lesion, leads to an increase of the friction that occurs between moving tissues as well as to a release of chemical mediators, both of which may start the inflammatory process.

This process may present macroscopically with a number of signs, particularly (a) pain (b) swelling, and (c) redness and warmth. However, microtrauma may not present with any of these signs, particularly during the early stages, even though the inflammation is proceeding at the microscopic level.” (p. 125)

“The injured tissues next undergo remodeling, which can take up to one year to complete in the case of major tissue disruption.

The remodeling stage blends with the later part of the regeneration stage, which means that motion of the injured tissues will influence their structure when they are healed.

This is one reason why it is necessary to consider using controlled motion during the recovery stage.

If a limb is completely immobilized during the recovery process, the tissues may emerge fully healed but poorly adapted functionally, with little chance for change, particularly if the immobilization has been prolonged.

Another reason for encouraging controlled motion is that any adhesions that develop will be flexible and will thus allow the tissues to move easily on each other.

Caution should be observed during the first two weeks, as mentioned previously, as the tensile strength of the tissues may be markedly reduced.” (p.127)

In 1986, physician John Kellett notes (9):

Acute inflammation is beneficial when one has acute infection. However, the “acute inflammatory phase of the body’s response to trauma is apparently of no benefit.”

“The micropathology of acute soft tissue trauma has been investigated. Healing of ligaments and soft tissue injuries in general has been shown to occur by fibrous repair (scar tissue) and not by regeneration of the damaged tissue.”

“Early mobilization, guided by the pain response, promotes a more rapid return to full activity.”

“Early mobilization, guided by the pain response, promotes a more rapid return to full functional recovery.”

“The collagen is remodeled to increase the functional capabilities of the tendon or ligament to withstand the stresses imposed upon it.”

“It appears that the tensile strength of the collagen is quite specific to the forces imposed on it during the remodeling phase: i.e. the maximum strength will be in the direction of the forces imposed on the ligament.”

Dr. Kellett summarizes the benefits of early mobilization following soft tissue injury as follows:

1) Improvement of bone and ligament strength, reducing recurrence of injury.

2) The strength of repaired ligaments is proportional to the mobility of the ligament, resulting in larger diameter collagen fiber bundles and more total collagen.

3) “Collagen fiber growth and realignment can be stimulated by early tensile loading of muscle, tendon, and ligament.”

4) Collagen formation is not confined to the healing ligaments, but adheres to surrounding tissues. The formation of these adhesions between repairing tissues and adjacent structures is minimized by early movement.

5) With motion, “joint proprioception is maintained or develops earlier after injury, and this may be of importance in preventing recurrences of injuries and in hastening full recovery to competitive fitness.”

6) The nutrition to the cartilage is better maintained with early mobilization.

7) Following this acute inflammatory phase and largely guided by the pain response of the patient, early mobilization is commenced, based upon the premise that the stress of movement on repairing collagen is largely responsible for the orientation and tensile strength of the tendons and ligaments.

Dr. Cohen (5) and associates also comment even further on the value of range of motion exercises in the management of soft tissue injury, by stating:

“During the phase of wound contraction, the active cellular process is locked into position by increasing amounts of rigid collagenous scar. Frequent, gentle exercise can be used to put an extremity joint through a full range of motion and keep the newly developing scar tissue stretched and remodeled. Frequent use of the range of motion exercises is important to keep the developing and contracting scar tissue from becoming a rigid, fixed scar contracture. Range of motion exercises concentrate on remodeling the newly laid collagen before it develops into a rigid scar contracture.” (p. 110)

In 1994, Halldor Jonsson and associates (10) performed surgical evaluations of 50 patients with chronic whiplash symptoms, showing a “high incidence of discoligamentous injuries in whiplash-type distortions.” The authors noted:

“The injured spinal segments had become increasingly stiffer over 5 years, which may reflect healing of unrecognized soft tissue injuries.”

“The most likely source of radicular symptoms is perineural scarring.

Therefore, patients with neck distortions after traffic accidents should be mobilized early within the limits of pain to prevent scar transformation of hidden injuries.”

In 1996, orthopedic surgeon Joseph Buckwalter, MD, from the University of Iowa, adds to the concepts with the following points from an article published in the journal Hand Clinics (11):

1) Treatment of tissue injuries with prolonged rest delays recovery and can cause irreversible changes in tissue strength and function.

2) Early motion of tissue injuries maintains the structure and composition of normal bone, tendon, ligament, articular cartilage and muscle.

3) Immobilization of dense fibrous tissues (tendon, ligament, and joint capsule) causes the tissues to be weaker and stiffer.

4) Complete restoration of normal ligament insertion structure and mechanical properties require up to one year of activity, which can mean some patients may require a year of management following these injuries.

5) Ageing decreases the adaptive response to repetitive loading, indicating that older patients do not respond as well to the same treatment delivered to younger patients, and that older patients may require more treatment and have a worse prognosis for complete recovery.

6) Early motion during the repair and remodeling phases of healing can decrease or prevent adhesions.

In 1997, US President Bill Clinton tore the tendon of his quadriceps at the attachment to the patella. After surgical repair, President Clinton was put into a passive range of motion device to improve the timing and quality of healing of his injury.

The device used to treat Mr. Clinton was researched by Canadian orthopedic surgeon Robert Salter. Dr. Salter has published many primary research studies on the physiological effects of passive motion.

Much of this research is summarized in his 1993 book Continuous passive Motion, A Biological Concept for the Healing and Regeneration of Articular Cartilage, Ligaments, and Tendons; From Origination to Research to Clinical Applications (12).

It can be reasonably assumed that President Clinton received the best treatment in the world for his injuries. All indications reflect that he enjoyed a speedy and complete recovery.

Lastly, as presented here, an excellent review on The Concept Of Motion was published in the journal The Physician and Sports Medicine in 2000 by Pekka Kannus, MD, Ph.D. (13).

Dr. Kannus is chief physician and head of the Accident and Trauma Research Center and sports medicine specialist at the Tampere Research Center of Sports Medicine at the UKK Institute in Tampere, Finland. His article titled “Immobilization or Early Mobilization After an Acute Soft-Tissue Injury?” notes:

“Experimental and clinical studies demonstrate that early, controlled mobilization is superior to immobilization for primary treatment of acute musculoskeletal soft-tissue injuries and postoperative management.”

Prolonged inflammation may lead to excessive scarring. Therefore, early, effective treatment seeks to prevent prolonged inflammation and excessive scarring.

“The current literature on experimental acute soft-tissue injury speaks strongly for the use of early, controlled mobilization rather than immobilization for optimal heating.”

Experimentally induced ligament tears in animals heal much better with early, controlled mobilization than with immobilization.

“The superiority of early controlled mobilization has been especially clear in terms of quicker recovery and return to full activity without jeopardizing the subjective or objective long-term outcome.”

“Controlled experimental and clinical trials have yielded convincing evidence that early, controlled mobilization is superior to immobilization for musculoskeletal soft-tissue injuries. This holds true not only in primary treatment of acute injuries, but also in their postoperative management. The superiority of early controlled mobilization is especially apparent in terms of producing quicker recovery and return to full activity, without jeopardizing the long-term rehabilitative outcome. Therefore, the technique can be recommended as the method of choice for acute soft-tissue injury.”

Two Additional Supportive Studies…

Suportive Study #1

Early Mobilization of Acute Whiplash Injuries (14)

British Medical Journal

March 1986

In this study, 61 whiplash-injured patients were randomized to treatment with either “a period of immobility using a soft collar and simple analgesia before gradual mobilization” (standard treatment), or a alternative treatment involving “daily neck exercises and mobilization.” The authors concluded that:

“Results showed that eight weeks after the accident the degree of improvement seen in the actively treated group compared with the group given standard treatment was significantly greater for both cervical movement and intensity of pain.”

“Our results confirmed expectations that initial immobility after whiplash injuries gives rise to prolonged symptoms whereas a more rapid improvement can be achieved by early active management without any consequent increase in discomfort.”

Supportive Study #2

Early Intervention in Whiplash-Associated Disorders

A Comparison of Two Treatment Protocols (15)

Spine

July 15, 2000

This study was designed as a prospective randomized trial in 97 patients with a whiplash injury caused by a motor vehicle collision. Patients were randomly assigned to initial cervical collar or to early active mobilization. The authors concluded:

“In patients with whiplash-associated disorders caused by a motor vehicle collision, treatment with frequently repeated, active submaximal movements combined with mechanical diagnosis and therapy is more effective in reducing pain than a standard program of initial rest, recommended use of a soft collar, and gradual self-mobilization.”

“The main finding in this study was that active treatment of whiplash associated disorder resulted in a significantly greater pain reduction than standard [initial immobilization] treatment.”

“In patients with WAD caused by a motor vehicle collision, early treatment with frequently repeated active submaximal movements combined with mechanical diagnosis and therapy is more effective in reducing pain than treatment with initial rest, recommendation of a soft collar, and a gradual introduction of home exercises.”

Conclusions

The discussion and references above support the concept that adverse pathogens cause tissue destruction and subsequent inflammation. The body appears to respond in a manner to wall-off the area of inflammation by over healing the region with a fibrous response.

The fibrous response appears to be a physical barrier, reducing the ability of the pathogens to spread to other regions of the body, thereby improving the host’s chances for survival.

However, when inflammation is caused by non-infectious mechanisms, the same fibrotic tissue response occurs. In such cases, without infectious pathogens, the fibrotic tissue response is excessive, resulting in mechanical harm to the host.

This harmful tissue fibrosis is worsened with early immobilization of the affected tissues.

This tissue fibrosis is minimized with early persistent controlled mobilization.

Established harmful tissue fibrosis is best managed with specific controlled motion for purpose of adhesion rupture and remodeling. The motion to treat established harmful fibrotic tissue should be individualized to the needs of the patient.

Different fibrotic tissues respond optimally to different categories of controlled motion application:

1) Periarticular tissue fibrosis responds optimally to joint adjustments / specific line-of-drive manipulation.

2) Muscle fibrosis responds well to active resistive exercise.

3) Non-contractile tissue (tendon, fascia, ligament, etc.) fibrosis responds best to manually applied tissue friction.

Most patients have a combination of tissues that are adversely affected, depending on the mechanism of injury or stress.

Consequently, a combination of these applications of controlled motion, by someone who is expertly trained, is often required to achieve timely, efficient, and long-lasting clinical improvements.

REFERENCES

1) Cyriax, James; Textbook of Orthopaedic Medicine, Diagnosis of Soft Tissue Lesions, Bailliere Tindall, Volume 1, eighth edition, 1982.

2) Boyd, William, Pathology, Lea and Febiger, 1952.

3) Guyton, Arthur, Textbook of Medical Physiology, Saunders, 1986.

4) Roy, Steven; Irvin, Richard; Sports Medicine: Prevention, Evaluation, Management, and Rehabilitation, Prentice-Hall, 1983.

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

6) Melham TJ, Sevier TL, Malnofski MJ, Wilson JK, Helfst RK, Chronic ankle pain and fibrosis successfully treated with a new noninvasive augmented soft tissue mobilization technique (ASTM); Medicine Science Sports Exercise, June 1998; 30(3): 801-4.

7) 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.

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

9) Kellett J, Acute soft tissue injuries–a review of the literature;

Medicine and Science in Sports and Exercise. Oct. 1986;18(5):489-500.

10) 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.

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

12) 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.

13) 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.

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

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

Back Pain, Acute Soft Tissue Injuries, Mobilization, & Fibromyalgia A Review Of The Literature

Medicine and Science in Sports and Exercise. Oct. 1986;18(5):489-500.

John Kellett

FROM ABSTRACT:

The pathological processes [of soft tissue injury and repair] at a cellular level are described in three phases: acute inflammatory, repair, and remodelling.

The management of acute soft tissue trauma is embodied in the acronym RICE for rest, ice, compression, and elevation during the first 48 to 72 h.

Additional benefit from anti-prostaglandin medications has not been clearly demonstrated in clinical trials, and if used, these medications should be restricted to the first 3 days.

Cryotherapy (crushed ice) for 10 to 20 min, 2 to 4 times/day for the first 2 to 3 days is helpful in promoting early return to full activity.

Early mobilization, guided by the pain response, promotes a more rapid return to full activity.

Early mobilization, guided by the pain response, promotes a more rapid return to full functional recovery.

Progressive resistance exercises (isotonic, isokinetic, and isometric) are essential to restore full muscle and joint function.

Rehabilitation is complete when the injured and adjacent tissues are restored to full pain-free functional capacity under competitive conditions in association with the necessary level of cardiovascular respiratory fitness.

THIS AUTHOR ALSO NOTES:

A common classification of soft tissue injuries is based on severity:

1) Grade 1 (first degree)

“Mild pain at the time of injury or within 24 h of injury, especially when stress is applies to the injury; local tenderness may or may not be present.”

2) Grade 2 (second degree)

“The person notices pain during activity and usually has to stop; pain and local tenderness are moderate to severe when the injury is stressed.”

3) Grade 3 (third degree)

“Complete or near complete rupture or avulsion of at least a portion of a ligament or tendon with severe pain or loss of function; a palpable defect may be present; stressing a ruptured ligament may, paradoxically, be painless due to the loss of continuity of the tissue.”

In a third degree ligament sprain, “the ligament may appear intact macroscopically yet have complete loss of load-carrying ability.”

Third degree ligament injury may require surgical management.

In inter-muscular hematoma, the blood tracks distally from the site of injury and appears as a bruise some distance from the site of injury, after some time.

Intra-muscular hematoma remains confined by epimysium and may take three times longer to heal than inter-muscular hematoma.

In ligaments, microscopic collagen fiber failure begins at 7 to 8% strain.

Ligament strain greater than 7 to 8% results in failure of the ligament to resume its original length after removal of the load (plastic deformation), and to more extensive collagen failure.

Ligaments strains as high as 20 to 40% can occur before signs of failure are apparent.

“Continuity of ligaments may be macroscopically apparent (e.g. arthroscopically) even with complete loss of the load-carrying capacity of the ligament.”

“The micropathology of acute soft tissue trauma has been investigated. Healing of ligaments and soft tissue injuries in general has been shown to occur by fibrous repair (scar tissue) and not by regeneration of the damaged tissue.”

[The Fibrosis Of Repair]

The phases of soft tissue injury repair are:

Phase 1:

The Acute Inflammatory or Reaction Phase.

Lasts up to 72 hours.

Characterized by vasodilation, immune system activation of phagocytosis to remove debris, the release of prostaglandins and inflammation.

Prostaglandins play a prominent part in pain production and increased capillary permeability (swelling).

The wound is hypoxic, but macrophages can perform the phagocytosis duties anaerobically.

Phase 2:

The Repair or Regeneration Phase.

48 hours to 6 weeks.

Characterized by the synthesis and deposition of collagen.

The collagen that is deposited is “not fully oriented in the direction of tensile strength.

Collagen fibers tend to contract between 3 and 14 weeks after injury, and perhaps for as long as 6 months, decreasing tissue elasticity. [This is probably why we note reduced range of motion during this phase.]

This phase is “largely one of increasing the quantity of the collagen” but this collagen is not laid down in the direction of stress.

Phase 3:

The Remodeling Phase.

This phase may last up to “12 months or more.”

“The collagen is remodeled to increase the functional capabilities of the tendon or ligament to withstand the stresses imposed upon it.”

“It appears that the tensile strength of the collagen is quite specific to the forces imposed on it during the remodeling phase: i.e. the maximum strength will be in the direction of the forces imposed on the ligament.” [This could argue for the need for specific line-of-drive joint adjustments.] This phase is largely “an improvement of the quality” (orientation and tensile strength) of the collagen.

“Normal ligaments are composed of type I collagen, whereas damaged (and healed) ligaments contain a large proportion of immature type III collagen which is deficient in the number of cross-linkages between and within the tropocollagen subunits.”

The remodeled scar is deficient in both content and quality 40 weeks after injury, as there is a plateau in scar collagen concentration at about 70% of normal.

Acute inflammation is beneficial when one has acute infection. However, the “acute inflammatory phase of the body’s response to trauma is apparently of no benefit.” [Most Important]

“Numerous studies have shown the effectiveness of ice therapy in reducing the pain and period of disability to soft tissue injuries.”(4 references)[Important]

In contrast, “early heat treatment leads to an increase in the blood flow to the injured area with an exaggerated acute inflammatory response.” [Important]

“The advantages of cryotherapy in treating soft tissue injuries have been well documented.” Ice within 48 hours of injury reduces disability of ankle sprains from 15 days to 10 days.

Cryotherapy is superior to heat, especially when applied within 24 hours of injury.

Cryotherapy should be limited to a maximum duration of 30 minutes.

“The use of anti-prostaglandin medications or nonsteroidal anti-inflammatory drugs (NSAIDs) in the management of acute soft tissue injury has become increasingly common in recent years despite a lack of adequate clinical studies to support such a practice.” [Important]

Prostaglandins, especially E2, are responsible for the acute inflammatory response to trauma. [Very Important]

The use of anti-prostaglandin medications or nonsteroidal anti-inflammatory drugs (NSAIDs) should be used for no more than 72 hours or they become detrimental to the second phase of healing. [Important]

“It is well to remember that all of these types of medications have adverse effects, some minor (e.g. gastrointestinal intolerance) and some major (e.g. fatalities from bone marrow suppression).” [This is really important: common pain drugs suppress the bone marrow, the sole producer of immune system cells. In another context, taking these pain drugs when suffering from colds or flu would suppress the immune system’s ability to neutralize the pathogens.] The use of these drugs “should be restricted to a maximum of 3 days following injury.”

Corticosteroids have been shown to cause destructive changes in articular cartilage. “Steroids have a deleterious effect on collagen and direct injection into collagen may produce a permanent decrease in tensile strength.” The use of steroids for soft tissue injury has “no sound biological basis.” Steroids delay collagen repair. Steroids “retard fibroblastic activity and may well delay healing.” “Corticosteroids have little part to play in the management of soft tissue injuries.”

BENEFITS OF EARLY MOBILIZATION

1) Improvement of bone and ligament strength, reducing recurrence of injury.

2) The strength of repaired ligaments is proportional to the mobility of the ligament, resulting in larger diameter collagen fiber bundles and more total collagen.

3) “Collagen fiber growth and realignment can be stimulated by early tensile loading of muscle, tendon, and ligament.” [Important]

4) Collagen formation is not confined to the healing ligaments, but adheres to surrounding tissues. The formation of these adhesions between repairing tissues and adjacent structures is minimized by early movement.

5) With motion, “joint proprioception is maintained or develops earlier after injury, and this may be of importance in preventing recurrences of injuries and in hastening full recovery to competitive fitness.” [Important, especially for chiropractors]

6) The nutrition to the cartilage is better maintained with early mobilization.

ADVERSENESS OF IMMOBILIZATION

1) A decrease in aerobic capacity.

2) Muscle wasting and loss of strength.

3) One study showed that 8 weeks of immobilization of the anterior cruciate ligament delayed the return to full tensile strength for more than one year.

4) “Immobilization leads to a higher incidence of avulsion fractures of bony attachments of ligaments rather than ligament failure.” [Important]

MANAGEMENT RECOMMENDATIONS:

1) “The principles of management of acute soft tissue injuries have been embodied in the acronym RICE (for rest, ice, compression, and elevation) during the first 48 to 72 hours following injury.”

2) Following this acute inflammatory phase and largely guided by the pain response of the patient, early mobilization is commenced, based upon the premise that the stress of movement on repairing collagen is largely responsible for the orientation and tensile strength of the tendons and ligaments.

3) The goal of stressing repairing tissues with controlled motion is to induce adaptive response of functionally stronger connective tissues. However, excessive stressing of the repairing tissues may result in further damage. Consequently, any sign or symptom which suggests a worsening of the injury (severe pain) is a clear indication to reduce the motion stress on the tissues.

4) “The masking of such symptoms by analgesics is contraindicated.” [Important]

5) Drinking alcohol increases local hemorrhage and the acute inflammatory response, and should therefore be avoided.

KEY POINTS FROM DAN MURPHY

1) Ligaments collagen fibers begin to fail at 7 to 8% strain.

2) Ligament strains as high as 20 to 40% can occur before signs of failure are apparent.

3) The healing of ligaments and soft tissue injuries in general has been shown to occur by fibrous repair or scar tissue, [The Fibrosis Of Repair] and not by regeneration of the damaged tissue.

4) There are three primary phases of soft tissue injury repair:

A) Phase 1, The Acute Inflammatory or Reaction Phase.

Lasts up to 72 hours, is characterized by pain and swelling, and mediated primarily by prostaglandin E2.

B) Phase 2, The Repair or Regeneration Phase.

48 hours to 6 weeks, characterized by the synthesis and deposition of collagen, but this collagen is not fully oriented in the direction of tensile strength.

C) Phase 3, The Remodeling Phase.

This phase may last up to “12 months or more.”

“The collagen is remodeled to increase the functional capabilities to withstand the stresses imposed upon it;” this remodeling occurs in response to specific forces applied to the tissues.

5) Healed ligaments still have problems. There are residual weaknesses as compared to normal ligaments because of reduced cross-linkages and a plateau in scar collagen concentration at about 70% of normal.

6) When one has an infection, acute inflammation is beneficial because it helps the body neutralize the pathogen. However, the “acute inflammatory phase of the body’s response to trauma is apparently of no benefit,” and results in adverse fibrosis. Early management should therefore include ice, not heat.

7) The use of anti-prostaglandin medications or nonsteroidal anti-inflammatory drugs (NSAIDs) in the management of acute soft tissue injury should NOT be used for more than 72 hours or they become detrimental to the second phase of healing. [Important]

8) Common pain drugs suppress the bone marrow [production of immune system cells]. [This is really important]

9) Corticosteroids damage articular cartilage, weaken the collagen repair, delay collagen repair, produce a permanent decrease in collagen strength, and should therefore never be used in the management of soft tissue injuries.

10) Early mobilization of soft tissue injuries improves the healing of bone, cartilage, tendon, ligament; reduces the adverseness of adhesions, and restores joint proprioception.

11) Immobilization of soft tissue injures decreases aerobic capacity, causes muscle wasting and loss of strength that may delay full recovery for a year or more.

Chiropractic Adjuncts To Managing Patients With Fibromyalgia Syndrome

Fibromyalgia Syndrome is the third most commonly diagnosed rheumatologic disorder, following osteoarthritis and rheumatoid arthritis. Fibromyalgia is characterized by widespread pain and tenderness, fatigue, morning stiffness, and sleep disturbance. Fibromyalgia is often disabling. Fibromyalgia is often treatment resistant. Fibromyalgia can be triggered by trauma (Greenfield, Waylonis, Buskila, Neumann). Studies report that between 25% and 50% of subjects with fibromyalgia recall physical trauma immediately prior the onset of their symptoms (Al-Allaf).

Chiropractors usually manage patients with fibromyalgia by attempting to enhance the quality of mechanical neurological afferentation by improving the sagittal and horizontal planes of spinal posture and motion. However, these efforts will often worsen patient symptoms, at least temporarily.

This article reviews several adjunct approaches to the management of patients with fibromyalgia syndrome.

MALIC ACID and MAGNESIUM

In 1992, Abraham and Flechas propose that fibromyalgia is caused by a deficiency of substances needed for ATP synthesis. The nociceptive nervous system requires a steady flow of ATP to remain subthreshold. Therefore, reductions in ATP supplies could account for the lowered pain thresholds that fibromyalgia patients experience.

Abraham and Flechas explain the synergistic role of magnesium and malic acid in the genesis of ATP. They detail the biochemistry of how reductions in magnesium and malic acid would result in APT deficiency.

Abraham and Flechas then treat 15 fibromyalgia patients with daily 300-600 mg of magnesium plus 1200-2400 mg malic acid. “All patients reported significant subjective improvement of pain within 48 hours of starting” supplementation.

In 1995, Russell et al in a randomized, double blind, placebo controlled, crossover study, also used magnesium and malic acid to treat 29 patients with fibromyalgia, noting “significant reductions in the severity of all 3 primary pain/tenderness measures were observed.” Better results were observed in those taking 600 mg of magnesium and 2400 mg of malic acid, as compared to those who took lower doses. The authors note that this supplementation should continue for al least 2 months, and often for as long as 6 months.

THE SEROTONIN PATHWAY

In 2004, Borut Banic and colleagues, writing in the journal Neurology, present extensive evidence suggesting that fibromyalgia is the consequence of reduced levels of the brain neurotransmitter serotonin.

In 1998, osteopath John H Juhl also proposed that fibromyalgia could be related to reduced serotonin. He notes that researchers have found low serum levels of serotonin in fibromyalgia patients. Low serum serotonin levels have been found to have an inverse correlation with clinical measures of pain.

The serotonin pathway begins with the essential amino acid tryptophan.

Tryptophan is the least common of the 8 essential amino acids, accounting for about 1% of protein content.

After absorption, about 90% of tryptophan is used at the peripheral tissues for protein synthesis.

About 9% of absorbed tryptophan is used to produce niacin. The RDA for niacin is 15 mg. It takes 60 mg of tryptophan to produce 1 mg of niacin. This is important, because if niacin levels are adequate in the diet, the body will not need to use this 9% to make niacin.

In fact, the higher the dietary levels of niacin, the less tryptophan is converted to this pathway. This increases the tryptophan available to be converted to serotonin.

About 1% of absorbed tryptophan is converted to serotonin.

In the body, tryptophan is converted to 5-hydroxy-tryptophan (5-HPT). 5-HTP easily crosses the blood-brain barrier for conversion to serotonin in the central nervous system. The conversion of 5-HPT to serotonin requires vitamin B6. Consequently, inadequate levels of B6 impair the conversion of tryptophan to serotonin.

Currently, tryptophan is available by prescription only in the United States. However, 5-HTP is sold, and as noted above, still crosses the blood brain barrier for conversion to serotonin. Commercially, 5-HTP is extracted from the seeds of Grifonia simplicifolia, a plant grown in West Africa.

Dr. Juhl notes 2 published studies where supplementation of 5-HTP in the dose of 100 mg 3 times per day in patients with fibromyalgia resulted in significant improvement of clinical symptoms after 30-90 days. The effective daily dose range appears to be 200-1000 mg total per day, and that it should be taken with meals.

These patients should also be given vitamin B6 to increase conversion of 5-HTP to serotonin, and niacinamide to inhibit the need for tryptophan to convert to niacin.

Dr. Rodger Murphree supports the tryptophan to 5HTP to serotonin pathway noted by Dr. Juhl. In his 2003 book titled Treating and beating Fibromyalgia and Chronic Fatigue Syndrome, Dr. Murphree suggests supplementing with 100-300 mg of 5HTP on an empty stomach 30 minutes before bed. He notes that it can take several nights to two weeks before supplementing with 5HTP starts to work.

LOW LEVEL LASER THERAPY

Below are 3 studies that show significant benefit to management of chronic pain and fibromyalgia using low-level laser therapy. The first article is by Green, et al in 2000. The authors claim excellent positive therapeutic results in treating patients with chronic painful diabetic neuropathy, chronic myofascial pain, or complex regional pain syndrome.

Green et al conclude, “It appears that photon stimulation carries with it a significant potential for amelioration of chronic pain in which autonomic and neurovascular abnormalities are, in fact, present.”

The second article is a randomized controlled clinical trial done in 2002 by Gur et al on patients with fibromyalgia. The laser group of patients were treated for 3 minutes at each tender point daily for 2 weeks. The authors note “Significant improvements were indicated in all clinical parameters in the laser group,” and that “laser therapy can be used as a monotherapy or as a supplementary treatment to other therapeutic procedures in fibromyalgia.”

Gur and others also publish the third article published in 2002. It is a single-blinded placebo-controlled trial of low power laser therapy in 40 female patients with fibromyalgia. The authors note that there was a “significant difference was in parameters as pain, muscle spasm, morning stiffness and tender point numbers in favour of laser group.” These authors conclude “Our study suggests that laser therapy is effective on pain, muscle spasm, morning stiffness, and total tender point number in fibromyalgia and suggests that this therapy method is a safe and effective way of treatment in the cases with fibromyalgia.”

According to Jan Tuner, and Lars Hode’s 2002 text titled Laser Therapy, Clinical Practice and Scientific Background, the first low level laser to be awarded 510K market clearance by the United States Food and Drug Administration is from Erchonia Medical. Erchonia medical is located in McKinney, TX: (888) 242-0571.

According to a book chapter titled “Low-Power Laser Therapy” by Tina Karu, low-level laser therapy physiologically increases the mitochondrial production on cellular energy ATP. This is similar to the proposed mechanism of supplementing with malic acid and magnesium, as noted above.

EXCITOTOXINS

Below are listed 5 books that deal extensively with dietary excitotoxins and their deleterious effects on human physiology. These deleterious effects include chronic fibromyalgia pain because dietary excitotoxins also function as excitatory neurotransmitters for chronic pain (Dickenson).

In a nutshell, dietary excitotoxins are added to food because they function as excitatory neurotransmitters, enhancing the flavor of food. The two main dietary excitotoxins are glutamate (often labeled monosodium glutamate or MSG, and aspartame because it is metabolized to the excitotoxin aspartate).

In excess, these substances can literally excite neurons to death, and therefore have been associated with neurodegenerative diseases such as Alzheimer and Parkinson diseases, as well as a plethora of other symptoms, including fibromyalgia chronic pain. Unfortunately, excitotoxins such as glutamate can have dozens of names on food labels.

In 2001, Smith reports on 4 cases of chronic pain fibromyalgia patients who where successfully treated after avoiding all products that contain the excitotoxins glutamate and aspartame. Some of these patients had suffered for as long as 17 years, and were taking as many as 13 different drugs for their symptoms.

Smith notes the following:

“Excitotoxins are molecules, such as MSG and aspartate that act as excitatory neurotransmitters, and can lead to neurotoxicity when used in excess.”

“MSG, the sodium salt of the amino acid glutamic acid or glutamate, is an additive used to enhance the flavor of certain foods.”

The US Food and Drug Administration (FDA) grandfathered MSG, like salt and baking powder, as harmless food substances in 1959.

Aspartame was first marketed in 1981, and is a dipeptide of aspartate and phenylalanine used in foods, beverages, and drugs.

“In animal models, aspartame has been associated with an increased incidence of brain tumors.”

“Anecdotally, aspartame use in humans has been linked with head aches, seizures, dizziness, movement disorders, urticaria, angioedema, and anaphylaxis.”

“Much of the research performed proving that glutamate was safe for human consumption may have been flawed.”

Glutamate has a role in chronic pain sensitization:

“MSG is nearly ubiquitous in processed food, appearing under many names, including gelatin, hydrolyzed vegetable protein, textured protein, and yeast extract.”

Aspartame is the dominant artificial sweetener on the market since 1981.

Fibromyalgia can be caused by exposure to dietary excitotoxins in susceptible individuals.

Aspartate and glutamate taken together have additive neurotoxic effects.

The elimination of MSG and other excitotoxins from the diets of patients with fibromyalgia offers a benign treatment option that has the potential for dramatic results in a subset of patients.

There are dozens of names for glutamate as it is added to foods. A partial list of names seen on food packaging are listed below, from the website 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

The MSG-reaction is a reaction to free glutamic acid that occurs in food as a consequence of manufacture. MSG-sensitive people do not react to protein (which contains bound glutamic acid) or any of the minute amounts of free glutamic acid that might be found in unadulterated, unfermented, food.

These ALWAYS contain MSG
Glutamate
Glutamic acid
Gelatin
Monosodium glutamate
Calcium caseinate
Textured protein
Monopotassium glutamate
Sodium caseinate
Yeast nutrient
Yeast extract
Yeast food
Autolyzed yeast
Hydrolyzed protein (any protein that is hydrolyzed) Hydrolyzed corn gluten

These OFTEN contain MSG or create MSG during processing

Carrageenan
Maltodextrin
Malt extract
Natural pork flavoring
Citric acid Malt flavoring
Bouillon and Broth Natural chicken flavoring Soy protein isolate
Natural beef flavoring
Ultra-pasteurized Soy sauce
Stock Barley malt
Soy sauce extract
Whey protein concentrate Pectin
Soy protein
Whey protein Protease
Soy protein concentrate
Whey protein isolate
Protease enzymes
Anything protein fortified
Flavors(s) & Flavoring(s)
Anything fermented Anything enzyme modified
Enzymes anything
Seasonings Natural flavor & flavoring (the word “seasonings”)

The website further notes that “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.”

“MSG reactions have been reported to soaps, shampoos, hair conditioners, and cosmetics, where MSG is hidden in ingredients that include the words ‘hydrolyzed,’ ‘amino acids,’ and ‘protein.’ Low fat and no fat milk products often include milk solids that contain MSG. Drinks, candy, and chewing gum are potential sources of hidden MSG and of aspartame and neotame.”

“Aspartic acid, found in neotame and aspartame (NutraSweet), ordinarily causes MSG type reactions in MSG sensitive people. Aspartame is found in some medications, including children’s medications.”

“According to the manufacturer, Varivax–Merck chicken pox vaccine (Varicella Virus Live), contains L-monosodium glutamate and hydrolyzed gelatin both of which contain processed free glutamic acid (MSG) which cause brain lesions in young laboratory animals, and cause endocrine disturbances like obesity and reproductive disorders later in life. It would appear that most, if not all, live virus vaccines contain MSG.”

Fibromyalgia patients are often quite resistant to traditional treatment approaches. Today’s chiropractors used all or some of the above adjuncts, along with traditional joint adjusting, tissue work, postural improvement and exercise. Most patients so treated experience substantial benefit and achieve acceptable clinical improvement.

REFERENCES

Abraham GE, Flechas JD. Management of Fibromyalgia: Rationale for the Use of Magnesium and Malic Acid. J of Nutritional Med. 1992 (3) 49-59.

A. W. Al-Allaf, K. L. Dunbar, N. S. Hallum, B. Nosratzadeh, K. D. Templeton and

T. Pullar. A case–control study examining the role of physical trauma in the onset of fibromyalgia syndrome Rheumatology 2002; 41: 450-453.

Borut Banic, Steen Petersen-Felix, Ole K. Andersen, Bogdan P. Radanov, P. M. Villiger, Lars Arendt-Nielse and Michele Curatolo. Evidence for spinal cord hypersensitivity in chronic pain after whiplash injury and in fibromyalgia. Pain. January 2004, Pages 7-15.

Buskila D, Neumann L, Vaisberg G, Alkalay D, Wolfe F. Increased rates of fibromyalgia following cervical spine injury. A controlled study of 161 cases of traumatic injury. Arthritis Rheum. 1997 Mar;40(3):446-52.

Dickenson AH. Gate Control Theory of pain stands the test of time British Journal of Anaesthesia, Vol. 88, No. 6, June 2002, Pgs. 755-757.

Green J, Fralicker D, Clewell W, Horowitz E, Lucey T, Yannacone V, Haber C. INFRARED PHOTON STIMULATION: A NEW FORM OF CHRONIC PAIN

THERAPY. American Journal of Pain Management, Vol. 10, No. 3 July 2000,113-120;

Greenfield S, Fitzcharles MA, Esdaile JM. Reactive fibromyalgia syndrome.

Arthritis Rheum. 1992 Jun;35(6):678-81.

Gur A, Karakoc M, Nas K, Cevik R, Sarac J, Ataoglu S. Effects of low power laser and low dose amitriptyline therapy on clinical symptoms and quality of life in fibromyalgia: a single-blind, placebo-controlled trial. Rheumatol Int. 2002 Sep;22(5):188-93.

Gur A, Karakoc M, Nas K, Cevik R, Sarac J, Demir E. Efficacy of low power laser therapy in fibromyalgia: a single-blind, placebo-controlled trial. Lasers Med Sci. 2002;17(1):57-61.

Juhl JH, (1998-10-01). “Fibromyalgia and the serotonin pathway”,

Altern Med Rev;3(5):367-75.

Karu, Tina, “Low-Power Laser Therapy”, Chapter 48 in Biomedical Photonics Handbook, Tuan Vo-Dinh, CRS Press, 2003.

Murphree, Rodger, Treating and beating Fibromyalgia and Chronic Fatigue Syndrome, The Definitive Guide for Patients and Physicians, Harrison and Hampton Publishing, 2003.

Neumann L, Zeldets V, Bolotin A, Buskila D. Outcome of posttraumatic fibromyalgia: A 3-year follow-up of 78 cases of cervical spine injuries.

Semin Arthritis Rheum. 2003 Apr;32(5):320-5.

Russell IJ, Michalek JE, Flechas JD, Abraham GE. Treatment of fibromyalgia syndrome with Super Malic: a randomized, double blind, placebo controlled, crossover pilot study. J Rheumatol. 1995 May;22(5):953-8.

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

Tuner, Jan and Hode, Lars, Laser Therapy, Clinical Practice and Scientific Background, Prima Books, 2002.

Waylonis GW, Perkins RH. Post-traumatic fibromyalgia. A long-term follow-up.

Am J Phys Med Rehabil. 1994 Nov-Dec;73(6):403-12.

Excitotoxin Books

Excitotoxins, The Taste That Kills by Russell Blaylock (University of Mississippi neurosurgeon), Health Press, 1997

In Bad Taste, The MSG Symptom Complex, by George Schwartz, Health Press, 1999

The Crazy Makers, How the Food Industry Is Destroying Our Brains and Harming Our Children, by Carol Simontacchi, Tarcher Putnam, 2000

Food Allergies by William Walsh, Wiley, 2000

Health and Nutrition Secrets by Russell Blaylock, Heath press, 2006

Fibromyalgia Article Summary

A case–control study examining the role of physical
trauma in the onset of fibromyalgia syndrome
Rheumatology 2002; 41: 450-453

 

A. W. Al-Allaf, K. L. Dunbar, N. S. Hallum, B. Nosratzadeh, K. D. Templeton and

T. Pullar

FROM ABSTRACT

Objective.

To investigate whether physical trauma may precipitate the onset of fibromyalgia syndrome (FMS).

Design.

A case–control study was carried out to compare fibromyalgia out-patients with controls attending non-rheumatology out-patient clinics.

Method.

136 FMS patients and 152 age- and sex-matched controls completed a postal questionnaire about any physical trauma in the 6 months before the onset of their symptoms.

Results.

Fifty-three (39%) FMS patients reported significant physical trauma in the 6 months before the onset of their disease, compared with only 36 (24%) of controls (P<0.007).

There was no significant difference between FMS patients who had a history of physical trauma and those who did not have physical trauma with regard to age, sex, disease duration, employment status and whether their job at onset was manual.

Conclusion.

Physical trauma in the preceding 6 months is significantly associated with the onset of FMS.

KEY POINTS

(1) Fibromyalgia is the 3rd or 4th most common rheumatological referral.

(2) 2% of the population has fibromyalgia, primarily in women.

(3) Physical trauma is a significantly etiological trigger for FMS onset.

(4) 25% to 50% of those with FMS note physical trauma immediately prior the onset.

(5) The risk of developing FMS is more than 10-fold higher in adults with neck injuries than in other adults (1997 study).

(6) Those who develop FMS after trauma may be “genetically predisposed.”

(7) Physical trauma is also increases the risk for osteoarthritis, rheumatoid arthritis, psoriasis and ankylosing spondylitis.

Treatment of fibromyalgia syndrome with Super Malic:
a randomized, double blind, placebo controlled, crossover pilot study
Journal of Rheumatology, May 1995;22(5):953-8

Russell IJ, Michalek JE, Flechas JD, Abraham GE.

FROM ABSTRACT

OBJECTIVE.

To study the efficacy and safety of Super Malic, a proprietary tablet containing malic acid (200 mg) and magnesium (50 mg), in treatment of primary fibromyalgia syndrome.

The 3 primary outcome variables were measures of pain and tenderness but functional and psychological measures were also assessed.

RESULTS.

With dose escalation and a longer duration of treatment in the open label trial, significant reductions in the severity of all 3 primary pain/tenderness measures were obtained without limiting risks.

CONCLUSIONS.

These data suggest that Super Malic is safe and may be beneficial in the treatment of patients with fibromyalgia.

KEY POINTS FROM THIS ARTICLE

1) An explanation for the soft tissue pain experienced by patients with fibromyalgia was that muscle energy production of ATP may be compromised.

2) Also, abnormal blood flow may deprive muscle of sufficient oxygen and other nutrients.

3) The muscles of patients with fibromyalgia are deficient in ATP and magnesium.

4) Malic acid and magnesium “play a pivotal role in mitochondrial ATP synthesis.”

5) Malic acid is “widely distributed in the vegetable kingdom including concentrations of 4 to 8 g/l of apple juice.”

6) Malic acid plus magnesium can increase mitochondrial production of ATP energy.

7) The best results were observed from “use of a higher dosage and longer duration of treatment” with malic acid and magnesium.

8) Study results “indicate that it may be beneficial on the painful fibromyalgia symptoms in dosages in excess of 8 tablets/day for up to 6 months.”

[8 tablets X 200 mg per tablet = 1600 mg malic acid per day]

[8 tablets X 50 mg per tablet = 400 mg magnesium per day]

9) The proposed mechanism for the benefit of malic acid plus magnesium supplementation is that they “increase production of ATP.”

Evidence for spinal cord hypersensitivity in chronic pain after whiplash injury and in fibromyalgia

Pain, January 2004, Pages 7-15

Borut Banic, Steen Petersen-Felix, Ole K. Andersen, Bogdan P. Radanov, P. M. Villiger, Lars Arendt-Nielse and Michele Curatolo
FROM ABSTRACT:

Patients with chronic pain after whiplash injury and fibromyalgia patients display exaggerated pain after sensory stimulation.

Because evident tissue damage is usually lacking, this exaggerated pain perception could be explained by hyperexcitability of the central nervous system.

The nociceptive withdrawal reflex (a spinal reflex) may be used to study the excitability state of spinal cord neurons.

We tested the hypothesis that patients with chronic whiplash pain and fibromyalgia display facilitated withdrawal reflex and therefore spinal cord hypersensitivity.

Three groups were studied: whiplash (n=27), fibromyalgia (n=22) and healthy controls (n=29).

Two types of transcutaneous electrical stimulation of the sural nerve were applied: single stimulus and five repeated stimuli at 2 Hz. Electromyography was recorded from the biceps femoris muscle. The main outcome measurement was the minimum current intensity eliciting a spinal reflex (reflex threshold).

Reflex thresholds were significantly lower in the whiplash compared with the control group, after both single and repeated stimulation.

The same was observed for the fibromyalgia group, after both stimulation modalities.

We provide evidence for spinal cord hyperexcitability in patients with chronic pain after whiplash injury and in fibromyalgia patients.

This can cause exaggerated pain following low intensity nociceptive or innocuous peripheral stimulation.

Spinal hypersensitivity may explain, at least in part, pain in the absence of detectable tissue damage.

KEY POINTS FROM THIS ARTICLE

1) Whiplash causes tissue damage.

2) This tissue damage is not recognized by available diagnostic procedures.

3) Whiplash tissue damage produces inflammation.

4) This inflammation alters the thresholds of the nociceptive afferent system, increasing pain.

5) This inflammation also induces a gene expression in the dorsal root ganglion resulting in increased peripheral receptor fields. [Receptive Field Enlargement]

This also increases pain.

6) This inflammation also increases the expression (production) of cyclooxygenase-2 (COX-2) in the spinal cord, which is an enzyme that converts the omega-6 fatty acid arachidonic acid into the pro-inflammatory eicosanoid prostaglandin E2. The pro-inflammatory eicosanoid prostaglandin E2 further alters the thresholds of the nociceptive afferent system, sending more pain afferentation into the spinal cord.

7) This increased COX-2 expression is not confined to the neural structures connected to the site of inflammation, but is observed in the whole spinal cord and in supraspinal centers. This alters the pain sensitivity of the entire body, including non-injured regions.

8) All of this induces profound plasticity changes [synaptogenesis/neuroplasticity] in the spinal cord that result in increased pain that can persist after all possible tissue healing has occurred.

9) Some of these spinal plastic changes may be irreversible (permanent chronic pain syndromes).

10) This article objectively proves that patients with chronic pain have hypersensitivity of the spinal cord neurons.

11) The absence of evident tissue damage does not necessarily mean that there is no tissue damage.

12) Elevated levels of excitatory amino acids, like glutamate, are often found in the cerebrospinal fluid of chronic pain patients, and cause generalized spinal cord hyperexcitability.

14) Serotonin inhibits pain and inhibits depression. Reduced serotonin may explain while chronic pain patients often suffer from psychological distress.

Relief of Fibromyalgia Symptoms Following Discontinuation of Dietary Excitotoxins

The Annals of Pharmacotherapy: Vol. 35, No. 6, pp. 702–706.

June 2001

 

Jerry D Smith, Chris M Terpening, Siegfried OF Schmidt and John G Gums

FROM ABSTRACT:

BACKGROUND:

Fibromyalgia is a common rheumatologic disorder that is often difficult to treat effectively.

CASE SUMMARY:

Four patients diagnosed with fibromyalgia syndrome for two to 17 years are described. All had undergone multiple treatment modalities with limited success.

All had complete, or nearly complete, resolution of their symptoms within months after eliminating monosodium glutamate (MSG) or MSG plus aspartame from their diet.

All patients were women with multiple comorbidities prior to elimination of MSG.

All have had recurrence of symptoms whenever MSG is ingested.

DISCUSSION:

Excitotoxins are molecules, such as MSG and aspartate that act as excitatory neurotransmitters, and can lead to neurotoxicity when used in excess.

We propose that these four patients may represent a subset of fibromyalgia syndrome that is induced or exacerbated by excitotoxins or, alternatively, may comprise an excitotoxin syndrome that is similar to fibromyalgia.

CONCLUSIONS:

The elimination of MSG and other excitotoxins from the diets of patients with fibromyalgia offers a benign treatment option that has the potential for dramatic results in a subset of patients.

KEY POINTS FROM THIS ARTICLE:

1) Fibromyalgia is common difficult to treat.

2) Fibromyalgia can be caused by exposure to dietary excitotoxins in susceptible individuals.

3) Excitotoxins are molecules, such as MSG and aspartate, that act as excitatory neurotransmitters.

4) MSG is found in nearly all processed food and can have many names, including gelatin, hydrolyzed vegetable protein, textured protein, and yeast extract.”

5) Aspartame is the dominant artificial sweetener on the market since 1981.

6) Glutamate and other dietary excitotoxins primarily enter the brain at the hypothalamus that is not well protected by the blood-brain barrier.

7) Glutamate is the neurotransmitter that causes dorsal horn spinal cord chronic pain sensitization.

8) Aspartate and glutamate taken together have additive neurotoxic effects.

9) Much of the research done to show that glutamate was safe for human consumption may have been flawed.

10) The elimination of MSG and other excitotoxins from the diets of patients with fibromyalgia offers a benign treatment option that has the potential for dramatic results in a subset of patients.