OUTLINE

1. Abstract
2. Introduction
3. Trigger Point Terminology
4. A Common Error
5. A Historical Perspective
6. Histopathologic and Ultrastructural Changes
7. Evidence for the Oxidative-Dysoxygenative Pathogenetic Model of ODTP
8. Anatomic Sites of ODTPs
9. Fundamentals of ODTP Injection Therapy
10. Procedural Steps for ODTP Injection Therapy
11. Colchicine and Steroid Injections
12. Systemic Therapies for Oxidative-Dysoxygenative Dysfunction
13. Clinical Outcome of Injection Therapies
14. Summary

1. ABSTRACT

An oxidative-dysoxygenative dysfunction (ODD) is proposed in this issue of the Journal as the systemic molecular pathogenetic model of fibromyalgia for all of its symptom-complexes. The three primary molecular phenomena in ODD are oxidosis, dysoxygenosis (abnormal oxygen metabolism), and acidosis. In this article, a review of the pathogenetic mechanisms proposed in the past for trigger points (TPs) is presented. Clinical, laboratory, and experimental evidence is marshaled for the view that trigger points in fibromyalgia are caused and perpetuated by localized areas of oxidative-dysoxygenative (OD) injury affecting interstitial fluid, lymph, and cell membranes in the involved tissues. The term oxidative-dysoxygenative trigger points (ODTP) is introduced in this article to emphasize both the systemic nature of the disorder in which localized tender points develop and to challenge the validity of the diagnostic criteria of the American College of Rheumatology for fibromyalgia (presence of at least 11 of 18 established trigger points). The data showing efficacy of intra-ODTP injection of 50% glucose in equal volume of 2% lidocaine for resolving such points in a series of fifty patients with fibromyalgia are presented. The need for broad-based ecologic-integrative protocols for addressing the systemic OD phenomena in fibromyalgia along with TP injection therapy is underscored.

2. INTRODUCTION

An oxidative-dysoxygenative disorder (ODD) model of molecular pathogenesis of fibromyalgia is proposed in this issue of the Journal.1 The ODD model evolved as an extension of the authors' previous studies of oxidative phenomena in health and disease.2-13 Important among such phenomena in the context of ODTP are oxidative cascades in the circulating blood (oxidative coagulopathy9), lymph (oxidative lymphopathy10), and those involving matrix, cell membranes, and mitochondria.11 In the ODD model, oxidosis, dysoxygenosis, and acidosis are the three primary systemic molecular mechanisms which initiate and perpetuate symptom-complexes of fibromyalgia. In this article, arguments are presented to support the hypothesis that the same three factors (oxidosis, dysoxygenosis, and acidosis) are the primary molecular pathogenetic mechanisms of ODTPs.

3. TRIGGER POINT TERMINOLOGY

A large number of terms have been used for trigger points in the European and American literature. Such terms are of considerable historical interest. Beyond that, such a perspective not only sheds light on the pathogenesis of TPs, it also has clear therapeutic implications. An incomplete list of such terms includes the following: myogelose, myogelosis, musklschwiele (muscle calluses), myogenic calluses, muskelharten (muscle hardening), myitis chronica, myofibrositis, myofascitis, myalgic rheumatism, myalgic spots, myalgic patches, myalgic encephalomyelitis, myofascial trigger points, myodysneuria, idiopathic myalgia, traumatic myalgia, rheumatic myalgia, rheumatic myositis, rheumatic polymyalgia, muscular rheumatism, occupational myalgia, fibromyositis, fibropathic syndrome, fibrositis, fibromyalgic trigger points, and interstitial myofibrositis. The first two terms in the preceding list, the German term myogelose and its English equivalent myogelosis, are of special interest in the context of the proposed ODTP hypothesis. Specifically, oxidative coagulopathy and oxidative lymphopathy, the two core components of the ODTP hypothesis, lead to stagnation of oxidized and denatured interstitium, lymph, and plasma within the ODTP tissues and create the clinically demonstrable sense of hardening of the involved tissues that is explicit in the terms myogelose and myogelosis. Some brief comments in the section on the historical perspective later in this article shed additional light on the ODTP hypothesis.

As a frame of reference for presenting the OD trigger point hypothesis, the following working definition, taken from Myofascial Pain and Dysfunction-The Trigger Point Manual14 by Janet Travell and David Simons, is adopted: A focus of hyper-irritability in a tissue that, when compressed, is locally tender and, if sufficiently hypersensitive, gives rise to referred pain and tenderness, and sometimes to referred autonomic phenomena and distortion of proprioception. Of course, 'hyper-irritability' in this definition should be interpreted as pain, which is the dominant problem from the patient's perspective.

4. A COMMON ERROR

"Trigger points" have been inadvertently discovered by patients, their spouses, therapists, nonmedical practitioners; yet, many of their physicians who have examined them have attributed their condition to various etiologies, and treated them with ineffectual therapies...For decades, Janet Travell has labored to document the scientific basis of myofascial pain and dysfunction. Her clinical reports have been ridiculed and ignored by some, but believed and confirmed by others. 15

There are three remarkable aspects of the above quote: First, trigger points (TPs) are commonly recognized by patients and those close to them. Second, physicians who examine them frequently fail to detect them. Third, when found and reported by some physicians, they are ridiculed by others. An amazing commentary on physicians' work for patients with TPs!

The first aspect is plainly troublesome: Self-detection of TPs, or discovery by some family member, should efface any doubt about the existence of such lesions in a given patient. Yet, this matter is dismissed or denied by his physician in many instances. The second aspect of the problem is more troublesome: physicians fail to detect TPs (evidently a critical physical finding) in situations in which non-physicians can do so. The third aspect is the most disturbing: even when an eminent physician writes scientific papers about her work, she is ridiculed or ignored (Janet Travell reportedly administered trigger point therapy to President John F. Kennedy).

The words quoted above were written 16 years ago in a foreword to Dr. Travell's landmark book. Regrettably, by and large, those words are as true today as when written. TP injection therapy, a highly successful therapy in most cases, is neither considered nor offered to most patients with such lesions, whether found as localized problems or as components of systemic disorders such as fibromyalgia and chronic fatigue syndrome.

5. A HISTORICAL PERSPECTIVE

As a young boy, the author first observed the practice of retired wrestlers "rubbing out knots" in soft tissues of young wrestlers to relieve acute and chronic painful muscle and soft tissue conditions. The old wrestlers seemed self-assured and worked with precision. To the author's young and curious eyes, they seemed to follow some invisible maps under the skin of their subjects. Later he learned that in other cultures, most notably in the ancient Chinese and Indian healing methods, practitioners treated pain syndromes with similar physical approaches. Undoubtedly, the art of diagnosis and treatment of such trigger points is as old as human suffering.

The "modern" medical writers addressing the subject of tender points often begin with an 1852 paper by Rudolf Virchow describing "serous exudate" in muscular rheumatism.16 Nine years earlier, Froriep coined the term muskelschwiele for what he thought were muscle calluses.17 The notions of demonstrable anatomic abnormalities underlying painful tender points seemed logical and intrigued many investigators. However, lacking clearly demonstrable evidence of such structural change (calluses or exudate could not be documented with histopathologic studies), the pendulum swung to what in today's language would be considered "imagined problems." Several papers and review articles concluded that Virchow's exudate and Froriep's muscular calluses theories were untenable.18,19 In the English literature, Gowers in 1904 introduced the term fibrositis,20 implying an inflammatory nature of tender trigger points, and rekindled interest in Froriep-Virchow exudate-callus theories. In the same year, Stockman put forth a different hypothesis, illustrating connective tissue responses and proposing that the histologic lesion in TPs was not inflammation but hyperplasia.21 The term fibrositis finally came of age with publication by Llewellyn and Jones of their famous book titled Fibrositis.22 What that book really achieved, as pointed out by Travell,23 was to lump diverse clinicopathologic entities, including lesions of rheumatoid arthritis and gout, into a catch-all term of fibrositis. A spate of biopsy studies which followed reported absence of serous and inflammatory lesions and challenged those theories.24,25 Not unexpectedly, the term fibrositis soon earned the designation of a "wastebasket" label used for non-organic and psychogenic pain syndromes (earlier versions of the prevailing all-in-the-head diseases).26 However, the term has proven to be resilient and continues to be used by many clinicians.

Of special interest to the ODTP hypothesis is the term myogelose introduced in a 1919 report by Schade,27 a German medical officer. He postulated increased viscosity and "colloid" of the muscle tissue involved in trigger points. That view, as will be evident later in this article, is fully consistent with the changes of oxidative coagulopathy and oxidative lymphopathy described as two important components of fibromyalgia as an oxidative-dysoxygenative disorder.

In 1921, two German investigators, Lange and Eversbusch,28 introduced the term muskelharten for painful tender points associated with palpable taut muscle bands. Lange likened those taut muscle bands to rigor mortis effect, subsequently described many case histories, and recommended a method of breaking up those bands (a technique he called gelotripsie)29 with direct, forceful digital or knuckle pressure, undoubtedly a therapy identical to the ancient Chinese method of acupressure. Several subsequent German biopsy studies described "non-specific" changes in regions designated myogelose by Schade and Lange.30,31 The subject of referred pain drew little, if any, attention. Those who acknowledged the presence of distant pain considered it as neuralgia.32,33

In late 1930s, Kellgreen and Lewis investigated the subject of referred pain by injecting 0.1 to 1.3 ml of 6% hypertonic saline into various locations in the muscles characteristically involved with TPs and documented patterns of referred pain.34-35 The concept of TP pain caused by vasospasm induced by sympathetic overactivity was introduced by Gutstein-Good in a series of papers between 1938 and 1957.36-38 A quite different pathogenetic view of TP pain involving a functional neurologic disturbance triggered by "myalgic lesions" was proposed by the Australian, Michael Kelly between 1941 and 1963.39,40 Travell initially proposed a fibroproliferative process secondary to a functional disorder 41 In the mid-and late 1970s,41-431 she summarized her extensive studies on the subject and postulated a feedback mechanism between the TP and the central nervous system.

In the area of TP treatment, Travell,44 Kraus,45 and others improvised and propagated vapocoolant therapy, emphasized the beneficial effects of exercise, and described effective stretch methods for involved muscles.

6. HISTOPATHOLOGIC AND ULTRASTRUCTURAL CHANGES IN TPs

Though earlier light microscopic studies of TP biopsies, by and large, failed to reveal significant abnormalities, subsequent biopsies with special stains and ultrastructural studies show one or more of the following changes: accumulation of fat droplets designated "fat dusting"; variations in width and intensity of staining of muscle fibers; nuclear enlargement and endomysial as well as perimysial nuclear clustering; fiber degeneration, contracture knots (club-like enlargement of myofibrils in vicinity of empty sarcolemmic tubes); and interstitial infiltration of metachromatic mucopol-ysaccharides.31,46,47 Ultrastructural abnormalities in TP tissues include the following: mitochondrial swelling, moth-eaten appearance of myofibrils, giant (double length) sarcomeres, disrupted sarcomeres, and excess collagen in advanced cases.48 It is noteworthy that both light microscopic and ultrastructural changes cited above are also characteristically seen in ischemic muscle49 and alcohol-induced muscle injury.50

7. EVIDENCE FOR THE OXIDATIVE-DYSOXYGENATIVE PATHOGENETIC MODEL OF ODTP

The evidence for the proposed hypothesis that fibromyalgia is an oxidative-dysoxygenative disorder is presented eslewhere in this issue of the Journal.11,12 Clinical experience makes it abundantly clear to the author that ODTPs in fibromyalgia in general resolve when all the systemic issues are effectively addressed and chronic points are managed with injection therapy employing 50% glucose in equal volume of 2% lidocaine. Indeed, such clinical observation form the primary basis of the proposed hypothesis. In this section, evidence for the ODTP hypothesis is presented under the following seven categories: (I) impaired perfusion (and hence oxidosis, dysoxygenosis, and acidosis) in ODTP tissues; (II) metabolic stress and demand/response dissonance; (III) calcium and mediator considerations; (IV) oxidative phenomena which initiate and perpetuate histopathologic lesions observed in ODTP tissues; (V) oxidative coagulopathy and oxidative lymphopathy; (VI) the role of trauma; and (VII) the oxidative phenomena involving 3M (matrix, membranes, and mitochondria) ecologies and 3C (coagulation, complement, and capsases) cascades.

I. Impaired Perfusion

The evidence for the role of ischemia in ODTP development and perpetuation is derived from clinical biopsy, and temperature studies. Clinically, the muscle spasm so commonly associated with ODTP can be expected to impair regional perfusion. A sense of resistance to fluid movement in involved tissues is regularly experienced by practitioners of deep massage therapy for fibromyalgia. For those and other reasons, many investigators have clinically suspected that TPs are zones of impaired perfusion.51-54

Direct experimental evidence for hypoperfusion is provided by radioisotopic studies.55 Studies with insertion of a thermocouple in the TP tissues revealed a higher initial temperature with return to normal within 15-60 seconds, suggesting increased metabolic rate and/or impaired perfusion. An autonomic dysfunction (sympathetic overdrive) has been proposed as one of the mechanisms involved.56 All of the above factors are known to be triggered or perpetuated by oxidative-dysoxygenative phenomena.

II. Metabolic Stress and Demand/Response Dissonance

That the TP tissues are zones of increased metabolic activity is self-evident in view of the pain and muscle spasms evoked by them. Enlargement of mitochondria observed in cells in TPs is a clear evidence for increased metabolic stress, as has been demonstrated in other cells in stress. The presence of fat droplets in TP tissues is yet another evidence for disturbance of fat metabolism. For the author, much more important than the above direct evidence is the indirect evidence of functional nutritional inadequacies. Travell and Simons observed that nearly half of their patients with myofascial pain syndromes required resolution of vitamin inadequacies for lasting relief.57 In patients with fibromyalgia, the author and his colleagues found it necessary to optimize nutritional support with large supplementation of vitamins and minerals.11 Indeed, such clinical observations constitute an important line of evidence for the central idea of oxidative-dysoxygenative dysfunction in fibromyalgia. It may be added here that some studies have documented hypovitaminosis (even by the woefully inadequate standards of the prevailing laboratory references) in up to 88 percent of randomly selected municipal hospital patient populations.58

III. Calcium and Mediator Considerations

Changes in calcium dynamics in TP pathogenesis have drawn much attention. Contractile activity of muscle fiber is intricately involved with the rapid release of calcium (triggered by a propagated action potential) and reabsorption of calcium stored in sarcoplasmic reticulum, the release initiating contractile activity and reabsorption terminating it. The sarcomeres exposed to prolonged periods of excess calcium so released may then be expected to undergo sustained contractile activity until the ATP supply is exhausted, regardless of ongoing changes in action potential.57,58

Various roles in the pathogenesis of TPs have been attributed to calcium-related mediator release. Such mediator molecules include molecules as histamine, kinins, prostaglandins, serotonin, and others.59 Thus, mast cell degranulation (putative source of histamine) and abundance of platelets in biopsy tissues (presumed source of serotonin) have been incriminated in the pathogenesis of TPs.

In the context of the ODTP hypothesis, the core question concerns the initial molecular triggers of all such molecular dynamics. The sarcoplasmic reticulum can be expected to be injured by oxidative-anoxic injury with resultant spilling of its calcium contents. Indeed, the author holds that oxidative-dysoxygenative dysfunction triggers all calcium-related cascades that not only trigger sustained contractile activity of sarcomeres but also myriad other calcium-related mediator cascades.

IV. Oxidative Phenomena Initiating and Perpetuating Histopathologic Abnormalities

In a series of articles, the author has described the fundamental oxygen order of human biology and has conducted a survey of a broad range of oxidative phenomena which initiate, potentiate, and perpetuate clinicopathologic syndromes as well as histopathologic entities.2,3,7-13 In those articles, high-resolution microscopic and biochemical data were presented and arguments marshaled to support the author's viewpoint that human health and disease issues should be seen as integrity, or lack thereof, of microecologic cellular and macroecologic tissue-organ ecosystems of the body rather than to continue to regard disruptions of such ecosystems as discrete diseases, as has been the case in the prevailing systems of disease classifications. When viewed in that light, it is evident that all of the histopathologic changes (such as fat dusting and endothelial swelling) or ultrastructural abnormalities (such as mitochondrial swelling) are initially triggered by oxidative phenomena. It may be added in this context that, in this issue of the Journal, an attempt is made to cast the observed oxidative (and associated dysoxygenative) phenomena within the much broader Darwinian concepts of competitive struggle for life, impact of ecologic factors of the health/dis-ease/disease continuum, and adaptive as well as maladaptive responses.

V. Oxidative Coagulopathy and Oxidative Lymphopathy:

Two Core Pathogenetic Mechanisms in Fibromyalgia

In 1997 and 1998, the author and his colleague, Omar Ali, introduced the terms oxidative coagulopathy12 and oxidative lymphopathy13 respectively. The relevance of those two pathologic processes to the oxidative-dysoxygenative disorder (ODD) hypothesis of fibromyalgia is discussed at length in a companion article in this issue of the Journal.1 Briefly, the term oxidative coagulopathy was coined for a host of oxidative phenomena which occur in blood and lead to structural damage to erythrocytes, polymorphonuclear cells, zones of congealed blood, fibrin needle and lattice network formation, and microclot and microplaque formation. The term oxidative lymphopathy was chosen for a state of stagnation of oxidized and denatured lymph in the interstitium as well as lymphatic channels of tissues involved with ODTP. We recognized that oxidative lymphopathy results from, and contributes to, oxidative phenomena occurring in the circulating blood as well as those involving the matrix, cell membranes, and mitochondria, the latter collectively designated AA oxidopathy.12 While the existence of oxidative coagulopathy can be readily documented with a high-resolution phase-contrast microscopy of freshly prepared peripheral blood smears, the evidence for oxidative lymphopathy is clinical and indirect, in the form of local signs of tenderness, increased tissue resistance as assessed by deep massage, and clinical response to ODTP injection therapy. (To date, there is no non-invasive technique for obtaining a sample of circulating lymph for conducting high-resolution microscopic studies comparable to those done with blood samples.)

In the authors' experience, the most effective therapy for ODTP in fibromyalgia, as is documented in this report, is the injection therapy employing 50% glucose solution with equal volume of 2% lidocaine.13 Other effective therapies are deep "stripping" massage of the ODTP tissues, myofascial release, hydrotherapy, repetitive stretching of the involved tissues, and acupuncture. Fifty percent glucose solution is a powerful temporary irritant (as shown by intense pain caused by it if injected without equal volumes of 2% lidocaine). Such a solution evokes a strong fibroproliferative response (as determined by long-lasting stabilizing effect of such therapy in joints weakened and rendered unstable by traumatic, chronic, non-healing sprains and tears in periarticular ligaments and tendons). How may such clinical observations be explained? It is noteworthy that all such responses, except acupuncture, clearly involve mechanical removal of stagnant (and, of necessity, oxidized, anoxic, and acidic) interstitial fluid, lymph, and venous blood. Especially noteworthy in this context are deep stripping massage, myofascial release, and hydrotherapy in which stagnant interstitial fluid, lymph, and venous blood are literally squeezed out of the affected tissues.

The ODTP hypothesis proposes that tender points develop as a result of accumulation of pools of oxidized and stagnant lymph (as well as oxidized and denatured blood components) within muscles, tendons and ligaments. Removal of such oxidized lymph clears the way for healing. Some clinicians report resolution of some trigger points with laser applications. It is further proposed that such laser applications also work by clearing the tissues of oxidized lymph and blood components.

A more important issue in this discussion is the well- established failure of ODTPs in fibromyalgia to respond to local therapies unless such therapies are vigorously supported by systemic oxygenative and antioxidant therapies which address all the systemic issues (including restorative measures for disrupted bowel, blood, and liver ecosystems) which feed the oxidative-dysoxygenative fires of fibromyalgia.

Trauma leading to the production of ODTPs in fibromyalgia may be localized to a few points or be more generalized. Local injury to tissues causes tears in the fibers of muscles, tendons, ligaments, and periosteum. Such tears do not heal due to continuing stress and other reasons. The generalized injury creates painful tender points in areas of chronic mechanical stress, such as the back of the upper neck, shoulders, lower back, knees, legs, and other tissues.

In both local and generalized trauma, the injured tissue fails to heal for a variety of reasons. First, the injured tissues are not allowed to rest adequately soon after the injury is sustained. Second, persistent spasm of muscles in close vicinity of TPs can compromise the flow of blood to the injured tissue and impair inflammatory and healing responses. Third, persistent muscle spasm continues to traumatize the injured tissues. Fourth, accelerated oxidative stress of associated clinical entities, such as CFS and fibromyalgia, increase the local acidosis of tissue injury and impair healing. Fifth, subliminal injury to injured tissue is another frequent cause of delayed healing.

Accelerated oxidative injury profoundly affects molecular dynamics of the intracellular matrix, cell membranes, and intracellular organelles, especially mitochondria (abbreviated as 3M ecologies13 by the author) as well as enzymatic pathways involving the complement, coagulation, and capsase cascades (3C cascades). Such oxidative modification of the structure and function have far-reaching pathophysiologic consequences in clinical states characterized by oxidosis and have been previously discussed.13 Though the occurrence of such oxidative phenomena involving ODTP tissues, to the author's knowledge, has not been investigated, it seems safe to predict that future research in this field will establish its role in the pathogenesis of ODTPs just as is the case in other "oxidotic" states.

8. ANATOMIC SITES OF ODTPs

When administering injection therapy for ODTPs, it is imperative that a diligent examination be conducted for detection of all existing ODTPs, even though only some of them can be injected at any given patient visit. Equally important is the issue of precise anatomic localization of the ODTPs so that the exact location can be injected. The following are the major anatomic sites of ODTPs in fibromyalgia:

I. Tendinous Trigger Points
II. Ligamentous Trigger Points
III. Periosteal Trigger Points
IV. Muscular Trigger Points
V. Subcutaneous Trigger Points
VI. Cutaneous Trigger Points

A diligent search frequently reveals the existence of trigger points in fibromyalgia patients in sites other than the 18 locations chosen by the American College of Rheumatology61 for defining its diagnostic criteria for fibromyalgia This is a point of considerable importance and is one of the two major reasons why the author considers the College's criteria unacceptable. Indeed, he has seen patients who were unsuccessfully treated for chronic backache, carpal tunnel syndrome, and a variety of other chronic pain syndromes for months or years before the true systemic nature of their illness was recognized and the diagnosis was revised to fibromyalgia. Equally important is the fact that, given a sufficiently large population of patients with fibromyalgia, careful examination will reveal ODTPs in nearly all locations in the body, including such unusual sites as the scalp at vertex, the lateral aspect of the lower radial extremity, and the thenar eminences in hands. (The second reason I consider the College criteria unacceptable is that its criteria do not address any of the systemic oxidative-dysoxygenative phenomena in fibromyalgia. This subject is discussed at length in the accompanying article in this issue of the Journal).

9. FUNDAMENTALS OF ODTP INJECTION THERAPY

9.1 Patients must be cared for as a whole person. Merely injecting the trigger points is not optimal management.

9.2 A sound knowledge of the regional anatomy is imperative for the clinicians administering ODTP injection therapy.

9.3 ODTPs must be precisely localized before such points are injected.

9.4 The composition of the injection solution employed in this study was as follows: 50% glucose with equal parts of 2% lidocaine, unless the existence of acute inflammatory response forces some other choice, such as Medrol solution.

9.5 It is imperative to remember that major ODTPs often mask minor ODTPs, which become more obvious and distressing after the major points are resolved, hence the need for close follow-up and subsequent additional therapy.

9.6 It is imperative to emphasize to the patient the absolute need for frequent, low-intensity stretching of muscle groups in the vicinity of trigger points; frequency of stretching is important; intensity and duration are not.

9.7 It is imperative that ODTP injection therapy be considered only as local therapy for a systemic disorder that requires effective systemic approach to address all oxidative-dysoxygenative issues involved.

The desired frequency and intervals for ODTP injection therapy depend upon how chronic the points are. In general, two to three sets of injections given at seven to 14 days apart are sufficient for near-complete healing. Of course, such trigger points develop in the same or other locations rapidly unless effective local measures for prevention (such as frequent stretching) as well as strong measures for addressing the underlying oxidative-dysoxygenative dysfunctions are vigorously implemented.

10. PROCEDURAL STEPS FOR ODTP INJECTION THERAPY

Equal volumes of 50% glucose and 2% lidocaine are drawn in a 10 ml syringe (amount of each to be determined by the number of injection sites to be injected). A 21-gauge needle is used for extra support so that the needle does not bend or break in the tissues. Localize the trigger points by direct digital pressure. Ask the patient to respond to the pressure by using one of the following response scores: (1) zero for no pain; (2) one for mild tenderness; (3) two for moderate tenderness; (4) three for marked tenderness; (5) four for exquisite tenderness. The author uses the following procedural steps: (1) the location of each ODTP is marked with a marking pen using the above scoring system; (2) all sites of the marked ODTPs are retested as if for the first time to assure the consistency of point identification; (3) the proximity of the intended sites of injection to major nerve trunks or vessels is determined carefully; (4) 0.3 to 1 ml of 50% glucose solution in equal volume of 2% lidocaine is injected exactly in the marked sites of ODTPs in a slow and sustained fashion, withdrawing the plunger at intervals to assure that the needle tip is not in a vein; (5) whenever possible, the needle is advanced until the periosteum of underlying bone is reached (the patient usually feels a sharp prick); (6) after completing the injection of the desired amount of the fluid, the needle is drawn expeditiously and direct, sustained pressure is applied over the site of injection for two-four minutes.

11. COLCHICINE AND STEROID INJECTIONS

One milligram of colchicine diluted in 10 ml of saline and given by a slow intravenous injection is valuable as an adjunct therapy to trigger points. It is imperative that all of the colchicine solution be administered cautiously, making certain that the needle is well placed within the vein. Colchicine is a very strong irritant and vasoconstrictant and may cause tissue sloughing if injected inadvertently into soft tissues. Regitine should be available for immediate injection into the tissues surrounding the site of colchicine extravasation to prevent tissue necrosis in case of an error.

In the author's experience, true indications for steroid (methylprednisolone or others) trigger point injections are extremely rare. Extensive experience has convinced me that results with glucose trigger points with adjunct therapies described here give far superior results. The only exception is when trigger points near small joints (fingers, hands and wrist) are accompanied with considerable acute inflammation. In those conditions, an injection of 20 to 40 mg methylprednisolone may be appropriate.

12. SYSTEMIC THERAPIES FOR
OXIDATIVE-DYSOXYGENATIVE DYSFUNCTION

Fibromyalgia is a systemic oxidative-dysoxygenative disorder (ODD)1 and requires a global ecologic-restorative management plan individualized for a given patient. Thus, treatment plans focused on local therapies for ODTPs rarely, if ever, yield long-lasting results. Specifically, it is necessary to institute a vigorous plan to restore damaged bowel, blood, and liver ecosystems. Most patients also require broad-based support for the thyroid, adrenals, and pancreas as the second trio of ecosystems. Finally, the third trio comprising sex hormones, neurotransmitters, and the limbic system requires functional assessment and enhancement. The need for such an ecologic-restorative management plan is discussed within the broader Darwinian ecologic perspective.62 An outline of such a program appears elsewhere in this issue of the Journal63 reporting clinical outcome data for 150 patients with fibromyalgia.

 13. CLINICAL OUTCOME OF INJECTION THERAPIES

14. SUMMARY

An oxidative-dysoxygenative pathogenetic model for trigger points characteristically seen in fibromyalgia is presented. This molecular model is fully consistent with the established biochemical, histopathologic, ultrastructural, and clinical features of chronic, intractable, painful, and tender points in soft tissues of the body. Beyond that, this pathogenetic model integrates as local phenomena ODTPs within the much broader context of the systemic nature of the oxidative-dysoxygenative dysfunction which fibromyalgia is. From the therapeutic perspective, the ODTP model emphasizes the absolute need of effective ecologic-restorative management protocols that address all the systemic issues for obtaining long-lasting relief of local symptomatology of trigger points. The outcome data obtained with ODTP injection therapy employing 50% solution of glucose in equal volume of 2% lidocaine demonstrates the efficacy of such approach when adopted as a part of a global ecologic-restorative management plan that addresses all of the oxidative-dysoxygenative dysfunctions encountered in fibromyalgia.