Research Review By Dr. Robert Rodine©

Date Posted:

July 2010

Study Title:

Fascia: a missing link in our understanding of the pathology of fibromyalgia.

Authors:

Liptan G

Author's Affiliations:

Department of Medicine, Oregon Health & Science University.

Publication Information:

Journal of Bodywork and Movement Therapies 2010; 14: 3-12.

Background Information:

Fibromyalgia (FM) is a chronic and painful disorder characterized by widespread muscle pain. It is controversial. Its etiology is unknown and pathogenesis obscure. As a clinical condition, FM is a diagnosis of exclusion, often a last resort as a label/cause of a patient’s symptoms when all other conditions have been ruled out.

Research has found that, when compared to controls, patients with FM feel pain at lower pressure point thresholds, experience stronger pain and experience larger referral patterns. As the central nervous system appears to be responding with exaggerated pain responses, central sensitization (CS) is proposed as at least a partial mechanism in this disorder (1,2).

To date, no evidence of muscle pathology has been found to date in FM patients. Therefore, in the midst of recent interest in fascial research, the search has extended towards intramuscular connective tissue in search of answers about FM.

The following narrative review presents a hypothesis that inflammation and dysfunction of the fascial system leads to CS, therefore playing a role in the etiology FM. The authors therefore, review literature supporting their theory and the role of manual therapy in addressing this relationship.

Summary:

  • The term FM was coined in 1976 and adopted by the American College of Rheumatology with diagnostic criteria in 1990.
  • No consistent differences have been found within the muscle tissue of FM patients compared to controls.
  • While trigger points have been often labeled as the peripheral source of nociception which leads to CS, not all patients with FM have trigger points. Triggers points are also common in patients without FM.
  • Fascia, a dense connective tissue, is composed of fibroblasts, macrophages and mast cells in addition to extracellular matrix (ECM). Fascia is intertwined with, and linked to, muscle proteins as it surrounds muscle tissue, and is continuous with both tendons and periosteum.
  • 25% of muscle stretch receptors and 75% of free nerve endings are located within the fascia, indicating that this connective tissue is not an inert substance (3).
  • Fascia consists primarily of fibroblasts, which regulate inflammation and wound repair following tissue injury. They play a crucial role in the homeostasis of ECM.
  • Fibroblasts respond to mechanical stretch with altered shape and alignment and through increased producing of inflammatory cytokines.
  • Dysregulation of fibroblasts is seen within chronic inflammation and Rheumatoid Arthritis.
  • As fascia can remodel under stress and inflammation, the formation of adhesions can result through disorganized collagen. This pattern of disorganization is familiar from research surrounding plantar fasciitis and elbow tendinopathy (4).
  • Recent research has identified an increase in the amount of collagen surrounding muscle cells in FM patients versus controls. An increase in immuno-histochemical staining is suggestive of inflammation within the fascial system. Given that evidence of local myofascial inflammation has been l inked to CS in the case of chronic low back pain, generalized myofascial inflammation may play a role in generalized CS, or FM (5).
  • It is additionally important to consider the effect of sleep deprivation on FM patients and the course of FM. FM patients experience reduced and interrupted sleep. This reduces the production of growth hormone in this patient subset, as GH is primarily produced in late stage sleep.
  • 90% of FM patients have reduced GH levels, and GH replacement therapy improves symptoms in FM patients (6,7).
  • Fibroblasts have GH receptors. When stimulated, fibroblasts produce IG-1 a major mediator of wound healing.

Clinical Application & Conclusions:

A summary of some general research points is summarized above - presented by the author to support the hypothesis that fascial dysfunction may be caused by impaired healing due to insufficient GH production. When combined with chronic tension and microtrauma, fascial dysfunction leads to inflammation and eventually CS. This may result in FM.

The hypothesis proposes that some patients may be genetically predisposed to a prolonged stress response subsequent to trauma. This link is backed by research indicating a genetic component to FM as well as the significant association to preceding trauma to FM onset. As a result of the prolonged stress response, a hyper-arousal state is entered. This disrupts sleep (inhibiting GH secretion) and disturbs function of the HPA axis (inhibiting GH secretion). Inhibited GH in turn affects wound healing and connective tissue.

Additionally, a state of ‘chronic tension’ as a result of hyper-arousal (sympathetic dominance) that is combined with continued microtrauma/fascial tension may result in the overproduction of collagen and ECM, leading to disorganization leading to increased mechanical stress.

Combined, these factors result in a body wide ‘fasciitis’ and generalized pain – in other words, Fibromyalgia. The authors propose that the inflammation described here would not respond to NSAIDS or corticosteroids as these therapeutic modalities are not effective in states of chronic inflammation, or a ‘dysfunctional healing response.’ This provides a rational as to why FM patients do not typically respond to NSAIDs or corticosteroids.

Instead the authors revisit the phases of connective tissue healing: inflammatory, proliferative and remodeling, proposing that connective tissue fibrosis can be reversed through mechanical stimulation and manipulation of the healing process. This concept should be familiar to those in the manual medicine disciplines with the recent popularity of soft-tissue techniques like Active Release Techniques® and Graston®.

Additionally, research surrounding acupuncture has recently brought to light significant links between the fascial and nervous systems. The research of Helene Langevin proposes that acupuncture creates downstream effects via the ECM as a result of mechanical stimulation (8). Langevin reports that the mechanical aspects (pull-out force) are greater in subcutaneous tissue (fascia) than muscle; that connective tissue experiences “reorganization” with unilateral needle rotation; and that mechanical stimulation of the connective tissue results in cellular responses such as cell contraction, gene expression and signaling pathway activation (8).

These results point to a mechanical rationale for the therapeutic effect of acupuncture, linked to the fascial system. More importantly, it helps to signify that the fascial system is not an inert tissue as previously thought.

While Liptan’s hypothesis is of course speculative, sound rationale is provided. More clinical research could strengthen this area significantly. …Which is an excellent opportunity for manual therapists wishing to publish case study research.

Study Methods:

This study was a narrative literature review. No search strategy, inclusion/exclusion criteria, or quality appraisal of included studies or search results were presented.

Study Strengths / Weaknesses:

The study design is the strongest limitation of this manuscript, being a narrative literature review. No search strategy, inclusion/exclusion criteria or results are presented. Therefore, we must assume that the author has chosen to include only information which is in support of the paper’s hypothesis.

The strength of such a study could be improved with the use of more than one author and a detailed search strategy in which the reader may recreate.

The study however is strong with its innovation and interesting hypothesis into the role of fascia for FM, as well as for other soft-tissue disorders.

Additional References:

  1. Gracely et al. Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia. Arthitis & Rheumatism 2002; 46(5): 1333-1377.
  2. Sorensen et al. Hyperexcitability in fibromyalgia. Journal of Rheumatology 1998; 25(1): 152-155.
  3. Bonica. The management of pain. Lea & Febinger, Philidelphia. p. 34.
  4. Langevin et al. Potential role of fascia in chronic musculoskeletal pain. In: Audette, Bailey (eds.), Integrative Pain Medicine. Humana Press, p. 125.
  5. Spaeth et al. Increas of collagen IV in skeletal muscle of fibromyalgia patients. Journal of Musculoskeletal Pain 2005; 12(9S): 67.
  6. Paiva et al. Impaired growth hormone secretion in fibromyalgia patients: evidence for augmented hypothalamic somatostatin tone. Arthritis & Rhematism 2002; 46(5): 1344-1350.
  7. Bennett et al. A randomized, double-blind, placebo-controlled study of growth hormone in the treatment of fibromyalgia. American Journal of Medicine 1998; 104(3): 227-231.
  8. Langevin et al. Evidence of connective tissue involvement in acupuncture. The FASEB Journal 2002. Published Online: 10.1096/fj.01-0925fje.