As I perused the abstracts for the upcoming 4th International Fascial Research Congress (September 2015), I came upon one that made me stop and think. It related to a half-day post-conference workshop by Kirstie Segarra – Managing Fascial Health for Individuals in Fibromyalgia:
To demonstrate clearly that managing widespread pain must include treatment of the fascia as we are structured determined systems, and to decrease pain is to invite change in the structure through the fascial matrix in order to have a correlating change in the central nervous system. In this way we restore homeostasis in the client.
Could pathology within fascia have been overlooked in the search for a peripheral source of nociception in this condition? Well, it appears that this is no longer the case.
Liptan  hypothesized that fibromyalgia could be seen as a “bodywide fasciitis,” comparable to situations characterised by more focal fasciitis (e.g. plantar fasciitis).
The culprit appears to be chronic tension within the fascia responsible for causing micro-injuries (i.e. tears) in those with a “dysfunctional” healing response. Such a response is said to result from insufficient growth hormone release consequent upon inadequate deep sleep.
In summary, Liptan argued that: “Fascial dysfunction and inflammation may lead to widespread pain and central sensitization seen in fibromyalgia.”
She explained the tender points as possibly reflecting “areas that suffer the greatest microtrauma and mechanical stress from daily activities, and thus have higher levels of fascial inflammation.”
The main evidence put forward in support of her hypothesis derived from “recent biopsy studies [which] have found increased levels of collagen and inflammatory mediators in the fascia of fibromyalgia patients.”
But is this a novel hypothesis? In the Background section of her paper, Liptan harks back to the early 1900s when the aetiology of “muscular rheumatism” was indeed a hot topic.
In speculating upon the pathophysiology of low back pain, the great British neurologist, William Gowers  coined the term “fibrositis” and thus championed the central role of the fascia in this condition:
In all parts it seems it seems the most susceptible to the influence we call “rheumatism” … The relation of lumbago to rheumatism would alone, make us expect to find it an affection of the fibrous tissue of the muscles, the tissue in which the spindles are situated, rather than of these alone … important proof that the malady is an affection of fibrous tissue; it may spread, and it spreads by continuity of this tissue.
Gowers postulated both focal and generalised forms of “fibrositis”:
We are thus compelled to regard lumbago in particular, and muscular rheumatism in general, as a form of inflammation of the fibrous tissue of the muscles.
The pathological findings
Ralph Stockman , a Scottish pathologist, soon announced:
The essential lesion is a chronic inflammatory hyperplasia of white fibrous tissue in patches and as fibrous tissue is spread throughout the body the lesions may also be widely spread or may affect only a single limited area.
But after other researchers had repeatedly failed to find biopsy evidence of fibrous tissue inflammation, the “fibrositis” construct was eventually superseded by that of “fibromyalgia” [Hench, 1976] and classified in the nebulous category of non-articular rheumatism [Atkinson, 1981].
As did Gowers, Liptan  ascribed a limited role to anti-inflammatory drugs (NSAIDs and corticosteroids), which should be used only during the initial phase of injury repair.
According to Liptan  “only slow and sustained pressure will effect changes in the fascial tissue” and she recommended manual therapy techniques that “don’t cause further injury and inflammation, but rather gently break apart existing fascial restrictions and adhesions to promote tissue healing.”
She wondered whether techniques said to target the fascia, which included “Rolfing” (a technique of deep tissue manipulation) and “myofascial release,” could “help define the role of fascia in producing fibromyalgia pain.”
Based upon Liptan’s hypothesis, a pilot trial was undertaken comparing Swedish massage with myofascial release therapy (MFR), each administered over 90 minutes a week for 4 consecutive weeks [Liptan et al. 2013]. The former technique utilized moderate pressure stroking of the neck, back, arms and legs, whereas MFR consisted of “prolonged assisted stretching of painful areas of soft tissue” in the same regions.
The rationale given for MFR manoeuvres is that they are designed to “break up fascial adhesions” presumed to be the consequence of tissue injuries occurring in the fascia of patients with fibromyalgia [Liptan et al. 2013]. That for Swedish massage is to increase circulation and promote general relaxation.
Although numbers were small, both forms of treatment were found to be “safe, tolerable and acceptable” with MFR producing better symptom reduction.
By contrast, the mainstay of treatment recommended by Gowers was complete rest:
Not even passive movement should be employed until it causes no pain, and then it should be most gentle. The avoidance of pain should be made the standard for all local measures.
Gowers observed that counter-irritation (cautery being the most effective form) sometimes lessens the pain, as does deep hypodermic injection of cocaine, repeated daily for 2-3 weeks.
Other treatment strategies worth trying included a Turkish bath, mild aperients and, in the most acute cases, medicinal agents such as salicylates, nitrous ether, colchicum and perchloride of mercury.
Gowers conceded: “we are without any direct evidence of the real nature of these affections” but he did hope that opportunities for pathological research would be seized upon:
We cannot wonder at our ignorance, still less complain of it, for it is only quite recently that the minute structure of the sensory elements of muscle and tendon has been clearly perceived, and much of the normal structure remains obscure.
But over a century later, direct histological evidence to support the related concepts of “fibrositis” and “fascial adhesions” is still lacking.
Nonetheless, Liptan  calls for the use of existing methods of in vivo microdialysis to investigate the chemical composition of fascial interstitial fluid for evidence of inflammation, as well as for evidence of activation of fibroblasts removed from fascial tissues. She did not canvass the possibility that any such inflammation might in fact be “neurogenic” [Julius & Basbaum, 2001].
As for the role of manual therapy, Liptan et al.  hope that various measurement tools being developed “may provide insight into which symptom of function domains are most malleable to various types of massage intervention.”
To date, the search for underlying peripheral musculoskeletal pathology in fibromyalgia has not been fruitful. Yet, a recently published book – Fascial Dysfunction: Manual Therapy Approaches (2014) – is being advertised to manual therapists with this rather astounding claim appearing in the blurb:
Fascial dysfunction is now recognized as one of the main underlying causes of musculoskeletal pain leading to impaired and reduced mobility. [Link: http://www.amazon.com/Fascial-Dysfunction-Manual-Therapy-Approaches/dp/1909141100]
Could Gowers have been right after all? Should we now discard the term fibromyalgia and revert to his “fibrositis” model? It seems a most unlikely possibility but a critical review is urgently needed to once and for all resolve this important question.
Atkinson MH. Nonarticular rheumatism. Can Fam Physician 1981; 27: 254-258.
Gowers WR. A lecture on lumbago: its lessons and analogues. Brit Med J 1904; i: 117-121.
Hench PK. Nonarticular rheumatism, 22nd rheumatism review: review of the American and English literature for the years 1973 and 1974. Arthritis Rheum 1976; 19(suppl): 1081–1089.
Julius D, Basbaum AI. Molecular mechanisms of nociception. Nature 2001; 413: 203–210.
Liptan GL. Fascia: a missing link in our understanding of the pathology of fibromyalgia. J Bodywork Mov Ther 2010; 14: 3-12.
Liptan G, Mist S, Wright C, Arzt A, Jones KD. A pilot study of myofascial release therapy compared to Swedish massage in Fibromyalgia. J Bodywork Mov Ther 2013; 17: 365-370.
Stockman R. Discussion on fibrositis. Proc R Soc med 1913; 6: 36-39.