Scopingreviewandinterpretationofmyofascialpain/fibromyalgiasyndrome:Anattempttoassembleamedicalpuzzle

Myofascial Pain Syndrome (MPS) is one of the most common yet underdiagnosed and undertreated sources of chronic pain, affecting an estimated 37–65% of the population and costing the United States approximately $47 billion annually. Despite its prevalence, MPS lacks a clear definition, pathophysiology, or diagnostic criteria, leading many clinicians to dismiss it as psychosomatic. A particularly puzzling aspect is how localized MPS may evolve into the widespread pain of fibromyalgia, a condition similarly characterized by painful points, normal laboratory findings, and no systemic inflammation. While central sensitization is the most accepted theory for fibromyalgia, it fails to explain many empirical findings, including complete resolution after certain surgeries, strong associations with hypermobility syndrome, and specific anatomical patterns of tender points.

This scoping review systematically searched cross-disciplinary literature to explore mechanical, organic aspects of MPS and propose a unified mechanism explaining its pathophysiology and potential progression to fibromyalgia.

The author conducted a systematic search across MEDLINE, EMBASE, COCHRANE, PEDro, and medRxiv databases from September 2020 to September 2021, using keywords related to fascia tension, trigger points, biotensegrity, and myofascial pain. After removing duplicates and screening titles, abstracts, and full texts, 390 items were included from the systematic search. An additional 409 items from textbooks, UpToDate, and targeted database searches on side topics were added, totaling 799 included items. The review followed PRISMA-ScR guidelines for scoping reviews.

The author then synthesized findings across multiple domains—fascial biology, movement science, myofibroblast cellular biology, and clinical observations—to construct a theoretical model called "fascial armoring."

The review identified several key empirical findings that informed the proposed model. Fascia can reversibly change its biomechanical properties, with stress relaxation of approximately 90% achieved in about four minutes under experimental conditions. Hyaluronic acid within fascia undergoes gel-to-fluid transitions at 35–40°C, and its increased viscosity impairs normal tissue sliding. Myofibroblasts—contractile cells in connective tissue—generate sustained tension through alpha smooth muscle actin (α-SMA) in a positive feedback loop with TGF-β1 signaling.

Studies found that immobilization increases collagen and myofibroblast density within one week, and abnormal collagen arrangement appears after about four weeks. Trigger points were found in 100% of 224 non-specific neck pain patients, and 74–85% of pain clinic presentations had trigger points as the primary pain cause. Critically, fibromyalgia patients showed mean intramuscular pressure of 33.48 ± 5.90 mmHg in the trapezius—substantially higher than rheumatic disease controls (12.23 ± 3.75 mmHg) and exceeding all three diagnostic criteria for chronic exertional compartment syndrome. Studies also found that 21% of fibromyalgia patients discontinued all medications after parathyroidectomy, with 89% experiencing symptom relief as early as one week post-surgery.

Hypermobility syndrome showed 70–100% association with chronic widespread pain, with cells expressing increased myofibroblast transition. A genomic study found an odds ratio of 4.6 for fibromyalgia associated with a mitochondrial DNA variant affecting oxidative phosphorylation.

The "fascial armoring" model proposes that MPS represents a pathological state of fascial imbalance driven by myofibroblast-generated tension within a tensegrity framework. Sedentary lifestyle and disrupted biomechanics trigger this cascade, while movement normally prevents or reverses it. When widespread, this process creates a "global chronic compartment-like syndrome"—effectively fibromyalgia—characterized by mechanical compression of tissues, impaired perfusion, and peripheral nerve irritation rather than purely central nervous system dysfunction. The model has significant therapeutic implications: it suggests needling and other mechanical interventions work by disrupting stress-shielded myofibroblast networks and allowing fascial re-alignment, but emphasizes that treatment must respect tensegrity principles—gradual, systematic release rather than focal aggressive intervention.

The author proposes a "global percutaneous needle fasciotomy" approach, starting peripherally and working concentrically toward areas of highest tension. This framework also explains why certain surgeries unexpectedly resolve fibromyalgia (possible incidental fascial release) while others worsen it (disrupting tensegrity balance), and why hypermobility syndrome so strongly associates with fibromyalgia (altered collagen properties promoting myofibroblast differentiation). The model challenges the prevailing central sensitization paradigm and calls for renewed attention to peripheral mechanical factors in these common, debilitating conditions.