Trigger Point or Fibrous Adhesion?

Ask three providers to feel the same tender knot in your shoulder and you might get three answers: a trigger point, adhesion, or just tight muscle. Patients are left assuming these are competing diagnoses. Recent research points to a different picture. A trigger point is neurological. Fibrous adhesion is structural. The same spot can involve both, and the two may reinforce each other.

Trigger point: neurologically excited tissue

A trigger point is a localized knot of muscle fibers held in continuous contraction by nervous-system overactivity. It is tender and often refers pain to other areas of the body.

The classic explanation, formalized by Janet Travell and David Simons and later expanded by Gerwin, Dommerholt, and Shah, is the "integrated hypothesis." Dysfunctional motor endplates release excess acetylcholine and hold a small cluster of muscle fibers in contracture. The contracture compresses local capillaries, starves the tissue of oxygen, and triggers a release of sensitizing, inflammatory chemicals. Later microdialysis work by Jay Shah and colleagues gave this biochemical support. At active trigger points they measured significantly lower pH and elevated substance P, CGRP, bradykinin, and inflammatory markers like TNF-alpha and IL-1beta, compared with nearby normal tissue.

What remains unsettled is whether a trigger point is also a distinct physical lesion you could find on a biopsy. A 2015 critique in Rheumatology by Quintner, Bove, and Cohen argued that no such lesion has ever been reliably demonstrated, and that the phenomenon is better explained by ordinary nerve sensitization.

A small 2025 study in Scientific Reports biopsied clinically identified trigger points in five people. The researchers expected the classic "contraction knot." None were present. Instead, the tissue showed muscle fiber atrophy, fibrofatty replacement, and disorganized collagen and fibroblast activity. That is the signature of tissue remodeling, not a discrete neuromuscular lesion.

Fibrous adhesion: collagen "glue" in muscle

Fibrous adhesion is a structural problem. It is dense, disorganized collagen that binds muscle fibers together and to the surrounding tissue, restricting the normal glide between tissue layers. Clinically, that loss of glide shows up as reduced flexibility and range of motion. Because rigid, non-contractile collagen is standing in for tissue that should transmit force, adhesion can also leave the muscle mechanically weaker.

The mechanism is well described in the muscle fibrosis literature. Collagen production outpaces normal breakdown, typically after an injury, a period of immobilization, repetitive strain, or ongoing low-grade inflammation. Fibroblasts and resident fibro-adipogenic progenitor cells lay down excess extracellular matrix, driven substantially by TGF-beta signaling. Left alone, that restriction tends to persist and can worsen. We've written about how aging cells can worsen adhesion, and about fibrous adhesion as one possible contributor to chronic musculoskeletal pain.

How the same spot can be both

This is an active, still-developing area of research. A 2025 review in Frontiers in Pain Research proposes that fibrotic, densified fascia isn't a bystander in myofascial pain but a co-driver. When the ground substance between fascial layers thickens and loses its normal slipperiness, it stops absorbing movement. That abnormal mechanical tension is transmitted onto the sensory nerve endings woven through the tissue. This is a plausible mechanical route by which adhesion could produce the referred pain and tenderness we call a trigger point.

The 2025 biopsy findings point the same direction from the other side. A neurologically irritable spot sits in a chronic, low-grade inflammatory environment, with lower pH and elevated inflammatory signaling. That same environment also drives fibrotic collagen deposition. A longstanding trigger point may accumulate structural adhesion over time. A longstanding adhesion may create enough abnormal mechanical strain to keep the local nerve supply irritated. Neither model excludes the other. In a chronic case, they may reinforce each other in the same few square centimeters of tissue.

Why this matters more than the label

Physical exam findings for both have documented limits. A 2017 meta-analysis in the Clinical Journal of Pain, pooling data across 363 patients, found only fair-to-moderate agreement between examiners palpating for trigger points, with a pooled kappa around 0.45. Tenderness itself was reasonably reproducible. The taut band and twitch response that are supposed to confirm the diagnosis were considerably less so. Manual assessment of adhesion hasn't been studied nearly as rigorously, and there's no reason to expect it fares dramatically better by feel alone.

So "trigger point or adhesion?" may not have one right answer, especially when a problem has been present for months. A more useful question is whether both pieces are present. The structural piece is restricted glide and a dense or fibrotic feel to the tissue. The neurological piece is a taut band and reproducible referred pain on compression. When both are present, treatment aimed at only one may be one reason results stall.

That is the reasoning behind combining manual adhesion release with shockwave therapy.

In the neck, both sides have direct human evidence: surgical findings of trapezius fibrosis and measurably stiffer upper-trapezius tissue in myofascial pain, covered in trapezius fibrosis and tissue stiffness. For how we evaluate it, see chronic neck pain and tension headache treatment.

A 2025 scoping review of extracorporeal shockwave for myofascial pain found moderate-to-good efficacy across the studies it pooled. Proposed mechanisms include improved local blood flow, mechanotransduction effects on the tissue, and reduction of the same inflammatory substances Shah's group measured at active trigger points. These could plausibly address the structural and neurological sides of the same spot. The review's authors were candid that the underlying studies are still too inconsistent in method to call this settled.

Manual and instrument-assisted soft tissue techniques take a more direct route at the structural side. A 2017 review in the Journal of Exercise Rehabilitation describes how instrument-assisted mobilization appears to increase local fibroblast activity and encourage more organized collagen realignment. That evidence is mostly from animal models, alongside human studies showing acute improvements in range of motion. The authors note that more rigorous human research is still needed, a caveat that applies to most of this field.

If a sore spot in your shoulder, hip, or back has lasted months and nothing quite fits, it's worth an exam. It may be tender and refer pain like a trigger point, yet feel bound down and not loosen with stretching. Book a new patient exam and we'll assess what is going on in the tissue, whatever it's called.

Sources

• Travell, J.G. & Simons, D.G. — foundational "integrated hypothesis" of trigger point formation, later expanded by Gerwin, Dommerholt, and Shah. (link)
• Jay Shah and colleagues — microdialysis studies measuring elevated substance P, CGRP, bradykinin, and inflammatory markers at active trigger points. (link)
• Quintner, J.L., Bove, G.M., & Cohen, M.L. (2015). Rheumatology - critique of the trigger-point-as-lesion model. (link)
• 2025 biopsy study of clinically-identified trigger points, published in Scientific Reports. (link)
• 2025 review in Frontiers in Pain Research on fibrotic, densified fascia as a mechanical driver of myofascial pain. (link)
• 2017 meta-analysis in the Clinical Journal of Pain (363 patients) on inter-examiner reliability of trigger-point palpation. (link)
• 2025 scoping review of extracorporeal shockwave therapy for myofascial pain. (link)
• 2017 review in the Journal of Exercise Rehabilitation on instrument-assisted soft tissue mobilization. (link)