Myofascial pain syndrome (MPS) is familiar territory for physiotherapists, massage therapists and other musculoskeletal practitioners. Patients present with taut bands, trigger points, local or referred pain, stiffness and restricted movement. Yet a common clinical puzzle remains: why do some patients improve quickly with local treatment, while others experience recurrent pain, stress-related flares, poor sleep and progressively broader sensitivity?

A review by Ali Gur pubslihed in Frontiers in Pain Research
proposes a useful way of thinking about this problem: the Stress–Fascia–Pain (SFP) axis. Rather than replacing the traditional trigger-point model, it places trigger points within a wider system involving fascia, stress physiology, autonomic regulation and central pain processing.

Trigger points are biologically real

The strongest evidence still concerns the trigger point itself.

Human microdialysis studies show that active trigger points have a distinct biochemical environment, including lower pH and increased concentrations of substances such as bradykinin, substance P, CGRP, inflammatory cytokines, serotonin and norepinephrine.

In other words, an active trigger point is more than a tender “knot.” It represents an ischemic, hypoxic and chemically sensitised local environment capable of activating nociceptors and maintaining pain.

This supports the clinical value of appropriately selected local interventions, including manual therapy, dry needling, movement and load modification.

But it does not fully explain recurrence.

Fascia may help maintain stiffness

The review broadens the picture by considering the tissue surrounding muscle.

Fascia is richly innervated, contains nociceptive and sympathetic fibres and contributes to force transmission and normal sliding between tissue layers. Hyaluronan within loose connective tissue helps these layers glide smoothly.

Changes in tissue mechanics or hyaluronan behaviour may therefore contribute to persistent stiffness and reduced tissue excursion. Myofibroblasts may also influence fascial contractility.

This offers a more plausible interpretation of the sensation patients describe as “tightness” or “pulling.” Manual treatment may help by changing movement, load distribution, tissue glide or local nociceptive input rather than by literally breaking adhesions or repositioning tissue.

However, the evidence should not be overstated. The idea that psychological stress directly produces fascial fibrosis or persistent myofibroblast activity in people with MPS has not yet been demonstrated convincingly.

Stress can influence pain without making pain “psychological”

Patients frequently report that symptoms worsen during stressful periods.

The SFP framework provides a biological explanation. Stress can alter sympathetic nervous-system activity, catecholamine release, muscle tone, blood flow, sleep and inflammatory regulation. These changes could make already sensitised tissues more reactive or slower to recover.

The evidence in MPS itself remains limited, with much of it coming from temporomandibular myofascial pain. Even so, studies suggest altered cortisol and catecholamine responses and slower recovery from stress in some patients.

The key message is not that stress causes trigger points. Rather, stress may alter the physiological environment in which myofascial pain either settles or persists.

Do not overlook sleep

Sleep may be one of the most clinically important links in the model.

Poor sleep can increase pain sensitivity, reduce descending pain inhibition, alter cortisol rhythms and increase sympathetic activity. Pain itself then disrupts sleep, creating a vicious cycle:

pain → poor sleep → impaired recovery → greater pain sensitivity

For a patient with repeatedly recurring trigger-point pain, asking about sleep may therefore be just as important as asking about posture, training load or workstation ergonomics.

Local pain can become centrally amplified

Perhaps the most important clinical point is that peripheral and central mechanisms are not mutually exclusive.

Experimental studies show that sustained stimulation of a trigger point can reduce pressure-pain thresholds at distant sites. Persistent peripheral nociceptive input may therefore begin influencing the nervous system beyond the original painful region.

Over time, some patients develop broader mechanical sensitivity, poorer exercise tolerance, disturbed sleep and pain that appears increasingly disproportionate to local tissue findings.

This does not mean the original trigger point was imaginary or has become irrelevant. Instead, peripheral nociception and central amplification may begin reinforcing one another.

Repeatedly treating the same painful point in such a patient may consequently produce only temporary improvement.

Think in clinical phenotypes

The SFP model is perhaps most useful when it encourages therapists to stop treating all MPS as the same condition.

One patient may have a predominantly local phenotype: clear mechanical aggravation, reproducible local or referred pain and durable improvement with trigger-point treatment, movement restoration and load management.

Another may have a persistence-prone phenotype: recurrent symptoms, poor sleep, strong stress sensitivity, broader pain, reduced exercise tolerance and only short-lived responses to local treatment.

The second patient may still have active trigger points, but local treatment alone is unlikely to be enough.

Management may need to include graded activity, aerobic reconditioning, sleep restoration, pacing, stress regulation and strategies that improve confidence in movement and pain modulation.

What this means in the clinic

The review does not argue against manual therapy, dry needling or trigger-point treatment. It argues against repeatedly applying a local solution without considering why the problem keeps returning.

A useful question is:

Is this patient’s pain still predominantly local, or has the biological context become broader?

Myofascial pain may begin with a genuine peripheral lesion. Fascia may contribute to the mechanically sensitive environment. Stress and poor sleep may impair recovery. Persistent nociceptive input may then amplify pain processing.

The evidence is strongest for trigger-point biochemistry and considerably weaker for some of the proposed stress–fascia and autonomic pathways. The SFP axis should therefore be regarded as a useful working model rather than a proven causal chain.

For therapists, its central message is nevertheless valuable: myofascial pain can start locally without necessarily remaining local.

The clinical task is not to decide whether pain comes from muscle, fascia or the nervous system. It is to determine which mechanisms appear to matter most in this patient, at this stage of their condition.