Myofascial Pain Syndrome

Myofascial pain syndrome (MPS) is one of the most prevalent and most poorly understood musculoskeletal pain conditions in clinical practice — estimated to be a primary or contributing factor in up to 85% of patients presenting to pain clinics, and yet frequently dismissed, misdiagnosed, or treated with approaches that address only a fraction of what is actually happening in the tissue.

At our clinic, we take myofascial pain seriously — and we approach it through both the traditional trigger point model and the more recent and compelling fascial science that helps explain what that model was always pointing at but couldn't fully account for.

Ready to get on top of this?

📞 Call Now — speak with our team

🗓 Book Online — available 24/7

📄 Free 2-Week Rehab Program — request your copy

---

What Is Myofascial Pain Syndrome?

Myofascial pain syndrome is a chronic or recurrent pain condition characterised by the presence of myofascial trigger points — localised, hyperirritable spots within a taut band of skeletal muscle or its associated fascia that are tender on compression and that produce a predictable pattern of referred pain, autonomic phenomena, and motor dysfunction.

The term 'myofascial' is important and often glossed over: myo (muscle) and fascial (connective tissue). The pain is not purely muscular — it arises from the interface of muscle and the fascial matrix that surrounds, interpenetrates and interconnects it. This is why stretching the muscle alone may not fully address the underlying issue, and why treatments that incorporate the fascial component are increasingly recognised in the clinical literature.

Trigger points are classified as either active (spontaneously painful and producing referred pain with direct pressure) or latent (tender on pressure but not spontaneously painful — a significant source of movement restriction and motor inhibition even when pain is not the presenting complaint). The distinction matters clinically because latent trigger points are far more prevalent than active ones and represent a major but underappreciated driver of reduced performance and movement quality in otherwise 'healthy' active people.

Feature	Detail
Common locations in the low back region	Quadratus lumborum, iliopsoas, gluteus medius, gluteus minimus, piriformis, thoracolumbar erector spinae, multifidus
Referred pain patterns	QL refers to the iliac crest, buttock and lateral hip; glute minimus refers down the lateral or posterior leg (commonly mistaken for sciatica); iliopsoas refers to the lumbar spine and anterior thigh
Distinguishing features	Taut band palpable in the muscle belly; exquisite spot tenderness; reproducible referred pain; local twitch response with needling or firm pressure
Aggravating factors	Sustained postures, repetitive movements, psychological stress, poor sleep, dehydration, nutritional deficiencies
Prevalence	Found in 30–93% of patients presenting to pain clinics with regional pain as a primary complaint (Gerwin, 2001)

The Trigger Point Model — Its Strengths and Its Limits

The myofascial trigger point model, developed principally by Travell and Simons over several decades, describes trigger points as arising from a sustained depolarisation of motor end plates — a dysfunctional acetylcholine release cycle that creates a local energy crisis within the muscle sarcomere, sensitises local nociceptors, and generates the characteristic referred pain pattern via central sensitisation mechanisms.

This model has enormous clinical utility. The referred pain maps that Travell and Simons documented — where pressing the quadratus lumborum sends pain into the buttock and lateral hip, or where a trigger point in gluteus minimus mimics the distribution of an L5 or S1 radiculopathy — are reproducible and clinically valuable. They have helped countless practitioners avoid unnecessary imaging and interventions by explaining pain patterns that would otherwise seem neurological in origin.

However, the model has limitations. High-quality imaging and histological studies have struggled to consistently identify the structural 'knot' that the trigger point model proposes. The local energy crisis hypothesis, while plausible, has not been definitively confirmed. And perhaps most importantly, the traditional trigger point model places the primary pathology within the muscle belly — which does not fully account for why trigger point therapy, while effective for temporary relief, so frequently produces recurrence when the surrounding fascial environment is not addressed.

This is where Stecco's fascial science begins to complete the picture.

---

Who Typically Experiences Myofascial Pain Syndrome?

In practice, MPS presents across almost every demographic — but several patterns are particularly common:

The Chronically Stressed Desk Worker

Sustained isometric muscle contraction — the kind that occurs when you hold your shoulders elevated, your neck forward, and your breath shallow for eight hours a day — is one of the most potent triggers for myofascial pain. The muscles of the upper trapezius, levator scapulae, scalenes and posterior cervical group are loaded chronically at low levels without adequate recovery. The fascia surrounding them adapts to this sustained load by increasing its viscosity and reducing its gliding capacity. The result is a progressive accumulation of myofascial tension that, in the low back specifically, concentrates in the quadratus lumborum, thoracolumbar erector spinae and iliopsoas.

The Athlete with Recurring 'Muscle Tightness'

High-volume athletes — particularly those in sports involving repetitive unilateral loading (rowing, swimming, throwing sports, cycling) — frequently develop regional myofascial pain that they interpret simply as muscle tightness or delayed onset soreness. In our clinical experience, recurrent tightness in the same region despite adequate stretching and recovery is one of the most reliable indicators of myofascial dysfunction with a fascial component. The muscle is not simply tired — the fascial matrix surrounding it has adapted to the repeated strain and is no longer gliding freely, altering the mechanical environment of the muscle and perpetuating the taut band.

The Pilates and Yoga Practitioner with 'Unexplained' Pain

This is a population we see with particular frequency, and it is worth discussing in some detail. Pilates and yoga practitioners are often highly body-aware, flexible, and diligent about their practice — and they are frequently surprised and frustrated when they develop persistent regional pain that doesn't respond to the very interventions that are supposed to prevent it.

The explanation, in many cases, lies in a distinction that the fascia research has clarified: flexibility is not the same as fascial health. A yoga practitioner can have excellent range of motion at every joint and simultaneously have significant fascial densification — particularly at the myofascial junctions where muscle transitions to aponeurosis, or in the deep fascial layers that don't respond to passive stretching in the way that muscle-tendon units do. Furthermore, the repetitive end-range loading that characterises some yoga styles can actually increase fascial stiffness in certain planes, creating asymmetric tension patterns that manifest as localised myofascial pain.

The Person with a History of Trauma, Surgery, or Immobilisation

Physical trauma — whether from a motor vehicle accident, a fall, a surgical incision, or a prolonged period of immobilisation — reliably triggers fascial densification and the formation of myofascial trigger points in the affected region and in the compensatory patterns that develop around it. Post-surgical scar tissue is a particularly potent source of myofascial dysfunction: a scar anywhere along a fascial line can alter the tension transmitted through that entire line, producing pain and dysfunction at sites that seem anatomically unrelated to the original injury. A patient with an old appendectomy scar, for instance, may present with right hip and low back pain that has its mechanical origin in the altered fascial tension of the anterior abdominal wall.

The Person Under Significant Psychological Stress

The relationship between psychological stress and myofascial pain is bidirectional and well-documented. Elevated sympathetic nervous system tone increases muscle guarding, reduces pain thresholds, and promotes the sustained low-level muscle contraction that feeds the myofascial pain cycle. Chronic stress also directly affects fascial physiology — through its influence on cortisol, inflammatory cytokines and the autonomic innervation of the fascial matrix — making the fascia stiffer and less responsive to normal mechanical loading. A patient whose MPS consistently flares during periods of high life stress is not imagining the connection: the biology is real and it is directly relevant to management.

---

The Fascial Lens: Completing the Trigger Point Picture

The fascial science developed by Luigi Stecco, Carla Stecco and their collaborators over the past three decades does not replace the trigger point model — it contextualises and extends it. Where Travell and Simons described what was happening at the muscle end plate, the Steccos described what was happening in the connective tissue matrix surrounding and interpenetrating the muscle — and why that matrix, when dysfunctional, perpetuates exactly the conditions that produce trigger points in the first place.

Fascia Is Not Passive Wrapping — It Is a Mechanosensory Organ

The classical anatomical view of fascia as an inert packing material has been comprehensively overturned by the work of the last two decades. The deep fascia — the layer of dense connective tissue that invests the muscles and transmits force between them — contains a remarkable density of mechanoreceptors: Ruffini corpuscles, Pacinian corpuscles, Golgi tendon organ-like receptors, and free nerve endings. These receptors continuously monitor tension, pressure, vibration and stretch within the fascial matrix and feed this information into the central nervous system.

This means the fascia is not merely transmitting force — it is telling the nervous system what is happening to force distribution in the body. When fascial gliding is disrupted, these receptors receive abnormal mechanical input, the nervous system interprets this as a threat signal, and the local musculature responds with increased tone and guarding. The trigger point, in this model, is at least partly a neurological response to abnormal fascial mechanosensory input — which is why addressing the fascial matrix, not just the muscle, is essential for lasting resolution.

Hyaluronan, Densification and the Loss of Fascial Gliding

Between the layers of the deep fascia — and between the fascia and the underlying muscle — lies a thin layer of loose connective tissue rich in hyaluronic acid (hyaluronan, or HA). Hyaluronan is a large glycosaminoglycan molecule that, in its normal low-viscosity state, acts as a biological lubricant allowing the fascial layers to glide freely over one another as the body moves. This gliding is not a minor mechanical detail — it is essential for normal muscle function.

When fascial layers cannot glide, the muscles they surround cannot change shape freely, their force-generating capacity is compromised, and the mechanical environment for trigger point formation is created.

Stecco et al. demonstrated through both histological and biochemical analysis that in regions of fascial dysfunction, the hyaluronan changes from its normal fluid, low-molecular-weight form to a more viscous, aggregated, high-molecular-weight form — a state the Steccos termed densification. Densification reduces or eliminates fascial gliding and significantly increases the stiffness of the fascial matrix. Critically, the mechanoreceptors embedded within the densified fascia receive altered mechanical input, contributing to the pain and motor dysfunction that characterises MPS.

Why this matters clinically

If trigger points are perpetuated by fascial densification — by the inability of fascial layers to glide freely — then treating the trigger point in isolation (dry needling, ischaemic compression, massage) will produce temporary relief but not lasting resolution. The densification remains. The abnormal mechanosensory input continues. The trigger point returns.

This is the mechanism behind the frustrating recurrence that many patients with MPS experience after conventional treatment, and it is precisely why our approach targets the fascial matrix directly — not just the tender spot within it.

Centres of Coordination — The Stecco FM Model

Stecco's Fascial Manipulation model identifies specific anatomical points within the fascia — called centres of coordination (CCs) — where the vectors of myofascial force for a given movement direction converge. These CCs correspond closely to the trigger point locations documented by Travell and Simons — they are the points where fascial densification is most mechanically significant and where manual intervention produces the greatest change in regional fascial tension.

The key distinction between the FM approach and conventional trigger point therapy is not where the hands are placed — it is what the hands are doing and why. In FM, the practitioner applies sustained, specific pressure at the identified CC to generate heat within the local tissue, reduce hyaluronan viscosity, and restore fascial gliding. The intervention is guided by a systematic biomechanical assessment — not simply by where the patient reports the most pain — because the most painful point is frequently not the primary dysfunctional point in the fascial system.

The Thoracolumbar Fascia as a Myofascial Pain Amplifier

In the context of low back myofascial pain specifically, the thoracolumbar fascia deserves special attention. As the largest and most mechanically complex fascial structure in the trunk, the TLF is simultaneously the source of and the amplifier for myofascial dysfunction across the entire lumbopelvic region.

Densification within the TLF — whether in the posterior layer overlying the erector spinae, the middle layer adjacent to the quadratus lumborum, or at the lateral raphe where the layers converge — alters the mechanical environment for every muscle embedded within or attached to it.

Quadratus lumborum trigger points — among the most common sources of low back pain in practice — develop within a muscle that is almost entirely enveloped by the TLF and surrounded by the middle layer of that fascia. A densified middle TLF layer does not simply fail to glide; it compresses the QL, reduces its excursion, creates the sustained low-level contraction that feeds trigger point formation, and simultaneously alters the tension transmitted to the lumbar facets and SIJ via the myofascial slings that converge on the same fascial matrix.

This is why a single unresolved TLF densification can produce a seemingly unrelated cluster of symptoms: low back ache (QL and erector trigger points), buttock pain (gluteal referral), lateral hip discomfort (altered iliotibial band tension via the gluteal aponeurosis), and even anterior thigh referral (iliopsoas involvement via the anterior TLF layer). The pain appears to move or spread — but it is following the fascial anatomy.

• See also: Lumbar Facet Syndrome — The Thoracolumbar Fascia and Lateral Raphe
• See also: SIJ Syndrome — Force Closure and the Myofascial Slings

The fascial picture — Myofascial Pain Syndrome

Trigger points are real. The referred pain maps are real. The clinical relief from trigger point therapy is real. But the full picture requires the fascial layer: densified hyaluronan reduces fascial gliding, creating the mechanical environment in which trigger points form and persist. Abnormal mechanosensory input from densified fascia amplifies the pain signal and perpetuates muscle guarding. And the TLF — as the master fascial structure of the trunk — sits at the centre of almost every low back myofascial pain presentation.

Treating the trigger point without treating the fascia is like removing the smoke without addressing the fire.

---

What the Research Says

Prevalence and Clinical Significance

Gerwin (2001) reviewed the epidemiological literature on myofascial pain and concluded that trigger points were a primary pain source in 30–93% of patients presenting with regional pain syndromes — a wide range reflecting the significant variation in diagnostic criteria used across studies, but consistent in confirming that MPS is among the most prevalent pain conditions in clinical practice.

Simons, Travell and Simons (1999) in their definitive clinical manual documented referred pain patterns from over 200 muscles, providing the foundational atlas that remains in use across multiple manual therapy disciplines.

The Hyaluronan Densification Model

Stecco C et al. (2011) published histological analysis of cadaveric fascial specimens showing that in regions of reported myofascial pain, the loose connective tissue between fascial layers contained significantly higher concentrations of aggregated, high-molecular-weight hyaluronan compared to asymptomatic regions. This provided histological support for the densification model and the proposed mechanism by which manual therapy — specifically, the sustained friction applied in Fascial Manipulation — generates sufficient local heat to reduce HA viscosity and restore fascial gliding.

Cowman et al. (2015) reviewed the biophysical properties of hyaluronan and confirmed that HA viscosity is temperature-dependent and mechanically responsive — that is, sustained mechanical load applied at appropriate depth and duration can shift HA from a high-viscosity aggregated state back toward its normal low-viscosity form. This paper provides the biophysical rationale for why the duration and specificity of manual pressure in FM techniques matters — and why brief or superficial pressure does not produce the same effect.

Fascia as a Sensory Organ

Stecco C et al. (2008) conducted a systematic histological study of receptor populations within the deep fascia of the limbs, confirming the presence of Ruffini corpuscles, Pacinian corpuscles and free nerve endings in significantly higher densities than previously recognised.

Tesarz et al. (2011) confirmed free nerve endings within the thoracolumbar fascia and proposed a direct nociceptive role for TLF in low back pain — a finding with significant implications for understanding why low back pain so often has a diffuse, poorly-localised quality that does not map cleanly onto a single structure.

Central Sensitisation and MPS

Shah et al. (2008) used microdialysis to sample the biochemical milieu at active trigger points and found significantly elevated concentrations of substance P, calcitonin gene-related peptide (CGRP), bradykinin, serotonin and noradrenaline — a nociceptive soup consistent with a state of peripheral sensitisation at the trigger point site. Prolonged peripheral sensitisation is a well-established driver of central sensitisation — the process by which the central nervous system amplifies pain signals and reduces pain thresholds — which explains why longstanding MPS frequently has features of widespread pain sensitivity that extend well beyond the original trigger point locations.

Fascial Manipulation — Clinical Evidence

Romanini et al. (2016) conducted a randomised controlled trial of Fascial Manipulation versus conventional physiotherapy for non-specific low back pain and found significantly greater improvements in pain and disability in the FM group at both short and medium-term follow-up.

Stecco A et al. (2013) published a systematic review of FM outcomes across multiple musculoskeletal conditions, concluding that the available evidence supported FM as an effective manual therapy approach with a plausible and well-described mechanistic basis.

---

Our Approach to Myofascial Pain Syndrome

Our approach to MPS is guided by the principle that trigger points are symptoms of a fascial environment, not isolated pathological events. We treat the trigger point — but we treat the fascial matrix around it first, and we assess the entire myofascial chain to understand why that region has become dysfunctional.

Assessment

• Detailed pain history — duration, behaviour, aggravating and easing factors, previous treatments and their effects
• Movement screening — identifying the specific movement directions that reproduce or provoke the pain, which guides the FM assessment toward the relevant myofascial segments
• Fascial palpation using Stecco FM protocols — systematic assessment of centres of coordination across the relevant body segments to identify densification; the most dysfunctional point is often not the most painful one
• Muscle palpation — identification of taut bands, active and latent trigger points, and referred pain patterns
• Postural and movement habit assessment — identifying the sustained positions or repetitive movement patterns that are maintaining the fascial dysfunction
• Screening for contributing factors — sleep quality, stress levels, hydration, nutritional status, and exercise load as perpetuating factors

Treatment

• Fascial Manipulation by Stecco (FM) — the cornerstone of our approach; sustained, specific manual pressure at identified centres of coordination to restore hyaluronan fluidity and fascial gliding
• Treatment is directed by the biomechanical assessment, not by the location of maximum tenderness — this is a fundamental departure from conventional trigger point therapy
• Trigger point therapy — direct manual pressure, muscle energy techniques, or dry needling (where indicated) to address active trigger points once the surrounding fascial environment has been prepared
• Movement rehabilitation — progressive loading of the affected myofascial region within its newly restored range, to reinforce fascial gliding and prevent redensification. Movement is not optional in MPS management — it is the primary mechanism by which fascial health is maintained
• Load and lifestyle management — addressing the perpetuating factors that are maintaining the dysfunction: posture, ergonomics, training load, stress, sleep and hydration

AHPRA Note

The above describes our general clinical approach. Individual presentations vary, and the specific assessment and management of your condition will be determined in consultation with your practitioner at your first visit. Nothing on this page constitutes clinical advice for your specific situation.

---

Self-Help Starting Point — What You Can Do Right Now

Managing myofascial pain is ultimately about creating the conditions in which the fascial system can recover and maintain its health. The following strategies address the most common perpetuating factors and represent a meaningful starting point before — or alongside — professional care.

1. Move More — And More Variably

The single most powerful anti-myofascial-pain intervention available to you is varied movement. Fascia adapts to the loads it regularly receives: sustained postures create directional densification; varied, multi-planar movement maintains hyaluronan fluidity and fascial gliding.

This does not require formal exercise. It requires that you do not sustain any single position — especially sitting — for more than 30–40 minutes without a movement break. The break does not need to be long: 2–3 minutes of gentle movement in multiple directions is sufficient to mechanically stimulate the fascial matrix and prevent progressive densification.

2. Hydration Is Not Trivial — Hyaluronan Depends on It

Hyaluronan is a highly hydrophilic molecule — it binds water and relies on adequate hydration to maintain its lubricating properties. Chronic mild dehydration is a genuine and underappreciated perpetuating factor for myofascial pain: it directly increases HA viscosity and promotes fascial densification.

The clinical literature does not specify a precise daily water intake, but 2–3 litres of water per day — more with exercise or heat — is a reasonable starting point. If your urine is consistently dark yellow, you are almost certainly contributing to your myofascial symptoms through dehydration.

3. Slow, Sustained Loading — Not Rapid Stretching

Rapid, ballistic stretching does not effectively address fascial densification. The viscoelastic properties of HA mean that it responds to sustained load over time — not to brief, high-velocity deformation.

A slow, sustained stretch held for 90–120 seconds in the direction of restriction, with conscious attention to the sensation of gradual release rather than a sharp pull, is more likely to produce a meaningful change in fascial viscosity than a conventional 20-second stretch repeated multiple times. This principle — which aligns with the slower, more sustained work of yin yoga or certain restorative Pilates practices — has a genuine biomechanical rationale.

4. Address the Stress Component — It Is Not in Your Head

If your myofascial pain reliably worsens during periods of psychological stress, this is not coincidence and it is not weakness — it is biology. Elevated sympathetic tone directly increases muscle guarding and fascial stiffness. Stress management strategies — adequate sleep, regulated breathing practices, regular low-intensity movement — are not adjuncts to treating myofascial pain; they are part of the treatment.

A diaphragmatic breathing practice of 5–10 minutes per day has been shown to reduce sympathetic tone and, through the mechanical effect of diaphragmatic excursion on the TLF and psoas, directly influences the fascial tension of the lumbar region.

Want to know where to start?

Download our free 2-week Myofascial Pain & Low Back Mobility Intro Program — a practitioner-designed starting point that combines graded movement, fascial loading strategies, and habit recommendations we commonly offer in the early stages of managing myofascial pain. Enter your email below to receive it as a PDF instantly.

---

Ready to Take the Next Step?

If you have been living with persistent, diffuse, or recurring muscle pain that hasn't responded to conventional treatment — or if you've had temporary relief from trigger point therapy or massage but the pain keeps returning — the fascial component of your pain may not yet have been addressed.

We would love to take a proper look.

Ready to get on top of this?

📞 Call Now — speak with our team

🗓 Book Online — available 24/7

📄 Free 2-Week Rehab Program — request your copy

Located in Melbourne, Victoria. Telehealth appointments available for initial assessment and rehab review.

---