What Is a Trigger Point?

What Is a Trigger Point?

A myofascial trigger point is a hyperirritable spot within a taut band of skeletal muscle that is painful on compression and that can elicit a referred pain response — a characteristic aching, burning, or tingling sensation perceived at a site distant from the point of pressure. The concept was systematically described by Janet Travell and David Simons, whose landmark two-volume work mapped referred pain patterns across virtually every skeletal muscle in the body and remains foundational to clinical practice today.

At a tissue level, a trigger point arises from a sustained contracture of a small group of sarcomeres — the fundamental contractile units of muscle fibres. This localised contracture persists without a normal action potential, consuming adenosine triphosphate (ATP) and failing to fully release. The result is a palpable nodule within a taut, rope-like band of muscle tissue, accompanied by a localised biochemical environment significantly more acidic and rich in inflammatory mediators — including substance P, calcitonin gene-related peptide, bradykinin, and prostaglandins — compared to surrounding tissue (Shah et al., 2008). These chemical changes sensitise local nociceptors and contribute to both local tenderness and the capacity to generate pain at remote sites.

Active vs Latent Trigger Points

Trigger points are classified as either active or latent. An active trigger point produces spontaneous pain without requiring external compression — clients often report a deep, diffuse aching that they recognise as their familiar pain, often in a pattern consistent with the known referral map of the affected muscle. The upper trapezius trigger point, for example, commonly refers pain up the lateral neck to the temple and behind the eye — a pattern that in many clients presents as a tension-type headache.

A latent trigger point does not produce spontaneous pain but is painful when directly compressed. Latent trigger points are not clinically insignificant: they restrict range of motion, alter recruitment patterns, and can become active under conditions of sustained postural loading, psychological stress, physical overexertion, or inadequate recovery.

Referred Pain Patterns

One of the most clinically significant features of trigger points is their capacity to generate pain at a location anatomically distinct from their origin. This referred pattern is not random; it follows consistent, reproducible maps documented across thousands of clinical observations by Travell and Simons and subsequently confirmed by other researchers.

Trigger points in the infraspinatus, for example, commonly refer pain to the anterior shoulder and upper arm in a pattern closely mimicking rotator cuff pathology. Gluteus minimus refers pain down the lateral and posterior thigh in a pattern essentially indistinguishable from sciatica. The soleus refers into the heel and calf in a manner overlapping with Achilles tendinopathy presentation. This overlap between trigger point referral patterns and other structural diagnoses is precisely why thorough clinical assessment is indispensable — pain location alone cannot attribute a complaint to a structural diagnosis without systematically assessing and excluding the myofascial contribution.

Why Do They Form?

Trigger points develop in response to mechanical, metabolic, or neurological stressors. Mechanical overload is most common — including both sudden high-force injury (acute overload such as a muscle strain) and sustained low-force repetitive loading (chronic overload such as sustained cervical and shoulder posture during prolonged computer work). Nutritional deficiencies — particularly in vitamin D, magnesium, iron, and B vitamins — impair normal muscle metabolism and perpetuate trigger point activity by reducing the efficiency of ATP production. Psychological stress elevates sympathetic nervous system tone, increases motor neurone excitability, and promotes sustained low-level cervical and shoulder girdle contraction. Poor sleep impairs restorative processes through which muscle tissue recovers from daily mechanical demands. Understanding these perpetuating factors is as clinically important as treating the trigger points themselves.

The Role of Central Sensitisation

In presentations where trigger points have been active and untreated for extended periods, central sensitisation may develop — a neuroplastic change in the spinal dorsal horn and supraspinal processing centres where repeated nociceptive input progressively lowers the threshold of central pain-processing neurones. The clinical result is a state in which pain is more easily generated, more widespread, and less proportionate to the degree of peripheral tissue involvement. Clients with well-established myofascial pain syndromes complicated by central sensitisation often describe diffuse, widespread pain disproportionate to apparent tissue findings — which is not an indication that the pain is not real, but that the nervous system itself has become a driver of the experience. Pain neuroscience education, graded activity, and addressing psychosocial contributors become essential components of management.

How Are They Treated?

Manual therapy — including ischaemic compression and trigger point pressure release — applies sustained mechanical pressure to the trigger point, hypothesised to mechanically deform the contracted sarcomere bundle, restore local circulation, and modulate pain through peripheral and central neurophysiological mechanisms. Dry needling uses a fine filiform needle inserted directly into the trigger point to elicit a local twitch response — an involuntary spinal reflex contraction of the taut band associated with an immediate reduction in the trigger point's electrical activity and a measurable decrease in the local concentration of pain-sensitising biochemicals. IASTM addresses the fascial environment surrounding trigger-point-laden muscles, improving tissue mobility and reducing mechanical loading concentration. Effective management does not end with deactivation of the nodule: correcting perpetuating factors and progressively restoring strength and endurance transforms short-term symptomatic improvement into lasting clinical outcome.