Novel Classification of Trigger Points

AAP Education


Here is the second article on 'Trigger Points' exploring a previously unmentioned idea that not all trigger points are the same. You can review article 1 here.

Novel Classification of Trigger Points (hypothesis)

Rather than considering all trigger points the same, I am exploring the idea that trigger points present similarly, but potentially with different underlying mechanisms.

I have divided trigger point presentations into 2 groups; Non traumatic and Traumatic.

Non Traumatic

In my opinion this is the much bigger of the two groups and I have divided it into 3 subgroups. These trigger points occur without any notable force, incident or direct injury and as a result I wouldn’t expect stimulation of the bradykinine/histamine system. Clinically these situations don’t seem to respond to NSAIDs. Is this because there are no pro-inflammatory chemicals present or as noted by others, is it the presence of local vasoconstriction, prevention the infiltration of the NSAID that accounts for the lack of response?

1. Chronic Low Load

Of the three subgroups, this is the most prevalent clinical category and includes postural low load/static situations, respiratory pathologies (asthma, COAD) and periods of enforced immobilizations (POPs and post surgical immobilisations).

Contributing Factors

  • Habit & Vocation

    neck pain

Humans by habit and by vocation perform a small range of repeated tasks. With increasing age, habitual motor patterns mean less movement variability, placing repeated load on a reduced group of muscles. Examples include students, female cleaners (9), and computer operators under stress (18). Many jobs are task specific by nature, to provide efficacy through familiarity. This entails the repeated usage of similar muscles that possibly leads to fatigue through shear volume/static overload, or precipitate on return from holiday or sickness (training error).

  • Cinderella Hypothesis

The Cinderella Hypothesis states that during low-level static continuous muscle contractions, smaller (type 1) muscle fibers are the first to be recruited and the last to be de-recruited and as a result only a fraction of the motor units available are used. These “Cinderella” fibers are then continuously activated and metabolically overloaded. Researchers using a customised oxygen sensor, determined there was a focal region with lower levels of oxygen, in the centre of the palpable nodule and hyperoxia compared to the surrounding area (14).

  • Ratio of Motor Units

The size of motor units* is highly variable, ranging from 100 - 200 muscle fibres per axon for intrinsic muscles of the hand, to 1500 - 2000 muscle fibres per axon for larger muscles like gastrocnemius (1). In the clinical situation, I find the more common muscles presenting are the larger muscles. Clinical relevance: Could this prevalence in some way relate to a poorer coordination or control of the larger muscles, due to a higher ratio of muscle fibres to axon, making them more susceptible?

*Motor unit – cell body, single motor nerve fibre and muscle fibres innervated by it. The ratio of muscle fibres varies with size and function (precision of movement) of the muscle. So the largest motor units are found in thigh and trunk muscles and smallest in hand and eye muscles.

2. Age

Trigger points are rarely seen in those less than 15 years of age (clinical observations) and very commonly found in the elderly (17). As we age, spontaneous trigger points (muscle cramps) that are well treated with dry needling, can launch people from bed in their 6th decade and beyond. Taken to the extreme, babies are born without trigger points, yet trigger points remain in the elderly after death, apparently untill rigor mortis is established. These clinical observations beg a plausible tissue explanation.

Could it be a metabolic reason, that with increasing age the reduced ability for water molecules to bond with collagen tissue leaves muscle stiffer, less flexible and more susceptible? Or could it be the higher repetition of tasks as we age as mentioned above in Non Traumatic: Habit and Vocation? By way of example if you give a 5 year old a toothbrush, what they do with it is a radom event, but give it to an adult and they invariable start and finish on exactly the same tooth - so much so that dentists can spot the increased tooth wear. Brushing teeth has become a habitual process.

Contributing Factors

  • Coexisting Medical Conditions

It has been shown that increased rates of cramps (and nerve compression injuries) occur in persons with metabolic disorders like uraemia and diabetes. These metabolic conditions place additional loads on the nervous system and could leave them susceptible to small compressions (alterations in axoplamic flow).

  • Habit & Vocation

These have previously been described and would play an increasing part with advancing years.

  • Medications

Could the side effects of common medications (e.g. statins) contribute to the increasing prevalence in older people?

3. Anatomy

The peripheral nervous system pervades all living tissues providing sensory, motor and autonomic functions, yet trigger points are remarkably regular in their clinical location.

Some reasons why some muscles maybe more susceptible include;Infraspinatous 2

  • Design: Muscles that twist on themselves (infraspinatus, subscupularis, upper trapezius, levator scapulae, latissimus dorsi)
  • Design: Muscles that have tight fasciae (supinator, extensor digitorum longus, flexor digitorum superficialis)
  • Design: Muscles that have bony boundaries (anconeus epitrochularis, fibularis longus)
  • Design: Possible regularity of trigger point relates to the commonality of neuromuscular junctions
  • Function: vocation, posture and ergonomics similarities means that a large proportion of the population are performing similar, repeated physical activities


Rather than talking about blunt trauma to tissues, this category relates more to sudden overload situations, like an acute hamstring ‘tear’ or a tennis calf ‘pop’. If there is a resultant trauma to the muscle, this should result in the release of pro inflammatory chemicals from neural and non-neural tissues; histamine, substance P, serotonin and bradykinin. The presence of these chemicals would lower the threshold of local peripheral nociceptors, making these nociceptors more responsive to subsequent temperature, chemical and mechanical stress.

However a proportion of these ‘traumatic’ injuries are nonresponsive to NSAIDs. A common scenario being the client presenting 2 weeks after injury, having been on NSAIDs and with no improvement e.g. acute hamstring tear while playing football. One proposed reason is that the pain is from a trigger point, and the muscle contraction of the trigger point reduces blood circulation, causing hypoxia (5) and preventing the NSAIDs from penetrating the injured tissue and having an effect. Countering this Mense 2008, says that muscle pain is assisted by NSAIDs, as it reduces the synthesis of prostaglandin (12). Not something that I agree with clinically.AFL Hamstring Injury

Another possibility is that there was no initial injury, even though your client will swear to the contrary. Rather, the sensation of tearing seems to be due to a sudden onset of a cramp like contraction. It was found that just over 30% of acutely diagnosed AFL players’, hamstring tears by a sports physician, were found to have no tissue damage at all on immediate MRI scans (15). So what caused the player to go down in a heap clutching the back of his thigh? Clinically I find this percentage approximates what I seen clinically for both the calf and hamstrings, but not the quadriceps. Perhaps the mechanism relates to the deceleration function of the hamstrings and gastrocnemius and I find these respond very well to dry needling.


1.              Bland J. Disorders of the Cervical spine: diagnosis and medical management. Philadelphia: W.B . Saunders, 1994.

2.              Gerber N, Sikdar S, Hammond J, and Shah J. A Brief Overview and Update of Myofascial Pain Syndrome and Myofascial Trigger Points. Journal of The Spinal Research Foundation 6: 55-64, 2011.

3.              Larrson B, Bjork J, Kadi F, Lindman R, and Gerdle B. Blood Supply and Oxidative Metabolism in Muscle Biopsies of Female Cleaners With and Without Myalgia. Clin J Pain 20: 440-446, 2004.

4.              Mense S. Muscle Pain: Mechanisms and Clinical Significance. Deutsches Ärzteblatt International 105: 214–219, 2008.

5.              Peirce S, and Skalak T. Microvascular remodeling: a complex continuum spanning angiogenesis to arteriogenesis. Microcirculation 10: 99-111, 2003.

6.              Schneider-Kolsky ME, Hoving JL, Warren P, and Connell DA. A comparison between clinical assessment and magnetic resonance imaging of acute hamstring injuries. Am J Sports Med 34: 1008-1015, 2006.

7.              Shah JP, and Gilliams EA. Uncovering the biochemical milieu of myofascial trigger points using in vivo microdialysis: an application of muscle pain concepts to myofascial pain syndrome. J Bodyw Mov Ther 12: 371-384, 2008.

8.              Travell JG, and Simon DG. Myofascial pain and dysfunction; the trigger point manual (vol 1). Baltimore: Williams & Wilkins, 1983.

9.              Treaster D, Marras WS, Burr D, Sheedy JE, and Hart D. Myofascial trigger point development from visual and postural stressors during computer work. Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology 16: 115-124, 2006.


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Specialist Musculoskeletal Physiotherapist (awarded by Australian College of Physiotherapy, 2009)
PhD Candidate Curtin University
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