The Science of Trigger Points

Paul Ingraham

It’s a while since I posted anything on this site, but my reading of recent articles by Paul Ingraham prompted me to post a link to them on this site.

Many practitioners seem to accept as gospel the neat representations of Trigger Points (TrPs) as illustrated in by Travell & Simons in ‘Myofascial Pain and Dysfunction – The Trigger Point Manual’but I have always had my doubts. Other practitioners vehemently deny their existence with the suggestion that they are a figment of the practitioner’s imagination.

As Paul mentioned in a Twitter post:

‘Most patients and professionals are oblivious to the whole mess”

In my own work as an occupational physician expressing opinions for medico-legal purposes the issue of validity of the TrP concept does come into focus at times, with poloarised views expressed. My position on this topic has shifted from ignorance to conversion’ and back to healthy scepticism.

I don’t have any doubt there are tender points in muscles, relevant to chronic pain states. The question for me, is what do they represent and are these points in muscle a primary manifestation of muscle pathology, amenable to local treatment or do they reflect a more central neurally based phenomenon.

Paul had sensibly chosen to ‘fence-sit’ on this issue, cautiously examining the evidence before publicising an opinion. He seems to be coming out with some sympathy for the concept that they represent a ‘tiny cramp’ affecting a muscle, based on scientific evidence. He doesn’t support dry needling or intense massage, but other milder treatments are OK.

He states:

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I commend the article for those interested in this issue.

Have a read:

Trigger Point Doubts

The Trigger Point Identify Crisis

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The Evolution of Office Technology & Screen Position Recommendations


I recently was given a copy of a monograph written by Bob Sellars, a New Zealand based physiotherapist with a particular interest in Functional Capacity Assessment. The Monograph is very useful as it provides a historical perspective of the introduction of typewriters and computers and an analysis of various recommendations about screen position in relation to the operator.

The monograph also discusses causes of ‘injuries’ to computer operators. The issues with classification of disorders and measurement of mechanical factors are flagged. There is reference to evidence about the inconclusive effects of various ergonomic measures on the incidence of neck, shoulder and arm musculoskeletal disorders amongst computer users. Evidence about the relative importance of psychosocial factors over the physical demands of computer tasks is presented with a caution about risks associated with any suggestion that computers are a serious risk to health.

From my perspective (as presented on this site), the underlying factor in most cases of neck/shoulder/arm pain related to computer use probably has a neurogenic basis due to postural loading of the brachial plexus at the level of the thoracic outlet. Psychological factors are also important modifiers of an individual’s physiological response to  postural demands associated with computer work. I agree that presenting computer use as a serious health hazard is unhelpful, but there are also hazards associated with presenting these types of disorders as purely psychological. Neck and shoulder posture at work remains an important consideration in ensuring the comfort,  health and well-being of employees and an understanding of the basis of current recommendations about screen position is very helpful.

I would like to thank Bob for allowing me to post his monograph on this site.

Here is a link:

Monograph by Bob Sellars

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Dr Quintner again!

Dr John Quintner asked that I post an article he has written commenting on acceptance of ‘RSI’ type disorders by the Accident Compensation Commission in New Zealand.

Here is a link to the article entitled


on my blog site ‘Insult and Injury’.

Here is the link:

No coverage by ACC in New Zealand for ‘RSI’ type disorders!

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Interesting blog from an RSI sufferer

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I came across an interesting blog today that deals with the day-to-day issues faced with a sufferer.

Although not recently updated, there are frequent references to lack of knowledge by the doctors in this subject (and some beautiful photography).

Well worth a look.

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Let’s Put Faces to the Neurogenic Hypothesis of RSI!

JQ in suit

John Quintner has kindly agreed that this article can posted on this site. It originally appeared in Mind in Body.

This article puts an important historical and personal perspective on the challenge to MPS and trigger point theories, an important alternative theory about the pathophysiology of ‘RSI’. It really assists understanding to follow John’s personal journey on this subject. I too had accepted the trigger point hypothesis until doubts were raised by reading John’s work.

Here it is:


“The study of fallacies … should attune the student to the omnipresent dangers to which we are exposed as a consequence of imprecise expressions – vague, ambiguous, or misdefined terms – or of unarticulated assumptions and presuppositions [1].

The 1980s was a watershed decade for me. I had a long-standing interest in what was then called Physical Medicine, and my most valued textbooks were those written by James Cyriax, Allen Stoddard and John Bourdillon.


At that time the Australian epidemic of repetitive strain injury (“RSI”) – a diagnosis applied to primarily upper limb (forearm and wrist) symptoms, the cause of which was attributed to keyboard and other occupational overuse – was raging. I was forced to admit that my training and subsequent experience as a rheumatologist did not help me to understand the clinical phenomena associated with “RSI” that I encountered daily.

Janet Travell with JFK standing together in Oval Office

By chance I came upon the first edition of The Trigger Point Manual by Janet Travell and David Simons [2]. Could their theory of “myofascial pain” arising from “trigger points” fill the large gap in my understanding of these complex clinical problems?

These authors expanded upon an earlier publication by Travell and Rinzler [3] in which patterns of “pain referral” from specific muscles were illustrated. However, as they did not publish the evidence upon which they based their patterns, it appeared to me that the illustrations were based on little more than inspired guesswork.

Nonetheless, taken at face value, the hypothesis for Myofascial Pain Syndrome (MPS) advanced by Travell and Simons seemed quite convincing: myofascial trigger points (MTrPs) were the sites of tissue damage, and resided within taut bands located in the culprit muscles. In hindsight, this is an excellent example of circular reasoning!

Many of the MTrPs (marked with an X), together with their respective patterns of pain “referral”, were impressively displayed. Treatments such as cold spray administered to the skin followed by gentle stretching of the involved muscle was said to be helpful, if not curative (page 63).

In addition, insertion of “dry” needles into the MTrPs followed by stretch of the involved muscle was recommended, as were ischaemic compression (page 86) and massage (page 87).

Bob Elvey 2008

But when I met the late Bob Elvey, he completely changed my way of thinking about these clinical problems. Bob’s mantra was that “muscles protect nerves.” He introduced me to the dynamics of the nervous system and I came to understand that peripheral nerves of the upper limb had evolved to be able to adapt to the various changes in limb position and length and that they were vulnerable at certain anatomical points along their course. His pioneering work on methods of assessing the mechanosensitivity of peripheral nerve trunks has greatly enhanced the clinical examination of the upper limb.

In addition to these important clinical insights, I became aware of the large mechanical forces that could potentially be generated within the cervical spinal canal by the maintenance of fixed head/neck postures being adopted by those who performed repetitive manual work.

On a closer reading of The Trigger Point Manual, I discovered that the authors had made at least three fundamental epistemological errors that cast considerable doubt upon their theory of MPS.

These three errors are not directly related to MTrPs, which are in any event yet to be validated, but rather to poor diagnostic reasoning.

Firstly, they implied that pain of peripheral nerve origin could be diagnosed only with accompanying clinical evidence of neurological deficit (page 22), as defined by loss of muscle power and wasting, loss of myotatic reflexes, and diminished sensibility in the distribution of the relevant peripheral nerve, thus enabling the clinician to distinguish such pain from that said to arise from MTrPs. Travell and Simons did not appear to appreciate that pain of peripheral nerve origin could be present without such clinical evidence.

Secondly, they believed that a normal conventional electrodiagnostic examination effectively ruled out the possibility of peripheral nerve pain (page 22). Such an examination does not provide any information as to the state either of the small diameter nerve fibres responsible for nociceptive input or that of the nerve interstitium.

Thirdly, they announced in Table 3.2 (page 63) that taut bands within muscles that contained MTrPs could entrap peripheral nerves in the vicinity. The existence of such bands had never been demonstrated and it was therefore highly speculative and erroneous to attribute nerve entrapment to such a mechanism.

Other weaknesses in their theory included the somewhat metaphysical concepts of “latent trigger points,” “secondary trigger points,” “satellite trigger points” and even “metastasising” trigger points.

To further confuse matters, it was later shown that “experts” in MPS diagnosis could not agree as to the location of or even the presence of individual MTrPs in a given patient.

The mind-boggling list of possible causative and perpetuating factors for MTrPs was completely devoid of scientific evidence and therefore lacked credibility. But at least any of a myriad of factors could be drawn upon to exempt from blame those well-meaning therapists who were finding that the recommended treatment regimen was ineffective.

Finally, those who became “dry needlers” appeared to be unaware that when justifying their assault on MTrPs they were following the “like cures like” tenet of homeopathy. In their parlance, physical therapists (including physicians) were obliged to create a lesion in muscle tissue in order to cure (“desensitise”) a lesion (for which there was no pathological evidence).

Milton Cohen

Meanwhile there were important developments on the “RSI” front. Taken together, our work and that of Milton Cohen’s group in Sydney provided scientifically credible and testable hypotheses for “RSI” [4,5]. But that is for the next installment.

Early in the 1990s, Milton and I decided to challenge myofascial pain theory. At the time, another concern of ours was that the fibromyalgia construct was also logically and epistemologically flawed.

In our 1994 paper we deconstructed the MPS hypothesis of Travell and Simons, found it wanting, and offered scientifically credible explanations for the observed clinical phenomena [6].


The pioneering studies of nerve inflammation conducted by Geoffrey Bove and the publication by Geoff, together with Alan Light, of the “nervi nervorum” hypothesis [7] attracted our interest and culminated in an alliance with Geoff that has continued.

In brief, Geoff’s studies have had two major impacts on how we think about pain felt in muscles or other deep structures.

Firstly, he confirmed the presence of nociceptors with multiple receptive fields that branch within the nerve sheaths and extend to other deep tissues (nervi nervorum) [7]. The implication of this finding is that activity in a receptor in one structure could be perceived in another.

Secondly, he showed that inflammation of nerves has profound effects on these same axons, the nociceptors to deep structures. These effects include ongoing activity and abnormal mechanical sensitivity [8, and others]. The implication of this finding is that this activity will be perceived by the brain in the area of the normal receptive fields, not in the area of the problem.

Both of these mechanisms are critical to the concepts being discussed, as they open more plausible possibilities for pain perceived as coming from muscles (see Figure 1).

However our challenge to the MPS theorists failed to evoke a response, which we thought surprising, given that we raised serious doubts about their construct. Not only was the MPS/MTrP literature expanding in volume but also the editors of journals that published papers based on MPS theory appeared reluctant to countenance any criticism of the authors.

But this subsequent literature was also notable for its failure to acknowledge that the underlying hypothesis was flawed – no one has ever succeeded in demonstrating nociceptive input from putative myofascial trigger points. All subsequent “research” simply assumed the truth of what started out – and remains – as conjecture.

Early in 2013, Milton, Geoff and I joined forces and decided that another paper was needed to refute the MTrP dogma. The three most prominent North American pain journals did not accept our offerings. Eventually our paper was published online, with open access, in Rheumatology [9].

Now we are left with a major challenge – how to explain the pain previously attributed in error to MTrPs. We hope that in our latest paper we have pointed the way towards a theoretical model that will explain the clinical phenomena by incorporating our knowledge of the mechanisms of referred pain and tenderness, along with the well-documented clinical findings of nerve trunk allodynia, and the experimental evidence derived from studies of nerve inflammation.

John Quintner, Physician in Rheumatology and Pain Medicine (retired)

I gratefully acknowledge the assistance of Geoff Bove and Milton Cohen when preparing this article.

John Quintner is a retired physician in Rheumatology and Pain Medicine who is currently a volunteer with Arthritis and Osteoporosis WA. He is now interested in contributing to pain education for health professionals and consumers. John has long been active as an iconoclast in the field of pain theory and practice. The prime targets have been myofascial pain theory and the North American fibromyalgia construct. His skeptical approach has been well balanced by Milton Cohen’s critical analytical skills. Most of John’s useful ideas have come to him whilst “in the zone” atop his long-cherished bicycle.


[1] Toulmin S, Rieke R, Janik A. An Introduction to Reasoning, 2nd ed. New York: Macmillan Publishing Co., 1979.

[2] Travell JG, Simons DG. The Trigger Point Manual. Baltimore: Williams and Wilkins, 1983.

[3] Travell J, Rinzler SH. The myofascial genesis of pain. Post-Grad Med 1952; 11: 425-434.
[4] Elvey RL, Quintner JL, Thomas AN. A clinical study of RSI. Aust Fam Physician 1986; 15: 1314-1312.
[5] Cohen ML, Arroyo JF, Champion GD, Browne CD. In search of the pathogenesis of refractory cervicobrachial pain. A deconstruction of the RSI phenomenon. Med J Aust 1992; 156: 432-436.

[6] Quintner JL, Cohen ML. Referred pain of peripheral neural origin: an alternative to the “Myofascial Pain” construct. Clin J Pain 1994; 10: 243-251.

[7] Bove GM, Light AR. The nervi nervorum. Missing link for neuropathic pain? Pain Forum 1997; 6: 181-190.

[8] Bove GM, Ransil BJ, Lin HC, & Leem JG. Inflammation induces ectopic mechanical sensitivity in axons of nociceptors innervating deep tissues. Journal of Neurophysiology 2003; 90: 1949-1955.

[9] Quintner JL, Bove GM, Cohen ML. A critical evaluation of the trigger point phenomenon. Rheumatology 2014 Dec 3. doi: 10.1093/rheumatology/keu471 First published online: December 3, 2014.


Figure 1. Proposed hypothesis for the development of focal muscle sensitivity and possible alteration in muscle texture with a proximal neural cause. Inflammation affecting a peripheral nerve (red spot) results in spontaneous and mechanically evoked afferent and efferent action potentials in small caliber sensory neurons innervating non-cutaneous structures, and decreased sympathetic discharge (-). These processes may cause reflex motor discharge sufficient to cause a palpable contraction (?), which combined with clinical phenomena associated with neurogenic inflammation (+), could explain the clinical phenomenon that has become known as a “trigger point.”

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Text Neck – The stresses in the cervical spine due to head/neck posture


The ABC recently carried a story about ‘Text Neck”:

The story refers to a publication ‘Assessment of Stresses in the Cervical Spine Caused by Posture and Position of the Head’ by Kenneth Hansraj, Chief of Surgery at New York Spine Surgery & Rehabilitation Medicine.

The paper discusses the increased pressure associated with the forward cervical posture seen with use of technology.

Worth a read.

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Are Trigger Points Real?


The first post on this site details the neurogenic hypothesis of ‘RSI’ as expounded by John Quintner back in 1991 in the aftermath of the Australian ‘RSI epidemic’.

Before providing accounts of alternative hypotheses from Hunter Fry, Yolande Lucire and others about the pathogenesis of RSI, I thought it might be useful to digress to consider a very recent paper by John Quintner, Geoffrey Bove and Milton Cohen about myofascial trigger points (TrP), the purported hallmark of Myofascial Pain Syndrome (MPS), an explanation of some forms of ‘RSI’.

The construct of MPS certainly has superficial appeal to practitioners and patients alike. The concept has been accepted by many pain physicians and rheumatologists.

Dommerholt and Shah, in the recent 4th edition of Bonica’s Management of Pain (Chapter 35, page 451) state:

‘ A survey of physician members of the American Pain Society showed overwhelming agreement that myofascial pain is a distinct clinical entity’.

Clinical experience suggests utility of ‘dry needling’ in the treatment of painful muscles. There has been widespread uptake of such treatments by a variety of health practitioners.

Quintner et al argue that the MPS hypothesis is based on faulty circular logic:

‘TrPs cause myofascial pain because painful muscles contain them’

Their recent paper suggests that the explanation for any apparent response to treatments to inactivate TrP’s is due to a ‘counterirritant’ effect i.e.

‘……elicit a transient reduction in pain intensity by recruiting those higher order brain regions responsible for nociception’

Given the extent of disability and work incapacity associated with muscle pain syndromes and the resources directed towards their treatment, the existence, or otherwise, of TrPs is an important issue in modern medical practice.

Reading Quintner et al’s recent paper is well worthwhile.

Here is the link: 

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Quintner & Elvey – The Neurogenic Hypothesis of RSI

There is continuing controversy about the pathophysiological basis of what has been widely labelled ‘RSI’, the terminology that remains in common usage in Australia.

As an occupational physician who often sees these conditions in my clinical practice,  I had considered that there were neurogenic and muscular aspects to this condition. Quintner and Elvey’s hypothesis that dates to the aftermath of the Australian ‘RSI Epidemic’ however provides a unifying hypothesis that can explain the full gamut of features seen in clinical practice in the true tradition of William of Occam.

Quintner and Elvey’s paper was one of a series Working Papers edited by Gabriele Bammer and published by the Australian National University in the early 1990’s. It has only recently been made available on-line.

To provide a detailed account of this paper seems to me to be a good place to start in considering the pathophysiology of ‘RSI’. The paper articulates an informed and well thought though hypothesis utilising evidence from a variety of sources to support the conclusions.

In her introduction to this paper Ms Bammer stated in relation to the ‘RSI Controversy”:

‘In late 1989 I conceived the idea of inviting some of the leading protagonists of different viewpoints to write detailed expositions of their hypotheses. These were to be circulated amongst a variety of people with different expertise, to encourage discussion from a number of perspectives. The protagonists were also invited to respond to these commentaries’

Quintner and Elvey expound the hypothesis that entrapment can affect neural tissues in the cervical region with distal pain and ‘sensory-neural’ irritability. They also suggest that entrapment can affect more distal tissues with proximal spread of pain and irritability.

In their introduction, the authors refer to the work of one of the co-authors, Elvey in relation to a physical examination technique, the brachial plexus tension test, considered valuable in diagnosis of patients with widespread cervicobrachial pain. This work was seen as a stimulus to the development of the neurogenic hypothesis of RSI.

Quintner and Elvey’s hypothesis is stated as follows:

“1. The clinical features of ‘RSI’ arise from irritable neural tissues related to the upper limb. These tissues exhibit the properties of increased mechanosensitivity and ectopic impulse formation. Other pathophysiological mechanisms relevant to neuropathic pain may be involved and are outlined in this discussion paper.

2. The sensori-neural tissues related to the painful arm have become irritable as a result of pathological changes induced by excessive mechanical tension and/or friction generated during manual work of a repetitive nature, usually performed with postural fixity of the head and neck.

3. The neural tissues predominantly affected by these forces are proximally situated (cervical spinal nerve, nerve root complex, brachial plexus), however, an identical clinical presentation (widespread neural pain) may result from entrapment of distal upper limb neural tissues.”

The authors discuss the evidence to support their hypothesis.

They refer to experimental evidence about referred somatic pain that can accompany chemical injection of muscles, deep fascia, tendons, periosteum and interspinous ligaments (Kellegren). Such pain can be misinterpreted causing difficulties with medical diagnosis. The characteristics of somatic referred pain i.e. dull, aching, boring quality, difficult to describe feeling deep and radiating widely are described. Such pain does not correspond to a peripheral or spinal nerve root distribution and may be accompanied by a sensation of numbness, heaviness, local muscle soreness/tenderness, muscle spasm, tenderness of bony prominences in addition to secretomotor and vasomotor changes. They refer to the hypothesis of Asbury and Fields that peripheral nerve damage can be associated with either dysesthetic pain or nerve trunk pain. Dysesthetic pain is burning, tingling, searing or raw, while nerve trunk pain is a deep aching pain along the course of the nerve which is often tender.

The persistent pain state of neuropathic pain associated with traumatised or irritated peripheral nerves is discussed. Such pain can be severe and spread widely and associated with muscle tenderness and cutaneous hypersensitivity. Pain onset may be delayed followed nerve injury and persist long after the original insult with a paroxysmal stabbing component, allodynia and hyperalgesia. There follows some discussion about possible mechanisms of neuropathic pain with reference to changes within the dorsal root ganglion as one possibility. Quintner drew attention to the similarity between RSI and brachial neuralgia.

There follows discussion of relevant case studies published by Ferguson, Taylor, Stone, Browne and Fry. They point out the failure by some authors to recognise that muscle/tendon pain or tenderness can be explained by referred somatic or neural pathology. Fry in particular described musicians with painful overuse disorders presumed to arise in overused muscles.

Quintner and Elvey refer to their own work which demonstrated that symptoms were provoked by the brachial plexus tension tests, sustained neck postures and palpation over the transverse processes of the related cervical levels. They point out:

“…Upper limb symptoms may have been referred from structures ‘at fault’  within the neck or the brachial plexus of many patients was not discussed by the authors of most of the Australian studies, although the evidence they presented is compatible with this explanation”

After reviewing Australian Studies, the authors briefly review the overseas experience of RSI, in particular Japanese and Swedish publications where the term occupational cervicobrachial disorder is used for the same disorders. Some overseas authors emphasised the importance of working posture over repetitive work tasks.

Field studies, particularly those relating to the role of posture in causation, are discussed. In particular, the authors refer to studies of symptom development after sustained occupational neck flexion with the spread of symptoms from the neck into the thoracic region and shoulders and, in some subjects, associated with upper limb neurological symptoms.

An interesting, non-occupational,  case history is presented:

‘a man who had been tied up for 12 hours with his head forced and held in extreme forward flexion. This man developed a partial motor and sensory loss (C5-T1 on the right, C3-T1 on the left). Investigations did not reveal evidence of underlying pre-existing cervical disease.’

This case and others were presented as evidence that extreme positions of the neck were damaging to the cervical cord due to high tension that develops with biomechanically induced stretching of the cord, presumably due to interference with spinal cord vasculature.

Following a review of occupational health field studies of accounting machine operators, electronic industry workers, television assembly workers, sewers and keyboard/VDU operators, the authors concluded that these studies confirmed the association between manual work in a seated position and the associated postural immobility with head, neck, upper back, shoulder and arm symptoms, particularly when the work was undertaken with head/neck flexion.

In their discussion of biomechanical considerations, the authors discuss studies relevant to the effects of tension on cervical and peripheral neural tissues. There is evidence of a change in length of the spinal canal between flexion and extension (by 7cm) and the effects from lateral flexion and rotation of the cervical spine on the cervical nerve roots. Of particular note was the evidence that the movement of the cervical nerve roots with cervical flexion was more marked during abduction of the shoulder or downward traction on the arm.

“The evidence from these studies supports the hypothesis that a high physical tension may develop within the cervical spinal neural tissues of those who perform repetitive manual work which is accompanied by elements of cervical forward flexion, rotation and lateral flexion.”

In their discussion about tension and peripheral neural tissue, the authors refer to the evidence about resting tension in peripheral nerves and the mechanisms by which nerve lengths adapt to limb movement and are protected from the forces generated during normal limb use. Peripheral nerves are vulnerable where they cross the extensor aspect of a joint, pass over ligamentous bands, travel through canals or tunnels, thorough two closely applied muscles or through deep fascia to become a superficial nerve. They refer in particular to risk of entrapment of the lower cervical spinal nerves (anterior primary rami) at the level of the gutters of the transverse processes of the cervical vertebrae, the ulnar nerve in the cubital tunnel, the posterior interosseous nerve in the radial tunnel, the anterior interosseous branch of the median nerve between the heads of pronator trees and the median nerve in the carpal tunnel.

Neural tissue responds to stretch with varying degrees of structural damage to blood vessels, nerve fibres and perineurium. In particular the authors present evidence about stretch impairing epineural blood flow:

“which, in turn, may compromise the intramural microvascular flow leading to endoneurial anoxia and oedema formation”

The authors suggest that an inflammatory reaction due to chronic irritation may affect nerves at vulnerable points with changes in myelin sheaths associated with intramural fibrosis and axon degeneration. They note that axonal degeneration is usually only apparent in the presence of severe compression neuropathy, but that fibrosis has potential consequences – constricting nerve fibres and forming adhesions at the injury site. Traction of the damaged nerve during limb movements can deform a hyper-sensitive focus within the nerve generating pain.

“…. there is evidence that the microcirculation of peripheral nerves, spinal nerve roots and the dorsal root ganglia can be seriously impeded by mechanical forces. Both acute and chronic mechanical irritation have been shown to cause varying degrees of damage to peripheral nerve and spinal nerve roots.”

A marked increase in the sensitivity of inflamed nerve roots has been demonstrated in the lumbar and cervical spine. Both the dorsal and ventral roots are sensitive. Irritation of the dorsal roots causes ‘neuralgic’ pain in a dermatomal distribution, while irritation of the ventral root causes ‘myalgic’ pain with pain radiating into upper limb muscles in a non-dermatomal distribution consistent with the patterns seen in the upper limb symptoms of ‘RSI’ sufferers.

The authors describe the brachial plexus tension tests developed by Elvey designed to differentiate between painful local upper limb disorders and cervical/brachial plexus disorders causing referred pain along neural tissues into the upper limb. Cadaver studies have shown the positioning of the upper quarter that places maximum tension of the cervical nerve roots, particularly C5 and C6. Studies in health volunteers showed that at maximum tension subjects experienced a deep stretch or ache in the cubital fossa extending down the anterior and radial aspects of the forearm into the radial side of the hand and a definite tingling sensation in the thumb and first three fingers.

The authors state that the differential diagnosis of RSI includes cervical radiculopathy associated with cervical spondylosis and following cervical injury, thoracic outlet syndrome, and the various upper limb entrapment neuropathies. The recognised entrapment neuropathies include those of the median nerve, the radial/posterior interosseous nerve and the ulnar nerve.

In their conclusion, the authors discuss the difficulties in distinguishing the level of entrapment:

‘Entrapment may affect either the neural tissues in the cervical region, with ensuing distal spread of pain and sensory-neural irritability, or more distal neural tissues (e.g. median nerve in carpal tunnel) followed by proximal spread of pain and sensori-neural irritability. The end result of both processes may be indistinguishable’

Quinter and Elvey detail the implications for treatment from the ‘Neurogenic Hypothesis’ including the following:

‘It is reasonable to state a stage of early reversible peripheral neural dysfunction related to occupation which may respond to rest of the limb with or without local corticosteroid therapy’

and, most importantly for occupational medicine:

‘Based on current knowledge and understanding of ‘RSI’, emphasis must be placed upon its prevention by identifying all possible risk factors which relate both to occupation and to the potentially affected worker. The increasingly sedentary nature of employment occurring throughout many industries exposes an increasing number of workers to the risk of developing “RSI”‘


While this paper is more than 20 years old, the ideas put forward remain relevant to understanding the pathophysiology of ‘RSI’ and its management.

A link to the article is included below.

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Why T.I.P.S.?

In every facet of modern life humans are interfacing with technology. Many people earn their living operating computers or utilising other electronic devices including smart phones, tablet computers and various other devices. Recreational use of such devices is increasing as well. These devices are increasingly used by children who are likely to be using such devices over their lifetimes often starting in Primary School or even before.

This blog aims to publicise health and medical literature about the various pain disorders that have been associated with human interfaces with technology from an Australian perspective. The best known example is what is know as ‘Repetitive Strain Injury’ or ‘RSI’, but the history of controversy about such disorders goes back much further with conditions such as ‘telegraphist’s cramp’.

Australia has a unique place in the understanding of such disorders. The ‘RSI’ epidemic of the 1980’s in Australia received international attention and resulted in a polarisation of views about the phenomenon within the medical community, leading to pejorative labels such as ‘kangaroo paw’.

It is important that accurate scientific information is available about the risks to musculoskeletal health associated with use of such devices. While the popular media may discuss ‘iInjuries’ or ‘Blackberry Thumb’, there is limited accurate information about such conditions available to health professionals, the organisations that design electronic devices and employers that expect their employees to use such devices at work.

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