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”‘

Conclusion

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.

http://hdl.handle.net/1885/12092