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:

http://rheumatology.oxfordjournals.org/content/early/2014/12/03/rheumatology.keu471.short?rss=1