Dr John Quintner, Consultant Physician in Rheumatology and Pain
Medicine in Australia, has sent this very interesting article
which I thought you would like to see.

Thanks to Dr Quintner for sending the article. I will upload it
to the website later today.

Regards,
Ellen Mizzell
Listowner

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RSI IN THE Y2K

There is an entrenched belief in the Australian community that "RSI" in the
1980s was a mass psychogenic illness, particularly affecting women who had
difficulty coping with the demands of their work. Having once acquired the
label of "RSI" from sympathetic doctors, they then had an acceptable and
compensable way out of their predicament.

There were vocal members of the medical profession, including some
rheumatologists, who fostered this mythology and, as large sums of money were
at stake, employers, insurers and Governments gratefully embraced it.
Consequently, "RSI" as a diagnosis has disappeared but the problem of
occupationally induced upper limb pain remains.

It is now clear that the fundamental error made by the "psychalgic
fundamentalists" (those doctors who believe that ideas per se can cause
persistent pain) was their unwillingness to accept that the widespread pain
and other sensory phenomena, such as tingling and numbness, that characterise
"RSI", could ever be explained in terms of bodily dysfunction.[1,2] Hence
the monumental leap they made into the minds of sufferers in their attempt
to provide an explanation.

It is true that the pain syndrome "RSI" does not accord with the accepted
"injury model" of disease (there being no objective evidence of tissue
damage), but it also sits uneasily alongside contemporary psychiatric
diagnoses for unexplained pain (eg. conversion or somatoform disorders).[3]
That the criteria for diagnosis of these psychiatric conditions could not
be met in most patients was not enough to save them. It is true that many
were already distressed by their predicament, but the insinuation of
imaginary pain ("it's all in your mind, dear!") was enough to complete
their demoralisation.

There is a third explanatory model, wherein the clinical phenomena are seen
as originating in the nervous system.[4] This model was put forward late
in the 19th century,[5] but remained largely neglected until the time of
the "RSI" epidemic. This neglect was due to poor understanding of the
mechanisms responsible for chronic pain. Over the past two decades,
neuroscientists have largely redressed this situation. Sadly for the "RSI"
sufferers, these advances in knowledge came too late to prevent the ignominious
treatment that Australian society meted out to them. "RSI" became a stigmatic
label.

A considerable body of scientific evidence now supports the neurogenic model
of "RSI". A number of studies of the relationship between the characteristics
or patterns of physical stimuli and the resultant sensation in these patients
have provided valuable clues as to underlying pain mechanisms.

Under normal circumstances, feeling gently over peripheral nerve trunks is a
painless examination technique. By contrast, in the painful upper limb(s) of
"RSI" sufferers, this part of the physical examination is usually found to be
painful.[4] It appears that nerve trunks can become sensitive to mechanical
forces when they have been exposed to a number of insults. These include their
exposure to repeated increases in tension at specific anatomical sites (such
as in the carpal tunnel at the wrist, the radial tunnel in the forearm, and
the cubital tunnel at the elbow).

Upper limb tension tests, which were originally devised by Perth
physiotherapist, Robert Elvey, are somewhat analogous to the
straight-leg-raising tests long used in the diagnosis of lower limb pain.
The tests are deemed positive when they are both limited in their range of
excursion and do reproduce the patient's pain.

In 1986, Elvey and his co-researchers in Perth reported that upper limb
tension tests were usually positive in the symptomatic arms of their patients
with "RSI".[6] Since then, others have confirmed this finding.[7,8] It
appears to reflect the same state of increased mechanosensitivity of the
nerves in the painful arm as is detectable when they are gently palpated.

Jesus Arroyo and Milton Cohen, from St Vincent's Hospital, Darlinghurst,
Sydney, showed that in patients with typical "RSI", perception threshold and
pain tolerance to non-noxious electrical stimulation of the skin in the
unaffected limbs did not differ from those observed in normal subjects.[9]

By contrast, in the affected limbs Arroyo and Cohen consistently noted
reduction in pain tolerance to electrical stimulation, which was invariably
accompanied by spread of arm pain and persistence of unpleasant abnormal
sensations after cessation of the stimulus. From these results they inferred
that dysfunction within the nervous system, either peripheral and/or central,
may be involved in the development of "RSI".

Jane Greening and Bruce Lynn, from the Department of Physiology, University
College, London, found that detection thresholds for vibration were
significantly raised in the distribution of the median and ulnar nerves in
the symptomatic arms of these patients. This finding is consistent with
there being a minor degree of nerve damage.

They also found that increased intensity of vibratory stimulation caused a
painful response in 82% of subjects.[10] As vibration is never a painful
stimulus under normal circumstances, these findings suggest altered
processing of non-noxious sensory information is occurring in these
patients.

Stephen Gibson, Sandra LeVasseur, and Robert Helme from the National
Institute of Gerontology and Geriatric Medicine, Mount Royal Hospital,
Parkville, Victoria, measured the brain responses to potentially noxious
thermal stimulation of the hands of those suffering unilateral cervicobrachial
(neck and arm) pain.[11]

When compared to controls, subjects showed both a reduced detection threshold
activity and a reduction in amplitude of the positive waveform in the cerebral
cortex on the affected side, but not on the unaffected side. Importantly, the
alterations were restricted to pain perception and were more related to
the severity of the reported pain than to the general mood state of the
patients.[11] These findings are consistent with an alteration of central
nervous system processing, and subjective appraisal of acute experimental
pain, in the painful limbs of "RSI" patients.

The Victorian researchers also found that the area of spreading flush or
redness of the skin produced by injected chilli pepper (known as the flare
response) was reduced in the pain-affected limbs of patients, whilst the
unaffected limb showed increased size of the flare response when compared
to controls.[12]

The reported severity of cervicobrachial pain was significantly correlated
with the reduction in flare size. The results were thought to signify a
disturbance in function of the primary apparatus for the detection of tissue
damage in the painful arms of these patients.

Taken together, the scientific evidence refutes the sole argument of the
"psychalgic fundamentalists" - that the pain of "RSI" cannot be explained
in terms of bodily dysfunction. The evidence points to there being significant
alterations in the function of both nociceptive and non-nociceptive pathways
related to the painful arms of patients. These alterations probably involve
both peripheral and central neural processes connected with sensation, an
explanation in accordance with current understanding of the neurobiology of
chronic pain.[13,14]

The possibility that psychic trauma, strongly held personal beliefs, or even
involvement in medico-legal systems can together or in part change the way
in which the nervous system functions, resulting in persistent pain and other
sensory phenomena, has yet to be addressed by the "psychalgic fundamentalists".
Will, or can, they respond, now that their own scientific credibility has
been challenged?

John Quintner MRCP FFPMANZCA
Physician in Rheumatology and Pain Medicine.

References:
1. Lucire Y. Neurosis in the work place. Med J Aust 1986; 145: 323-328.
2. Bell DS. "Repetition strain injury: an iatrogenic epidemic of simulated injury. Med J Aust 1989: 151: 280-284.
3. Cohen ML, Arroyo JF, Champion GD, Browne CD. In search of the pathogenesis of refractory cervicobrachial pain syndrome. Med J Aust 1992; 156: 432-436.
4. Quintner JL, Elvey RL. The neurogenic hypothesis of RSI. Canberra: ANU National Centre for Epidemiology and Population Health, Working Paper No. 24, May 1991.
5. Quintner JL, Cohen ML. Occupation neuroses and the psychogenic connotation of "Repetition Strain Injury": the misconstruction of neurosis. Integrative Psychiatry 1994; 10: 165-176.
6. Elvey RL, Quintner JL, Thomas AN. A clinical study of RSI. Aust Fam Phys 1986; 15: 1319-1322.
7. Champion GD, Cornell J, Browne CD, Garrick R, Herbert TJ. Clinical observations in patients with the syndrome "repetition strain injury." J Occup Health Safety - Aust NZ 1986; 2: 107-113.
8. Grieve E. The cervical contribution to arm pain in a sample of industrial workers. Physiotherapy Theory and Practice 1993; 9: 223-234.
9. Arroyo JF, Cohen ML. Unusual responses to electrocutaneous stimulation in refractory cervicobrachial pain: clues to a neuropathic pathogenesis. Clin Exp Rheum 1992; 10: 475-482.
10. Greening J, Lynn B. Vibration sense in the upper limb in patients with repetitive strain injury and a group of at-risk office workers. Int Arch Occup Environ Health 1998; 71: 29-34.
11. Gibson SJ, LeVasseur SA, Helme RD. Cerebral event-related responses induced by CO2 laser stimulation in subjects suffering from cervico-brachial pain. Pain 1991: 173-182.
12. Helme RD, LeVasseur SA, Gibson SJ. RSI revisited: evidence for psychological and physiological differences from an age, sex and occupation matched control group. Aust NZ J Med 1992; 22: 23-29
13. Coderre TJ, Katz J, Vaccarino AL, Melzack R. Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence. Pain 1993; 52: 259-285.
14. Woolf CJ, Doubell TP. The pathophysiology of chronic pain - increased sensitivity to low threshold A?-fibre inputs. Curr Opin Neurobiol 1994; 4: 525-534.


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