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In their correspondence about pain in the rheumatic diseases, Thompson and Carr report that some of their cohort of 100 patients with inflammatory arthritis show a disassociation between reported pain and objective measures of disease activity.1In most patients there was a close linear relation between change of reported pain, the number of swollen joints, and C reactive protein over two years. However 18 patients reported high pain scores despite no evidence of C reactive protein or swollen joint activity. On the other hand 10 patients reported no pain despite active disease. The difference could not be explained on the grounds of joint deformity. Thompson and Carr do not set out to explain their finding.
However their previous writings on subjects such as handicap2 indicate they are well aware of the importance of psychosocial factors in the manifestations of disease and, by implication, the weakness of rigid application of the medical model to chronic disease. Only a small proportion of patients with the mechanical low back pain or tender fibromyalgic spots develops chronic pain syndromes and becomes severely disabled. Psychosocial factors rather than clinical findings or treatment prescribed are the strongest predictors of chronicity in mechanical low back pain.3 In patients with fibromyalgia Wolff et al have demonstrated that the number of tender spots is proportional to the degree of distress. They suggest that the tender point count could be considered as the erythrocyte sedimentation rate of distress.4
Even in osteoarthritis, disease severity accounts for only a proportion of the individual variability in clinical outcome. After controlling for disease severity, psychological variables remain strong predictors of individual differences in functional impairment and pain.5
Thus it is well established that psychosocial factors are important predictors of ongoing pain in non-inflammatory musculoskeletal conditions. There is no reason to anticipate that people will behave differently whether responding to pain of an inflammatory or non-inflammatory nature. Thus it can be assumed that a proportion of those with rheumatoid arthritis will develop a chronic pain syndrome. This is almost certainly what has happened in the 18% of Thompson and Carr’s patients with high pain scores in the presence of inactive disease.
The appropriate treatment of these patients is not by first, second or third line drugs combined or otherwise but by paying attention to self management strategies, coping skills, etc, etc. No doubt a proportion of those with active disease will also have developed chronic pain behaviours and associated disability that require as much attention as the raised C reative protein and number of swollen joints.
And what are we to make of the 10% of RA patients who do not express pain despite active disease? Although they are a delight for the rheumatologist to deal with, such pain related behaviour may also be pathological. It is well recognised that a proportion of patients with rheumatoid arthritis battle on regardless and develop what has been called arthritis robustus with rapid aggressive joint destruction. Might these patients be found among Thompson and Carr’s pain free 10% with active joints?
We agree with Dr Jones that psychological factors are likely to be important in self reported pain and disability in chronic musculoskeletal conditions. However, the available clinical data are controversial in this area. Current studies variously report an absent1-1 or only weak1-2 correlation between disease activity and pain scores, that disease activity is a strong predictor of pain1-3 and that disease activity influences pain indirectly via depression.1-4
Therefore we feel that the cause and effect relation between psychosocial distress and self reported pain and disability remains a hypothesis that would explain our findings rather than a conclusion of the findings themselves.
We are currently studying these relations in more detail.
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