Central nervous system involvement in perceived joint stiffness.

juvenile idiopathic arthritis, Kikuchi's disease and haemophagocytic lym-phohistiocytosis—is there a link? Case report and literature review. SIR, Haigh et al. [1] state that measurement of objective joint stiffness does not relate to that experienced by the patient in rheumatoid arthritis (RA). This premise underlies their paper on phantom limb stiffness in amputees who have RA. However, more recent studies by our group have shown that objective joint stiffness does correlate with subjective stiffness providing appropriate correction for muscle wasting is made [2]. Furthermore, the changes observed can reflect local joint inflammation and the response to intra-articular steroids [3]. People may also use a variety of descriptors to relate the deterioration they experience after a night in bed and may, in some cases, find it difficult to distinguish between stiffness and pain [4]. I agree that cortical plasticity may explain some of the symptoms experienced in the presence of chronically inflamed joints, but the physical evidence suggests that joint stiffness is a real phenomenon and that distal sensory function in large fibre afferents is normal in this group of patients [5]. Use of an objective measure of articular stiffness to record changes in finger joints after intra-articular injection of corticosteroid. Reply We thank Helliwell for his considered arguments. Our premise was that central nervous system changes governed the subjective experience of stiffness in a limb even after it is amputated, and in support of the hypothesis, maintain that current evidence fails to confirm a consistent relationship between objective and subjective measures of joint stiffness. Indeed, local treatments of inflammation, such as aspiration and injection of corticosteroid into a joint, have a number of consequences in addition to a local anti-inflammatory effect that may influence both peripheral and central nervous systems, resulting in altered sensory feedback and a modified motor output. In addition, our subject reported a reduction in stiffness in the joints in her intact limb as well as her phantom limb following systemic steroid therapy. Thus, it is difficult to accept that peripheral mechanisms alone generate and perpetuate stiffness. Furthermore, distal sensory function may not be normal in rheumatoid arthritis at all [1], despite biothesiometer vibration perception thresholds being normal in the cited study [2]. We agree that semantics, terminology and understanding of the concept(s) of stiffness can complicate the issue and Helliwell suggests that our subjects may have found it difficult to differentiate between pain and stiffness, particularly on …