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Rheumatology Advance Access originally published online on July 16, 2003
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Rheumatology 2003; 42: 1279-1286
© 2003 British Society for Rheumatology

Review

A review of contralateral responses to a unilateral inflammatory lesion

N. Shenker, R. Haigh, E. Roberts1, P. Mapp1, N. Harris and D. Blake

Royal National Hospital for Rheumatic Diseases and 1Department of Medical Sciences, University of Bath, Bath, UK.

Correspondence to: N. Shenker. Royal National Hospital for Rheumatic Diseases, Bath, BA1 1RL, UK. E-mail: mpxns@bath.ac.uk

The first 150 words of the full text of this article appear below.


   Introduction
 
Symmetry is a remarkably constant clinical feature of chronic inflammatory disease. Rheumatoid arthritis is almost by definition symmetrical [1]. Osteoarthritis, psoriasis and some of its associated arthritides are also symmetrical [2–4]. Pulmonary fibrosis, glomerulonephritis and sympathetic ophthalmia are also symmetrical inflammatory conditions. Whilst the pathophysiology behind this symmetry is unexplained, we and others have speculated that it is likely to be mediated via neurological mechanisms crossing through the spinal cord [5, 6]. The two sides of the spinal column have largely been thought to function independently of each other. There are three lines of evidence to suggest that this is not true.

Careful anatomical studies of the spinal cord show transmedian fibres decussating posteriorly at all levels of the spinal cord to synapse in the laminae on the contralateral dorsal horn. These neuronal connections have been seen in many different species, . . . [Full Text of this Article]


   Methods
 

   Results
 

   Discussion
 

   Conclusion
 

   Appendix 1. Papers excluded after appraisal
 

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