A considerable number of biochemical differences have been shown between connective tissues from CTS patients and normal individuals. In CTS there are increased local levels of the cytokines interleukin-6 (IL-6), prostaglandin e2 (PG-e2), vascular endothelial growth factor (VEGF), transforming growth factor beta-R1 (TGF-beta-R1), and matrix mettalloproteinases (Freeland 2002, Ettema 2004) and upregulation of the enzyme cyclo-oxygenase 2(COX-2) which is important in the production of prostaglandins (Talmor 2003). There is proliferation of fibroblasts and small blood vessels, and increased accumulation of glycosaminoglycans in the interstitial matrix. Interleukin-6, VEGF and prostagladin e2 are released from small blood vessels in response to ischaemia. Cultured fibroblasts from CTS patients also increase their production and release of VEGF and PG-e2 in response to mechanical stress applied to the cells (Hirata 2005). The extent to which such molecules are released in response to a given insult is likely to be at least partially under genetic control and is also known to be influenced by oestrogens and progestogens.

In one particularly interesting experiment connective tissue from CTS patients wrists was cultured for a few hours in a phosphate buffered saline solution. Compared to samples from patients without CTS the tissue pieces from the CTS wrists absorbed and retained much more of the culture fluid and swelled considerably (Tucci 2001). The connective tissue from the CTS subjects is there showing exactly the sort of physical properties which could explain a sustained increase in carpal tunnel pressure.

We can now propose a theory of CTS causation

Revision date - 4th March 2012

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