1999 Clinical and Scientific Meeting

Neil McGregor [1], High Dunstan [1], Henry Butt [1], Tim Roberts [1], Iven Klineberg [1], Phillip Clifton-Bligh [2], Greg Fulcher [2], Julie Dunemore [2], Leigh Hoskin [2]

1 Collaborative Pain Research Unit (CPRU) Universities of Newcastle and Sydney
2 Royal North Shore CFS Unit

Chronic Pain and Protein Turnover in Polysymptomatic Patients

Chronic pain is one of the major reasons for seeking medical treatment, however the mechanisms by which chronic pain occurs are very poorly understood. Onset of chronic pain has been associated with infectious events, trauma and increasing life stresses, each of which may induce an increased host energy demand suggesting that dysregulation of protein turnover is associated with chronic pain. The data from three studies will be presented that assess the potential mechanisms of chronic pain seen in chronic polysymptomatic patients.

The metabolic events associated with chronic pain are distinct from those associated with chronic fatigue. The three studies show that alteration in the tyrosine:leucine ratio, a marker of the relationship between proteolysis and protein synthesis, is strongly associated with chronic muscle pain. Enhanced proteolysis is associated with diuresis and an increase in the secretion of excitatory amino acids, such as glutamic and aspartic acids. Prolonged muscle pain is associated with increases in ALT, AST, urea-markers of tissue damage.

These data support an alteration in nitric oxide production and enhanced NMDA activation, two factors essential for the initiation of spinal column hyperalgesia. The inhibition of these responses is mediated by noradrenaline and the opioids, and may explain why certain tricyclic antidepressants may be useful in management of the pain response. Understanding of the mechanism behind chronic pain is essential for the development of appropriate therapies.


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