The perception of pain is a complex process involving central integration of nociceptive sensory signals with autonomic, emotional, motor and behavioural cortical networks. The principal aim of this thesis was to explore how this process contributes to the presenting clinical phenotype in complex regional pain syndrome (CRPS), and whether this extends to other chronic pain conditions in rheumatic disease such as osteoarthritis (OA) and rheumatoid arthrits (RA). The first study established baseline quantitative sensory testing parameters and autonomic function. It found that allodynia was absent in controls, present in some OA and RA patients and most marked in CRPS patients. Autonomic function was normal in controls, with some impairment in OA and RA and most dysfunction in CRPS. The second study used an optokinetic visuo-motor challenge induced by a mirror-whiteboard device. The presence or absence of sensory disturbances and/or new/worsening pain was used to generate a vulnerability scale. Controls were the least vulnerable followed by RA, then OA with CRPS the most vulnerable. Autonomic responses, sensory disturbances and new/worsening pain to a pure visual conflict in the form of ambiguous visual stimuli (AVS) were used for the third study. Sensory disturbances, pain enhancement and abnormal asymmetric autonomic responses occurred only in the CRPS cohort. The final study investigated parietal lobe function in CRPS patients. It showed clinical evidence of parietal lobe dysfunction present in a substantial number of CRPS patients, and that this was reflected both in symptoms and impact upon activities of daily living. Overall, the thesis findings support the concept that perterbation of central somaesthetic integration may induce cortical network dysfunction, reflected in different patterns of autonomic and pain responses. This might contribute to the differing clinical presentations seen in CRPS. Similar processes may also occur in OA and RA. This work provides an approach to the clinical phenotyping of CRPS and other chronic painful rheumatic diseases. Appreciation of the potential mechanisms described may allow better targeting of therapy.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:579161 |
| Date | January 2012 |
| Creators | Cohen, Helen |
| Contributors | McCabe, Candy ; Judge, Kenneth |
| Publisher | University of Bath |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
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