The perception of pain is a complex process involving central integration ofnociceptive sensory signals with autonomic, emotional, motor and behaviouralcortical networks. The principal aim of this thesis was to explore how this processcontributes to the presenting clinical phenotype in complex regional pain syndrome(CRPS), and whether this extends to other chronic pain conditions in rheumaticdisease such as osteoarthritis (OA) and rheumatoid arthrits (RA).The first study established baseline quantitative sensory testing parameters andautonomic function. It found that allodynia was absent in controls, present in someOA and RA patients and most marked in CRPS patients. Autonomic function wasnormal in controls, with some impairment in OA and RA and most dysfunction inCRPS. The second study used an optokinetic visuo-motor challenge induced by amirror-whiteboard device. The presence or absence of sensory disturbances and/ornew/worsening pain was used to generate a vulnerability scale. Controls were theleast vulnerable followed by RA, then OA with CRPS the most vulnerable. Autonomicresponses, sensory disturbances and new/worsening pain to a pure visual conflict inthe form of ambiguous visual stimuli (AVS) were used for the third study. Sensorydisturbances, pain enhancement and abnormal asymmetric autonomic responsesoccurred only in the CRPS cohort. The final study investigated parietal lobe functionin CRPS patients. It showed clinical evidence of parietal lobe dysfunction present in asubstantial number of CRPS patients, and that this was reflected both in symptomsand impact upon activities of daily living.Overall, the thesis findings support the concept that perterbation of centralsomaesthetic integration may induce cortical network dysfunction, reflected indifferent patterns of autonomic and pain responses. This might contribute to thediffering clinical presentations seen in CRPS. Similar processes may also occur inOA and RA. This work provides an approach to the clinical phenotyping of CRPS andother chronic painful rheumatic diseases. Appreciation of the potential mechanismsdescribed may allow better targeting of therapy.
|Date of Award||31 Jul 2012|
|Supervisor||Candy McCabe (Supervisor) & Kenneth Judge (Supervisor)|