Complex Regional Pain Syndrome (CRPS) is a debilitating pain condition of unknown aetiology, usually occurring post-traumatically. Early diagnosis of CRPS remains a challenge with adverse implications on rehabilitation and recovery. The main goals of my research were to help develop clinically useful bedside tests as well as objective biomarkers to improve the early diagnosis of CRPS.

The first research project in this thesis, ‘Novel signs in CRPS and their diagnostic clinical utility’ was a prospective observational cohort study which defined the four novel signs (finger misperception, abnormal hand laterality, astereognosis and abnormal body scheme report) in CRPS, examined their prevalence in CRPS and other chronic pain conditions and assessed their diagnostic utility (Sensitivity, Specificity, Predictive values and Likelihood ratios) for identifying patients at risk of CRPS within a Fracture cohort. This study demonstrates that novel signs are present in the majority of CRPS patients and can be reliably detected following simple training. They are practical and have significant clinical utility in diagnosing persistent pain in a fracture group. They can be used to identify patients at high risk of developing chronic pain post-fracture thereby allowing targeted early intervention.

Cortical reorganisation, defined as structural and functional changes within the cerebral cortex, is implicated in many chronic pain conditions including CRPS. The second research project in this thesis ‘Cortical reorganisation and finger misperception in CRPS- a high density electroencephalogram study’ was a prospective case control design study which investigated the EEG parameters suggestive of cortical reorganisation in CRPS patients by studying the somatosensory ERPs (Event Related Potentials) elicited on painless finger stimulation. There was no significant difference in the GFP (Global Field Power) latency in the patient group compared to healthy subjects or between affected and unaffected sides of the patient group suggesting there was no impairment of somatosensory conduction from the periphery to the somatosensory cortex. However, GFP amplitude corresponding to P300 was significantly higher in the patient affected side compared to the healthy subjects suggesting cognitive dysfunction possibly related to increased allocation of attentional resources.