It has an incidence of 26/100,000 in European population. It has its peak in people aged 55–75 years. It may be triggered by a variety of insults, such as trauma, surgery, inflammation, stroke, nerve injury and immobilisation. The syndrome occurs frequently in young adults and more frequently in women than in men.

Some features of acute/early CRPS are because of sympathetic hypofunction and can be explained by an exaggerated localised inflammatory process, especially in the early phase. Blister fluid contains high levels of IL-6 and TNF alpha in the involved extremity as compared to the uninvolved extremity. CRPS is characterised by disproportionate spontaneous and evoked pain (hyperalgesia and mechanical allodynia). Sensory impairment occurs in 70 % of CRPS patients. An acute nociceptive barrage from an inciting trauma or due to peripheral sensitisation and/or neurogenic inflammation can cause rapid changes in CNS (brain/spinal cord) known as central sensitisation. In acute CRPS, vasodilatation and sudomotor dysfunction is observed in contrast to chronic CRPS where vasoconstriction and hyperhidrosis are seen. Nerve dropout and osteopenia may be seen. Most CRPS patients show weakness, spasm, tremor, bradykinesia and motion abnormalities. Minority may show dystonia. Weakness of skeletal muscles of the affected distal extremity is common. Tremor may occur in 70 % of patients.

There are three sequential stages seen in CRPS: