The author describes subjects concerning the clinical manifestation of reflex sympathetic dystrophy (RSD) and the possible factors of the development of RSD. Lack of consensus is definitely based on lack of knowledge in both the clinical field and the basic mechanism by which the clinical picture of RSD is generated. The following factors may be involved in the development of the RSD: the NMDA receptor in dorsal horn neurones of the spinal cord with respect to Ca2+, substance P, L-glutamate, nitric oxide, and synaptic plasticity; and cellular immediate early gene with respect to c-fos, fos-B, c-jun, jun-B, jun-D, Krox 24 and hippocampus and memory.