Orlando Workshop, November 1993

Interest in the sympathetic nervous system (SNS) during the past few years has not only increased exponentially but it has been responsible for sparking a resurgence of laboratory activity to answer the question, “in what way and how might the SNS be involved in this activity”? (Basbaum and Besson 1991; Fields and Liebeskind 1992; Jänig and Schmidt 1992). This has had the salutary effect of dispelling many of the previously held controversies and has also laid to rest the idea that the SNS is the primary instigator of the clinical entities RSD and Causalgia. Without understanding the mechanistic basis by which the SNS interacts with the neuropathic, nociceptive and inflammatory processes already identified in the pathophysiology of the syndrome, there is little to question why sympathetic blocks have been successfully used over the preceding decades to manage pain in a comparatively large number of patients. Certainly, the focus for the Orlando workshop was to address this issue which amongst all the other topics that are discussed below provided a redefinition of RSD that would have only an indirect but most likely, multiple interactions with the SNS.