Abstract
Relentlessly progressive sympathetically maintained pain (SMP) with dystonia in a patient with CRPS1 was consistently responsive to systemic phentolamine, but not responsive at all to regional intravenous phentolamine. Sympatholysis was only transiently effective. Our observations suggest that neural activity that caused the pain and drove the dystonia probably originated in sympathetic-sensory coupling within dorsal root ganglia (DRGs) rather than in abnormally adrenosensitive afferent endings in the extremity.