Theories on the etiology of reflex sympathetic dystrophy (RSD) are reviewed and presented in three categories: peripheral, spinal, and supraspinal. The peripheral pathophysiology involves a prolonged inflammatory, response to injury due to the axon reflex with release of vasoactive neuropeptides and sensitized nociceptors. The spinal component of RSD genesis involves nociceptive spinal cord neurons with lowered thresholds due to chronic pain input. These sensitized spinal neurons respond in turn by signaling pain reflexes through the sympathetic system. A physical-emotional diathesis may predispose individuals to respond to stress through autonomic arousal. Autonomic arousal, coupled with injury, signals the supraspinal influence on this syndrome. Since the puzzle of RSD remains to be solved, measurement and treatment strategies are suggested to provide intervention at each level. Measurement techniques should include a battery of static tests and stress tests. Static tests are used to quantify a physiological parameter at one point in time. Stress tests access physiological response to various neuro-vaso-motor challenges. A "hands off" treatment regime is presented that includes pain control, methods to reset sensory thresholds, vasomotor challenges, and an active motion program.