Objective
To determine whether the cause of sympathetic dysfunction is due to increased regional sympathetic outflow or receptor supersensitivity to circulating catecholamines in the pathogenesis of reflex sympathetic dystrophy in hemiplegia.

Method
Ten hemiplegic patients with reflex sympathetic dystrophy were instructed to refrain from smoking or using caffeine and alcohol, and medications that influence catecholamine metabolism were witheld for 24 hours before blood sampling. Patients with cardiovascular disease, diabetes or abnormal liver and renal function tests were excluded from the study. Patients with a history of sympathectomy were also excluded. Ten hemiplegic patients without reflex sympathetic dystrophy served as the control group. Both groups of patients rested in supine position in a quiet room for 30 minutes. A needle with heparin cap was inserted into the dorsal venous arches of the affected hand and patients rested for another 20 minutes, after which blood was drawn through the heparin cap. The blood samples were assayed using high-performance liquid chromatography (HPLC) and norepinephrine and epinephrine were detected electrochemically. 24 hour urine was collected during rest and vanillylmandelic acid (VMA) and metanephrine were also detected using HPLC.

Results
The mean plasma norepinephrine levels were 1.05⁑0.24 ng/ml and 0.47⁑0.06 ng/ml in RSD affected and unaffected groups respectively, and the plasma norepinephrine level was significantly higher in the patient group with reflex sympathetic dystrophy (p＜0.05). The plasma epinephrine and 24-hour urine VMA and metanephrine levels were not significantly different in two groups.

Conclusion
These results may support a hypothesis of increased regional sympathetic outflow in the pathogenesis of reflex sympathetic dystrophy in hemiplegia.