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May 1999

Explaining Reflex Sympathetic Dystrophy

Arch Neurol. 1999;56(5):521-522. doi:10.1001/archneur.56.5.521

THE ARTICLE by Wasner and colleagues1 clearly demonstrates a complete functional loss of cutaneous sympathetic vasoconstrictor activity in a very early stage of reflex sympathetic dystrophy/complex regional pain syndrome type I (RSD/CRPS I) that returns with clinical recovery. They also present compelling evidence that this autonomic dysfunction is located within the central nervous system. This elegant clinical study of 1 patient and 2 control subjects addresses the role of the sympathetic nervous system in the early stages of RSD/CRPS I by measuring cutaneous blood flow (laser Doppler flowmetry) under phasic and tonic conditions that parallels vasoconstrictor innervation. Two weeks after the onset of RSD/CRPS I, the skin temperature of the patient's affected extremity was higher than that measured on the contralateral side at room temperature and during controlled thermoregulation, which demonstrated maximal vasodilation. Phasic stimulation (deep respiration) that causes cutaneous vasoconstriction and tonic cutaneous vasoconstriction (controlled body hypothermia) did not decrease skin blood flow or temperature on the affected side but induced both on the normal contralateral side. Venous norepinephrine levels were lower from the venous effluent on the affected side. This physiological evaluation convincingly demonstrated a complete functional loss of cutaneous vasoconstrictor activity in the affected extremity in the early stages of RSD/CRPS I. Furthermore, they demonstrated that antidromic firing of nociceptive afferents by iontophoresis of histamine dihydrochloride into the skin and the consequent release of the vasoactive neuropeptides calcitonin gene-related peptide and substance P does not cause complete depression of sympathetic vasoconstrictor reflex activity. Therefore, it is unlikely that the suffused hot extremities Wasner and colleagues observed in their patient and that others have seen in a great number of patients with early onset of RSD/CRPS I are caused by neurogenic inflammation.

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