THE SPINAL COMPONENT TO SKIN BLOOD-FLOW ABNORMALITIES IN REFLEX SYMPATHETIC DYSTROPHY

Objective: To determine whether the mechanisms of reflex sympathetic d ystrophy, a neuropathic pain syndrome characterized by skin blood flow abnormalities associated with sympathetic vasoconstrictor and antidro mic vasodilator mechanisms, are solely of peripheral origin or have an additional spinal component and act exclusively through neural or als o involve humoral pathways. Patients: The 54 patients with unilateral reflex sympathetic dystrophy were divided into the following three sta ges according to their perception of skin temperature in the clinicall y affected hand: stage I, stationary warmth sensation; stage II, inter mittent warmth and cold sensation; and stage III, stationary cold sens ation. Methods: Investigation of basal skin blood flow and vasoconstri ctive response to dependency of skin microvessels in the clinically un affected hand and the clinically affected hand of patients with reflex sympathetic dystrophy and the left hand of 16 control subjects. Micro circulation was investigated at the predominantly neurally controlled thermoregulatory level (Doppler laser flowmetry) and at the predominan tly humorally controlled nutritive level (capillary microscopy). Resul ts: In the clinically unaffected hand, at the thermoregulatory level o f the microcirculation: (1) basal skin blood flow was increased at sta ge I compared with the control subjects, whereas no differences could be observed at this stage compared with the clinically affected hand; (2) the vasoconstrictive response to dependency (defined as skin blood flow at heart level divided by skin blood flow in the dependent posit ion) was attenuated at stage I compared with the control subjects, whe reas no differences could be observed at this stage compared with the clinically affected hand; and (3) basal skin blood flow and the vasoco nstrictive response to dependency did not differ from the control subj ects at stages II and III. In the clinically unaffected hand, at the n utritive level, no differences could be observed at any stage of the s yndrome compared with the control subjects. Conclusions: This study in dicates that there is a spinal component to microcirculatory abnormali ties at stage I of the reflex sympathetic dystrophy syndrome that most likely acts through neural (antidromic vasodilator) mechanisms and th at may be initiated by traumatic excitation of a peripheral nerve on t he clinically affected side.