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Published on: March 13, 2012
Sympathetic vasoconstrictor reflex pattern in patients with complex regional pain syndrome
Frank Birklein1, Bernhard Riedl, Bernhard Neundörfer
1Neurologische Klinik, Friedrich-Alexander-Universität Erlangen, Erlangen, Germany Institut für Physiologie und experimentelle Pathophysiologie, Friedrich-Alexander-Universität Erlangen, Erlangen, Germany.
Abstract:
Twenty patients suffering from complex regional pain syndrome (CRPS) and 21 healthy control subjects were examined to evaluate sympathetic reflex vasoconstriction. The mean age of the 12 female and eight male patients was 48.9 (21-72) years. At the time of investigation the median duration of the disease was 8.5 weeks (2-70). Twenty-one healthy subjects were investigated for control. Different maneuvers, such as the veno-arteriolar reflex (VAR), inspiratory gasp (IG), cold pressor test (CP) and mental arithmetic (MA), were employed to induce vasoconstriction while the cutaneous blood flow of the affected and the contralateral limb was recorded. In addition, the skin temperature of both limbs was measured by infrared thermography. In 14 of 20 patients and in 14 of 21 control subjects vasoconstriction due to the provocation tests could be measured, while the remaining six patients and seven controls showed vasodilatation in at least one test, and by that they were excluded from analysis of vasoconstrictor reflex pattern. After thermoregulatory adaptation skin temperature was not different between the affected and the unaffected limb. Sympathetic reflex vasoconstriction triggered by MA which represents cortical generated, moderate vasoconstrictor stimulus, was significantly reduced on the affected limb (102.9% of prestimulus period) when compared to the control limb (85.0%, P < 0.002) or to controls (84.8%, P < 0.001). VAR (pure postganglionic), IG and CP (both spinal and supraspinal), representing stronger vasoconstrictor stimuli, revealed no significant side to side difference of sympathetic vasoconstriction and no significant difference as compared to controls. In conclusion our findings prove impairment of sympathetic vasoconstrictor activity after central vasoconstrictor stimulation in CRPS, and possible mechanisms are discussed.
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