Abstract

Complex regional pain syndrome type I (CRPS I) is a frequent complication after injuries of the upper limbs. The pathophysiology of this disease remains unclear, although disturbances of the sympathetic nervous system have been detected in several clinical studies, and sympathetic blocks resolve the symptoms in many of the cases. To investigate the meaning of sympathetic dysfunction at the beginning of the disease, 27 patients with distal radial fracture were examined prospectively during the course of the disease with regard to their clinical symptoms and their peripheral sympathetic nervous function. Sympathetic nervous function was examined by testing the vasoconstrictor response to sympathetic stimuli — recorded with laser Doppler fluxmetry — of the fingertips of both hands. Four patients developed CRPS I during the 12-week observation time and two patients presented an incomplete clinical CRPS I picture (‘borderline patients’). The complaints of all patients (normal fracture patients, CRPS I patients, borderline patients) were similar during the first week after trauma with focus on pain, motoric disturbances and autonomic symptoms. After 1or 2 weeks, a larger clinical difference developed between normal fracture patients and CRPS I or ‘borderline patients’. In CRPS I patients and ‘borderline patients’, the sympathetic vasoconstrictor response was diminished or absent from the first posttraumatic day throughout the observation time, whereas the normal fracture patients revealed slightly impaired sympathetic nervous function on the first posttraumatic day and normal results during the rest of the observation time. With regard to the unaffected contralateral hand, CRPS I patients also showed impaired sympathetic nervous function. The results of the present study suggest that the disturbances in the sympathetic nervous system in CRPS I patients are systemic and not limited to the affected limb. Their occurrence before the clinical breakout of the disease may serve as a marker that might be useful for early therapy and lead to further understanding of the pathophysiology of CRPS I.

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