• F Birklein, W Künzel, and N Sieweke.
• Neurologische Klinik, Friedrich-Alexander-Universität Erlangen, Universitätsstrasse 17, D-91054 Erlangen, Germany. birklein@physiologie1.uni-erlangen.de
• Pain. 2001 Aug 1;93(2):165-71.

AbstractIn order to analyze the pathophysiology behind the clinical similarity acutely after limb trauma and in acute stages of complex regional pain syndrome (CRPS), 20 patients with external fixation after distal radius fracture (3.5 days after surgery) without signs of CRPS and 24 patients suffering from acute CRPS I (without nerve lesion; duration, 5 weeks) were investigated. Hyperalgesia to heat was tested by a feedback-controlled thermode, and to mechanical stimuli by an impact stimulator. The sympathetic nervous system was examined by measuring skin temperature (infra-red thermography), testing different sympathetic vasoconstrictor reflexes (laser-Doppler flowmetry) and quantitative sudometry after thermal load (thermoregulatory sweat test). We found hyperalgesia to heat after trauma (P<0.001), but not in CRPS, whereas mechanical hyperalgesia was present in both patient groups (trauma: P<0.001; CRPS: P<0.005). Skin temperature was significantly increased on the affected side in both patient groups (acute trauma: P<0.001; CRPS: P<0.005). However, sympathetic failure, as indicated by impairment of sympathetic vasoconstrictor reflexes (P<0.02) and hyperhidrosis (P<0.01), was found exclusively in CRPS patients. Our results indicate that pain and vasomotor disturbances may be generated by different mechanisms acutely after trauma and in acute CRPS. Despite the clinical similarity, additional changes in the peripheral or central nervous system are required for CRPS. In the light of our observations, it seems unlikely that CRPS is a simple exaggeration of post-traumatic inflammation.

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