• Birgitta Tuveson, Ann-Sofie Leffler, and Per Hansson.
• Section of Clinical Pain Research, Department of Molecular Medicine and Surgery, Karolinska Institute, SE-171 76 Stockholm, Sweden. Birgitta.Tuveson@ds.se
• Eur J Pain. 2007 May 1;11(4):452-62.

AbstractIn 15 patients with painful peripheral neuropathy and dynamic mechanical allodynia, the influence of spontaneous ongoing neuropathic pain on pain sensitivity in a remote pain-free area was examined, as was the influence of ischemia-induced heterotopic noxious conditioning stimulation (HNCS) on the intensity of ongoing pain and brush-evoked allodynia. In addition, the modulating effect of HNCS on pain sensitivity in a pain-free area was investigated. Pain thresholds to pressure and heat as well as the sensitivity to suprathreshold pressure- and heat pain were assessed in the pain-free area. Dynamic mechanical allodynia was induced by a recently developed semi-quantitative brushing technique and the patients continuously rated the intensity of the allodynia using a computerized visual analogue scale (VAS). The total brush-evoked pain intensity was calculated as the area under the VAS curve. At baseline, no significant difference in pain sensitivity was found between patients and their healthy controls in the pain-free area, indicating a lack of activation of pain modulatory systems from the spontaneous pain. Compared to baseline, the patients rated the ongoing neuropathic pain intensity significantly lower during the HNCS-procedure (p<0.05). In contrast, there was no influence from HNCS on the total brush-evoked pain intensity. In the pain-free area higher pressure pain thresholds were demonstrated during conditioning stimulation in patients and controls alike (p<0.01). In controls only, a significantly higher heat pain threshold was found during the HNCS-procedure (p<0.01). The main finding of the present study was that HNCS altered differentially spontaneous and brush-provoked pain in patients with painful peripheral neuropathy.

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