Gunnar Wasner1, Anne Kleinert, Andreas Binder, Jörn Schattschneider, Ralf Baron. 1. Dept. of Neurological Pain Research and Therapy, Neurological Clinic, Universitätsklinikum Schleswig-Holstein, Campus Kiel, Schittenhelmstrasse 10, 24105 Kiel, Germany. g.wasner@neurologie.uni-kiel.de
Abstract
OBJECTIVES: Topical lidocaine is effective in postherpetic neuralgia (PHN). The aim of the present investigation was to classify patients according to their predominant peripheral nociceptor function and to compare these data with the results of a controlled study using dermal lidocaine patch. METHODS: Within the skin area of maximal pain QST (thermotest) and QCART (histamine iontophoresis and laser Doppler flowmetry) were performed prospectively in 18 PHN patients. A controlled study using cutaneous lidocaine (lidocaine 5% patch, IBSA) followed. RESULTS: Six patients (group I, sensitised nociceptors) had no sensory loss. Heat pain thresholds were equal or lower than on the contralateral side. Histamine-induced flare and axon reflex vasodilatation were not different on both sides. Histamine evoked pain increased. In 12 patients (group II, nociceptor impairment) heat pain thresholds were higher than contralateral. Histamine-induced flare was impaired or abolished. Histamine did not induce any sensation. Lidocaine was efficacious in the entire group of patients. Subgroup analysis revealed that patients with impairment of nociceptor function had significantly greater pain reduction under lidocaine vs placebo. Patients with preserved and sensitised nociceptors demonstrated no significant pain relief. CONCLUSIONS: PHN patients differ concerning their cutaneous nociceptor function: In the group I pain is caused by pathologically sensitised nociceptors. In subset II there is a loss of function of cutaneous C-nociceptors within the allodynic skin. Patients responded well to topical lidocaine even if the skin was completely deprived of nociceptors. Different underlying mechanisms of lidocaine action in nociceptor-deprived skin are discussed.
OBJECTIVES: Topical lidocaine is effective in postherpetic neuralgia (PHN). The aim of the present investigation was to classify patients according to their predominant peripheral nociceptor function and to compare these data with the results of a controlled study using dermal lidocaine patch. METHODS: Within the skin area of maximal pain QST (thermotest) and QCART (histamine iontophoresis and laser Doppler flowmetry) were performed prospectively in 18 PHN patients. A controlled study using cutaneous lidocaine (lidocaine 5% patch, IBSA) followed. RESULTS: Six patients (group I, sensitised nociceptors) had no sensory loss. Heat pain thresholds were equal or lower than on the contralateral side. Histamine-induced flare and axon reflex vasodilatation were not different on both sides. Histamine evoked pain increased. In 12 patients (group II, nociceptor impairment) heat pain thresholds were higher than contralateral. Histamine-induced flare was impaired or abolished. Histamine did not induce any sensation. Lidocaine was efficacious in the entire group of patients. Subgroup analysis revealed that patients with impairment of nociceptor function had significantly greater pain reduction under lidocaine vs placebo. Patients with preserved and sensitised nociceptors demonstrated no significant pain relief. CONCLUSIONS: PHN patients differ concerning their cutaneous nociceptor function: In the group I pain is caused by pathologically sensitised nociceptors. In subset II there is a loss of function of cutaneous C-nociceptors within the allodynic skin. Patients responded well to topical lidocaine even if the skin was completely deprived of nociceptors. Different underlying mechanisms of lidocaine action in nociceptor-deprived skin are discussed.
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