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Preinjury treatment with morphine or ketamine inhibits the development of experimentally induced secondary hyperalgesia in man

Warncke, Torhilda,*; Stubhaug, Audunb; Jørum, Ellena

doi: 10.1016/S0304-3959(00)00260-8

We examine the effect of morphine or ketamine (N-methyl-D-aspartate receptor antagonist; NMDA) treatment on secondary hyperalgesia. Drug treatment started preinjury and continued into the early postinjury period. Hyperalgesia was induced by a local 1° burn injury covering 12.5 cm2 on the medial side of the calf. In this double-blind, cross-over study, 12 healthy volunteers received, on 3 separate days and in randomized order: (1) placebo; (2) morphine, bolus 150 μg/kg+infusion 1 μg/kg per min and 0.5 μg/kg per min; and (3) ketamine, bolus 60 μg/kg+infusion 6 μg/kg per min and 3 μg/kg per min. Bolus+infusion started 30 min before injury and ended 50 min after it. The area of secondary hyperalgesia was quantitated using punctate (von Frey filaments) and brush stimuli (electric brush). On the day of placebo, all subjects developed an area of hyperalgesia to punctate and brush stimuli outside the thermal injury (secondary hyperalgesia). We show that ketamine or morphine treatment starting preinjury significantly reduces this development (P<0.01, both). In a previous study, we found that postinjury treatment alone with morphine did not affect secondary hyperalgesia, whereas ketamine did so significantly. The differential response to morphine administered pre- or postinjury may be relevant to the recently shown NMDA receptor mediated interaction of central hyperexcitability and morphine antinociception. The effect of ketamine supports the hypothesis of the role of NMDA receptor mediation in central hyperexcitability.

aDepartment of Neurology, The National Hospital, University of Oslo, N-0027 Oslo, Norway

bDepartment of Anaesthesiology, The National Hospital, University of Oslo, N-0027 Oslo, Norway

*Corresponding author. Fax: +47-22868890

Received 5 January 1999; received in revised form 25 January 2000; accepted 5 February 2000.

© 2000 Lippincott Williams & Wilkins, Inc.
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