Spinal actions of NSAIDS in blocking spinally mediated hyperalgesia: the role of cyclooxygenase products.

Recent studies have shown that intrathecal NSAIDs can produce a significant, dose-dependent reduction in the second phase of the formalin response and block thermal hyperalgesia induced by spinally injected N-methyl-D-aspartate and substance P. These observations support the body of literature that indicate that sustained small fiber input yields a hyperalgesia through activation of spinal NMDA and NK1 receptors and that in turn a portion of this action is mediated by the spinal release of cyclooxygenase products.