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Vol. 280, Issue 2, 829-838, 1997
Anesthesiology Research Laboratory 0818, University of California,
San Diego, La Jolla, California
Neuropathic pain remains a significant clinical problem. Current
understanding implicates the spinal cord dorsal horn
N-methyl-d-aspartate (NMDA) receptor apparatus in its pathogenesis.
Previous reports have described NMDA antagonist reduction of nerve
injury-induced thermal hyperalgesia and formalin injection-related
electrical activity. We examined a panel of spinally administered NMDA
antagonists in two models: allodynia evoked by tight ligation of the
fifth and sixth lumbar spinal nerves (a model of chronic nerve injury pain), and the formalin paw test (a model wherein pretreatment with
drug may preempt the development of a pain state). A wide range of
efficacies was observed. In the nerve injury model, order of efficacy
(expressed as percent of maximum possible effect ± S.E.), at the
maximum dose not yielding motor impairment, was memantine (96 ± 5%) = AP5 (91 ± 7%) > dextrorphan (64 ± 11%) = dextromethorphan (65 ± 22%) > MK801 (34 ± 8%) > ketamine (18 ± 6%). For the formalin test, the order of
efficacy was AP5 (86 ± 9%) > memantine (74 ± 5%) 
MK801 (67 ± 16%) > dextrorphan (47 ± 16%) > dextromethorphan (31 ± 12%) > ketamine (17 ± 15%). In the nerve injury model, no supraspinal action was seen
after intracerebroventricular injections of
dextromethorphan and ketamine. NMDA antagonists by the
spinal route appear to be useful therapeutic agents for chemically
induced facilitated pain as well as nerve injury induced tactile
allodynia. It is not known what accounts for the wide range of
efficacies.
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