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Department of Anesthesiology Allegheny General Hospital Pittsburgh, PA 15212
To the Editor:
The article by Guirimand et al. (1) demonstrates the link between seemingly esoteric laboratory research and clinical experience. The authors evaluated the effects of small systemic doses of ketamine on the temporal summation (wind-up) of both the nociceptive flexion reflex and sensations of pain in volunteers. The glutamate N-methyl-D-aspartase (NMDA) receptor blockers, such as ketamine, are adjunctive analgesics. The existence of a spinal reflex arc whose afferent limb is nociceptive input, which is routed through and amplified by glutamate NMDA signaling to then exit in an efferent motor limb, suggests several conclusions. First, a neurophysiologic basis for muscle spasm associated with pain states is suggested. Likewise the use of an NMDA receptor antagonist might be doubly beneficial in the treatment of pain—as an analgesic adjuvant and as a means of relieving muscle spasm. Perhaps the effect of the addition of dextromethorphan to analgesia regimens for back pain may be helpful.
There may also be relevance for epidural anesthesia. Epidural neural blockade is not complete as evidenced by the continued ability to record lower limb somatosensory-evoked potentials. If the incomplete neural blockade of epidural anesthesia allows a small amount of nociceptive afferent input to reach the spinal cord, then it is conceivable that this continued input could gradually amplify through an NMDA receptor-based mechanism to ultimately express clinically as patient complaint of pain and surgeon complaint of increased muscle tone (i.e., poor relaxation). Because of the role of the NMDA receptor in both wind-up and in this reflex arc, it has been my practice for the past several years to use a "poor man’s infusion" of IV ketamine (ketamine 10–15 mg/L of IV fluids) in conjunction with epidural anesthesia. My experience with this epidural + small-dose IV ketamine technique has been most gratifying both in terms of patient comfort and maintaining adequate muscle relaxation. I suspect the mechanism of this is that which Guirimand et al. have so clearly demonstrated.
Footnotes
Dr. Guirimand did not wish to respond to this letter.
References
This article has been cited by other articles:
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  S. Sivaramakrishnan, S. J. Sterbing-D'Angelo, B. Filipovic, W. R. D'Angelo, D. L. Oliver, and S. Kuwada GABAA Synapses Shape Neuronal Responses to Sound Intensity in the Inferior Colliculus J. Neurosci., May 26, 2004; 24(21): 5031 - 5043. [Abstract] [Full Text] [PDF]
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