| JOURNAL HOME | CME HOME | THIS MONTH | PAST ISSUES | ETOC | COLLECTIONS |
| AUTHORS | REVIEWERS | EDITORIAL BOARD | FEEDBACK | RSS | HELP |
| ||||||||||||||
| ||||||||||||||
|
|
|
|
||||||||||||
|
||||||||||||||
From the Department of Anesthesiology, University of California San Diego, San Diego, California.
Address correspondence to Mark S. Wallace, MD, 9500 Gilman Drive #0924, La Jolla, CA 92093-0924. Address e-mail to mswallace{at}ucsd.edu.
Abstract
Preclinical and clinical studies have emphasized that persistent small afferent input will induce a state of central facilitation that can be attenuated by systemically administered nonsteroidal antiinflammatory drugs. However, these studies have been performed using cutaneous models of hyperalgesia. In this study we evaluated the effects of IV ketorolac on an experimental model of deep tissue hyperalgesia using IM capsaicin. We used a double-blind, placebo-controlled, crossover design. Ten subjects received 60 mg of ketorolac or placebo in 2 sessions separated by 1 wk. Capsaicin (100 µg in 10 µL) was then injected into the flexor carpi ulnaris muscle of the left forearm. After injection, spontaneous pain scores, pressure pain scores, gripping pain, pain distribution, and pain quality were recorded at 0, 5, 10, 15, 20, and 25 min. Cutaneous allodynia and dysesthesia were then mapped and thermal and mechanical thresholds were measured. The IM injection of capsaicin resulted in a reliable report of pain, hyperalgesia, and referred pain. Ketorolac had no effect on spontaneous pain, elicited pain, pain distribution, or secondary hyperalgesia induced by capsaicin. The findings of this study support the feasibility of further pharmacological studies using the IM capsaicin pain model.
|
