BLOCKADE OF PERIPHERAL NEURONAL BARRAGE REDUCES POSTOPERATIVE PAIN

Peripheral afferent neuronal barrage from tissue injury produces centr al nervous system hyperexcitability which may contribute to increased postoperative pain. Blockade of afferent neuronal barrage has been rep orted to reduce pain following some, but not all, types of surgery. Th is study evaluated whether blockade of sensory input with a long-actin g local anesthetic reduces postoperative pain after the anesthetic eff ects have dissipated. Forty-eight patients underwent oral surgery with general anesthesia in a parallel group, double-blind, placebo-control led study. Subjects randomly received either 0.5% bupivacaine or salin e intraoral injections, general anesthesia was induced with propofol, a non-opioid anesthetic, and 2-4 third molars extracted. Subjects were assessed at 24 and 48 h for postoperative pain and analgesic intake. Blood samples were collected at baseline, intraoperatively and at I-h intervals postoperatively for measurement of beta-endorphin as an inde x of CNS response to nociceptor input. Plasma beta-endorphin levels in creased significantly from baseline to the end of surgery in the salin e group in comparison to the bupivacaine group (P < 0.05), indicating effective blockade of nociceptor input into the CNS by the local anest hetic. Pain intensity was not significantly different between groups a t 24 h. Pain at 48 h was decreased in the bupivacaine group as measure d by category scale and graphic rating scales for pain and unpleasantn ess (P < 0.05). Additionally, subjects in the bupivacaine group self-a dministered fewer codeine tablets for unrelieved pain over 24-48 h pos toperatively (P < 0.05). These data support previous animal studies de monstrating that blockade of peripheral nociceptive barrage during and immediately after tissue injury results in decreased pain at later li me points. The results suggest that blockade of nociceptive input by a dministration of a long-acting local anesthetic decreases the developm ent of central hyperexcitability, resulting in less pain and analgesic intake. (C) 1997 International Association for the Study of Pain.