Attenuation of Pain in a Randomized Trial by Suppression of Peripheral Nociceptive Activity in the Immediate Postoperative Period

Peripheral neuronal barrage from tissue injury produces central nervous system changes that contribute to the maintenance of postoperative pain. The therapeutic approaches to blocking these central changes remain controversial, because previous studies have not differentiated presurgical interventio...

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Published inAnesthesia and analgesia Vol. 95; no. 5; pp. 1351 - 1357
Main Authors Gordon, Sharon M., Brahim, Jaime S., Dubner, Ronald, McCullagh, Linda M., Sang, Christine, Dionne, Raymond A.
Format Journal Article
LanguageEnglish
Published United States International Anesthesia Research Society 01.11.2002
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ISSN0003-2999
DOI10.1097/00000539-200211000-00047

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Abstract Peripheral neuronal barrage from tissue injury produces central nervous system changes that contribute to the maintenance of postoperative pain. The therapeutic approaches to blocking these central changes remain controversial, because previous studies have not differentiated presurgical interventions from those administered after tissue injury, yet before pain onset. In this study, we evaluated the relative contributions of blockade of nociceptive input during surgery or during the immediate postoperative period on pain suppression. Subjects were randomly allocated to one of four groupspreoperative 2% lidocaine, postoperative 0.5% bupivacaine, both, or placebo injections. General anesthesia was induced and third molars extracted. Pain was assessed over 4 h and at 24 and 48 h. The β-endorphin in blood samples increased twofold during surgery, which is indicative of activation of the peripheral nociceptive barrage in response to painful stimuli. Pain was decreased in the immediate postoperative period in the bupivacaine groups, whereas it increased in the lidocaine group over time. Pain intensity was less 48 h after surgery in the groups whose postoperative pain was blocked by the administration of bupivacaine, but no effect was demonstrated for the preoperative administration of lidocaine alone. These results in the oral surgery pain model suggest that minimizing the peripheral nociceptive barrage during the immediate postoperative period decreases pain at later time periods. In contrast, blocking the intraoperative nociceptive barrage does not appear to contribute significantly to the subsequent reduction in pain.
AbstractList Peripheral neuronal barrage from tissue injury produces central nervous system changes that contribute to the maintenance of postoperative pain. The therapeutic approaches to blocking these central changes remain controversial, because previous studies have not differentiated presurgical interventions from those administered after tissue injury, yet before pain onset. In this study, we evaluated the relative contributions of blockade of nociceptive input during surgery or during the immediate postoperative period on pain suppression. Subjects were randomly allocated to one of four groupspreoperative 2% lidocaine, postoperative 0.5% bupivacaine, both, or placebo injections. General anesthesia was induced and third molars extracted. Pain was assessed over 4 h and at 24 and 48 h. The β-endorphin in blood samples increased twofold during surgery, which is indicative of activation of the peripheral nociceptive barrage in response to painful stimuli. Pain was decreased in the immediate postoperative period in the bupivacaine groups, whereas it increased in the lidocaine group over time. Pain intensity was less 48 h after surgery in the groups whose postoperative pain was blocked by the administration of bupivacaine, but no effect was demonstrated for the preoperative administration of lidocaine alone. These results in the oral surgery pain model suggest that minimizing the peripheral nociceptive barrage during the immediate postoperative period decreases pain at later time periods. In contrast, blocking the intraoperative nociceptive barrage does not appear to contribute significantly to the subsequent reduction in pain.
Peripheral neuronal barrage from tissue injury produces central nervous system changes that contribute to the maintenance of postoperative pain. The therapeutic approaches to blocking these central changes remain controversial, because previous studies have not differentiated presurgical interventions from those administered after tissue injury, yet before pain onset. In this study, we evaluated the relative contributions of blockade of nociceptive input during surgery or during the immediate postoperative period on pain suppression. Subjects were randomly allocated to one of four groups: preoperative 2% lidocaine, postoperative 0.5% bupivacaine, both, or placebo injections. General anesthesia was induced and third molars extracted. Pain was assessed over 4 h and at 24 and 48 h. The beta-endorphin in blood samples increased twofold during surgery, which is indicative of activation of the peripheral nociceptive barrage in response to painful stimuli. Pain was decreased in the immediate postoperative period in the bupivacaine groups, whereas it increased in the lidocaine group over time. Pain intensity was less 48 h after surgery in the groups whose postoperative pain was blocked by the administration of bupivacaine, but no effect was demonstrated for the preoperative administration of lidocaine alone. These results in the oral surgery pain model suggest that minimizing the peripheral nociceptive barrage during the immediate postoperative period decreases pain at later time periods. In contrast, blocking the intraoperative nociceptive barrage does not appear to contribute significantly to the subsequent reduction in pain.UNLABELLEDPeripheral neuronal barrage from tissue injury produces central nervous system changes that contribute to the maintenance of postoperative pain. The therapeutic approaches to blocking these central changes remain controversial, because previous studies have not differentiated presurgical interventions from those administered after tissue injury, yet before pain onset. In this study, we evaluated the relative contributions of blockade of nociceptive input during surgery or during the immediate postoperative period on pain suppression. Subjects were randomly allocated to one of four groups: preoperative 2% lidocaine, postoperative 0.5% bupivacaine, both, or placebo injections. General anesthesia was induced and third molars extracted. Pain was assessed over 4 h and at 24 and 48 h. The beta-endorphin in blood samples increased twofold during surgery, which is indicative of activation of the peripheral nociceptive barrage in response to painful stimuli. Pain was decreased in the immediate postoperative period in the bupivacaine groups, whereas it increased in the lidocaine group over time. Pain intensity was less 48 h after surgery in the groups whose postoperative pain was blocked by the administration of bupivacaine, but no effect was demonstrated for the preoperative administration of lidocaine alone. These results in the oral surgery pain model suggest that minimizing the peripheral nociceptive barrage during the immediate postoperative period decreases pain at later time periods. In contrast, blocking the intraoperative nociceptive barrage does not appear to contribute significantly to the subsequent reduction in pain.Suppression of postoperative pain immediately after surgery attenuates the pain experienced 1 to 2 days after surgery. These findings suggest that pain after minor surgery can be prevented by blocking the development of pain processes that amplify pain for days after surgery.IMPLICATIONSSuppression of postoperative pain immediately after surgery attenuates the pain experienced 1 to 2 days after surgery. These findings suggest that pain after minor surgery can be prevented by blocking the development of pain processes that amplify pain for days after surgery.
Peripheral neuronal barrage from tissue injury produces central nervous system changes that contribute to the maintenance of postoperative pain. The therapeutic approaches to blocking these central changes remain controversial, because previous studies have not differentiated presurgical interventions from those administered after tissue injury, yet before pain onset. In this study, we evaluated the relative contributions of blockade of nociceptive input during surgery or during the immediate postoperative period on pain suppression. Subjects were randomly allocated to one of four groups: preoperative 2% lidocaine, postoperative 0.5% bupivacaine, both, or placebo injections. General anesthesia was induced and third molars extracted. Pain was assessed over 4 h and at 24 and 48 h. The beta-endorphin in blood samples increased twofold during surgery, which is indicative of activation of the peripheral nociceptive barrage in response to painful stimuli. Pain was decreased in the immediate postoperative period in the bupivacaine groups, whereas it increased in the lidocaine group over time. Pain intensity was less 48 h after surgery in the groups whose postoperative pain was blocked by the administration of bupivacaine, but no effect was demonstrated for the preoperative administration of lidocaine alone. These results in the oral surgery pain model suggest that minimizing the peripheral nociceptive barrage during the immediate postoperative period decreases pain at later time periods. In contrast, blocking the intraoperative nociceptive barrage does not appear to contribute significantly to the subsequent reduction in pain. Suppression of postoperative pain immediately after surgery attenuates the pain experienced 1 to 2 days after surgery. These findings suggest that pain after minor surgery can be prevented by blocking the development of pain processes that amplify pain for days after surgery.
Author Sang, Christine
Dubner, Ronald
McCullagh, Linda M.
Gordon, Sharon M.
Dionne, Raymond A.
Brahim, Jaime S.
AuthorAffiliation National Institute of Dental and Craniofacial Research, Bethesda, Maryland; †University of Maryland, School of Dentistry, Baltimore, Maryland; ‡Department of Nursing, National Institutes of Health Clinical Center, National Institutes of Health, Bethesda, Maryland; and §Department of Anesthesia, Massachusetts General Hospital, Boston, Massachusetts
AuthorAffiliation_xml – name: National Institute of Dental and Craniofacial Research, Bethesda, Maryland; †University of Maryland, School of Dentistry, Baltimore, Maryland; ‡Department of Nursing, National Institutes of Health Clinical Center, National Institutes of Health, Bethesda, Maryland; and §Department of Anesthesia, Massachusetts General Hospital, Boston, Massachusetts
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  organization: National Institute of Dental and Craniofacial Research, Bethesda, Maryland; †University of Maryland, School of Dentistry, Baltimore, Maryland; ‡Department of Nursing, National Institutes of Health Clinical Center, National Institutes of Health, Bethesda, Maryland; and §Department of Anesthesia, Massachusetts General Hospital, Boston, Massachusetts
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  givenname: Jaime
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Snippet Peripheral neuronal barrage from tissue injury produces central nervous system changes that contribute to the maintenance of postoperative pain. The...
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SubjectTerms Acetaminophen - administration & dosage
Acetaminophen - therapeutic use
Adult
Analgesics, Non-Narcotic - administration & dosage
Analgesics, Non-Narcotic - therapeutic use
Analgesics, Opioid - administration & dosage
Analgesics, Opioid - therapeutic use
Anesthesia, General
Anesthesia, Local
beta-Endorphin - blood
Codeine - administration & dosage
Codeine - therapeutic use
Double-Blind Method
Female
Humans
Male
Nociceptors - drug effects
Pain Measurement
Pain, Postoperative - drug therapy
Peripheral Nervous System - drug effects
Surveys and Questionnaires
Title Attenuation of Pain in a Randomized Trial by Suppression of Peripheral Nociceptive Activity in the Immediate Postoperative Period
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https://www.ncbi.nlm.nih.gov/pubmed/12401625
https://www.proquest.com/docview/72628831
Volume 95
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