Analgesic effects of dexamethasone in burn injury☆

Werner, Mads U.; Lassen, Birgit; Kehlet, Henrik

doi:10.1053/rapm.2002.30664

Cited by 19 publications

(31 citation statements)

References 33 publications

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“…Dexamethasone alone lacks any analgesic property in thermal injury and secondary hyperalgesia [17]. Inclusion of dexamethasone in bupivacaine microspheres injected in animal experiments results in prolonged duration of analgesia.…”

Section: Discussionmentioning

confidence: 99%

Adjuvant dexamethasone with bupivacaine prolongs the duration of interscalene block: a prospective randomized trial

et al. 2011

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Section: Discussionmentioning

confidence: 99%

Adjuvant dexamethasone with bupivacaine prolongs the duration of interscalene block: a prospective randomized trial

et al. 2011

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“…3,5,6 Fourth, a number of previous studies applying BI model were also unable to demonstrate analgesic or antihyperalgesic effects of otherwise well-documented analgesics, such as local anesthetics, nonsteroidal anti-inflammatory drugs, and glucocorticoids. 24,28,30,45,49 These negative pharmacodynamic findings using the BI model may therefore be explained by the limited and quite superficial tissue damage provided in this model. It is not unlikely that other human pain models with more extensive tissue damage, such as the incision model 16 or the third molar extraction model, 23 could be used to document possible analgesic or antihyperalgesic properties of melatonin.…”

Section: Limitationsmentioning

confidence: 97%

Analgesic and antihyperalgesic effects of melatonin in a human inflammatory pain model

Andersen

Gögenur

Fenger

et al. 2015

Pain

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Antinociceptive effects of melatonin have been documented in a wide range of experimental animal models. The aim of this study was to investigate the analgesic, antihyperalgesic, and anti-inflammatory properties of melatonin using a validated burn injury (BI) model in healthy male volunteers. The design was a randomized, double-blind, placebo-controlled, three-arm crossover study. Each volunteer participated in 3 identical study sessions with intravenous administration of placebo, melatonin 10 mg, or melatonin 100 mg. Sixty minutes after bolus injection of study medication, a BI was induced by a computerized contact thermode (47.0°C, 420 seconds, 5.0 × 2.5 cm). Pain ratings during the BI and quantitative sensory testing at baseline and at 1, 2, 4, and 6 hours after the BI were performed. Quantitative sensory testing included assessments of secondary hyperalgesia areas, mechanical and thermal thresholds in the BI area, and pressure algometry. Furthermore, markers of inflammation, skin-reflectance spectrophotometry, and high-resolution ultrasonography were applied to measure skin erythema and dermal thickness in the BI area. Pain during the BI and secondary hyperalgesia areas were defined as primary outcomes. Twenty-nine volunteers were randomized and completed the study. While the BI induced large secondary hyperalgesia areas and significantly increased the markers of inflammation, no significant effects of melatonin were observed with respect to primary or secondary outcomes, compared with placebo. The administration of melatonin was not associated with any adverse effects. Melatonin did not demonstrate any analgesic, antihyperalgesic, or anti-inflammatory properties in the BI model.

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“…Superficial cutaneous heat injury is a well-characterized and validated inflammatory model of human peripheral nociceptor sensitization, primary hyperalgesia ( PHA ) and SHA. It has been used extensively for pharmacodynamic research (Brennum et al, 2001, Werner et al, 2001, Dirks et al, 2002a, Dirks et al, 2002b, Werner et al, 2002a, Werner et al, 2002b, Dirks et al, 2003, Ravn et al, 2012, Ravn et al, 2013). Sensitization is transient, reversible and replicable (Werner et al, 2013).…”

Section: Conceptual Model Conclusion and Clinical Significancementioning

confidence: 99%

Endogenous Analgesia, Dependence, and Latent Pain Sensitization

Taylor

Corder

2014

Current Topics in Behavioral Neurosciences

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Endogenous activation of μ-opioid receptors (MORs) provides relief from acute pain. Recent studies have established that tissue inflammation produces latent pain sensitization (LS) that is masked by spinal MOR signaling for months, even after complete recovery from injury and re-establishment of normal pain thresholds. Disruption with MOR inverse agonists reinstates pain and precipitates cellular, somatic and aversive signs of physical withdrawal; this phenomenon requires N-methyl-D-aspartate receptor-mediated activation of calcium-sensitive adenylyl cyclase type 1 (AC1). In this review, we present a new conceptual model of the transition from acute to chronic pain, based on the delicate balance between LS and endogenous analgesia that develops after painful tissue injury. First, injury activates pain pathways. Second, the spinal cord establishes MOR constitutive activity (MORCA) as it attempts to control pain. Third, over time, the body becomes dependent on MORCA, which paradoxically sensitizes pain pathways. Stress or injury escalates opposing inhibitory and excitatory influences on nociceptive processing as a pathological consequence of increased endogenous opioid tone. Pain begets MORCA begets pain vulnerability in a vicious cycle. The final result is a silent insidious state characterized by the escalation of two opposing excitatory and inhibitory influences on pain transmission: LS mediated by AC1 (which maintains accelerator), and pain inhibition mediated by MORCA (which maintains the brake). This raises the prospect that opposing homeostatic interactions between MORCA analgesia and latent NMDAR–AC1-mediated pain sensitization create a lasting vulnerability to develop chronic pain. Thus, chronic pain syndromes may result from a failure in constitutive signaling of spinal MORs and a loss of endogenous analgesic control. An overarching long-term therapeutic goal of future research is to alleviate chronic pain by either: a) facilitating endogenous opioid analgesia, thus restricting LS within a state of remission; or b) extinguishing LS altogether.

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Analgesic effects of dexamethasone in burn injury☆

Abstract: The study indicates that systemic administration of dexamethasone 2 hours before a burn injury does not reduce the inflammatory-mediated changes in quantitative sensory thresholds, pain perception, or skin erythema in humans.

Cited by 19 publications

References 33 publications

Adjuvant dexamethasone with bupivacaine prolongs the duration of interscalene block: a prospective randomized trial

Adjuvant dexamethasone with bupivacaine prolongs the duration of interscalene block: a prospective randomized trial

Analgesic and antihyperalgesic effects of melatonin in a human inflammatory pain model

Endogenous Analgesia, Dependence, and Latent Pain Sensitization

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