Relevant bibliographies by topics / Hyperalgesia

Academic literature on the topic 'Hyperalgesia'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 August 2024

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Journal articles on the topic "Hyperalgesia"

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Alvarez, Pedro, Xiaojie Chen, Oliver Bogen, Paul G. Green, and Jon D. Levine. "IB4(+) nociceptors mediate persistent muscle pain induced by GDNF." Journal of Neurophysiology 108, no. 9 (November 1, 2012): 2545–53. http://dx.doi.org/10.1152/jn.00576.2012.

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Skeletal muscle is a well-known source of glial cell line-derived neurotrophic factor (GDNF), which can produce mechanical hyperalgesia. Since some neuromuscular diseases are associated with both increased release of GDNF and intense muscle pain, we explored the role of GDNF as an endogenous mediator in muscle pain. Intramuscularly injected GDNF induced a dose-dependent (0.1–10 ng/20 μl) persistent (up to 3 wk) mechanical hyperalgesia in the rat. Once hyperalgesia subsided, injection of prostaglandin E2 at the site induced a prolonged mechanical hyperalgesia (>72 h) compared with naïve rats (<4 h; hyperalgesic priming). Selective neurotoxic destruction of IB4(+) nociceptors attenuated both GDNF hyperalgesia and hyperalgesic priming. Ergonomic muscular injury induced by eccentric exercise or mechanical vibration increased muscle GDNF levels at 24 h, a time point where rats also exhibited marked muscle hyperalgesia. Intrathecal antisense oligodeoxynucleotides to mRNA encoding GFRα1, the canonical binding receptor for GDNF, reversibly inhibited eccentric exercise- and mechanical vibration-induced muscle hyperalgesia. Finally, electrophysiological recordings from nociceptors innervating the gastrocnemius muscle in anesthetized rats, revealed significant increase in response to sustained mechanical stimulation after local GDNF injection. In conclusion, these data indicate that GDNF plays a role as an endogenous mediator in acute and induction of chronic muscle pain, an effect likely to be produced by GDNF action at GFRα1 receptors located in IB4(+) nociceptors.
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Klamt, Jyrson G. "Effects of Intrathecally Administered Lamotrigine, a Glutamate Release Inhibitor, on Short- and Long-term Models of Hyperalgesia in Rats." Anesthesiology 88, no. 2 (February 1, 1998): 487–94. http://dx.doi.org/10.1097/00000542-199802000-00028.

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Background Lamotrigine is a sodium channel blocker that inhibits the neuronal release of glutamate. Systemic administration of lamotrigine induces analgesia in short- and long-term models of hyperalgesia in rats. Considering the key role of N-methyl-D-aspartate receptors in the sensitization of dorsal horn neurons that leads to hyperalgesia, the author hypothesizes that intrathecally injected lamotrigine would be effective in reducing the hyperalgesia. Methods Short-term hyperalgesia was induced by unilateral intraplantar injection of prostaglandin E2. Long-term hyperalgesia was produced by treating rats with streptozotocin, which causes diabetic neuropathy and, in a different group of animals, by loose ligation of the sciatic nerve (chronic constriction injury). Hyperalgesia was assessed by measuring withdrawal reaction time after paw pressure, and analgesia was measured by the thermal tail-flick test. Results In the short-term model, intrathecally administered lamotrigine (12.5, 25.0, and 100.0 microg) produced a dose-dependent increase in the reaction time of the hyperalgesic paw. The highest dose that completely restored the reaction time to control levels (26-29 s) from the hyperalgesic levels (12-15 s) did not affect the reaction time of the normal contralateral paw. In the tail-flick test, a consistent effect could be observed only with doses of 200 microg, which caused transient motor impairment of the hind paws. In the long-term models of hyperalgesia, intrathecally administered lamotrigine produced a dose-dependent and long-lasting (24-48 h) antihyperalgesic effect. Conclusions Intrathecally administered lamotrigine produced a spinal, dose-dependent, and long-lasting antihyperalgesic effect in short- and long-term neuropathic models of hyperalgesia.
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Hans, Guy H., Everhard Vandervliet, Kristof Deseure, and Paul M. Parizel. "Cerebral Activation during Von Frey Filament Stimulation in Subjects with Endothelin-1-Induced Mechanical Hyperalgesia: A Functional MRI Study." BioMed Research International 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/610727.

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Endothelin-1 (ET-1) is an endogenously expressed potent peptide vasoconstrictor. There is growing evidence that ET-1 plays a role in the pain signaling system and triggers overt nociception in humans. The underlying neuronal pathways are still a matter of great debate. In the present study, we applied an intradermal ET-1 sensitization model to induce mechanical hyperalgesia in healthy subjects. Functional magnetic resonance imaging (fMRI) was used to tease out the cortical regions associated with the processing of ET-1-induced punctate hyperalgesia, as compared to a nonnoxious mechanical stimulation of the contralateral arm. Von Frey hair testing revealed the presence of increased responsiveness to punctate stimulation in all subjects. Activational patterns between nonpainful control stimulation and hyperalgesic stimulation were compared. Two major observations were made: (1) all cortical areas that showed activation during the control stimulation were also present during hyperalgesic stimulation, but in addition, some areas showed bilateral activation only during hyperalgesic stimulation, and (2) some brain areas showed significantly higher signal changes during hyperalgesic stimulation. Our findings suggest that injection of ET-1 leads to a state of punctate hyperalgesia, which in turn causes the activation of multiple brain regions. This indicates that ET-1 activates an extended neuronal pathway.
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Roman, K., M. Yang, and Robert L. Stephens. "Characterization of the Visceral Antinociceptive Effect of Glial Glutamate Transporter GLT-1 Upregulation by Ceftriaxone." ISRN Pain 2013 (December 25, 2013): 1–10. http://dx.doi.org/10.1155/2013/726891.

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Recent studies demonstrate that glial glutamate transporter-1 (GLT-1) upregulation attenuates visceral nociception. The present work further characterized the effect of ceftriaxone- (CTX-) mediated GLT-1 upregulation on visceral hyperalgesia. Intrathecal pretreatment with dihydrokainate, a selective GLT-1 antagonist, produced a reversal of the antinociceptive response to bladder distension produced by CTX. The hyperalgesic response to urinary bladder distension caused by intravesicular acrolein was also attenuated by CTX treatment as was the enhanced time spent licking of abdominal area due to intravesicular acrolein. Bladder inflammation via cyclophosphamide injections enhanced the nociceptive to bladder distension; cohorts administered CTX and concomitant cyclophosphamide showed reduced hyperalgesic response. Cyclophosphamide-induced bladder hyperalgesia correlated with a significant 22% increase in GluR1 AMPA receptor subunit expression in the membrane fraction of the lumbosacral spinal cord, which was attenuated by CTX coadministration. Finally, neonatal colon insult-induced hyperalgesia caused by intracolonic mustard oil (2%) administration at P9 and P11 was attenuated by CTX. These studies suggest that GLT-1 upregulation (1) attenuates the hyperalgesia caused by bladder irritation/inflammation or by neonatal colonic insult, (2) acts at a spinal site, and (3) may produce antinociceptive effects by attenuating GluR1 membrane trafficking. These findings support further consideration of this FDA-approved drug to treat chronic pelvic pain syndromes.
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Masue, Tatsuhiko, Shuji Dohi, Toshio Asano, and Hiroyuki Shimonaka. "Spinal Antinociceptive Effect of Epidural Nonsteroidal Antiinflammatory Drugs on Nitric Oxide-induced Hyperalgesia in Rats." Anesthesiology 91, no. 1 (July 1, 1999): 198–206. http://dx.doi.org/10.1097/00000542-199907000-00028.

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Background Nonsteroidal antiinflammatory drugs (NSAIDs) suppress various hyperalgesia perhaps via inhibition of cyclooxygenase activity at the spinal cord. The present study aimed to examine whether epidural application of NSAIDs affects hyperalgesia induced by nitric oxide. Methods The authors studied the antinociceptive effects of epidurally administered NSAIDs in rats with a chronically in-dwelling epidural catheter by three hyperalgesic models, including nitric oxide-induced hyperalgesia by nitroglycerin (10 microg) or l-arginine (100 microg), and the biphasic response in the formalin test. Results Epidural, but not systemic, nitroglycerin induced hyperalgesia that was completely blocked by methylene blue but not by N(omega)-nitro-L-arginine methyl ester (L-NAME). Epidural l-arginine, but not d-arginine, also induced hyperalgesia that was completely blocked by L-NAME. Epidural S(+)ibuprofen (100-1,000 microg) suppressed the nitroglycerin- and l-arginine-induced thermal hyperalgesia and also the second phase response in the formalin test. Neither systemic S(+)ibuprofen nor epidural R(-)ibuprofen suppressed the hyperalgesia Epidural indomethacin (10-100 microg) or diclofenac (10-1,000 microg) dose-dependently suppressed nitroglycerin-induced thermal hyperalgesia The order of potency for this suppression (ID50 in microg) was indomethacin = didofenac &gt; S(+)ibuprofen &gt; R(-)ibuprofen. Conclusions The antinociceptive action of epidurally administered NSAIDs could be the result of suppression of spinal sensitization, perhaps induced with nitric oxide in the spinal cord. The ID50 values for epidural indomethacin, diclofenac, and S(+)ibuprofen were about 10 times higher than those reported in other studies for intrathecal NSAIDs in hyperalgesia models. (Key words: Cyclooxygenase inhibitors; NO donor; NO precursor; optical isomers; neuroplasticity.)
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Khasar, Sachia G., Gordon McCarter, and Jon D. Levine. "Epinephrine Produces a β-Adrenergic Receptor-Mediated Mechanical Hyperalgesia and In Vitro Sensitization of Rat Nociceptors." Journal of Neurophysiology 81, no. 3 (March 1, 1999): 1104–12. http://dx.doi.org/10.1152/jn.1999.81.3.1104.

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Epinephrine produces a β-adrenergic receptor-mediated mechanical hyperalgesia and in vitro sensitization of nociceptor-like neurons in the rat. Hyperalgesic and nociceptor sensitizing effects mediated by the β-adrenergic receptor were evaluated in the rat. Intradermal injection of epinephrine, the major endogenous ligand for the β-adrenergic receptor, into the dorsum of the hindpaw of the rat produced a dose-dependent mechanical hyperalgesia, quantified by the Randall-Selitto paw-withdrawal test. Epinephrine-induced hyperalgesia was attenuated significantly by intradermal pretreatment with propranolol, a β-adrenergic receptor antagonist, but not by phentolamine, an α-adrenergic receptor antagonist. Epinephrine-induced hyperalgesia developed rapidly; it was statistically significant by 2 min after injection, reached a maximum effect within 5 min, and lasted 2 h. Injection of a more β-adrenergic receptor-selective agonist, isoproterenol, also produced dose-dependent hyperalgesia, which was attenuated by propranolol but not phentolamine. Epinephrine-induced hyperalgesia was not affected by indomethacin, an inhibitor of cyclo-oxygenase, or by surgical sympathectomy. It was attenuated significantly by inhibitors of the adenosine 3′,5′-cyclic monophosphate signaling pathway (the adenylyl cyclase inhibitor, SQ 22536, and the protein kinase A inhibitors, Rp-adenosine 3′,5′-cyclic monophosphate and WIPTIDE), inhibitors of the protein kinase C signaling pathway (chelerythrine and bisindolylmaleimide) and a μ-opioid receptor agonist DAMGO ([d-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin). Consistent with the hypothesis that epinephrine produces hyperalgesia by a direct action on primary afferent nociceptors, it was found to sensitize small-diameter dorsal root ganglion neurons in culture, i.e., to produce an increase in number of spikes and a decrease in latency to firing during a ramped depolarizing stimulus. These effects were blocked by propranolol. Furthermore epinephrine, like several other direct-acting hyperalgesic agents, caused a potentiation of tetrodotoxin-resistant sodium current, an effect that was abolished by Rp-adenosine 3′,5′-cyclic monophosphate and significantly attenuated by bisindolylmaleimide. Isoproterenol also potentiated tetrodotoxin-resistant sodium current. In conclusion, epinephrine produces cutaneous mechanical hyperalgesia and sensitizes cultured dorsal root ganglion neurons in the absence of nerve injury via an action at a β-adrenergic receptor. These effects of epinephrine are mediated by both the protein kinase A and protein kinase C second-messenger pathways.
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Koppert, Wolfgang, Reinhard Sittl, Karin Scheuber, Monika Alsheimer, Martin Schmelz, and Jürgen Schüttler. "Differential Modulation of Remifentanil-induced Analgesia and Postinfusion Hyperalgesia by S -Ketamine and Clonidine in Humans." Anesthesiology 99, no. 1 (July 1, 2003): 152–59. http://dx.doi.org/10.1097/00000542-200307000-00025.

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Background Experimental studies and clinical observations suggest a possible role for opioids to induce pain and hyperalgesia on withdrawal. The authors used a new experimental pain model in human skin to determine the time course of analgesic and hyperalgesic effects of the mu-receptor agonist remifentanil alone or in combination with the N-methyl-D-aspartate-receptor antagonist S-ketamine or the alpha(2)-receptor agonist clonidine. Methods Thirteen volunteers were enrolled in this randomized, double-blind, placebo-controlled study. Transcutaneous electrical stimulation at a high current density (2 Hz, 67.3 +/- 16.8 mA, mean +/- SD) induced acute pain (numerical 11-point rating scale: 5-6 out of 10) and stable areas of mechanical hyperalgesia to punctate stimuli and touch (allodynia). The magnitude of pain and area of hyperalgesia were assessed before, during, and after drug infusion (remifentanil at 0.1 microg x kg-1 x min-1 and S-ketamine at 5 microg x kg-1 x min-1 over a period of 30 min, respectively; clonidine infusion at 2 microg/kg for 5 min). Results Remifentanil reduced pain and areas of punctate hyperalgesia during infusion. In contrast, postinfusion pain and hyperalgesia were significantly higher than control. During infusion of S-ketamine, pain and hyperalgesia decreased and gradually normalized after infusion. When given in combination, S-ketamine abolished postinfusion increase of punctate hyperalgesia but did not reduce increased pain ratings. Clonidine alone did not significantly attenuate pain or areas of hyperalgesia. However, when given in combination with remifentanil, clonidine attenuated postinfusion increase of pain ratings. Conclusions Opioid-induced postinfusion hyperalgesia could be abolished by S-ketamine, suggesting an N-methyl-d-aspartate-receptor mechanism. In contrast, elevated pain ratings after infusion were not reduced by ketamine but were alleviated by the alpha(2)-receptor agonist clonidine. The results of this study suggest different mechanisms of opioid-induced postinfusion antianalgesia and secondary hyperalgesia.
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Aghade, Karveer Babanrao. "Effect of caffeine on capsaicin induced hyperalgesia in mice." Indian Journal of Pharmacy and Pharmacology 10, no. 3 (October 15, 2023): 197–203. http://dx.doi.org/10.18231/j.ijpp.2023.037.

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Caffeine is the most widely consumed behaviorally active substance in the world. In the past several pharmaceutical companies used caffeine along with other drugs to get analgesic effect. The present research work was undertaken to investigate the effect of interaction of caffeine and capsaicin on animal model of hyperalgesia in mice. To meet these objectives, effect of drugs was studied using tail immersion test, an animal model of thermal hyperalgesia and tail withdrawal test in mice, an animal model of cold hyperalgesia. The efficacy of three active principles alone and in combination of indomethacin, caffeine and prochlorperazine in reverting hyperalgesia was studied. Indomethacin 0.3 mg/ kg, i.p., caffeine 0.1 & 0.3 mg/ kg, i.p. and prochlorperazine 0.1 mg/ kg as well as combination reverted morphine withdrawal induced hyperalgesia. Initial application of capsaicin was found to be algesic leading to noxious stimulation in peripheral nervous system, which may cause allodynia and hyperalgesia. Thus this mechanism is also being studied in this study. Since most of the centrally acting analgesics act by way of their effect on dopaminergic mechanism and modifying calcium release, further studies on hyperalgesic activity were carried out using caffeine, capsaicin, amlodipine, haloperidol in the tail immersion (hot water of 55°C) and the tail withdrawal test (cold ethanol -14°C).
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Hughes, Sam W., Meirvaan Basra, Calvin Chan, Callum Parr, Felyx Wong, Sofia Gomes, and Paul H. Strutton. "Capsaicin-Induced Changes in Electrical Pain Perception Threshold Can Be Used to Assess the Magnitude of Secondary Hyperalgesia in Humans." Pain Medicine 21, no. 11 (April 26, 2020): 2830–38. http://dx.doi.org/10.1093/pm/pnaa082.

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Abstract Objectives Areas of secondary hyperalgesia can be assessed using quantitative sensory testing (QST). Delivering noxious electrocutaneous stimulation could provide added benefit by allowing multiple measurements of the magnitude of hyperalgesia. We aimed to characterize the use of electrical pain perception (EPP) thresholds alongside QST as a means by which to measure changes in pain thresholds within an area of secondary mechanical hyperalgesia. Methods EPP and heat pain thresholds (HPTs) were measured at five distinct points at baseline and following 1% capsaicin cream application, one within a central zone and four within a secondary zone. Areas of secondary mechanical hyperalgesia were mapped using QST. In a further 14 participants, capsaicin-induced reduction in EPP thresholds was mapped using a radial lines approach across 24 points. Results There was a reduction in EPP threshold measured at the four points within the secondary zone, which was within the mapped area of mechanical secondary hyperalgesia. The magnitude of secondary hyperalgesia could be split into a mild (∼4% reduction) and severe (∼21% reduction) area within an individual subject. There was no reduction in HPT within the secondary zone, but there was a reduction in both HPT and EPP threshold within the primary zone. EPP mapping revealed differences in the magnitude and spread of hyperalgesia across all subjects. Conclusions Measuring capsaicin-induced reduction in EPP thresholds can be used to map hyperalgesic areas in humans. This semi-automated approach allows rapid assessment of the magnitude of hyperalgesia, both within an individual subject and across a study population.
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Holtman, Joseph R., and Elzbieta P. Wala. "Characterization of the Antinociceptive and Pronociceptive Effects of Methadone in Rats." Anesthesiology 106, no. 3 (March 1, 2007): 563–71. http://dx.doi.org/10.1097/00000542-200703000-00022.

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Background Recently, it has been appreciated that in addition to their antinociceptive properties, opioid analgesics also can enhance pain sensitivity (opioid-induced hyperalgesia [OIH]). OIH may enhance preexisting pain and contribute to dose escalation, tolerance, and misuse/abuse of opioids. Better information is needed to determine which opioid or opioid combinations may be least likely to produce OIH and therefore possibly represent better choices for pain management. Herein the authors have examined the hyperalgesic and antinociceptive properties of racemic methadone and its enantiomers alone and in combination with morphine in rats. Methadone is of particular interest because it possesses both micro-receptor agonist and N-methyl-d-aspartate receptor antagonist activities. Methods The antinociceptive and hyperalgesic properties of d,l-methadone, l-methadone, and d-methadone were characterized by dose and sex using the thermal tail-flick test (high and low intensity). The responses to l- and d-methadone combinations with morphine were also determined with this model. Results Antinociceptive and hyperalgesic effects of d,l-methadone were demonstrated. These effects were related to dose but not to sex. The degree of hyperalgesia was greater with l-methadone compared with d,l-methadone. In contrast, d-methadone (N-methyl-d-aspartate antagonist) did not produce hyperalgesia. Furthermore, d-methadone blocked morphine hyperalgesia, enhanced antinociception, and abolished sex-related differences. This seems to be the result of antagonistic activity of d-methadone at the N-methyl-d-aspartate receptor. Conclusion The current findings with methadone are supportive of previous findings implicating mu-opioid and N-methyl-d-aspartate receptor mechanisms in OIH. Better understanding of OIH may help in choosing the most appropriate opioids for use in the treatment of pain.
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Dissertations / Theses on the topic "Hyperalgesia"

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McConaghy, Paul M. "Secondary hyperalgesia and postoperative pain." Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387878.

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Ramos, Khara M. "Spinally-mediated hyperalgesia in experimental diabetes." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3258831.

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Thesis (Ph. D.)--University of California, San Diego, 2007.
Title from first page of PDF file (viewed June 8, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 193-221).
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Stein, Alexander T. "Nerve growth factor produces hyperalgesia through phosphoinositide 3-kinase-dependent recruitment of TRPV1 ion channels /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/10631.

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MIZUMURA, KAZUE. "Peripheral Mechanism of Hyperalgesia : Sensitization of Nociceptors." Nagoya University School of Medicine, 1997. http://hdl.handle.net/2237/16753.

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Freshwater, Jason D. "Spinal mechanisms of hyperalgesia in experimental diabetes /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2004. http://wwwlib.umi.com/cr/ucsd/fullcit?p3120722.

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Isherwood, Ruth Jayne. "Opioid-related side-effects and opioid-induced hyperalgesia." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/6598/.

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Introduction: Opioids are widely used for the management of cancer and chronic non-cancer pain and the maintenance management of patients with a history of substance misuse. Increasingly the use of opioids is being scrutinised as patients are prescribed opioids for longer periods and the long-term effects of the opioids becomes clinically more relevant and evident. Our work has explored the prevalence of opioid-related side-effects in patients who are prescribed opioids and explored the clinically relevant phenomenon of opioid-induced hyperalgesia. . Methods: Patients were recruited who were prescribed opioids for the management of cancer and non-cancer pain or substance misuse. Quantitative data was collected to explore the prevalence and severity of opioid related side-effects, the impact of opioids on cognitive function and the effect of opioids on peripheral nerve function through quantitative sensory testing. Testing the sensory processing of patients who are on opioids has revealed altered thermal thresholds and the presence of wind-up at non-painful sites indicating central sensitisation. Qualitative description was used to explore the patient experience of an episode of opioid toxicity. Results: Patients have a significant burden of side-effects which have often not been recognised by clinicians. Using the Addenbrooke’s Cognitive Examination much more cognitive impairment has been revealed than has previously been recognised. Altered thermal thresholds and wind-up at non-painful sites suggests altered pain processing as a result of opioids. Themes from the qualitative description highlighted the coping strategies patients’ develop when managing with significant side-effects and toxicity, the covert self-management of their pain and the need to exert control. One of the most significant findings from the qualitative research was the finding of altered sensation and pain description associated with other features of opioid toxicity. Conclusions: The impact of opioids on the cognitive function of patients has significant implications in terms of patients’ involvement in decision-making and functioning in everyday life. The qualitative data reflects the burden of side effects and the descriptions of patients suggest that opioid-induced hyperalgesia exists as part of the spectrum of opioid toxicity. This finding may help physicians identify patients who are developing opioid-induced hyperalgesia and allow them to intervene earlier with a proactive approach.
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McNamee, Kay Edwina. "The role of IL-17 in inflammatory hyperalgesia." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/7066.

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Rheumatoid arthritis (RA) is a chronic autoimmune disease that affects up to 1% of the population. The importance of tumour necrosis factor (TNF) in RA has been established and anti-TNF biologics have proved to be highly effective in reducing inflammation. However, a proportion of RA patients fail to adequately respond to anti-TNF and even those who do respond have residual pain. This has prompted the investigation into other cytokines, such as interleukin-17 (IL-17), as potential new targets. This study sought to investigate the contribution of IL-17 to acute or chronic hyperalgesia. C57BL/6 mice were injected with recombinant IL-17. This induced a transient hyperalgesia, which was found to be dependent both on neutrophil migration and signalling through TNFR1. Using the air pouch model of cell migration, it was confirmed that the cell infiltration was associated with increased expression of the chemokine keratinocyte attractant (KC). These results suggest that IL-17 induces acute hyperalgesia by inducing TNF from resident cells. To investigate IL-17 and chronic hyperalgesia, the collagen induced arthritis mouse model (CIA) was used. IL-17RA was found to be up regulated in both the paw and in the dorsal root ganglia in arthritis, suggesting a role for IL-17 in chronic hyperalgesia. IL-17 blockade proved to be anti-arthritic and analgesic during CIA and potently reduced expression of pro-inflammatory cytokines. This study confirms that IL-17 contributes to acute and chronic hyperalgesia but acts in part via the induction of TNF.
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Vardanyan, Anna. "Opioid-induced Hyperalgesia: Underlying Mechanisms and Clinical Relevance." Diss., The University of Arizona, 2007. http://hdl.handle.net/10150/195034.

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Metastatic bone cancer causes severe pain that is primarily treated with opioids. A recently developed model of bone cancer pain was used to evaluate the effects of sustained morphine treatment. In cancer-treated mice, morphine enhanced spontaneous and evoked pain; these effects were dose-dependent and naloxone-sensitive. SP and CGRP positive DRG cells did not differ between sarcoma or control mice, but were increased following morphine in both groups. Morphine increased ATF-3 expression only in DRG cells of sarcoma mice. Morphine did not alter tumor growth in vitro or in vivo but increased sarcoma-induced bone destruction and incidence of spontaneous fracture in a dose- and naloxone-sensitive manner. Morphine increased osteoclast activity suggesting enhancement of sarcoma-induced osteolysis. Thus, morphine treatment may "add-on" additional mechanisms of pain beyond those induced by sarcoma. Despite the potential clinical significance, the exact mechanisms of opioid-induced hypersensitivity remain unknown. The vanilloid 1 receptor (TRPV1) is a molecular integrator of noxious stimuli. Sustained morphine elicited thermal and tactile hypersensitivity in WT, but not TRPV1 KO mice. Sustained morphine enhanced capsaicin-induced flinching and plasma extravasation in rats, indicating increased activity of these receptors in the periphery. Immunohistochemical studies indicate increase in TRPV1 expression in DRG and sciatic nerve, but not spinal cord, suggesting increased trafficking of TRPV1 channel to the periphery. Possible mechanisms of this enhanced expression and function of TRPV1 channels is activation of p38 MAPK. Sustained intrathecal infusion of p38 MAPK inhibitor prevents morphine-induced hypersensitivity and enhanced capsaicin-induced flinching, indicating the role of p38MAPK in the development of morphine-induced pain, possibly through sensitization of TRPV1 receptors. Acute administration of p38 MAPK inhibitor reversed morphine-induced pain suggesting the importance of p38 MAPK in the maintenance of morphine-induced hypersensitivity, likely through activation of TRPV1 channel. Sustained morphine also up-regulates NGF content in skin, which is then transported to DRG neurons where phosporilation of p38MAPK takes place. Single injection of anti-NGF peptibody blocked the development of morphine-induced hypersensitivity, enhanced capsaicin-induced flinching and plasma extravasation. Co-treatment with these compounds blocks the development of morphine-induced hyperalgesia and may optimize treatment of chronic pain states, like bone cancer pain.
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Ernberg, Malin. "Significance of serotonin for pain, allodynia, and hyperalgesia in the human masseter muscle /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3779-6/.

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Duedahl, Tina Hoff. "Anti-hyperalgesic drugs in postoperative pain /." Cph. : The Danish University of Pharmaceutical Sciences, Department of Pharmaceutics, 2005. http://www.dfuni.dk/index.php/Tina_Hoff_Duedahl/1732/0/.

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Books on the topic "Hyperalgesia"

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Jianren, Mao, ed. Opioid-induced hyperalgesia. New York: Informa Healthcare USA, 2010.

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Jianren, Mao, ed. Opioid-induced hyperalgesia. New York: Informa Healthcare USA, 2009.

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Lars, Lundberg. Pain and hyperalgesia in the human skin. Uppsala: Uppsala Universitet, 1992.

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Leonardo, Vecchiet, Albe-Fessard Denise G, and Lindblom Ulf, eds. New trends in referred pain and hyperalgesia. Amsterdam: Elsevier, 1993.

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Bristol-Myers Squibb Symposium on Pain Research (2nd 1991 Galveston, Tex.). Hyperalgesia and allodynia: The Bristol-Myers Squibb Symposium on Pain Research. Edited by Willis William D. 1934-. New York: Raven Press, 1992.

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universitet, Aalborg, ed. Fundamentals of muscle pain, referred pain and deep tissue hyperalgesia. Oslo: Taylor & Francis, 2006.

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1934-, Willis William D., ed. Hyperalgesia and allodynia: The Bristol-Myers Squibb Symposium on Pain Research. New York: Raven Press, 1992.

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1966-, Malmberg Annika B., and Chaplan Sandra R, eds. Mechanisms and mediators of neuropathic pain. Basel: Birkhäuser Verlag, 2002.

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Ziegler, Esther Anja. Die Bedeutung nozizeptiver A- und C-Fasern für die Mechanismen der sekundären Hyperalgesie. [s.l.]: [s.n.], 1999.

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Bannister, Kirsty. Opioid-induced hyperalgesia. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0061.

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The landmark paper discussed in this chapter is ‘Opioid-induced hyperalgesia: Abnormal or normal pain?’, published by Simonnet and Rivat in 2003. Morphine remains the analgesic of choice for those patients suffering moderate-to-severe pain, but it is increasingly recognized that worsening pain can be associated with chronic opioid consumption—the so-called phenomenon of opioid-induced hyperalgesia (OIH). This paper combined knowledge from clinical studies and experimental evidence from animal research in order to delve deeper into the workings of OIH and ask whether it represented normal or abnormal pain. The authors, intrigued by evidence indicating that exogenous opioids could activate both inhibitory and facilitatory pain systems, looked to reassess the role of such enhancement in pain sensitivity. As the debate regarding the very existence of OIH rages on, we pain specialists can take comfort in the knowledge that for many before us, over a decade ago, the reality of OIH was never in question.
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Book chapters on the topic "Hyperalgesia"

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Torebjörk, Erik. "Hyperalgesia." In Information Processing in the Somatosensory System, 399–404. London: Macmillan Education UK, 1991. http://dx.doi.org/10.1007/978-1-349-11597-6_29.

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Bloch, Michael H., Michael H. Bloch, Mark A. Geyer, David C. S. Roberts, Eileen M. Joyce, Jonathan P. Roiser, John H. Halpern, et al. "Hyperalgesia." In Encyclopedia of Psychopharmacology, 606. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1403.

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Treede, Rolf-Detlef. "Hyperalgesia." In Encyclopedia of Pain, 1518–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_1806.

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Compton, Peggy. "Methadone Hyperalgesia." In Handbook of Methadone Prescribing and Buprenorphine Therapy, 91–107. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6974-2_9.

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Handwerker, Hermann O., and Michaela Kress. "Cutaneous hyperalgesia." In Pain and Neurogenic Inflammation, 39–60. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8753-3_3.

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Sørensen, Jakob, and Per Sjøgren. "Opioid-Induced Hyperalgesia." In Cancer Pain, 131–42. London: Springer London, 2013. http://dx.doi.org/10.1007/978-0-85729-230-8_10.

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Murphy, Melisa Z., David A. Edwards, and Puneet Mishra. "Opioid-Induced Hyperalgesia." In Hospitalized Chronic Pain Patient, 15–17. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08376-1_5.

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Poole, Stephen, Fernando de Queiroz Cunha, and Sergio Henriques Ferreira. "Hyperalgesia from subcutaneous cytokines." In Cytokines and Pain, 59–87. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8749-6_4.

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Campbell, James N., and Richard A. Meyer. "Primary Afferents and Hyperalgesia." In Spinal Afferent Processing, 59–81. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-4994-5_3.

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Ferreira, Sergio H., Daniela Sachs, Fernando Q. Cunha, and B. B. Lorenzetti. "Persistent Hyperalgesia and Cytokines." In Pain and Neuroimmune Interactions, 3–8. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4225-4_1.

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Conference papers on the topic "Hyperalgesia"

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Murray-Brown, F. "19 Management of opioid induced hyperalgesia." In Accepted Oral and Poster Abstract Submissions, The Palliative Care Congress 1 Specialty: 3 Settings – home, hospice, hospital 19–20 March 2020 | Telford International Centre. British Medical Journal Publishing Group, 2020. http://dx.doi.org/10.1136/spcare-2020-pcc.19.

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Tianyao, Zhang, Dong Shuhua, Cui Chang, Zhang Yongjun, and Zeng Ling. "OP002 PAK4 inhibitor reduces remifentanil-induced postoperative hyperalgesia in rat." In ESRA Abstracts, 40th Annual ESRA Congress, 6–9 September 2023. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/rapm-2023-esra.2.

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"Effects of treadmill exercise on thermal hyperalgesia in CCI male rats." In International Conference on Medicine, Public Health and Biological Sciences. CASRP Publishing Company, Ltd. Uk, 2016. http://dx.doi.org/10.18869/mphbs.2016.146.

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Nagao, N., H. Wakabayashi, S. Kato, G. Miyamura, Y. Naito, and A. Sudo. "FRI0566 Teriparatide and alendronate improved bone loss and hyperalgesia in a mouse model of osteoporosis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4628.

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Ilari, Sara S., Filomena A. Lauro, Luigino Giancotti, Concetta Dagostino, Valentina Malafoglia, Lucia C. Passacatini, Cinzia Garofalo, et al. "Mitochondrial SIRT3 and morphine induced hyperalgesia and tolerance: the effect of polyphenol fraction of bergamot." In ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.553360.

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Guarino, B. B., H. A. Baig, J. L. Branconi, and B. A. Winkelstein. "Repeated whole-body vibration exposure induces prolonged mechanical hyperalgesia & increased spinal COX-2: A novel rat model." In 2012 38th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2012. http://dx.doi.org/10.1109/nebc.2012.6207133.

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Nicholson, Kristen J., Taylor M. Gilliland, and Beth A. Winkelstein. "Duration of Nerve Root Compressive Trauma Modulates the Subsequent Thermal Hyperalgesia and Spinal Expression of the Glutamate Transporter, GLT1." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14110.

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Mechanical compression of the cervical nerve roots is a common injury modality [1] and a frequent source of neck pain, affecting 30–50% of adults each year [2]. Since the nerve root is viscoelastic in compression (Fig. 1) [3,4], its response to loading from different injury scenarios is also likely a function of the duration of the applied tissue insult, which varies with the type of injury. For example, the nerve root undergoes brief periods of compression during sports and auto-related trauma, whereas a more prolonged compression occurs for a bulging disc or foraminal stenosis [1]. Similarly, mechanical sensitivity (i.e. pain) after root compression is has been shown to be duration-dependent [3,4]. Compression of the cervical nerve root is only sufficient to induce mechanical sensitivity in a rat model if the compression is applied for more than 3 minutes [3]. Yet, mechanical sensitivity is only one behavioral sequelae of radicular pain and it is not known whether the duration dependent response is similar for other types of evoked pain, such as thermal sensitivity.
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Bevan, J., T. Abdelmaksoud, J. O’Sullivan, and P. Ecimovic. "B208 Management of a rare case of fentanyl induced hyperalgesia (FIH) undergoing re-excision mastectomy four weeks later: a case report." In ESRA Abstracts, 39th Annual ESRA Congress, 22–25 June 2022. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/rapm-2022-esra.283.

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Guimarães, Mário Vicente Campos, Josué Andrade Martins, Ana Lívia Piovezan de Oliveira, and Cecília Procópio Cardoso. "Neuropathic pain as consequence of rifle injury: a case report and literature review." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.585.

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Rifle injuries are relatively common in emergency cases. It may result in several acute damages or it could lead to chronic consequences to the patient. This paper reports a case of a rifle injury on the leg that resulted in neuropathic pain and venous insufficiency. To treat this patient, a multidimensional approach was prefered, using comprehensive therapy, drug treatment and neuromodulation. The case reported in this paper was gathered by appreciation of the patient’s records and interviews and was discussed in the light of the most recent literature. Neuropathic pain is caused by lesion or disease of the somatosensory nervous system, according to The International Association for Study of Pain that affects over 7 to 8 percent of general populations and corresponds to 20 to 25 percent of chronic pain, most frequently in women and man older than 50-years, diagnosed exclusively via clinical criteria. It might be classified by the clinical manifestations: spontaneous pain, evoked pain, after sensations, hyperpathia and referred pain. The details of pathophysiology of neuropathic pain are yet to be clarified once most of the data in the matter comes from animal testing and should be interpreted carefully, majorly in the long-term assessments. It is clear, though, that several mechanisms are involved in the pathogenic process, depending on anatomical location and etiology, and that different classifications of neuropathic pain could be clustered to form several subgroups based on the symptoms combination, each reflecting different mechanisms. Understanding these underlying mechanisms is crucial to a proper treatment of the patient. In this paper, we report a patient who suffered from a fire gun injury in the left feet resulting in a neuropathic pain. A 40-year-old male comes to the office referring to allodynia, hyperalgesia, burning pain and paroxysmal pain, characterizing persistent neuropathic pain, intensity 8 in the one-to-ten scale, and edema during the day in the left inferior member. The patient reports being shot, one year and half before, with a 5.56 caliber rifle at the left feet, riching the fifth metatarsal No remarkable finding was present in the medical history prior to the incident. At physical examination, it was perceived that the patient developed venous insufficiency, for which was prescribed a ⅞ compression socks (30- 40 mmhg). The neuropathic pain was firstly treated with pregabalin 50 mg/ day and Duloxetine 30 mg/day, showing relevant response. Then, electroneuromyography revealed intermedial dorsal cutaneous nerve injury, being managed with a local block, prepared with 8 ml of 2% Lidocaine and 2 ml of 4 mg Dexamethasone, and a 30 Hz neuromodulation, terminating the pain. Ballistic knowledge is essential to a proper management of gunshots injury. In this case report, the patient suffered a 5.56 caliber rifle injury, a high-velocity gun, resulting in an intermediate dorsal cutaneous nerve and the fifth metatarsal lesion. In these injuries, the projectile transfers energy to the affected tissue, expanding and crushing it. This brief expansion creates a subatmospheric pressure resulting in bacterial and foreign material suction into the wound. It is worth to note that gunshot-related injuries in the feet, due to scarce soft tissue, numerous bones and articulations, are more propense to vascular and neural lesions. Although pathophysiological mechanisms of neuropathic pain are not fully understood, it is described post-traumatic peripheral ectopic nerve activity and central sensitization that could help to understand the pain origin. Moreover, coexisting psychological and emotional triggers might be associated with neuropathic pain association. As the electroneuromyography shows, the intermediate dorsal cutaneous nerve, the smallest branch of the fibular nerve, was injured at the fifth metatarsal level rising neuropathic pain. In addition, as mentioned above, gunshot injuries might lead to bacterial invasion, triggering the inflammatory response. In this setting, it is important to point out that evidence suggests inflammatory mediators and proinflammatory cytokines as an inductor factor for pain hypersensitivity. Another possible gunshot related etiology that must be considered is lead toxicity in the composition of gun projectiles, which is reportedly associated with neuropathies. For its heterogeneity of etiologies, mechanisms and presentations, it is essential to understand the underlying causes and its consequences to a proper treatment resulting in partial or full pain relief. In this case, the patient was treated with Duloxetine, a serotonin-norepinephrine reuptake inhibitor and first line to treat neuropathic pain, and pregabalin, an anticonvulsant used to inhibit neuronal excitatory transmission. The synergistic action of these drugs is superior compared to monotherapy. Auxiliary, a local block was performed using Lidocaine analgesic, sodium channel blocker, and Dexamethasone, an antiinflammatory corticosteroid, testifying in favor of mechanical and inflammatory pathogenic mechanism originated by the gunshot injury. Finally, it is worth noting that gunshot wounds might give rise to venous insufficiency as a result of vascular injury and must be carefully considered in order to provide the proper treatment, revascularization for exemple. Another possible cause is deep venous thrombosis and leg injury accounts as a risk factor. In this case, it was opted for compression therapy, a conservative treatment, for increased venous return. Concluding that, neuropathic pain is a heterogeneous condition with a limited action mechanism understanding. It is required from the physicians to comprehend the multiple dimensions and main etiology of this disease in order to provide a proper treatment. As gunshots may contribute to the rise of several damage mechanisms, this case report highlights the importance of acknowledging ballistic properties and possibilities wound-related.
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