• Neuropathic pain is a disease of the somatosensory system that is characterized by heightened sensitivity to innocuous and noxious stimuli (allodynia and hyperalgesia). (elifesciences.org)
  • We hypothesized that CRF-CRFR1 signaling in central amygdala (CeA) mediates stress-induced hyperalgesia in rats with high stress reactivity. (nature.com)
  • We used pharmacological, molecular, and immunohistochemical techniques to assess the role of CRF-CRFR1 signaling in CeA in stress-induced hyperalgesia. (nature.com)
  • Intra-CeA CRF infusion mimicked stress-induced hyperalgesia. (nature.com)
  • Enhanced nociception and pain sensitivity due to exposure to physical or psychological stressors is described as stress-induced hyperalgesia (SIH) [ 4 ]. (biomedcentral.com)
  • In this study, we show that genetic deletion or pharmacological inhibition of DLK greatly reduces the development of mechanical allodynia as well as the spinal cord microgliosis resulting from spared nerve injury. (elifesciences.org)
  • Electroacupuncture treatment alleviates the remifentanil-induced hyperalgesia by regulating the activities of the ventral posterior lateral nucleus of the thalamus neurons in rats. (mpg.de)
  • Finally, intra-CeA infusion of tetrodotoxin produced thermal hyperalgesia in unstressed rats and blocked the anti-hyperalgesic effect of systemic CRFR1 antagonist in stressed rats. (nature.com)
  • These data suggest that rats with high stress reactivity exhibit hyperalgesia that is mediated by CRF-CRFR1 signaling in CeA. (nature.com)
  • In rats with endometriosis plus ureteral calculosis, oral ultramicronized palmitoylethanolamide vs placebo significantly reduces viscerovisceral hyperalgesia by downregulating mast cell activity in endometriotic lesions. (lww.com)
  • Once daily administration of morphine (3 mg/kg, s.c.) in CCI rats led to the development of tolerance within 6 days. (aspetjournals.org)
  • Ipsilateral hind paws of all rats operated on CCI/SNI displayed mechanoallodynia and thermal hyperalgesia while contralateral hind paws and forepaws of both sides exhibited no significant hypersensitivity. (muni.cz)
  • This study inquired into whether and how GPR30 and GABA A -α4β1δ in the PAG promote preoperative anxiety-induced postoperative hyperalgesia in female rats. (biomedcentral.com)
  • After microinjection of G1 into the PAG, female rats with plantar incision continued to exhibit significant hyperalgesia until postoperative 48 h. (biomedcentral.com)
  • On the other hand, microinjection of G15 with SPS and plantar incision procedure relieved postoperative hyperalgesia in female rats. (biomedcentral.com)
  • Our results indicate that the GPR30-PKA-GABA A α4β1δ pathway in the PAG promotes preoperative anxiety-induced postoperative hyperalgesia in female rats. (biomedcentral.com)
  • It is well known that microglia are involved in the development of neuropathic pain after peripheral nerve injury [ 5 ]. (hindawi.com)
  • The development of treatments for neuropathic pain has been hindered by our limited understanding of the basic mechanisms underlying abnormalities in nociceptor hyperexcitability. (jneurosci.org)
  • Neuropathic pain induction was tested by measurement of mechanoallodynia and thermal hyperalgesia. (muni.cz)
  • Neuropathic pain resulting from nerve injury can become persistent and difficult to treat but the molecular signaling responsible for its development remains poorly described. (elifesciences.org)
  • Despite recent advances, the mechanisms underlying the development of neuropathic pain are still not fully understood. (elifesciences.org)
  • However, to date, a role for DLK in the development of neuropathic pain has not been examined. (elifesciences.org)
  • We are also interested in exploring the contribution of these pathways in the development of opioid-induced hyperalgesia and antinociceptive tolerance known to hamper the effective use of opioids for pain management. (slu.edu)
  • SIGNIFICANCE STATEMENT The development of hyperalgesia and antinociceptive tolerance during prolonged opioid use are noteworthy opioid-induced adverse effects that reduce opioid efficacy for treating chronic pain and increase the risk of dependence and abuse. (unime.it)
  • In addition, 8,9-EET sensitized AITC-induced calcium increases in DRG neurons and AITC-induced calcitonin gene related peptide (CGRP) release from sciatic nerve axons, indicating that 8,9-EET sensitizes TRPA1-expressing neurons, which are known to contribute to mechanical hyperalgesia. (uni-frankfurt.de)
  • The infiltration of blood MDMs in the spinal cord may promote the development of painful neuropathy in diabetes. (hindawi.com)
  • MDMs in spinal cord promotes the hyperalgesia based on different models of chronic pain [ 10 ]. (hindawi.com)
  • Using the monocyte-depletion approach, the present study aimed at characterizing the dynamic changes and the role of infiltrated MDMs in the spinal cord during the development of diabetic neuropathy. (hindawi.com)
  • Hyperalgesia is an exaggerated and prolonged response to noxious stimuli that can be produced by plasticity at peripheral sites (eg, reduced threshold and/or amplified nociceptor response to noxious stimuli) and centrally in the spinal cord or brain. (nature.com)
  • Neuropeptide changes persist in spinal cord despite resolving hyperalgesia in a rat model of mononeuropathy. (ox.ac.uk)
  • We have previously described the changes in spinal cord neuropeptides in the unilateral sciatic chronic constriction injury (CCI) model of Bennett and Xie [Pain, 33 (1988) 87-108] at 28 days, a time of maximum mechanical hyperalgesia. (ox.ac.uk)
  • Mechanical hyperalgesia was assessed with a Ugo-Basile analgesymeter and immunohistochemistry performed on the spinal cord sections of the animals and quantified using a confocal microscope. (ox.ac.uk)
  • Cyclooxygenase-2 (COX-2)-dependent prostaglandin (PG) E2 synthesis in the spinal cord plays a major role in the development of inflammatory hyperalgesia and allodynia. (uni-frankfurt.de)
  • Tolerance, another condition that can arise from prolonged exposure to opioids, can often be mistaken for opioid-induced hyperalgesia and vice versa, as the clinical presentation can appear similar. (wikipedia.org)
  • Although tolerance and opioid-induced hyperalgesia both result in a similar need for dose escalation to receive the same level of effect to treat pain, they are nevertheless caused by two distinct mechanisms. (wikipedia.org)
  • Under chronic opioid treatment, a particular individual's requirement for dose escalation may be due to tolerance, opioid-induced hyperalgesia, or a combination of both. (wikipedia.org)
  • In addition, what appears to be opioid tolerance can be caused by opioid-induced hyperalgesia lowering the baseline pain level, thus masking the drug's analgesic effects. (wikipedia.org)
  • Whereas increasing the dose of opioid can be an effective way to overcome tolerance, doing so to compensate for opioid-induced hyperalgesia may worsen the patient's condition by increasing sensitivity to pain while escalating physical dependence. (wikipedia.org)
  • However, the conclusion of a report published in the Journal of Pain & Palliative Care Pharmacotherapy suggests that "[h]yperalgesia shares a common mechanism with tolerance and it may be that hyperalgesia is a manifestation of tolerance itself. (wikipedia.org)
  • Molecular pathways and mechanisms tied to neuroinflammation appear to play similar, yet distinct roles in the development of both opioid tolerance and opioid-induced hyperalgesia. (taylorfrancis.com)
  • This suggests that mediating neuroinflammation would prove beneficial in treating opioid tolerance and opioid-induced hyperalgesia. (taylorfrancis.com)
  • The development of tolerance, the potential for abuse and misuse, and a lack of understanding as to the indications for use all contribute to physician angst. (ama-assn.org)
  • The development of physiologic tolerance can be expected following repeated exposure to exogenous agents that occupy receptor sites normally responsive to endogenous substances. (ama-assn.org)
  • Most importantly, the development of tolerance is by no means equivalent to addiction. (ama-assn.org)
  • Dose escalation due to tolerance is common and not necessarily directly related to the development of an obsession for the procurement and compulsive use of the drug, hallmarks of addiction. (ama-assn.org)
  • The recommendations from the APS have subsequently been revised to reflect the clinical importance and frequency of tolerance development to opioid therapy [8]. (ama-assn.org)
  • The pharmacology for opioid-induced hyperalgesia is more complicated, and is believed to involve the activation of NMDA receptors and increased excitatory peptide neurotransmitters (such as cholecystokinin). (wikipedia.org)
  • Systemic blockade of corticotropin-releasing factor (CRF) type 1 receptors (CRFR1s) reduces stress-induced thermal hyperalgesia. (nature.com)
  • Regular physical activity increases the percentage of M2 macrophages and prevents the development of chronic muscle hyperalgesia through activation of muscle interleukin-10 receptors. (lww.com)
  • This enhanced responsiveness to nociceptive input of the central nervous system primarily manifests as an increased sensitivity to painful mechanical pinprick stimuli extending beyond the site of injury (secondary mechanical hyperalgesia) and is thought to be a key mechanism in the development of chronic pain, such as persistent post-operative pain. (iasp-pain.org)
  • HFS induced an increased sensitivity to mechanical pinprick stimuli at both forearms, directly (T1) and 20 min (T2) after HFS, confirming the successful induction of secondary hyperalgesia at both forearms. (iasp-pain.org)
  • Hyperalgesia is an exaggerated response to noxious stimuli produced by peripheral or central plasticity. (nature.com)
  • Introduction: Several factors are cited as capable to influence the development of Temporomandibular Disorders (TMD), among them, the psychological, systemic, genetic, and occlusal factors. (bvsalud.org)
  • We used murine models of cancer and inflammatory muscle pain to examine whether the cannabinoid receptor agonist WIN55,212-2 reduces hyperalgesia originating in deep tissues. (umn.edu)
  • After controlling for the difference in magnitude of hyperalgesia between the two models, WIN55,212-2 was still more potent at reducing hyperalgesia in the inflammatory model. (umn.edu)
  • These data show that cannabinoids attenuate deep tissue hyperalgesia produced by both cancer and inflammatory conditions. (umn.edu)
  • Professor Ferreira also discovered the mechanism in which non-steroidal anti-inflammatory drugs (NSAIDs) work and studied a basic mechanism involving the inflammatory hyperalgesia. (princemahidolaward.org)
  • Secondary hyperalgesia phenotypes exhibit differences in brain activation during noxious stimulation. (mpg.de)
  • Maladaptive neuroplasticity of the descending pain modulatory systems in dysmenorrhic women that might be relevant to the development of co-occurring functional disorders later in life. (lww.com)
  • Once again, individual variability characterizes the development of addiction, making outcome prediction difficult [3], but some features are associated with increased risk for addiction: increasing dose requirement, younger age, preexisting mental health disorders, and prior substance abuse [4]. (ama-assn.org)
  • At some point during the syndrome's development, both show evidence of edema, changes in skin blood flow revealed by color changes and skin temperature changes greater than 1.1°C from the homologous body part, or abnormal sudomotor activity in the painful region. (medscape.com)
  • Described herein are methods and compositions relating to inhibition of mechanically-induced TRPV4 activation, e.g., for the treatment of pulmonary edema, edema, inflammation, hypertension, and/or hyperalgesia. (google.com)
  • This study was designed to investigate any correlation between the mechanism of pain development and changes of histochemically-reactive zinc contents in the rat spinal cords following peripheal nerve ligation. (koreamed.org)
  • This mechanism might be a potential novel therapeutic target for hyperalgesia in females. (biomedcentral.com)
  • Background IMI2-PainCare-BioPain-RCT2 is one of four similarly designed clinical studies aiming at profiling a set of functional biomarkers of drug effects on specific compartments of the nociceptive system that could serve to accelerate the future development of analgesics. (researchgate.net)
  • These results suggest that TRPV4 plays a crucial role in a painful peripheral neuropathy, making it a very promising target for the development of a novel class of analgesics. (jneurosci.org)
  • His study led to the development of a selected class of analgesics, particularly the COX 2 inhibitor, considered to be a remarkable progress for all NSAIDs. (princemahidolaward.org)
  • It has been shown that estrogen-induced mechanical hyperalgesia is produced by selective agonists of the GPR30 receptor, and is inhibited by knockdown of the GPR30 receptor [ 7 ]. (biomedcentral.com)
  • Opioid-induced hyperalgesia (OIH) or opioid-induced abnormal pain sensitivity, also called paradoxical hyperalgesia, is an uncommon condition of generalized pain caused by the long-term use of high dosages of opioids such as morphine, oxycodone, and methadone. (wikipedia.org)
  • We suggest that these changes may form a substrate for subsequent development of abnormal pain states. (ox.ac.uk)
  • Interestingly, cannabinoids differentially modulated carrageenan- and tumor-evoked hyperalgesia in terms of potency and receptor subtypes involved suggesting that differences in underlying mechanisms may exist between these two models of deep tissue pain. (umn.edu)
  • G-protein coupled estrogen receptor 30 (GPR30) was proved the specific estrogen receptor relating to mechanical hyperalgesia. (biomedcentral.com)
  • Taxol is the most widely used drug for the treatment of a variety of tumor types, but the dose of Taxol that can be tolerated is limited by the development of a small-fiber painful peripheral neuropathy. (jneurosci.org)
  • Because TRPV4 appears to be more important in pathological pain conditions than in normal mechanical nociception, we investigated whether TRPV4 also is involved in mechanical hyperalgesia associated with painful peripheral neuropathy. (jneurosci.org)
  • October 2006 The presence of increased activated and degranulating mast cells in deeply infiltrating endometriosis, which are the most painful lesions, and the close histological relationship between mast cells and nerves strongly suggest that mast cells could contribute to the development of pain and hyperalgesia in endometriosis, possibly by a direct effect on nerve structures. (endometriosis.org)
  • In opioid-induced hyperalgesia, sensitization of pronociceptive mechanisms occurs, resulting in a decrease in the pain threshold, or allodynia. (wikipedia.org)
  • Early life stress (ELS) is a risk-factor for the development of IBS, however the mechanisms responsible for the persistent effects of ELS on visceral perception in adulthood remain incompletely understood. (frontiersin.org)
  • Both hyperalgesia (lower pain threshold) and allodynia (pain perceived in non-sensory pathways) are involved in the development of visceral (gut) hypersensitivity. (helpforibs.com)
  • Ribeirão Preto, PAHO/WHO Collaborating Centre for Nursing in pressure pain threshold, with significant differences in Research Development, Ribeirão Preto, SP, Brazil. (bvsalud.org)
  • Attenuation of capsaicin-induced ongoing pain and secondary hyperalgesia during exposure to an immersive virtual reality environment. (mpg.de)
  • The focus of spatial attention during the induction of central sensitization can modulate the subsequent development of secondary hyperalgesia. (iasp-pain.org)
  • Both types demonstrate continuing pain, allodynia, or hyperalgesia that is usually disproportionate to the inciting event. (medscape.com)
  • We also demonstrate that Taxol-induced TRPV4-mediated hyperalgesia is essentially dependent on integrin/Src tyrosine kinase signaling. (jneurosci.org)
  • By tracking the development of primary and secondary hyperalgesia as well as allodynia in the sensory cortex, we demonstrate the usefulness of our new neural interface and its capability to differentially and simultaneously record neural signals in different cortical laminae in awake freely moving animals. (lu.se)
  • In paper V, sensory processing in primary somatosensory cortex during an episode of hyperalgesia was monitored using implanted neural interfaces in order to further evaluate the probe functionality and usefulness in neurophysiological research. (lu.se)
  • Surprisingly, in the COX-2-dependent zymosan-evoked hyperalgesia model, the nociceptive behavior was not reduced in mPGES-1-deficient mice despite a marked decrease of the spinal PGE2 synthesis. (uni-frankfurt.de)
  • This indicates that top-down attentional factors can modulate the development of central sensitization by peripheral nociceptive input, and that the focus of spatial attention, besides its modulatory effects on perception, can affect activity-dependent neuroplasticity. (iasp-pain.org)
  • In addition, Dr. Sullivan would like to disclose that he is consulting with Chrono Therapeutics concerning development and testing of an opioid taper device. (cdc.gov)
  • To address this challenge, a novel, polymer-based neural probe, with protrusions tailored to the target tissue, was developed to investigate which probe properties affect the development of a glial scar and neuronal cell death surrounding probes. (lu.se)
  • Development of a polymer based neural probe - How to record intracortical neural activity while minimizing the tissue response. (lu.se)
  • Attenuation of capsaicin-induced ongoing pain and secondary hyperalgesia by virtual reality stimulation is related to the activity within endogenous pain inhibitory pathways. (mpg.de)
  • Characterization of signaling pathways immediately downstream of nerve injury could thus help understand the molecular and cellular changes that are critical for its development and uncover new targets for the treatment of chronic pain. (elifesciences.org)
  • Current model based on over 50 years of expertise and continuous product development. (ugobasile.com)
  • In this study we examine the same model 100-120 days post injury by which time resolution of the hyperalgesia and peripheral nerve injury has occurred according to previous studies. (ox.ac.uk)
  • Identifying the development of hyperalgesia is of great clinical importance since patients receiving opioids to relieve pain may paradoxically experience more pain as a result of treatment. (wikipedia.org)
  • While participants performed a somatosensory detection task that required focusing attention towards one of the forearms, secondary hyperalgesia was induced at both forearms using bilateral and simultaneous high-frequency electrical stimulation (HFS) of the skin. (iasp-pain.org)
  • Most importantly, at T2, the HFS-induced increase in pinprick sensitivity as well as the area of secondary hyperalgesia was greater at the attended arm as compared to the non-attended arm. (iasp-pain.org)
  • These findings suggest A3AR-dependent adenosine signaling is compromised during sustained morphine to allow the development ofmorphine-induced adverse effects. (unime.it)
  • A 10mg/kg dose of WIN55,212-2 fully reversed carrageenan-evoked muscle hyperalgesia. (umn.edu)
  • In contrast, both antagonists blocked antihyperalgesic effects of WIN55,212-2 on carrageenan-evoked muscle hyperalgesia. (umn.edu)