The Experts below are selected from a list of 2823 Experts worldwide ranked by ideXlab platform
Juliana Geremias Chichorro - One of the best experts on this subject based on the ideXlab platform.
-
The opposing contribution of neurotrophin-3 and nerve growth factor to orofacial Heat Hyperalgesia in rats.
Behavioural pharmacology, 2020Co-Authors: Renata Cristiane Dos Reis, Carina Fernanda Mattedi Nones, Caroline Machado Kopruszinski, Débora Assunção Aguiar, Juliana Geremias ChichorroAbstract:It has been proposed that neurotrophin-3 acts in a manner that is opposed to nerve growth factor, especially in the modulation of Heat Hyperalgesia. Injury to the constriction of the infraorbital nerve (CION) is a well-established model of trigeminal neuropathic pain that leads to robust Heat, cold, and mechanical Hyperalgesia. Here, we assessed the effect of local neurotrophin-3 treatment on CION-induced Hyperalgesia, and we examined some mechanisms related to the effect of neurotrophin-3. Neurotrophin-3 (1 µg/50 µl) injected into the upper lip of CION rats caused a significant and long-lasting reduction of CION-induced Heat Hyperalgesia, but failed to affect cold and mechanical Hyperalgesia. Increased levels of neurotrophin-3 were detected in the injured nerve at the time point that represents the peak of Heat Hyperalgesia. The anti-hyperalgesic effect of neurotrophin-3 was markedly reduced in the presence of an antagonist of TrkA receptors (K-252a, 1 μg/50 μl). Moreover, association of lower doses of neurotrophin-3 with an antibody anti-nerve growth factor resulted in a synergistic anti-hyperalgesic effect in CION rats. Local injection of nerve growth factor (3 µg/50 µl) or the TRPV1 agonist capsaicin (1 μg/50 μl), but not neurotrophin-3 injection (1 µg/50 µl), resulted in long-lasting facial Heat Hyperalgesia, which was both significantly reduced by previous neurotrophin-3 local treatment. In conclusion, we suggest that neurotrophin-3 is a potent modulator of facial Heat Hyperalgesia, which may exert an inhibitory influence on the trkA pathway. Neurotrophin-3 treatment may represent a promising approach, especially in pain conditions associated with increased levels of nerve growth factor.
-
Comparison of antinociceptive effects of plain lidocaine versus lidocaine complexed with hydroxypropyl-β-cyclodextrin in animal models of acute and persistent orofacial pain.
Naunyn-Schmiedeberg's archives of pharmacology, 2019Co-Authors: Stéphani Batista De Oliveira, Erika Ivanna Araya, Luiz Eduardo Nunes Ferreira, Eder Gambeta, Michele Franz-montan, Rafaela Franco Claudino, Juliana Geremias ChichorroAbstract:Herein, it was investigated whether a complex of lidocaine with 2-hydroxypropyl-β-cyclodextrin (HP-β-CD) would present a better antinociceptive profile in vivo when compared with plain lidocaine in models of orofacial pain. Plain lidocaine (LDC) and complexed lidocaine (LDC:HP-β-CD) were initially evaluated in vitro to determine the release rate of the two formulations. Subsequently, the effect of both formulations was evaluated in independent groups of rats submitted to the orofacial formalin test, induction of facial Heat Hyperalgesia by capsaicin and carrageenan, and induction of facial Heat and mechanical Hyperalgesia by constriction of the infraorbital nerve. LDC:HP-β-CD led to a reduction in the lidocaine release assessed in the in vitro release assay compared to plain LDC. Both formulations presented an antinociceptive effect in all models, but LDC:HP-β-CD showed a better effect in the second phase of the formalin response, in carrageenan-induced Heat Hyperalgesia, and in the Heat Hyperalgesia associated to infraorbital nerve constriction. Our results show that complexation improved in vivo antinociceptive effects of LDC, but further studies are necessary to elucidate what properties contribute to the better effect of the complexed formulation on this models and/or what characteristics of the pain model facilitate the action of the complexed formulation.
-
Blockade of peripheral endothelin receptors abolishes Heat Hyperalgesia and spontaneous nociceptive behavior in a rat model of facial cancer
Archives of oral biology, 2018Co-Authors: Caroline Machado Kopruszinski, Renata Cristiane Dos Reis, Giles A Rae, Juliana Geremias ChichorroAbstract:Abstract Objective To improve understanding of the pathophysiology of cancer-induced facial nociception, by evaluating the contribution of peripheral endothelin receptors in tumor-induced facial Heat Hyperalgesia, increased spontaneous grooming, as well as ongoing nociception in a rat model of facial cancer. Design The study was conducted using 396 rats. Facial cancer was induced by inoculating a suspension of Walker-256 cells into the rats’ right vibrissal pad. Facial Heat Hyperalgesia and spontaneous grooming were assessed on day 6, while the conditioned place preference (CPP) test was performed on days 3–6 after tumor cells inoculation. Rats received local injections of the non-peptidic dual ETA/ETB endothelin receptors antagonist, bosentan (10 and 30 μg/50 μL), single or combined injections of peptidic ETA and ETB endothelin receptors antagonists (BQ-123 and BQ-788, at 20 ug/50 μL, each), or of lidocaine (1 mg/50 μl) and morphine (30 μg/50 μL). Results Bosentan, lidocaine and morphine local treatment all attenuated tumor-induced Heat Hyperalgesia (p 0.05). Whether this difference in effectiveness is due to receptor affinity or to pharmacokinetic factors still needs to be explored. Local injection of bosentan, lidocaine or morphine failed to control ongoing nociception, as evidenced by the absence of CPP in tumor-bearing rats (p > 0.05). Conclusion Endothelins, acting through peripheral ETA and ETB receptors, may play a significant role on the development of Heat Hyperalgesia and increased spontaneous grooming associated to facial cancer in rats.
-
Facial Hyperalgesia due to direct action of endothelin-1 in the trigeminal ganglion of mice.
Journal of Pharmacy and Pharmacology, 2018Co-Authors: Lenyta Oliveira Gomes, Erika Ivanna Araya, Juliana Geremias Chichorro, Jade De OliveiraAbstract:OBJECTIVE: This study assessed the ability of endothelin-1 (ET-1) to evoke Heat Hyperalgesia when injected directly into the trigeminal ganglia (TG) of mice and determined the receptors implicated in this effect. The effects of TG ETA and ETB receptor blockade on alleviation of Heat Hyperalgesia in a model of trigeminal neuropathic pain induced by infraorbital nerve constriction (CION) were also examined. METHODS: Naive mice received an intraganglionar (i.g.) injection of ET-1 (0.3-3 pmol) or the selective ETB R agonist sarafotoxin S6c (3-30 pmol), and response latencies to ipsilateral Heat stimulation were assessed before the treatment and at 1-h intervals up to 5 h after the treatment. Heat Hyperalgesia induced by i.g. ET-1 or CION was assessed after i.g. injections of ETA R and ETB R antagonists (BQ-123 and BQ-788, respectively, each at 0.5 nmol). KEY FINDINGS: Intraganglionar ET-1 or sarafotoxin S6c injection induced Heat Hyperalgesia lasting 4 and 2 h, respectively. Heat Hyperalgesia induced by ET-1 was attenuated by i.g. BQ-123 or BQ-788. On day 5 after CION, i.g. BQ-788 injection produced a more robust antihyperalgesic effect compared with BQ-123. CONCLUSIONS: ET-1 injection into the TG promotes ETA R/ETB R-mediated facial Heat Hyperalgesia, and both receptors are clearly implicated in CION-induced Hyperalgesia in the murine TG system.
-
Mechanisms involved in facial Heat Hyperalgesia induced by endothelin-1 in female rats
Archives of oral biology, 2017Co-Authors: Rafael Fernandes De Souza, Erika Ivanna Araya, Giles A Rae, Luana Lechenakoski De Oliveira, Carina Fernanda Mattedi Nones, Renata Cristiane Dos Reis, Caroline Machado Kopruszinski, Juliana Geremias ChichorroAbstract:Abstract Objective Pronociceptive responses to endothelins in the trigeminal system seem to be mediated by ETA and ETB receptors, which have been shown to be expressed in neurons of the trigeminal ganglion of humans and rats. The present study aimed to evaluate the ability of endothelin-1 (ET-1) to induce facial Heat Hyperalgesia in female rats, the contribution of ETA and ETB receptors to this response, as well as the mechanisms underlying Heat Hyperalgesia induced by ET-1. Design ET-1 (100 pmol/50 μL) was injected into the upper lip and Heat Hyperalgesia was evaluated for up to 6 h. Facial Heat Hyperalgesia induced by ET-1 was assessed in rats pre-treated locally with BQ-123 or BQ-788 (selective ETA and ETB receptor antagonists, respectively, 30 nmol/50 μL); BCTC (TRPV1 receptor antagonist; 300 μg/50 μL); anti-NGF (3 μg/50 μL); K252a (TrkA inhibitor, 1 μg/50 μL); or in rats that received intraganglionar resiniferatoxin injection (RTX, 200 ng/10 μL) to promote C-fibers ablation. Results ET-1 induced facial Heat Hyperalgesia that persisted up to 6 h and was prevented by BQ-123, BQ-788 or by intraganglionar RTX injection. Likewise, local pre-treatment with BCTC abolished ET-1 induced facial Heat Hyperalgesia up to 3 h. Local pre-treatment with anti-NGF or K252a was effective to prevent ET-1 induced Heat Hyperalgesia. Conclusions In conclusion, ET-1 is able to induce Heat hyperagelsia in trigeminal primary afferents of female rats, which is mediated by ETA and ETB receptors. Activation of TRPV1 receptors and NGF-signaling pathways may contribute to Heat Hyperalgesia induced by ET-1.
Kathleen A. Sluka - One of the best experts on this subject based on the ideXlab platform.
-
asic3 in muscle mediates mechanical but not Heat Hyperalgesia associated with muscle inflammation
Pain, 2007Co-Authors: Kathleen A. Sluka, Rajan Radhakrishnan, Christopher J Benson, Jayasheel O Eshcol, Margaret P Price, Kazimierz Babinski, Katherine M Audette, David C Yeomans, Steven P WilsonAbstract:Abstract Peripheral initiators of muscle pain are virtually unknown, but likely key to development of chronic pain after muscle insult. The current study tested the hypothesis that ASIC3 in muscle is necessary for development of cutaneous mechanical, but not Heat, Hyperalgesia induced by muscle inflammation. Using mechanical and Heat stimuli, we assessed behavioral responses in ASIC3−/− and ASIC3+/+ mice after induction of carrageenan muscle inflammation. ASIC3−/− mice did not develop cutaneous mechanical Hyperalgesia after muscle inflammation when compared to ASIC3+/+ mice; Heat Hyperalgesia developed similarly between groups. We then tested if the phenotype could be rescued in ASIC3−/− mice by using a recombinant herpes virus vector to express ASIC3 in skin (where testing occurred) or muscle (where inflammation occurred). Infection of mouse DRG neurons with ASIC3-encoding virus resulted in functional expression of ASICs. Injection of ASIC3-encoding virus into muscle or skin of ASIC3−/− mice resulted in ASIC3 mRNA in DRG and protein expression in DRG and the peripheral injection site. Injection of ASIC3-encoding virus into muscle, but not skin, resulted in development of mechanical Hyperalgesia similar to that observed in ASIC3+/+ mice. Thus, ASIC3 in primary afferent fibers innervating muscle is critical to development of Hyperalgesia that results from muscle insult.
-
Acetazolamide, a carbonic anhydrase inhibitor, reverses inflammation-induced thermal Hyperalgesia in rats.
The Journal of pharmacology and experimental therapeutics, 2005Co-Authors: Rajan Radhakrishnan, Kathleen A. SlukaAbstract:Inflammatory pain is linked to reduction in tissue pH. Tissue proton generation is mainly mediated by carbonic anhydrases (CAs). We therefore hypothesized that inhibition of CAs with acetazolamide (ACTZ) increases the tissue pH and reverses inflammation-induced pain. CAs are also present in the central nervous system and control anion concentrations. Furthermore, ACTZ has direct effects on ion channels involved in nociception. In the current study, responses to Heat and mechanical stimuli (von Frey filaments) of the paw were assessed before and after carrageenan-induced muscle inflammation and after treatment with ACTZ in rats. ACTZ was administered systemically, locally, or intrathecally 24 h after the induction of inflammation. In separate studies, pH was measured in the inflamed and noninflamed muscles and after administration of ACTZ. Carrageenan injection to the gastrocnemius muscle produced Heat Hyperalgesia and mechanical allodynia of the paw. Systemic ACTZ reversed the Heat Hyperalgesia but not mechanical allodynia. Similarly, injections of ACTZ into the inflamed muscle or intrathecally reversed the Heat Hyperalgesia but not mechanical allodynia. Surprisingly, the pH in the inflamed muscle was not reduced compared with noninflamed muscle. Thus, the current data do not support our hypothesis that ACTZ reduces inflammatory Hyperalgesia by raising the reduced pH in muscle. Although the possibility of pH changes and the role of CAs in the microenvironment cannot be ruled out, the mechanism of ACTZ-induced antiHyperalgesia is not clear from this study. It is possible that the inhibition of ion channels and/or the inhibition of spinally located CAs contribute to the observed antiHyperalgesia.
-
BLOCKADE OF N- AND P/Q-TYPE CALCIUM CHANNELS REDUCES THE SECONDARY Heat Hyperalgesia INDUCED BY ACUTE INFLAMMATION
The Journal of pharmacology and experimental therapeutics, 1998Co-Authors: Kathleen A. SlukaAbstract:High voltage calcium channels are implicated in nociceptive transmission after nerve injury, capsaicin or formalin injection. The purpose of this study was to investigate the role of calcium channels in secondary Heat Hyperalgesia associated with acute joint inflammation. After induction of acute inflammation (knee joint injection of kaolin and carrageenan), decreased paw withdrawal latency (PWL) to radiant Heat ( i . e . , secondary Heat Hyperalgesia), increased guarding of the limb and increased joint circumference occurs. Spinal administration (through a microdialysis fiber placed in dorsal horn) of an N-type calcium channel blocker (MVIIA, SNX 111, ziconotide, 0.001–0.1 mM), before induction of inflammation, prevents the decrease in PWL. Treatment with SNX 111 4 hr after inflammation reverses Heat Hyperalgesia. A small reduction in spontaneous pain-related behaviors (guarding of the limb) occurs after pre- or post-treatment with SNX 111. Spinal blockade of P/Q-type calcium channels (with ω-agatoxin IVA) had no effect on the decrease in PWL to radiant Heat when administered after induction of inflammation. However, pre-treatment with ω-agatoxin IVA prevents secondary Heat Hyperalgesia. ω-Agatoxin IVA has no effect on spontaneous pain-related behaviors whether administered before or after induction of inflammation. In contrast, pre or post-treatment with nifedipine (L-type calcium channel blocker, 0.01–1.0 mM), had no effect on Heat Hyperalgesia or spontaneous pain-related behaviors induced by acute inflammation. There were no differences in joint circumference between groups with any treatment. Thus, N-type calcium channels contribute to both the development and maintenance of secondary Heat Hyperalgesia while P-type calcium channels are only involved during development of Hyperalgesia.
-
Differential roles of neurokinin 1 and neurokinin 2 receptors in the development and maintenance of Heat Hyperalgesia induced by acute inflammation
British Journal of Pharmacology, 1997Co-Authors: Kathleen A. Sluka, M. A. Milton, William D. Willis, Karin N. WestlundAbstract:1. Following induction of acute inflammation by intraarticular injection of kaolin and carrageenan into the knee joint in rats, there was a significant decrease in the withdrawal latency to radiant Heat applied to the paw (i.e. Heat Hyperalgesia), an increased joint circumference and increased joint temperature. 2. A neurokinin1 (NK1) receptor antagonist (CP-99,994, 10 mM) had no effect on the paw withdrawal latency when it was administered spinally through a microdialysis fibre before the induction of inflammation. Pretreatment with a NK2 receptor antagonist (SR48968, 1 mM) administered spinally through the microdialysis fibre prevented the Heat Hyperalgesia from developing in the early stages of the inflammation. 3. Post-treatment through the microdialysis fibre with the NK1 receptor antagonist (0.01-10 mM) was effective in reversing the Heat Hyperalgesia. In contrast, post-treatment spinally with the NK2 receptor antagonist (0.01-1 mM) had no effect on the Heat Hyperalgesia. The inactive stereoisomers of the NK1 receptor antagonist, CP100,263, or the NK2 receptor antagonist, SR48965, administered at the same doses, had no effect on the joint inflammation or the Heat Hyperalgesia. 4. Pretreatment systemically with the NK1 receptor antagonist (30 mg kg-1) had no effect on the Heat Hyperalgesia or pain-related behaviour ratings where 0 is none and 5 is non weight bearing and complete avoidance of limb contact. Pretreatment with a NK2 receptor antagonist (10 mg kg-1) systemically prevented the Heat Hyperalgesia and pain-related behaviour ratings from developing in the early stages of the inflammation. The inactive stereoisomers of NK1 receptor antagonist, CP100,263, or the NK2 receptor antagonist, SR48965, administered at the same doses, had no effect on the joint inflammation or the Heat Hyperalgesia. 5. Post-treatment systemically with either the NK1 (0.1-30 mg kg-1) or the NK2 (0.1-10 mg kg-1) receptor antagonist resulted in a dose-dependent reversal of the Heat Hyperalgesia. Pain-related behaviour ratings were reduced by post-treatment only with the NK1 receptor antagonist. The inactive stereoisomers of the NK1 receptor antagonist, CP100,263, or the NK2 receptor antagonist, SR48965, administered at the same doses, had no effect on the behavioural responses. 6. Direct pretreatment of the knee joint with either the NK1 (30 mg) or the NK2 (10 mg) receptor antagonist prevented the Heat Hyperalgesia from developing without affecting joint swelling. The inactive stereoisomers of the NK1 receptor antagonist, CP100,263, or the NK2 receptor antagonist, SR48965, administered at the same doses, had no effect on the joint inflammation or the Heat Hyperalgesia. 7. There appears to be a differential role for the spinal tachykinin receptors in the development and maintenance of the Heat Hyperalgesia associated with acute joint inflammation. The NK2 receptors appear to be activated early in the development of the Heat Hyperalgesia and NK1 receptors are involved in the maintenance of the Heat Hyperalgesia. 8. Peripherally, both NK1 and NK2 receptors are involved in the development of Heat Hyperalgesia and pain-related behaviour ratings induced by acute inflammation.
-
Joint inflammation and Hyperalgesia are reduced by spinal bicuculline.
Neuroreport, 1993Co-Authors: Kathleen A. Sluka, W. D. Willis, Karin N. WestlundAbstract:Knee joint injection of kaolin and carrageenan produces acute inflammation with localized joint swelling and increased temperature. This inflammation results in behavioral changes, including limping and guarding of the limb, and Heat Hyperalgesia. Prior spinal cord infusion of bicuculline, a gamma amino butyric acidA (GABAA) receptor antagonist, significantly reduces the severity of joint inflammation and prevents the development of Heat Hyperalgesia. In contrast, infusion of a GABAB receptor antagonist does not alter the arthritis. Therefore, these data support the existence of a central pathway involving GABAA receptors in the spinal cord that influences the development of peripheral inflammation. We suggest that primary afferent depolarization and accompanying dorsal root reflexes play a significant role in the development of peripheral inflammation.
Marcel Chauvin - One of the best experts on this subject based on the ideXlab platform.
-
the evolution of primary Hyperalgesia in orthopedic surgery quantitative sensory testing and clinical evaluation before and after total knee arthroplasty
Anesthesia & Analgesia, 2007Co-Authors: Valeria Martinez, Dominique Fletcher, Didier Bouhassira, Daniel I Sessler, Marcel ChauvinAbstract:BACKGROUND: Quantitative sensory testing (QST) allows precise characterization of sensory deficits and painful symptoms and may offer additional information on the pathophysiology of postoperative pain. METHODS: We evaluated 20 patients scheduled for total knee arthroplasty clinically and with QST before surgery, at 1 and 4 days after surgery, and at 1 and 4 mo after surgery. The clinical evaluation included preoperative pain and inflammation of the operative knee, postoperative assessment of pain at rest and during movement (Visual Analog Scale score), cumulative morphine consumption, and circumference and temperature of both knees. QST included thermal and mechanical (pressure) pain threshold measurements and assessment of responses to suprathreshold stimuli. Brush-evoked allodynia was also evaluated. Measurements were taken on the operative knee, contralateral knee, and on the hand as a control site. RESULTS: All patients had prolonged and severe pain before surgery and inflammation of the operative knee. Preoperative QST provided evidence of Heat Hyperalgesia in the inflammatory area on the operative knee, but absence of punctate or brush-evoked allodynia in the adjacent noninflamed area. Patients had intense postoperative pain, mostly induced by movement. Primary Heat Hyperalgesia was present on the operative knee on the first and fourth day after surgery, and was associated with punctate mechanical allodynia in the inflammatory area, but not in the adjacent noninflamed area. Postoperative morphine consumption was correlated with preoperative Heat Hyperalgesia (r = 0.63; P = 0.01). QST returned to baseline at the 4-mo evaluation. Only four patients had moderate knee pain induced by movement at that time. CONCLUSION: Heat Hyperalgesia was the predominant QST symptom associated with perioperative pain after total knee arthroplasty, and was predictive of postoperative morphine consumption.
-
The evolution of primary Hyperalgesia in orthopedic surgery: quantitative sensory testing and clinical evaluation before and after total knee arthroplasty.
Anesthesia and Analgesia, 2007Co-Authors: Valeria Martinez, Dominique Fletcher, Didier Bouhassira, Daniel Sessler, Marcel ChauvinAbstract:BACKGROUND: Quantitative sensory testing (QST) allows precise characterization of sensory deficits and painful symptoms and may offer additional information on the pathophysiology of postoperative pain. METHODS: We evaluated 20 patients scheduled for total knee arthroplasty clinically and with QST before surgery, at 1 and 4 days after surgery, and at 1 and 4 mo after surgery. The clinical evaluation included preoperative pain and inflammation of the operative knee, postoperative assessment of pain at rest and during movement (Visual Analog Scale score), cumulative morphine consumption, and circumference and temperature of both knees. QST included thermal and mechanical (pressure) pain threshold measurements and assessment of responses to suprathreshold stimuli. Brush-evoked allodynia was also evaluated. Measurements were taken on the operative knee, contralateral knee, and on the hand as a control site. RESULTS: All patients had prolonged and severe pain before surgery and inflammation of the operative knee. Preoperative QST provided evidence of Heat Hyperalgesia in the inflammatory area on the operative knee, but absence of punctate or brush-evoked allodynia in the adjacent noninflamed area. Patients had intense postoperative pain, mostly induced by movement. Primary Heat Hyperalgesia was present on the operative knee on the first and fourth day after surgery, and was associated with punctate mechanical allodynia in the inflammatory area, but not in the adjacent noninflamed area. Postoperative morphine consumption was correlated with preoperative Heat Hyperalgesia (r = 0.63; P = 0.01). QST returned to baseline at the 4-mo evaluation. Only four patients had moderate knee pain induced by movement at that time. CONCLUSION: Heat Hyperalgesia was the predominant QST symptom associated with perioperative pain after total knee arthroplasty, and was predictive of postoperative morphine consumption.
David Andrew - One of the best experts on this subject based on the ideXlab platform.
-
Sensitization of lamina I spinoparabrachial neurons parallels Heat Hyperalgesia in the chronic constriction injury model of neuropathic pain
The Journal of Physiology, 2009Co-Authors: David AndrewAbstract:It has been proposed that spinal lamina I neurons with ascending axons that project to the midbrain play a crucial role in Hyperalgesia. To test this hypothesis the quantitative properties of lamina I spinoparabrachial neurons in the chronic constriction injury (CCI) model of neuropathic pain were compared to those of unoperated and sham-operated controls. Behavioural testing showed that animals with a CCI exhibited Heat Hyperalgesia within 4 days of the injury, and this Hyperalgesia persisted throughout the 14-day post-operative testing period. In the CCI, nociceptive lamina I spinoparabrachial neurons had Heat thresholds that were significantly lower than controls (43.0 ± 2.8°C vs. 46.7 ± 2.6°C; P < 10−4, ANOVA). Nociceptive lamina I spinoparabrachial neurons were also significantly more responsive to graded Heat stimuli in the CCI, compared to controls (P < 0.02, 2-factor repeated-measures ANOVA), and increased after-discharges were also observed. Furthermore, the Heat-evoked stimulus–response functions of lamina I spinoparabrachial neurons in CCI animals co-varied significantly (P < 0.03, ANCOVA) with the amplitude of Heat Hyperalgesia determined behaviourally. Taken together these results are consistent with the hypothesis that lamina I spinoparabrachial neurons have an important mechanistic role in the pathophysiology of neuropathic pain.
-
Sensitization of lamina I spinoparabrachial neurons parallels Heat Hyperalgesia in the chronic constriction injury model of neuropathic pain.
The Journal of physiology, 2009Co-Authors: David AndrewAbstract:It has been proposed that spinal lamina I neurons with ascending axons that project to the midbrain play a crucial role in Hyperalgesia. To test this hypothesis the quantitative properties of lamina I spinoparabrachial neurons in the chronic constriction injury (CCI) model of neuropathic pain were compared to those of unoperated and sham-operated controls. Behavioural testing showed that animals with a CCI exhibited Heat Hyperalgesia within 4 days of the injury, and this Hyperalgesia persisted throughout the 14-day post-operative testing period. In the CCI, nociceptive lamina I spinoparabrachial neurons had Heat thresholds that were significantly lower than controls (43.0 +/- 2.8 degrees C vs. 46.7 +/- 2.6 degrees C; P < 10(-4), ANOVA). Nociceptive lamina I spinoparabrachial neurons were also significantly more responsive to graded Heat stimuli in the CCI, compared to controls (P < 0.02, 2-factor repeated-measures ANOVA), and increased after-discharges were also observed. Furthermore, the Heat-evoked stimulus-response functions of lamina I spinoparabrachial neurons in CCI animals co-varied significantly (P < 0.03, ANCOVA) with the amplitude of Heat Hyperalgesia determined behaviourally. Taken together these results are consistent with the hypothesis that lamina I spinoparabrachial neurons have an important mechanistic role in the pathophysiology of neuropathic pain.
Valeria Martinez - One of the best experts on this subject based on the ideXlab platform.
-
the evolution of primary Hyperalgesia in orthopedic surgery quantitative sensory testing and clinical evaluation before and after total knee arthroplasty
Anesthesia & Analgesia, 2007Co-Authors: Valeria Martinez, Dominique Fletcher, Didier Bouhassira, Daniel I Sessler, Marcel ChauvinAbstract:BACKGROUND: Quantitative sensory testing (QST) allows precise characterization of sensory deficits and painful symptoms and may offer additional information on the pathophysiology of postoperative pain. METHODS: We evaluated 20 patients scheduled for total knee arthroplasty clinically and with QST before surgery, at 1 and 4 days after surgery, and at 1 and 4 mo after surgery. The clinical evaluation included preoperative pain and inflammation of the operative knee, postoperative assessment of pain at rest and during movement (Visual Analog Scale score), cumulative morphine consumption, and circumference and temperature of both knees. QST included thermal and mechanical (pressure) pain threshold measurements and assessment of responses to suprathreshold stimuli. Brush-evoked allodynia was also evaluated. Measurements were taken on the operative knee, contralateral knee, and on the hand as a control site. RESULTS: All patients had prolonged and severe pain before surgery and inflammation of the operative knee. Preoperative QST provided evidence of Heat Hyperalgesia in the inflammatory area on the operative knee, but absence of punctate or brush-evoked allodynia in the adjacent noninflamed area. Patients had intense postoperative pain, mostly induced by movement. Primary Heat Hyperalgesia was present on the operative knee on the first and fourth day after surgery, and was associated with punctate mechanical allodynia in the inflammatory area, but not in the adjacent noninflamed area. Postoperative morphine consumption was correlated with preoperative Heat Hyperalgesia (r = 0.63; P = 0.01). QST returned to baseline at the 4-mo evaluation. Only four patients had moderate knee pain induced by movement at that time. CONCLUSION: Heat Hyperalgesia was the predominant QST symptom associated with perioperative pain after total knee arthroplasty, and was predictive of postoperative morphine consumption.
-
The evolution of primary Hyperalgesia in orthopedic surgery: quantitative sensory testing and clinical evaluation before and after total knee arthroplasty.
Anesthesia and Analgesia, 2007Co-Authors: Valeria Martinez, Dominique Fletcher, Didier Bouhassira, Daniel Sessler, Marcel ChauvinAbstract:BACKGROUND: Quantitative sensory testing (QST) allows precise characterization of sensory deficits and painful symptoms and may offer additional information on the pathophysiology of postoperative pain. METHODS: We evaluated 20 patients scheduled for total knee arthroplasty clinically and with QST before surgery, at 1 and 4 days after surgery, and at 1 and 4 mo after surgery. The clinical evaluation included preoperative pain and inflammation of the operative knee, postoperative assessment of pain at rest and during movement (Visual Analog Scale score), cumulative morphine consumption, and circumference and temperature of both knees. QST included thermal and mechanical (pressure) pain threshold measurements and assessment of responses to suprathreshold stimuli. Brush-evoked allodynia was also evaluated. Measurements were taken on the operative knee, contralateral knee, and on the hand as a control site. RESULTS: All patients had prolonged and severe pain before surgery and inflammation of the operative knee. Preoperative QST provided evidence of Heat Hyperalgesia in the inflammatory area on the operative knee, but absence of punctate or brush-evoked allodynia in the adjacent noninflamed area. Patients had intense postoperative pain, mostly induced by movement. Primary Heat Hyperalgesia was present on the operative knee on the first and fourth day after surgery, and was associated with punctate mechanical allodynia in the inflammatory area, but not in the adjacent noninflamed area. Postoperative morphine consumption was correlated with preoperative Heat Hyperalgesia (r = 0.63; P = 0.01). QST returned to baseline at the 4-mo evaluation. Only four patients had moderate knee pain induced by movement at that time. CONCLUSION: Heat Hyperalgesia was the predominant QST symptom associated with perioperative pain after total knee arthroplasty, and was predictive of postoperative morphine consumption.
