The Experts below are selected from a list of 1719 Experts worldwide ranked by ideXlab platform
Luana Colloca - One of the best experts on this subject based on the ideXlab platform.
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Placebo Hypoalgesia: racial differences.
Pain, 2020Co-Authors: Chika Okusogu, Susan G. Dorsey, Yang Wang, Titilola Akintola, Nathaniel R Haycock, Nandini Raghuraman, Joel D. Greenspan, Jane Phillips, Claudia M. Campbell, Luana CollocaAbstract:No large-cohort studies that examine potential racial effects on placebo hypoalgesic effects exist. To fill this void, we studied placebo effects in healthy and chronic pain participants self-identified as either African American/black (AA/black) or white. We enrolled 372 study participants, 186 with a diagnosis of temporomandibular disorder (TMD) and 186 race-, sex-, and age-matched healthy participants to participate in a placebo experiment. Using a well-established paradigm of classical conditioning with verbal suggestions, each individual pain sensitivity was measured to calibrate the temperatures for high- and low-pain stimuli in the conditioning protocol. These 2 temperatures were then paired with a red and green screen, respectively, and participants were told that the analgesic intervention would activate during the green screens to reduce pain. Participants then rated the painfulness of each stimulus on a visual analog scale ranging from 0 to 100. Racial influences were tested on conditioning strength, reinforced expectations, and placebo Hypoalgesia. We found that white participants reported greater conditioning effects, reinforced relief expectations, and placebo effects when compared with their AA/black counterparts. Racial effects on placebo were observed in TMD, although negligible, short-lasting, and mediated by conditioning strength. Secondary analyses on the effect of experimenter-participant race and sex concordance indicated that same experimenter-participant race induced greater placebo Hypoalgesia in TMDs while different sex induced greater placebo Hypoalgesia in healthy participants. This is the first and largest study to analyze racial effects on placebo Hypoalgesia and has implications for both clinical research and treatment outcomes.
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Neural and behavioral changes driven by observationally-induced Hypoalgesia.
Scientific reports, 2019Co-Authors: Nandini Raghuraman, Yang Wang, Lieven A. Schenk, Andrew J. Furman, Christina Tricou, David A. Seminowicz, Luana CollocaAbstract:Observing successful pain treatment in others can induce anticipatory neural processes that, in turn, relieve pain. Previous studies have suggested that social learning and observation influence placebo Hypoalgesia. Here, we used electroencephalography (EEG) to determine the neurophysiological changes associated with pain relief acquired through the observation. Thirty-one participants observed a demonstrator undergo painful heat stimulations paired with a "control" cream and non-painful ones paired with a "treatment" cream, which actually were both Vanicreams. After their observation, the participants then received the same creams and stimulations. We found that the treatment cream led to lower self-reported pain intensity ratings than the control cream. Anticipatory treatment cues elicited smaller P2 in electrodes F1, Fz, FC1, and FCz than the control condition. The P2 component localization indicated a higher current density in the right middle frontal gyrus, a region associated with attentional engagement. In placebo responders, the sensorimotor cortex activity captured in electrodes C3, Cz, and C4 indicated that Hypoalgesia was positively correlated with resting state peak alpha frequency (PAF). These results suggest that observationally-induced placebo Hypoalgesia may be driven by anticipatory mechanisms that modulate frontal attentional processes. Furthermore, resting state PAF could serve as a predictor of observationally-induced Hypoalgesia.
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oprm1 rs1799971 comt rs4680 and faah rs324420 genes interact with placebo procedures to induce Hypoalgesia
Pain, 2019Co-Authors: Luana Colloca, Pedro E Martinez, Yen Pei C Chang, Kathleen A. Ryan, Colin A Hodgkinson, David Goldman, Susan G. DorseyAbstract:AbstractGenetics studies on the placebo hypoalgesic effect highlight a promising link between single nucleotide polymorphisms (SNPs) in the dopamine, opioid, and endocannabinoid genes and placebo Hypoalgesia. However, epistasis and replication studies are missing. In this study, we expanded on previ
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oprm1 rs1799971 comt rs4680 and faah rs324420 genes interact with placebo procedures to induce Hypoalgesia
Pain, 2019Co-Authors: Luana Colloca, Pedro E Martinez, Yen Pei C Chang, Kathleen A. Ryan, Colin A Hodgkinson, David Goldman, Yang Wang, Susan G. DorseyAbstract:Genetics studies on the placebo hypoalgesic effect highlight a promising link between single nucleotide polymorphisms (SNPs) in the dopamine, opioid, and endocannabinoid genes and placebo Hypoalgesia. However, epistasis and replication studies are missing. In this study, we expanded on previous findings related to the 3 SNPs in the opioid receptor mu subunit (OPRM1 rs1799971), catechol-O-methyltransferase (COMT rs4680), and fatty acid amide hydrolase (FAAH rs324420) genes associated with placebo Hypoalgesia and tested the effect of a 3-way interaction on placebo Hypoalgesia. Using 2 well-established placebo procedures (verbal suggestion and learning paradigm), we induced significant placebo hypoalgesic effects in 160 healthy participants. We found that individuals with OPRM1 AA combined with FAAH Pro/Pro and those carrying COMT met/met together with FAAH Pro/Pro showed significant placebo effects. Participants with COMT met/val alleles showed significant placebo effects independently of OPRM1 and FAAH allele combinations. Finally, the model that included the placebo procedure and genotypes predicted placebo responsiveness with a higher accuracy (area under the curve, AUC = 0.773) as compared to the SNPs alone indicating that genetic variants can only partially explain the placebo responder status. Our results suggest that the endogenous mu-opioid system with a larger activation in response to pain in the met/val allele carriers as well as the synergism between endogenous mu-opioid system and cannabinoids might play the most relevant role in driving hypoalgesic responses. Future epistasis studies with larger sample sizes will help us to fully understand the complexity of placebo effects and explain the mechanisms that underlie placebo responsiveness.
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The interplay of exercise, placebo and nocebo effects on experimental pain
Nature Publishing Group, 2018Co-Authors: Luana Colloca, Nicole Corsi, Mirta FiorioAbstract:Abstract Over the last few decades, placebo, and nocebo effects in general, have been investigated at rest. This proposed study explores whether they could work even when the experience of pain occurs during a movement. Exercise itself can have a hypoalgesic effect, suggesting that placebo- and exercise-induced Hypoalgesia could foster pain reduction. In the present study, we investigated the interplay of exercise, placebo and nocebo effects on pain. To this aim, we developed a machine-controlled isotonic motor task to standardize the exercise across participants and used a well-validated model of placebo and nocebo manipulations with reinforced expectations via a conditioning procedure including visual cues paired with heat painful stimulations. Participants reported expectations and pain on a trial-by-trial basis. We found that the standardized isotonic exercise elicited a reduction of pain intensity. Moreover, both exercise and placebo induced comparable hypoalgesic effects. When the exercise was added, placebo and nocebo effects were influenced by expectations but were not affected by fatigue or sex differences. Exercise-, placebo- and nocebo-induced pain modulation are likely to work through distinct mechanisms and neurophysiological research is needed to fully exploit the implications for sport, rehabilitation and pain management
Stephen D. Patterson - One of the best experts on this subject based on the ideXlab platform.
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the effect of blood flow restriction exercise on exercise induced Hypoalgesia and endogenous opioid and endocannabinoid mechanisms of pain modulation
Journal of Applied Physiology, 2020Co-Authors: Luke Hughes, Stephen D. PattersonAbstract:This study aimed to investigate and compare the magnitude of exercise-induced Hypoalgesia (EIH) with low-intensity blood flow restriction (BFR) resistance exercise (RE) at varying pressures to other intensities of resistance exercise and examine endogenous mechanisms of pain reduction. Twelve individuals performed four experimental trials involving unilateral leg press exercise in a randomized crossover design: low-load RE at 30% of one repetition maximum (1RM), high-load RE (70% 1RM), and BFR-RE (30% 1RM) at a low and high pressure. BFR pressure was prescribed relative to limb occlusion pressure at 40% and 80% for the low- and high-pressure trials. Pressure pain thresholds (PPT) were assessed before and 5 min and 24 h following exercise in exercising and nonexercising muscles. Venous blood samples were collected at the same timepoints to determine plasma concentrations of beta-endorphin and 2-arachidonoylglycerol. High-pressure BFR-RE increased PPTs in the exercising limb to a greater extent than all other trials. Comparable systemic EIH effects were observed with HLRE and both BFR-RE trials. PPTs in the exercising limb remained elevated above baseline at 24 h postexercise following both BFR-RE trials. Postexercise plasma beta-endorphin concentration was elevated during the BFR-RE trials. No changes to 2-arachidonoylglycerol concentration were observed. High pressure BFR-RE causes a greater EIH response in the exercising limb that persists for up to 24 h following exercise. The reduction in pain sensitivity with BFR-RE is partly driven by endogenous opioid production of beta-endorphin. BFR-RE should be investigated as a possible pain-modulation tool in individuals with acute and chronic pain.NEW & NOTEWORTHY High-pressure blood flow restriction (BFR) causes a greater Hypoalgesia response in the exercising limb (48%) compared with light and heavy load resistance exercise (10-34%). Performing light load resistance exercise with BFR causes systemic Hypoalgesia comparable with heavy load resistance exercise (10-18%). BFR resistance exercise prolonged the exercise-induced Hypoalgesia response for 24 h in the exercising limb (15% and 24%, respectively). Activation of endogenous opioid production and a conditioned pain modulation effect partly mediate the relationship between exercise and Hypoalgesia.
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Low intensity blood flow restriction exercise: Rationale for a Hypoalgesia effect
Medical hypotheses, 2019Co-Authors: Luke Hughes, Stephen D. PattersonAbstract:Exercise-induced Hypoalgesia is characterised by a reduction in pain sensitivity following exercise. Recently, low intensity exercise performed with blood flow restriction has been shown to induce Hypoalgesia. The purpose of this manuscript is to discuss the mechanisms of exercise-induced Hypoalgesia and provide rationale as to why low intensity exercise performed with blood flow restriction may induce Hypoalgesia. Research into exercise-induced Hypoalgesia has identified several potential mechanisms, including opioid and endocannabinoid-mediated pain inhibition, conditioned pain modulation, recruitment of high threshold motor units, exercise-induced metabolite production and an interaction between cardiovascular and pain regulatory systems. We hypothesise that several mechanisms consistent with prolonged high intensity exercise may drive the Hypoalgesia effect observed with blood flow restriction exercise. These are likely triggered by the high level of intramuscular stress in the exercising muscle generated by blood flow restriction including hypoxia, accumulation of metabolites, accelerated fatigue onset and ischemic pain. Therefore, blood flow restriction exercise may induce Hypoalgesia through similar mechanisms to prolonged higher intensity exercise, but at lower intensities, by changing local tissue physiology, highlighting the importance of the blood flow restriction stimulus. The potential to use blood flow restriction exercise as a pain modulation tool has important implications following acute injury and surgery, and for several load compromised populations with chronic pain.
Susan G. Dorsey - One of the best experts on this subject based on the ideXlab platform.
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Placebo Hypoalgesia: racial differences.
Pain, 2020Co-Authors: Chika Okusogu, Susan G. Dorsey, Yang Wang, Titilola Akintola, Nathaniel R Haycock, Nandini Raghuraman, Joel D. Greenspan, Jane Phillips, Claudia M. Campbell, Luana CollocaAbstract:No large-cohort studies that examine potential racial effects on placebo hypoalgesic effects exist. To fill this void, we studied placebo effects in healthy and chronic pain participants self-identified as either African American/black (AA/black) or white. We enrolled 372 study participants, 186 with a diagnosis of temporomandibular disorder (TMD) and 186 race-, sex-, and age-matched healthy participants to participate in a placebo experiment. Using a well-established paradigm of classical conditioning with verbal suggestions, each individual pain sensitivity was measured to calibrate the temperatures for high- and low-pain stimuli in the conditioning protocol. These 2 temperatures were then paired with a red and green screen, respectively, and participants were told that the analgesic intervention would activate during the green screens to reduce pain. Participants then rated the painfulness of each stimulus on a visual analog scale ranging from 0 to 100. Racial influences were tested on conditioning strength, reinforced expectations, and placebo Hypoalgesia. We found that white participants reported greater conditioning effects, reinforced relief expectations, and placebo effects when compared with their AA/black counterparts. Racial effects on placebo were observed in TMD, although negligible, short-lasting, and mediated by conditioning strength. Secondary analyses on the effect of experimenter-participant race and sex concordance indicated that same experimenter-participant race induced greater placebo Hypoalgesia in TMDs while different sex induced greater placebo Hypoalgesia in healthy participants. This is the first and largest study to analyze racial effects on placebo Hypoalgesia and has implications for both clinical research and treatment outcomes.
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oprm1 rs1799971 comt rs4680 and faah rs324420 genes interact with placebo procedures to induce Hypoalgesia
Pain, 2019Co-Authors: Luana Colloca, Pedro E Martinez, Yen Pei C Chang, Kathleen A. Ryan, Colin A Hodgkinson, David Goldman, Susan G. DorseyAbstract:AbstractGenetics studies on the placebo hypoalgesic effect highlight a promising link between single nucleotide polymorphisms (SNPs) in the dopamine, opioid, and endocannabinoid genes and placebo Hypoalgesia. However, epistasis and replication studies are missing. In this study, we expanded on previ
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oprm1 rs1799971 comt rs4680 and faah rs324420 genes interact with placebo procedures to induce Hypoalgesia
Pain, 2019Co-Authors: Luana Colloca, Pedro E Martinez, Yen Pei C Chang, Kathleen A. Ryan, Colin A Hodgkinson, David Goldman, Yang Wang, Susan G. DorseyAbstract:Genetics studies on the placebo hypoalgesic effect highlight a promising link between single nucleotide polymorphisms (SNPs) in the dopamine, opioid, and endocannabinoid genes and placebo Hypoalgesia. However, epistasis and replication studies are missing. In this study, we expanded on previous findings related to the 3 SNPs in the opioid receptor mu subunit (OPRM1 rs1799971), catechol-O-methyltransferase (COMT rs4680), and fatty acid amide hydrolase (FAAH rs324420) genes associated with placebo Hypoalgesia and tested the effect of a 3-way interaction on placebo Hypoalgesia. Using 2 well-established placebo procedures (verbal suggestion and learning paradigm), we induced significant placebo hypoalgesic effects in 160 healthy participants. We found that individuals with OPRM1 AA combined with FAAH Pro/Pro and those carrying COMT met/met together with FAAH Pro/Pro showed significant placebo effects. Participants with COMT met/val alleles showed significant placebo effects independently of OPRM1 and FAAH allele combinations. Finally, the model that included the placebo procedure and genotypes predicted placebo responsiveness with a higher accuracy (area under the curve, AUC = 0.773) as compared to the SNPs alone indicating that genetic variants can only partially explain the placebo responder status. Our results suggest that the endogenous mu-opioid system with a larger activation in response to pain in the met/val allele carriers as well as the synergism between endogenous mu-opioid system and cannabinoids might play the most relevant role in driving hypoalgesic responses. Future epistasis studies with larger sample sizes will help us to fully understand the complexity of placebo effects and explain the mechanisms that underlie placebo responsiveness.
Mark I. Johnson - One of the best experts on this subject based on the ideXlab platform.
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Hypoalgesia in response to transcutaneous electrical nerve stimulation tens depends on stimulation intensity
The Journal of Pain, 2011Co-Authors: Fidelma Moran, Tracey Leonard, Stephanie Hawthorne, Ciara Hughes, Evie Mccrumgardner, Mark I. JohnsonAbstract:Abstract Transcutaneous electrical nerve stimulation (TENS) is an electrophysical modality used for pain management. This study investigated the dose response of different TENS intensities on experimentally induced pressure pain. One hundred and thirty TENS naive healthy individuals (18–64 years old; 65 males, 65 females) were randomly allocated to 5 groups (n = 26 per group): Strong Non Painful TENS; Sensory Threshold TENS; Below Sensory Threshold TENS; No Current Placebo TENS; and Transient Placebo TENS. Active TENS (80 Hz) was applied to the forearm for 30 minutes. Transient Placebo TENS was applied for 42 seconds after which the current amplitude automatically reset to 0 mA. Pressure pain thresholds (PPT) were recorded from 2 points on the hand and forearm before and after TENS to measure Hypoalgesia. There were significant differences between groups at both the hand and forearm (ANOVA; P = .005 and .002). At 30 minutes, there was a significant hypoalgesic effect in the Strong Non Painful TENS group compared to: Below Sensory Threshold TENS, No Current Placebo TENS and Transient Placebo TENS groups ( P P = .001). There was no significant difference between Strong Non Painful TENS and Sensory Threshold TENS groups. The area under the curve for the changes in PPT significantly correlated with the current amplitude (r 2 = .33, P = .003). These data therefore show that there is a dose-response effect of TENS with the largest effect occurring with the highest current amplitudes. Perspective This study shows a dose response for the intensity of TENS for pain relief with the strongest intensities showing the greatest effect; thus, we suggest that TENS intensity should be titrated to achieve the strongest possible intensity to achieve maximum pain relief.
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does the pulse frequency of transcutaneous electrical nerve stimulation tens influence Hypoalgesia a systematic review of studies using experimental pain and healthy human participants
Physiotherapy, 2008Co-Authors: Chihchung Chen, Ghazala Tabasam, Mark I. JohnsonAbstract:Abstract Objectives To determine the hypoalgesic effect of pulse frequency of transcutaneous electrical nerve stimulation (TENS) when all other TENS parameters are held constant. Data sources Systematic review of studies using experimentally induced pain on healthy participants where there was a head-to-head comparison of different pulse frequencies. AMED, CINAHL, EMBASE, Inspec, PEDro, Pre-CINAHL, PsycARTICLES, PubMed, SPORTDiscus were searched in September 2006. Review methods Inclusion criteria were studies that directly compared two or more pulse frequencies head-to-head and recorded outcome as change in pain threshold or pain intensity. Studies were excluded if pulse intensity, pulse pattern, or pulse duration of TENS were not standardized between groups. Two reviewers judged the trial outcome independently. Primary outcome was a report of a statistically significant difference between pulse frequencies for pain threshold or intensity at any time point through the experiment. Results Twenty studies were identified, of which 13 experimental studies from 12 published reports were included for review. Ten studies found no statistically significant differences in Hypoalgesia between pulse frequencies. Of the three studies judged as positive outcome, one reported that 100 pulses per second (pps) was superior to 10 pps; one that 4 pps was superior to 100 pps; and one that 5 pps and 80 pps were superior to 2 pps. Conclusion Evidence from experimental pain studies suggests that TENS pulse frequency does not influence hypolagesia when its pulse intensity, pulse pattern, and pulse duration are kept constant. Inadequate sample sizes may have generated false negative findings in some studies.
Luke Hughes - One of the best experts on this subject based on the ideXlab platform.
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the effect of blood flow restriction exercise on exercise induced Hypoalgesia and endogenous opioid and endocannabinoid mechanisms of pain modulation
Journal of Applied Physiology, 2020Co-Authors: Luke Hughes, Stephen D. PattersonAbstract:This study aimed to investigate and compare the magnitude of exercise-induced Hypoalgesia (EIH) with low-intensity blood flow restriction (BFR) resistance exercise (RE) at varying pressures to other intensities of resistance exercise and examine endogenous mechanisms of pain reduction. Twelve individuals performed four experimental trials involving unilateral leg press exercise in a randomized crossover design: low-load RE at 30% of one repetition maximum (1RM), high-load RE (70% 1RM), and BFR-RE (30% 1RM) at a low and high pressure. BFR pressure was prescribed relative to limb occlusion pressure at 40% and 80% for the low- and high-pressure trials. Pressure pain thresholds (PPT) were assessed before and 5 min and 24 h following exercise in exercising and nonexercising muscles. Venous blood samples were collected at the same timepoints to determine plasma concentrations of beta-endorphin and 2-arachidonoylglycerol. High-pressure BFR-RE increased PPTs in the exercising limb to a greater extent than all other trials. Comparable systemic EIH effects were observed with HLRE and both BFR-RE trials. PPTs in the exercising limb remained elevated above baseline at 24 h postexercise following both BFR-RE trials. Postexercise plasma beta-endorphin concentration was elevated during the BFR-RE trials. No changes to 2-arachidonoylglycerol concentration were observed. High pressure BFR-RE causes a greater EIH response in the exercising limb that persists for up to 24 h following exercise. The reduction in pain sensitivity with BFR-RE is partly driven by endogenous opioid production of beta-endorphin. BFR-RE should be investigated as a possible pain-modulation tool in individuals with acute and chronic pain.NEW & NOTEWORTHY High-pressure blood flow restriction (BFR) causes a greater Hypoalgesia response in the exercising limb (48%) compared with light and heavy load resistance exercise (10-34%). Performing light load resistance exercise with BFR causes systemic Hypoalgesia comparable with heavy load resistance exercise (10-18%). BFR resistance exercise prolonged the exercise-induced Hypoalgesia response for 24 h in the exercising limb (15% and 24%, respectively). Activation of endogenous opioid production and a conditioned pain modulation effect partly mediate the relationship between exercise and Hypoalgesia.
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Low intensity blood flow restriction exercise: Rationale for a Hypoalgesia effect
Medical hypotheses, 2019Co-Authors: Luke Hughes, Stephen D. PattersonAbstract:Exercise-induced Hypoalgesia is characterised by a reduction in pain sensitivity following exercise. Recently, low intensity exercise performed with blood flow restriction has been shown to induce Hypoalgesia. The purpose of this manuscript is to discuss the mechanisms of exercise-induced Hypoalgesia and provide rationale as to why low intensity exercise performed with blood flow restriction may induce Hypoalgesia. Research into exercise-induced Hypoalgesia has identified several potential mechanisms, including opioid and endocannabinoid-mediated pain inhibition, conditioned pain modulation, recruitment of high threshold motor units, exercise-induced metabolite production and an interaction between cardiovascular and pain regulatory systems. We hypothesise that several mechanisms consistent with prolonged high intensity exercise may drive the Hypoalgesia effect observed with blood flow restriction exercise. These are likely triggered by the high level of intramuscular stress in the exercising muscle generated by blood flow restriction including hypoxia, accumulation of metabolites, accelerated fatigue onset and ischemic pain. Therefore, blood flow restriction exercise may induce Hypoalgesia through similar mechanisms to prolonged higher intensity exercise, but at lower intensities, by changing local tissue physiology, highlighting the importance of the blood flow restriction stimulus. The potential to use blood flow restriction exercise as a pain modulation tool has important implications following acute injury and surgery, and for several load compromised populations with chronic pain.