Pain Modulation

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David Yarnitsky - One of the best experts on this subject based on the ideXlab platform.

  • reliability of conditioned Pain Modulation a systematic review
    2016
    Co-Authors: Donna Kennedy, David Yarnitsky, Harriet I Kemp, Deborah Ridout, Andrew S C Rice
    Abstract:

    A systematic literature review was undertaken to determine if conditioned Pain Modulation (CPM) is reliable. Longitudinal, English language observational studies of the repeatability of a CPM test paradigm in adult humans were included. Two independent reviewers assessed the risk of bias in 6 domains; study participation; study attrition; prognostic factor measurement; outcome measurement; confounding and analysis using the Quality in Prognosis Studies (QUIPS) critical assessment tool. Intraclass correlation coefficients (ICCs) less than 0.4 were considered to be poor; 0.4 and 0.59 to be fair; 0.6 and 0.75 good and greater than 0.75 excellent. Ten studies were included in the final review. Meta-analysis was not appropriate because of differences between studies. The intersession reliability of the CPM effect was investigated in 8 studies and reported as good (ICC = 0.6-0.75) in 3 studies and excellent (ICC > 0.75) in subgroups in 2 of those 3. The assessment of risk of bias demonstrated that reporting is not comprehensive for the description of sample demographics, recruitment strategy, and study attrition. The absence of blinding, a lack of control for confounding factors, and lack of standardisation in statistical analysis are common. Conditioned Pain Modulation is a reliable measure; however, the degree of reliability is heavily dependent on stimulation parameters and study methodology and this warrants consideration for investigators. The validation of CPM as a robust prognostic factor in experimental and clinical Pain studies may be facilitated by improvements in the reporting of CPM reliability studies.

  • psychological factors and conditioned Pain Modulation a meta analysis
    2016
    Co-Authors: Hadas Nahmanaverbuch, Ronyreuven Nir, Elliot Sprecher, David Yarnitsky
    Abstract:

    Objective Conditioned Pain Modulation (CPM) responses may be affected by psychological factors such as anxiety, depression, and Pain catastrophizing; however, most studies on CPM do not address these relations as their primary outcome. The aim of this meta-analysis was to analyze the findings regarding the associations between CPM responses and psychological factors in both Pain-free individuals and Pain patients. Materials and methods After a comprehensive PubMed search, 37 articles were found to be suitable for inclusion. Analyses used DerSimonian and Laird's random-effects model on Fisher's z-transforms of correlations; potential publication bias was tested using funnel plots and Egger's regression test for funnel plot asymmetry. Six meta-analyses were performed examining the correlations between anxiety, depression, and Pain catastrophizing, and CPM responses in healthy individuals and Pain patients. Results No significant correlations between CPM responses and any of the examined psychological factors were found. However, a secondary analysis, comparing modality-specific CPM responses and psychological factors in healthy individuals, revealed the following: (1) pressure-based CPM responses were correlated with anxiety (grand mean correlation in original units r=-0.1087; 95% confidence limits, -0.1752 to -0.0411); (2) heat-based CPM was correlated with depression (r=0.2443; 95% confidence limits, 0.0150 to 0.4492); and (3) electrical-based CPM was correlated with Pain catastrophizing levels (r=-0.1501; 95% confidence limits, -0.2403 to -0.0574). Discussion Certain psychological factors seem to be associated with modality-specific CPM responses in healthy individuals. This potentially supports the notion that CPM paradigms evoked by different stimulation modalities represent different underlying mechanisms.

  • recommendations on practice of conditioned Pain Modulation cpm testing
    2015
    Co-Authors: David Yarnitsky, Serge Marchand, Michal Granot, Asbjorn Mohr Drewes, Didier Bouhassira, Roger B Fillingim, Per Hansson, Ruth Landau, Dagfinn Matre
    Abstract:

    Protocols for testing conditioned Pain Modulation (CPM) vary between different labs/clinics. In order to promote research and clinical application of this tool, we summarize the recommendations of interested researchers consensus meeting regarding the practice of CPM and report of its results.

  • conditioned Pain Modulation
    2015
    Co-Authors: Ronyreuven Nir, David Yarnitsky
    Abstract:

    Purpose of review Conditioned Pain Modulation (CPM) paradigms have been increasingly used over the past few years to assess endogenous analgesia capacity in healthy individuals and Pain patients. The current review concentrates on selected recent literature advancing our understanding and practice of CPM. Recent findings The main themes covered by the present CPM review include underlying mechanisms, approaches to experimental investigation, practicality in clinical practice, neurophysiological and psychophysiological correlates, and pharmacological solutions to Pain Modulation dysfunction. Summary The reviewed literature refines the methodology used for eliciting CPM responses and characterizing their physiological attributes in healthy individuals and Pain patients, and exemplifies the materializing concept of individualized Pain medicine through targeting impaired mechanisms of Pain Modulation by designated drugs for optimal Pain alleviation.

  • role of endogenous Pain Modulation in chronic Pain mechanisms and treatment
    2015
    Co-Authors: David Yarnitsky
    Abstract:

    Development and application of psychophysical test paradigms to assess endogenous Pain Modulation in healthy controls and in patients yielded large body of data over the last 2 decades. These tests can assist in predicting Pain acquisition, in characterizing Pain syndromes and related dysfunctions of Pain Modulation, and in predicting response to treatment. This chapter reviews the development of thought on Pain Modulation in the clinical setup, focusing on conditioned Pain Modulation, and update on accumulated data regarding the mechanism, protocols of administration, and applications in the clinic.

Felipe Fregni - One of the best experts on this subject based on the ideXlab platform.

  • defective endogenous Pain Modulation in fibromyalgia a meta analysis of temporal summation and conditioned Pain Modulation paradigms
    2018
    Co-Authors: Anthony Terrence Obrien, Alicia Deitos, Yolanda Trinanes Pego, Felipe Fregni, Maria T Carrillodelapena
    Abstract:

    Abstract To study the characteristics of temporal summation (TS) and conditioned Pain Modulation (CPM) in fibromyalgia (FM) patients, we systematically searched Pubmed and EMBASE for studies using TS or CPM comparing FM patients with healthy controls. We computed Hedges' g, risk of bias, sensitivity analysis, and meta-regression tests with 10,000 Monte-Carlo permutations. Twenty-three studies (625 female and 23 male FM patients and 591 female and 81 male healthy controls) were included. The meta-analyses showed an effect size of .53 for TS (P  Perspective This novel meta-analysis provides evidence for defective endogenous Pain Modulation in FM patients. We explored the effect of covariates on between-study variability in these paradigms. These biomarkers may aid in diagnosis, and treatment of patients. However, validation requires further investigation under strict methodological settings, and into individual patient covariates.

  • a framework for understanding the relationship between descending Pain Modulation motor corticospinal and neuroplasticity regulation systems in chronic myofascial Pain
    2016
    Co-Authors: Leonardo Monteiro Botelho, Alicia Deitos, Felipe Fregni, Leon Moralesquezada, Joanna Ripoll Rozisky, Aline Patricia Brietzke, Iraci Lucena Da Silva Torres, Wolnei Caumo
    Abstract:

    Myofascial Pain syndrome (MPS) is a leading cause of chronic musculoskeletal Pain. However, its neurobiological mechanisms are not entirely elucidated. Given the complex interaction between the networks involved in Pain process, our approach, to providing insights into the neural mechanisms of Pain, was to investigate the relationship between neurophysiological, neurochemical and clinical outcomes such as corticospinal excitability. Recent evidence has demonstrated that three neural systems are affected in chronic Pain: (i) motor corticospinal system; (ii) internal descending Pain Modulation system; and (iii) the system regulating neuroplasticity. In this cross-sectional study, we aimed to examine the relationship between these three central systems in patients with chronic MPS of whom do/do not respond to the Conditioned Pain Modulation Task (CPM-task). The CPM-task was to immerse her non-dominant hand in cold water (zero to 10C degree) to produce a heterotopic nociceptive stimulus. Corticospinal excitability was the primary outcome; specifically, the motor evoked potential (MEP) and intracortical facilitation (ICF) as assessed by transcranial magnetic stimulation (TMS). Secondary outcomes were the cortical excitability parameters [current silent period (CSP) and short intracortical inhibition (SICI)], serum brain-derived neurotrophic factor (BDNF), heat Pain threshold (HPT) and the disability related to Pain (DRP). We included 33 women, (18-65 years old). The MANCOVA model using Bonferroni’s Multiple Comparison Test revealed that non-responders (n=10) compared to responders (n=23) presented increased intracortical facilitation (ICF) (mean ± SD) 1.43(0.3) vs. 1.11 (0.12), greater motor-evoked potential amplitude (µV) 1.93 (0.54) vs. 1.40 (0.27), as well a higher serum BDNF (pg/Ml) 32.56 (9.95) vs. 25.59 (10.24), (P < 0.05 for all). Also, non-responders presented a higher level of DRP and decreased HPT (P < 0.05 for all). These findings suggest that the loss of net descending Pain inhibition was associated with an increase in ICF, serum BDNF levels, and DRP. We propose a framework to explain the relationship and potential directionality of these factors. In this framework we hypothesize that increased central sensitization leads to a loss of descending Pain inhibition that triggers compensatory mechanisms as shown by increased motor cortical excitability.

  • a framework for understanding the relationship between descending Pain Modulation motor corticospinal and neuroplasticity regulation systems in chronic myofascial Pain
    2016
    Co-Authors: Leonardo Monteiro Botelho, Alicia Deitos, Felipe Fregni, Leon Moralesquezada, Joanna Ripoll Rozisky, Aline Patricia Brietzke, Iraci Lucena Da Silva Torres, Wolnei Caumo
    Abstract:

    Myofascial Pain syndrome (MPS) is a leading cause of chronic musculoskeletal Pain. However, its neurobiological mechanisms are not entirely elucidated. Given the complex interaction between the networks involved in Pain process, our approach, to providing insights into the neural mechanisms of Pain, was to investigate the relationship between neurophysiological, neurochemical and clinical outcomes such as corticospinal excitability. Recent evidence has demonstrated that three neural systems are affected in chronic Pain: (i) motor corticospinal system; (ii) internal descending Pain Modulation system; and (iii) the system regulating neuroplasticity. In this cross-sectional study, we aimed to examine the relationship between these three central systems in patients with chronic MPS of whom do/do not respond to the Conditioned Pain Modulation Task (CPM-task). The CPM-task was to immerse her non-dominant hand in cold water (0-1°C) to produce a heterotopic nociceptive stimulus. Corticospinal excitability was the primary outcome; specifically, the motor evoked potential (MEP) and intracortical facilitation (ICF) as assessed by transcranial magnetic stimulation (TMS). Secondary outcomes were the cortical excitability parameters [current silent period (CSP) and short intracortical inhibition (SICI)], serum brain-derived neurotrophic factor (BDNF), heat Pain threshold (HPT), and the disability related to Pain (DRP). We included 33 women, (18-65 years old). The MANCOVA model using Bonferroni's Multiple Comparison Test revealed that non-responders (n = 10) compared to responders (n = 23) presented increased intracortical facilitation (ICF; mean ± SD) 1.43 (0.3) vs. 1.11 (0.12), greater motor-evoked potential amplitude (μV) 1.93 (0.54) vs. 1.40 (0.27), as well a higher serum BDNF (pg/Ml) 32.56 (9.95) vs. 25.59 (10.24), (P < 0.05 for all). Also, non-responders presented a higher level of DRP and decreased HPT (P < 0.05 for all). These findings suggest that the loss of net descending Pain inhibition was associated with an increase in ICF, serum BDNF levels, and DRP. We propose a framework to explain the relationship and potential directionality of these factors. In this framework we hypothesize that increased central sensitization leads to a loss of descending Pain inhibition that triggers compensatory mechanisms as shown by increased motor cortical excitability.

  • association of anxiety with intracortical inhibition and descending Pain Modulation in chronic myofascial Pain syndrome
    2014
    Co-Authors: Liliane Pinto Vidor, Alicia Deitos, Joanna Ripoll Rozisky, Aline Patricia Brietzke, Iraci Lucena Da Silva Torres, Liciane Fernandes Medeiros, Jairo Alberto Dussansarria, Letizzia Dallagnol, Gabriela Laste, Felipe Fregni
    Abstract:

    Background: This study aimed to answer three questions related to chronic myofascial Pain syndrome (MPS): 1) Is the motor cortex excitability, as assessed by transcranial magnetic stimulation parameters (TMS), related to state-trait anxiety? 2) Does anxiety modulate corticospinal excitability changes after evoked Pain by Quantitative Sensory Testing (QST)? 3) Does the state-trait anxiety predict the response to Pain evoked by QST if simultaneously receiving a heterotopic stimulus [Conditional Pain Modulation (CPM)]? We included females with chronic MPS (n = 47) and healthy controls (n = 11), aged 19 to 65 years. Motor cortex excitability was assessed by TMS, and anxiety was assessed based on the State-Trait Anxiety Inventory. The disability related to Pain (DRP) was assessed by the Profile of Chronic Pain scale for the Brazilian population (B:PCP:S), and the psychophysical Pain measurements were measured by the QST and CPM. Results: In patients, trait-anxiety was positively correlated to intracortical facilitation (ICF) at baseline and after QST evoked Pain (β =0 .05 andβ = 0.04, respectively) and negatively correlated to the cortical silent period (CSP) (β = -1.17 and β = -1.23, respectively) (P <0.05 for all comparisons). After QST evoked Pain, the DRP was positively correlated to ICF (β=0.02) (P<0.05). Pain scores during CPM were positively correlated with trait-anxiety when it was concurrently with high DRP (β= 0.39; P = 0.02). Controls’ cortical excitability remained unchanged after QST. Conclusions: These findings suggest that, in chronic MPS, the imbalance between excitatory and inhibitory descending systems of the corticospinal tract is associated with higher trait-anxiety concurrent with higher DRP.

  • association of anxiety with intracortical inhibition and descending Pain Modulation in chronic myofascial Pain syndrome
    2014
    Co-Authors: Liliane Pinto Vidor, Alicia Deitos, Joanna Ripoll Rozisky, Aline Patricia Brietzke, Iraci Lucena Da Silva Torres, Liciane Fernandes Medeiros, Jairo Alberto Dussansarria, Letizzia Dallagnol, Gabriela Laste, Felipe Fregni
    Abstract:

    This study aimed to answer three questions related to chronic myofascial Pain syndrome (MPS): 1) Is the motor cortex excitability, as assessed by transcranial magnetic stimulation parameters (TMS), related to state-trait anxiety? 2) Does anxiety modulate corticospinal excitability changes after evoked Pain by Quantitative Sensory Testing (QST)? 3) Does the state-trait anxiety predict the response to Pain evoked by QST if simultaneously receiving a heterotopic stimulus [Conditional Pain Modulation (CPM)]? We included females with chronic MPS (n = 47) and healthy controls (n = 11), aged 19 to 65 years. Motor cortex excitability was assessed by TMS, and anxiety was assessed based on the State-Trait Anxiety Inventory. The disability related to Pain (DRP) was assessed by the Profile of Chronic Pain scale for the Brazilian population (B:PCP:S), and the psychophysical Pain measurements were measured by the QST and CPM. In patients, trait-anxiety was positively correlated to intracortical facilitation (ICF) at baseline and after QST evoked Pain (β = 0.05 and β = 0.04, respectively) and negatively correlated to the cortical silent period (CSP) (β = -1.17 and β = -1.23, respectively) (P <0.05 for all comparisons). After QST evoked Pain, the DRP was positively correlated to ICF (β = 0.02) (P < 0.05). Pain scores during CPM were positively correlated with trait-anxiety when it was concurrently with high DRP (β = 0.39; P = 0.02). Controls’ cortical excitability remained unchanged after QST. These findings suggest that, in chronic MPS, the imbalance between excitatory and inhibitory descending systems of the corticospinal tract is associated with higher trait-anxiety concurrent with higher DRP.

Michele Curatolo - One of the best experts on this subject based on the ideXlab platform.

  • effects of conditioned Pain Modulation on spread of hyperalgesia after intramuscular capsaicin in humans
    2021
    Co-Authors: Michele Curatolo, Thomas Gravennielsen, Lars Arendtnielsen, Andreas Siegenthaler, Jurg Schliessbach
    Abstract:

    Muscle Pain can be associated with altered central Pain processing, leading to hyperalgesia both locally and at distant body sites. The role of endogenous inhibitory mechanisms in hyperalgesia associated with muscle Pain remains unclear. This study investigated the influence of conditioned Pain Modulation (CPM) on hyperalgesia at multiple body sites induced by intramuscular injection of capsaicin in the supraspinatus muscle. Thirty healthy males underwent CPM testing using the cold pressor test as conditioning stimulus and pressure Pain threshold (PPT) as test stimulus. Muscle Pain and hyperalgesia were induced by injection of capsaicin into the non-dominant supraspinatus muscle. Before and 5, 10, 15, 20, 30, 40, 50 and 60 min later, PPTs were recorded bilaterally at the supraspinatus, infraspinatus and deltoid muscles, ring finger and toe. Subjects were classified as inhibitory vs. facilitating CPM based on published reference values. Compared to baseline, PPTs decreased significantly at the supraspinatus, infraspinatus and deltoid muscle (p

  • conditioned Pain Modulation in patients with acute and chronic low back Pain
    2016
    Co-Authors: Sabine Mlekusch, Lars Arendtnielsen, Alban Y Neziri, Andreas Limacher, Peter Juni, Michele Curatolo
    Abstract:

    OBJECTIVES Disturbed endogenous Pain Modulation is likely one of the mechanisms underlying central hypersensitivity and might be a contributing factor for the development and maintenance of chronic Pain. To our knowledge, no study has investigated endogenous Pain Modulation in both acute and chronic low back Pain (LBP). We tested the hypothesis that endogenous Pain inhibition is impaired in patients with acute and chronic LBP. MATERIALS AND METHODS We evaluated 40 patients with acute LBP, 34 patients with chronic LBP and 30 Pain-free controls for their conditioned Pain Modulation (CPM), with pressure Pain tolerance and cold pressor as test and conditioning stimulus, respectively. Measurements were repeated up to 10 minutes after cold pressor test. RESULTS There was no difference in CPM among the groups immediately after cold pressor test. However, the decline in CPM effect was significantly faster in chronic and acute LBP patients than in controls, with no evidence for differences between Pain groups. DISCUSSION The present study provides evidence for some alterations of endogenous Modulation in both acute and chronic LBP. CPM was still detected in both patient groups, indicating that endogenous Modulation, although effective for a shorter duration, is partially functioning in patients with LBP.

  • is the conditioned Pain Modulation paradigm reliable a test retest assessment using the nociceptive withdrawal reflex
    2014
    Co-Authors: Jose Biurrun Manresa, Lars Arendtnielsen, Michele Curatolo, Ole Kaeseler Andersen, Raphael Fritsche, Pascal Henri Vuilleumier, Carmen Oehler, Carsten Dahl Morch
    Abstract:

    The aim of this study was to determine the reliability of the conditioned Pain Modulation (CPM) paradigm assessed by an objective electrophysiological method, the nociceptive withdrawal reflex (NWR), and psychophysical measures, using hypothetical sample sizes for future studies as analytical goals. Thirty-four healthy volunteers participated in two identical experimental sessions, separated by 1 to 3 weeks. In each session, the cold pressor test (CPT) was used to induce CPM, and the NWR thresholds, electrical Pain detection thresholds and Pain intensity ratings after suprathreshold electrical stimulation were assessed before and during CPT. CPM was consistently detected by all methods, and the electrophysiological measures did not introduce additional variation to the assessment. In particular, 99% of the trials resulted in higher NWR thresholds during CPT, with an average increase of 3.4 mA (p<0.001). Similarly, 96% of the trials resulted in higher electrical Pain detection thresholds during CPT, with an average increase of 2.2 mA (p<0.001). Pain intensity ratings after suprathreshold electrical stimulation were reduced during CPT in 84% of the trials, displaying an average decrease of 1.5 points in a numeric rating scale (p<0.001). Under these experimental conditions, CPM reliability was acceptable for all assessment methods in terms of sample sizes for potential experiments. The presented results are encouraging with regards to the use of the CPM as an assessment tool in experimental and clinical Pain. Trial registration: Clinical Trials.gov NCT01636440.

Alicia Deitos - One of the best experts on this subject based on the ideXlab platform.

  • defective endogenous Pain Modulation in fibromyalgia a meta analysis of temporal summation and conditioned Pain Modulation paradigms
    2018
    Co-Authors: Anthony Terrence Obrien, Alicia Deitos, Yolanda Trinanes Pego, Felipe Fregni, Maria T Carrillodelapena
    Abstract:

    Abstract To study the characteristics of temporal summation (TS) and conditioned Pain Modulation (CPM) in fibromyalgia (FM) patients, we systematically searched Pubmed and EMBASE for studies using TS or CPM comparing FM patients with healthy controls. We computed Hedges' g, risk of bias, sensitivity analysis, and meta-regression tests with 10,000 Monte-Carlo permutations. Twenty-three studies (625 female and 23 male FM patients and 591 female and 81 male healthy controls) were included. The meta-analyses showed an effect size of .53 for TS (P  Perspective This novel meta-analysis provides evidence for defective endogenous Pain Modulation in FM patients. We explored the effect of covariates on between-study variability in these paradigms. These biomarkers may aid in diagnosis, and treatment of patients. However, validation requires further investigation under strict methodological settings, and into individual patient covariates.

  • a framework for understanding the relationship between descending Pain Modulation motor corticospinal and neuroplasticity regulation systems in chronic myofascial Pain
    2016
    Co-Authors: Leonardo Monteiro Botelho, Alicia Deitos, Felipe Fregni, Leon Moralesquezada, Joanna Ripoll Rozisky, Aline Patricia Brietzke, Iraci Lucena Da Silva Torres, Wolnei Caumo
    Abstract:

    Myofascial Pain syndrome (MPS) is a leading cause of chronic musculoskeletal Pain. However, its neurobiological mechanisms are not entirely elucidated. Given the complex interaction between the networks involved in Pain process, our approach, to providing insights into the neural mechanisms of Pain, was to investigate the relationship between neurophysiological, neurochemical and clinical outcomes such as corticospinal excitability. Recent evidence has demonstrated that three neural systems are affected in chronic Pain: (i) motor corticospinal system; (ii) internal descending Pain Modulation system; and (iii) the system regulating neuroplasticity. In this cross-sectional study, we aimed to examine the relationship between these three central systems in patients with chronic MPS of whom do/do not respond to the Conditioned Pain Modulation Task (CPM-task). The CPM-task was to immerse her non-dominant hand in cold water (zero to 10C degree) to produce a heterotopic nociceptive stimulus. Corticospinal excitability was the primary outcome; specifically, the motor evoked potential (MEP) and intracortical facilitation (ICF) as assessed by transcranial magnetic stimulation (TMS). Secondary outcomes were the cortical excitability parameters [current silent period (CSP) and short intracortical inhibition (SICI)], serum brain-derived neurotrophic factor (BDNF), heat Pain threshold (HPT) and the disability related to Pain (DRP). We included 33 women, (18-65 years old). The MANCOVA model using Bonferroni’s Multiple Comparison Test revealed that non-responders (n=10) compared to responders (n=23) presented increased intracortical facilitation (ICF) (mean ± SD) 1.43(0.3) vs. 1.11 (0.12), greater motor-evoked potential amplitude (µV) 1.93 (0.54) vs. 1.40 (0.27), as well a higher serum BDNF (pg/Ml) 32.56 (9.95) vs. 25.59 (10.24), (P < 0.05 for all). Also, non-responders presented a higher level of DRP and decreased HPT (P < 0.05 for all). These findings suggest that the loss of net descending Pain inhibition was associated with an increase in ICF, serum BDNF levels, and DRP. We propose a framework to explain the relationship and potential directionality of these factors. In this framework we hypothesize that increased central sensitization leads to a loss of descending Pain inhibition that triggers compensatory mechanisms as shown by increased motor cortical excitability.

  • a framework for understanding the relationship between descending Pain Modulation motor corticospinal and neuroplasticity regulation systems in chronic myofascial Pain
    2016
    Co-Authors: Leonardo Monteiro Botelho, Alicia Deitos, Felipe Fregni, Leon Moralesquezada, Joanna Ripoll Rozisky, Aline Patricia Brietzke, Iraci Lucena Da Silva Torres, Wolnei Caumo
    Abstract:

    Myofascial Pain syndrome (MPS) is a leading cause of chronic musculoskeletal Pain. However, its neurobiological mechanisms are not entirely elucidated. Given the complex interaction between the networks involved in Pain process, our approach, to providing insights into the neural mechanisms of Pain, was to investigate the relationship between neurophysiological, neurochemical and clinical outcomes such as corticospinal excitability. Recent evidence has demonstrated that three neural systems are affected in chronic Pain: (i) motor corticospinal system; (ii) internal descending Pain Modulation system; and (iii) the system regulating neuroplasticity. In this cross-sectional study, we aimed to examine the relationship between these three central systems in patients with chronic MPS of whom do/do not respond to the Conditioned Pain Modulation Task (CPM-task). The CPM-task was to immerse her non-dominant hand in cold water (0-1°C) to produce a heterotopic nociceptive stimulus. Corticospinal excitability was the primary outcome; specifically, the motor evoked potential (MEP) and intracortical facilitation (ICF) as assessed by transcranial magnetic stimulation (TMS). Secondary outcomes were the cortical excitability parameters [current silent period (CSP) and short intracortical inhibition (SICI)], serum brain-derived neurotrophic factor (BDNF), heat Pain threshold (HPT), and the disability related to Pain (DRP). We included 33 women, (18-65 years old). The MANCOVA model using Bonferroni's Multiple Comparison Test revealed that non-responders (n = 10) compared to responders (n = 23) presented increased intracortical facilitation (ICF; mean ± SD) 1.43 (0.3) vs. 1.11 (0.12), greater motor-evoked potential amplitude (μV) 1.93 (0.54) vs. 1.40 (0.27), as well a higher serum BDNF (pg/Ml) 32.56 (9.95) vs. 25.59 (10.24), (P < 0.05 for all). Also, non-responders presented a higher level of DRP and decreased HPT (P < 0.05 for all). These findings suggest that the loss of net descending Pain inhibition was associated with an increase in ICF, serum BDNF levels, and DRP. We propose a framework to explain the relationship and potential directionality of these factors. In this framework we hypothesize that increased central sensitization leads to a loss of descending Pain inhibition that triggers compensatory mechanisms as shown by increased motor cortical excitability.

  • association of anxiety with intracortical inhibition and descending Pain Modulation in chronic myofascial Pain syndrome
    2014
    Co-Authors: Liliane Pinto Vidor, Alicia Deitos, Joanna Ripoll Rozisky, Aline Patricia Brietzke, Iraci Lucena Da Silva Torres, Liciane Fernandes Medeiros, Jairo Alberto Dussansarria, Letizzia Dallagnol, Gabriela Laste, Felipe Fregni
    Abstract:

    Background: This study aimed to answer three questions related to chronic myofascial Pain syndrome (MPS): 1) Is the motor cortex excitability, as assessed by transcranial magnetic stimulation parameters (TMS), related to state-trait anxiety? 2) Does anxiety modulate corticospinal excitability changes after evoked Pain by Quantitative Sensory Testing (QST)? 3) Does the state-trait anxiety predict the response to Pain evoked by QST if simultaneously receiving a heterotopic stimulus [Conditional Pain Modulation (CPM)]? We included females with chronic MPS (n = 47) and healthy controls (n = 11), aged 19 to 65 years. Motor cortex excitability was assessed by TMS, and anxiety was assessed based on the State-Trait Anxiety Inventory. The disability related to Pain (DRP) was assessed by the Profile of Chronic Pain scale for the Brazilian population (B:PCP:S), and the psychophysical Pain measurements were measured by the QST and CPM. Results: In patients, trait-anxiety was positively correlated to intracortical facilitation (ICF) at baseline and after QST evoked Pain (β =0 .05 andβ = 0.04, respectively) and negatively correlated to the cortical silent period (CSP) (β = -1.17 and β = -1.23, respectively) (P <0.05 for all comparisons). After QST evoked Pain, the DRP was positively correlated to ICF (β=0.02) (P<0.05). Pain scores during CPM were positively correlated with trait-anxiety when it was concurrently with high DRP (β= 0.39; P = 0.02). Controls’ cortical excitability remained unchanged after QST. Conclusions: These findings suggest that, in chronic MPS, the imbalance between excitatory and inhibitory descending systems of the corticospinal tract is associated with higher trait-anxiety concurrent with higher DRP.

  • association of anxiety with intracortical inhibition and descending Pain Modulation in chronic myofascial Pain syndrome
    2014
    Co-Authors: Liliane Pinto Vidor, Alicia Deitos, Joanna Ripoll Rozisky, Aline Patricia Brietzke, Iraci Lucena Da Silva Torres, Liciane Fernandes Medeiros, Jairo Alberto Dussansarria, Letizzia Dallagnol, Gabriela Laste, Felipe Fregni
    Abstract:

    This study aimed to answer three questions related to chronic myofascial Pain syndrome (MPS): 1) Is the motor cortex excitability, as assessed by transcranial magnetic stimulation parameters (TMS), related to state-trait anxiety? 2) Does anxiety modulate corticospinal excitability changes after evoked Pain by Quantitative Sensory Testing (QST)? 3) Does the state-trait anxiety predict the response to Pain evoked by QST if simultaneously receiving a heterotopic stimulus [Conditional Pain Modulation (CPM)]? We included females with chronic MPS (n = 47) and healthy controls (n = 11), aged 19 to 65 years. Motor cortex excitability was assessed by TMS, and anxiety was assessed based on the State-Trait Anxiety Inventory. The disability related to Pain (DRP) was assessed by the Profile of Chronic Pain scale for the Brazilian population (B:PCP:S), and the psychophysical Pain measurements were measured by the QST and CPM. In patients, trait-anxiety was positively correlated to intracortical facilitation (ICF) at baseline and after QST evoked Pain (β = 0.05 and β = 0.04, respectively) and negatively correlated to the cortical silent period (CSP) (β = -1.17 and β = -1.23, respectively) (P <0.05 for all comparisons). After QST evoked Pain, the DRP was positively correlated to ICF (β = 0.02) (P < 0.05). Pain scores during CPM were positively correlated with trait-anxiety when it was concurrently with high DRP (β = 0.39; P = 0.02). Controls’ cortical excitability remained unchanged after QST. These findings suggest that, in chronic MPS, the imbalance between excitatory and inhibitory descending systems of the corticospinal tract is associated with higher trait-anxiety concurrent with higher DRP.

Joanna Ripoll Rozisky - One of the best experts on this subject based on the ideXlab platform.

  • a framework for understanding the relationship between descending Pain Modulation motor corticospinal and neuroplasticity regulation systems in chronic myofascial Pain
    2016
    Co-Authors: Leonardo Monteiro Botelho, Alicia Deitos, Felipe Fregni, Leon Moralesquezada, Joanna Ripoll Rozisky, Aline Patricia Brietzke, Iraci Lucena Da Silva Torres, Wolnei Caumo
    Abstract:

    Myofascial Pain syndrome (MPS) is a leading cause of chronic musculoskeletal Pain. However, its neurobiological mechanisms are not entirely elucidated. Given the complex interaction between the networks involved in Pain process, our approach, to providing insights into the neural mechanisms of Pain, was to investigate the relationship between neurophysiological, neurochemical and clinical outcomes such as corticospinal excitability. Recent evidence has demonstrated that three neural systems are affected in chronic Pain: (i) motor corticospinal system; (ii) internal descending Pain Modulation system; and (iii) the system regulating neuroplasticity. In this cross-sectional study, we aimed to examine the relationship between these three central systems in patients with chronic MPS of whom do/do not respond to the Conditioned Pain Modulation Task (CPM-task). The CPM-task was to immerse her non-dominant hand in cold water (zero to 10C degree) to produce a heterotopic nociceptive stimulus. Corticospinal excitability was the primary outcome; specifically, the motor evoked potential (MEP) and intracortical facilitation (ICF) as assessed by transcranial magnetic stimulation (TMS). Secondary outcomes were the cortical excitability parameters [current silent period (CSP) and short intracortical inhibition (SICI)], serum brain-derived neurotrophic factor (BDNF), heat Pain threshold (HPT) and the disability related to Pain (DRP). We included 33 women, (18-65 years old). The MANCOVA model using Bonferroni’s Multiple Comparison Test revealed that non-responders (n=10) compared to responders (n=23) presented increased intracortical facilitation (ICF) (mean ± SD) 1.43(0.3) vs. 1.11 (0.12), greater motor-evoked potential amplitude (µV) 1.93 (0.54) vs. 1.40 (0.27), as well a higher serum BDNF (pg/Ml) 32.56 (9.95) vs. 25.59 (10.24), (P < 0.05 for all). Also, non-responders presented a higher level of DRP and decreased HPT (P < 0.05 for all). These findings suggest that the loss of net descending Pain inhibition was associated with an increase in ICF, serum BDNF levels, and DRP. We propose a framework to explain the relationship and potential directionality of these factors. In this framework we hypothesize that increased central sensitization leads to a loss of descending Pain inhibition that triggers compensatory mechanisms as shown by increased motor cortical excitability.

  • a framework for understanding the relationship between descending Pain Modulation motor corticospinal and neuroplasticity regulation systems in chronic myofascial Pain
    2016
    Co-Authors: Leonardo Monteiro Botelho, Alicia Deitos, Felipe Fregni, Leon Moralesquezada, Joanna Ripoll Rozisky, Aline Patricia Brietzke, Iraci Lucena Da Silva Torres, Wolnei Caumo
    Abstract:

    Myofascial Pain syndrome (MPS) is a leading cause of chronic musculoskeletal Pain. However, its neurobiological mechanisms are not entirely elucidated. Given the complex interaction between the networks involved in Pain process, our approach, to providing insights into the neural mechanisms of Pain, was to investigate the relationship between neurophysiological, neurochemical and clinical outcomes such as corticospinal excitability. Recent evidence has demonstrated that three neural systems are affected in chronic Pain: (i) motor corticospinal system; (ii) internal descending Pain Modulation system; and (iii) the system regulating neuroplasticity. In this cross-sectional study, we aimed to examine the relationship between these three central systems in patients with chronic MPS of whom do/do not respond to the Conditioned Pain Modulation Task (CPM-task). The CPM-task was to immerse her non-dominant hand in cold water (0-1°C) to produce a heterotopic nociceptive stimulus. Corticospinal excitability was the primary outcome; specifically, the motor evoked potential (MEP) and intracortical facilitation (ICF) as assessed by transcranial magnetic stimulation (TMS). Secondary outcomes were the cortical excitability parameters [current silent period (CSP) and short intracortical inhibition (SICI)], serum brain-derived neurotrophic factor (BDNF), heat Pain threshold (HPT), and the disability related to Pain (DRP). We included 33 women, (18-65 years old). The MANCOVA model using Bonferroni's Multiple Comparison Test revealed that non-responders (n = 10) compared to responders (n = 23) presented increased intracortical facilitation (ICF; mean ± SD) 1.43 (0.3) vs. 1.11 (0.12), greater motor-evoked potential amplitude (μV) 1.93 (0.54) vs. 1.40 (0.27), as well a higher serum BDNF (pg/Ml) 32.56 (9.95) vs. 25.59 (10.24), (P < 0.05 for all). Also, non-responders presented a higher level of DRP and decreased HPT (P < 0.05 for all). These findings suggest that the loss of net descending Pain inhibition was associated with an increase in ICF, serum BDNF levels, and DRP. We propose a framework to explain the relationship and potential directionality of these factors. In this framework we hypothesize that increased central sensitization leads to a loss of descending Pain inhibition that triggers compensatory mechanisms as shown by increased motor cortical excitability.

  • association of anxiety with intracortical inhibition and descending Pain Modulation in chronic myofascial Pain syndrome
    2014
    Co-Authors: Liliane Pinto Vidor, Alicia Deitos, Joanna Ripoll Rozisky, Aline Patricia Brietzke, Iraci Lucena Da Silva Torres, Liciane Fernandes Medeiros, Jairo Alberto Dussansarria, Letizzia Dallagnol, Gabriela Laste, Felipe Fregni
    Abstract:

    Background: This study aimed to answer three questions related to chronic myofascial Pain syndrome (MPS): 1) Is the motor cortex excitability, as assessed by transcranial magnetic stimulation parameters (TMS), related to state-trait anxiety? 2) Does anxiety modulate corticospinal excitability changes after evoked Pain by Quantitative Sensory Testing (QST)? 3) Does the state-trait anxiety predict the response to Pain evoked by QST if simultaneously receiving a heterotopic stimulus [Conditional Pain Modulation (CPM)]? We included females with chronic MPS (n = 47) and healthy controls (n = 11), aged 19 to 65 years. Motor cortex excitability was assessed by TMS, and anxiety was assessed based on the State-Trait Anxiety Inventory. The disability related to Pain (DRP) was assessed by the Profile of Chronic Pain scale for the Brazilian population (B:PCP:S), and the psychophysical Pain measurements were measured by the QST and CPM. Results: In patients, trait-anxiety was positively correlated to intracortical facilitation (ICF) at baseline and after QST evoked Pain (β =0 .05 andβ = 0.04, respectively) and negatively correlated to the cortical silent period (CSP) (β = -1.17 and β = -1.23, respectively) (P <0.05 for all comparisons). After QST evoked Pain, the DRP was positively correlated to ICF (β=0.02) (P<0.05). Pain scores during CPM were positively correlated with trait-anxiety when it was concurrently with high DRP (β= 0.39; P = 0.02). Controls’ cortical excitability remained unchanged after QST. Conclusions: These findings suggest that, in chronic MPS, the imbalance between excitatory and inhibitory descending systems of the corticospinal tract is associated with higher trait-anxiety concurrent with higher DRP.

  • association of anxiety with intracortical inhibition and descending Pain Modulation in chronic myofascial Pain syndrome
    2014
    Co-Authors: Liliane Pinto Vidor, Alicia Deitos, Joanna Ripoll Rozisky, Aline Patricia Brietzke, Iraci Lucena Da Silva Torres, Liciane Fernandes Medeiros, Jairo Alberto Dussansarria, Letizzia Dallagnol, Gabriela Laste, Felipe Fregni
    Abstract:

    This study aimed to answer three questions related to chronic myofascial Pain syndrome (MPS): 1) Is the motor cortex excitability, as assessed by transcranial magnetic stimulation parameters (TMS), related to state-trait anxiety? 2) Does anxiety modulate corticospinal excitability changes after evoked Pain by Quantitative Sensory Testing (QST)? 3) Does the state-trait anxiety predict the response to Pain evoked by QST if simultaneously receiving a heterotopic stimulus [Conditional Pain Modulation (CPM)]? We included females with chronic MPS (n = 47) and healthy controls (n = 11), aged 19 to 65 years. Motor cortex excitability was assessed by TMS, and anxiety was assessed based on the State-Trait Anxiety Inventory. The disability related to Pain (DRP) was assessed by the Profile of Chronic Pain scale for the Brazilian population (B:PCP:S), and the psychophysical Pain measurements were measured by the QST and CPM. In patients, trait-anxiety was positively correlated to intracortical facilitation (ICF) at baseline and after QST evoked Pain (β = 0.05 and β = 0.04, respectively) and negatively correlated to the cortical silent period (CSP) (β = -1.17 and β = -1.23, respectively) (P <0.05 for all comparisons). After QST evoked Pain, the DRP was positively correlated to ICF (β = 0.02) (P < 0.05). Pain scores during CPM were positively correlated with trait-anxiety when it was concurrently with high DRP (β = 0.39; P = 0.02). Controls’ cortical excitability remained unchanged after QST. These findings suggest that, in chronic MPS, the imbalance between excitatory and inhibitory descending systems of the corticospinal tract is associated with higher trait-anxiety concurrent with higher DRP.