Mo1559 - Conditioned Pain Modulation in Painful Functional Gastrointestinal Disorders: Systematic Review and Meta-Analysis

Objective: Patellofemoral pain has high recurrence rates and minimal long-term treatment success. Central sensitization refers to dysfunctional pain modulation that occurs when nociceptive neurons become hyper responsive. Research in this area in PFP has been increasingly productive in the past decade. The aim of this review is to determine whether evidence supports manifestations of central sensitization in individuals with PFP. Data sources: MeSH terms for quantitative sensory testing (QST) pressure pain thresholds, conditioned pain modulation, temporal summation, sensitization, hyperalgesia, and anterior knee pain or PFP were searched in PubMed, SportDiscus, CINAHL, Academic Search Complete, and Ebscohost. Study Selection: Peer reviewed studies written in English, published between 2005–2020 which investigated QST and/or pain mapping in a sample with PFP were included in this review. Data Extraction: The initial search yielded 140 articles. After duplicates were removed, 78 article abstracts were reviewed. Full-text review of 21 studies occurred, with 11 studies included in the meta-analysis and eight studies included in the systematic review. Data Synthesis: A random-effects meta-analysis was conducted for four QST variables (local pressure pain thresholds, remote pressure pain thresholds, conditioned pain modulation, temporal summation). Strong evidence supports lower local and remote pressure pain thresholds, impaired conditioned pain modulation, and facilitated temporal summation in individuals with PFP compared to pain-free individuals. Conflicting evidence is presented for heat and cold pain thresholds. Pain mapping demonstrated expanding pain patterns associated with long PFP symptom duration. Conclusions: Signs of central sensitization are present in individuals with PFP, indicating altered pain modulation. PFP etiological and treatment models should reflect the current body of evidence regarding central sensitization. Signs of central sensitization should be monitored clinically and treatments with central effects should be considered as part of a multi-modal plan of care. Registration Number: This review is registered with Prospero (CRD42019127548) Registration URL: https://www.crd.york.ac.uk/PROSPERO Key Points:

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Conditioned Pain Modulation in Populations With Chronic Pain: A Systematic Review and Meta-Analysis

Journal of Pain ◽

10.1016/j.jpain.2012.07.005 ◽

2012 ◽

Vol 13 (10) ◽

pp. 936-944 ◽

Cited By ~ 232

Author(s):

Gwyn N. Lewis ◽

David A. Rice ◽

Peter J. McNair

Keyword(s):

Systematic Review ◽

Chronic Pain ◽

Meta Analysis ◽

Pain Modulation ◽

Conditioned Pain Modulation

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Modulation of offset analgesia in patients with chronic pain and healthy subjects – a systematic review and meta-analysis

Scandinavian Journal of Pain ◽

10.1515/sjpain-2021-0137 ◽

2021 ◽

Vol 0 (0) ◽

Author(s):

Dennis Boye Larsen ◽

Xenia Jørgensen Uth ◽

Lars Arendt-Nielsen ◽

Kristian Kjær Petersen

Keyword(s):

Systematic Review ◽

Chronic Pain ◽

Subgroup Analysis ◽

Healthy Subjects ◽

Meta Analysis ◽

Pain Modulation ◽

Cochrane Library ◽

Conditioned Pain Modulation ◽

Qualitative Synthesis ◽

Current Systematic Review

Abstract Objectives Offset analgesia (OA) induces a brief pain inhibition and studies suggest OA impairment in patients with chronic pain when compared to healthy subjects. Conditioned pain modulation remains the most studied descending pain inhibitory control mechanism and is modulated by centrally-acting analgesics. Since OA may be mediated by similar neural substrates as conditioned pain modulation, understanding if OA is a peripheral or central proxy of pain modulation is important. The modulatory effect of centrally-acting drugs on OA in healthy and chronic pain populations has not yet been systematically reviewed and meta-analyzed, and this systematic review and meta-analysis aimed to identify studies employing interventions for modulating OA magnitude. Methods A systematic search of PubMed, Embase, Web of Science, and the Cochrane Library yielded 146 records of which 11 (172 healthy pain-free subjects, 106 chronic pain patients) were eligible for qualitative synthesis, and 10 for meta-analysis on overall modulatory effect of interventions on OA, and subgroup analysis of patients and healthy pain-free subjects. Results Risk of bias was evident for study participation and study confounding in the included studies. Several different methods for assessing and calculating OA magnitude were identified, which may affect interpretability of findings and warrants standardization. The meta-analysis showed no modulatory effects on OA overall (standardized mean difference (SMD) [95%CI]: 0.04 [−0.22, 0.30], Z=0.29, p=0.77), or in the subgroup analysis for patients (SMD [95%CI]: −0.04 [−0.63, 0.71], Z=0.13, p=0.90) or healthy pain-free subjects (SMD [95%CI]: 0.01 [−0.21, 0.24], Z=0.11, p=0.91). Moderate to substantial heterogeneity was found for the overall analysis (I2=47%, p=0.03) and patient subgroup analysis (I2=75%, p=0.003). Conclusions The current systematic review and meta-analysis conclude that centrally-acting drugs and exercise do not influence OA. Evidence on the peripheral contribution to OA response requires further investigations. Preclinical models of OA should be established to identify the neurophysiology and -biology behind OA.

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