Evidence map›Paper›PMID 19878863›Full record

ArticleThe journal of pain2009

Role of NFkappaB in an animal model of complex regional pain syndrome-type I (CRPS-I).

Marissa de Mos, André Laferrière, Magali Millecamps, Mercedes Pilkington, Miriam C J M Sturkenboom, Frank J P M Huygen, Terence J Coderre

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in The journal of pain, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07259382 (Neuro-Inflammation in Extremity Trauma), which is not on this map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT07259382 not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Neuro-Inflammation in Extremity Trauma: Risk Verification in Elbow Trauma: The NERVE Pilot Cohort Study

TypeobservationalSponsorUniversité de MontréalRan2026 to 2030Enrolled60ConditionsElbow Dislocation, Elbow Fractures, Inflammation Biomarkers, TBI Traumatic Brain InjuryArmsBiomarkers evaluation
3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 64 citations in OpenAlex.

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  6. [Effect and mechanism of glycyrrhizin on glial scar formation after spinal cord injury in rats].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2020
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  20. Activation of spinal NF-КB mediates pain behavior induced by plantar incision.International journal of clinical and experimental medicine · 2015
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Marissa de MosDepartment of Medical Informatics & Epidemiology and Biostatistics, Erasmus Medical Center, Rotterdam, the Netherlands. m.vrolijk-demos@erasmusmc.nl
André Laferrière
Magali Millecamps
Mercedes Pilkington
Miriam C J M Sturkenboom
Frank J P M Huygen
Terence J Coderre
McGill University · CAErasmus MC · NLMcGill University Health Centre · CA

Funding

CIHR 13236-2CIHR 13236-3CIHR 32536-1CIHR 53246-1CIHR 53246-2
6 · The paper itself

Abstract

unlabelledNFkappaB is involved in several pathogenic mechanisms that are believed to underlie the complex regional pain syndrome (CRPS), including ischemia, inflammation and sensitization. Chronic postischemia pain (CPIP) has been developed as an animal model that mimics the symptoms of CRPS-I. The possible involvement of NFkappaB in CRPS-I was studied using CPIP rats. Under sodium pentobarbital anesthesia, a tourniquet was placed around the rat left ankle joint, producing 3 hours of ischemia, followed by rapid reperfusion (IR injury). NFkappaB was measured in nuclear extracts of muscle and spinal cord tissue using ELISA. Moreover, the anti-allodynic (mechanical and cold) effect was tested for systemic, intrathecal, or intraplantar treatment with the NFkappaB inhibitor pyrrolidine dithiocarbamate (PDTC). At 2 and 48 hours after IR injury, NFkappaB was elevated in muscle and spinal cord of CPIP rats compared to shams. At 7 days, NFkappaB levels were normalized in muscle, but still elevated in spinal cord tissue. Systemic PDTC treatment relieved mechanical and cold allodynia in a dose-dependent manner, lasting for at least 3 hours. Intrathecal-but not intraplantar-administration also relieved mechanical allodynia. The results suggest that muscle and spinal NFkappaB plays a role in the pathogenesis of CPIP and potentially of human CRPS. PERSPECTIVE: Using the CPIP model, we demonstrate that NFkappaB is involved in the development of allodynia after a physical injury (ischemia and reperfusion) without direct nerve trauma. Since CPIP animals exhibit many features of human CRPS-I, this observation indicates a potential role for NFkappaB in human CRPS.

Indexed as

AnimalsCell NucleusCold TemperatureComplex Regional Pain SyndromesDisease Models, AnimalDose-Response Relationship, DrugMaleMuscle, SkeletalNF-kappa BPain MeasurementPhysical StimulationPyrrolidinesRatsRats, Long-EvansReperfusion InjurySpinal CordNF-kappa Bpyrrolidine dithiocarbamic acidPyrrolidinesThiocarbamates

Identifiers

PMID19878863
PMCPMC4531089
OpenAlexW2122240267

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.