Evidence map›Paper›PMID 30124090›Full record

ReviewMolecular pain

Autoinflammatory and autoimmune contributions to complex regional pain syndrome.

J David Clark, Vivianne L Tawfik, Maral Tajerian, Wade S Kingery

Registry-linked trialOpen access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07446712 (Hyperbaric Oxygen Therapy in Complex Regional Pain Syndrome), which is not on this map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
12.3field-weighted citation impact, top 1% 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.

NCT07446712 narecruitingnot on this map

Hyperbaric Oxygen Therapy in Complex Regional Pain Syndrome: a Randomised Controlled Trial

TypeinterventionalSponsorUniversity Hospital OstravaRan2026 to 2029Enrolled60ConditionsChronic Pain, Complex Regional Pain SyndromeArmsEarly hyperbaric oxygen therapy (HBOT), Delayed hyperbaric oxygen therapy (HBOT)
3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 98 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

J David Clark1 Anesthesiology Service, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA.
Vivianne L Tawfik2 Department of Anesthesiology, Perioperative & Pain Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Maral Tajerian2 Department of Anesthesiology, Perioperative & Pain Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Wade S Kingery3 Palo Alto Veterans Institute for Research, Palo Alto, CA, USA.
Stanford University · USPalo Alto Veterans Institute for Research · US

Funding

Neural Immunoregulation of Post-Traumatic AutoimmunityR01NS094438 · NINDS · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI DAVID J. CLARK, WADE S KINGERY · 2016 to 2026
$4.4M
Inflammasome Activation in Complex Regional Pain SyndromeR01NS072143 · NINDS · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI CLARK, DAVID J., KINGERY, WADE S · 2011 to 2015
$1.6M
Autonomic Regulation of the Immunological Response to Limb InjuryI01RX001475 · VA · VETERANS ADMIN PALO ALTO HEALTH CARE SYS · PI CLARK, DAVID J. · 2015 to 2025
–
NINDS NIH HHS R01 NS072143NINDS NIH HHS R01 NS094438RRD VA I01 RX001475
6 · The paper itself

Abstract

Complex regional pain syndrome (CRPS) is a highly enigmatic syndrome typically developing after injury or surgery to a limb. Severe pain and disability are common among those with chronic forms of this condition. Accumulating evidence suggests that CRPS may involve both autoinflammatory and autoimmune components. In this review article, evidence for dysfunction of both the innate and adaptive immune systems in CRPS is presented. Findings from human studies in which cytokines and other inflammatory mediators were measured in the skin of affected limbs are discussed. Additional results from studies of mediator levels in animal models are evaluated in this context. Similarly, the evidence from human, animal, and translational studies of the production of autoantibodies and the potential targets of those antibodies is reviewed. Compelling evidence of autoinflammation in skin and muscle of the affected limb has been collected from CRPS patients and laboratory animals. Cytokines including IL-1β, IL-6, TNFα, and others are reliably identified during the acute phases of the syndrome. More recently, autoimmune contributions have been suggested by the discovery of self-directed pain-promoting IgG and IgM antibodies in CRPS patients and model animals. Both the autoimmune and the autoinflammatory components of CRPS appear to be regulated by neuropeptide-containing peripheral nerve fibers and the sympathetic nervous system. While CRPS displays a complex neuroimmunological pathogenesis, therapeutic interventions could be designed targeting autoinflammation, autoimmunity, or the neural support for these phenomena.

Indexed as

AnimalsComplex Regional Pain SyndromesCytokinesDisease Models, AnimalHumansImmunity, InnateInflammationCytokinesautoimmunityAutoinflammationautonomiccytokinenerve growth factorpainperipheral nervous system

Identifiers

PMID30124090
PMCPMC6125849
OpenAlexW2888711096

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.