Evidence map›Paper›PMID 24335193›Full record

ReviewPharmacological reviews2014

Neuroinflammation and comorbidity of pain and depression.

A K Walker, A Kavelaars, C J Heijnen, R Dantzer

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Pharmacological reviews, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 213 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
213citing papers in PubMed, 9 pooled it
5.6field-weighted citation impact, top 2% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

213 citing papers in PubMed, 9 syntheses or guidelines pooled it, 451 citations in OpenAlex.

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  7. A Specific Inflammatory Profile Underlying Suicide Risk? Systematic Review of the Main Literature Findings.International journal of environmental research and public health · 2020
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  19. Opioidergic modulation of stress-induced hyperalgesia in adult zebrafish.Journal of neural transmission (Vienna, Austria : 1996) · 2026
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153 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

A K WalkerDepartment of Symptom Research Laboratory of Neuroimmunology of Cancer-Related Symptoms at the Institute of Biosciences and Technology, Texas A&M Health Sciences Center, 2121 W. Holcombe Boulevard, Room 1025, Houston, TX 77030. akwalker@mdanderson.org.
A Kavelaars
C J Heijnen
R Dantzer
The University of Texas MD Anderson Cancer Center · US

Funding

Neuroimmune Mechanisms of Recovery from Comorbid Depression and Chronic PainR01NS073939 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DANTZER, ROBERT, HEIJNEN, COBI J · 2011 to 2020
$4.0M
A novel molecular switch regulating transition from acute to chronic pain.R01NS074999 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KAVELAARS, ANNEMIEKE · 2011 to 2015
$1.7M
NINDS NIH HHS R01 NS073939NINDS NIH HHS R01-NS073939NINDS NIH HHS R01 NS074999NINDS NIH HHS R01-NS074999
6 · The paper itself

Abstract

Comorbid depression and chronic pain are highly prevalent in individuals suffering from physical illness. Here, we critically examine the possibility that inflammation is the common mediator of this comorbidity, and we explore the implications of this hypothesis. Inflammation signals the brain to induce sickness responses that include increased pain and negative affect. This is a typical and adaptive response to acute inflammation. However, chronic inflammation induces a transition from these typical sickness behaviors into depression and chronic pain. Several mechanisms can account for the high comorbidity of pain and depression that stem from the precipitating inflammation in physically ill patients. These mechanisms include direct effects of cytokines on the neuronal environment or indirect effects via downregulation of G protein-coupled receptor kinase 2, activation of the tryptophan-degrading enzyme indoleamine 2,3-dioxygenase that generates neurotropic kynurenine metabolites, increased brain extracellular glutamate, and the switch of GABAergic neurotransmission from inhibition to excitation. Despite the existence of many neuroimmune candidate mechanisms for the co-occurrence of depression and chronic pain, little work has been devoted so far to critically assess their mediating role in these comorbid symptoms. Understanding neuroimmune mechanisms that underlie depression and pain comorbidity may yield effective pharmaceutical targets that can treat both conditions simultaneously beyond traditional antidepressants and analgesics.

Indexed as

AnimalsBrainComorbidityDepressionHumansInflammationPain

Identifiers

PMID24335193
PMCPMC3880465
OpenAlexW2138452800

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.