Evidence map›Paper›PMID 34955170›Full record

ReviewBiological psychiatry2022

Role of Inflammation in Traumatic Brain Injury-Associated Risk for Neuropsychiatric Disorders: State of the Evidence and Where Do We Go From Here.

Victoria B Risbrough, Melonie N Vaughn, Samantha F Friend

Abstract readReview
In one paragraph

Review in Biological psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Chlorogenic acid attenuates TBI-induced neuroinflammation by suppressing cGAS-STING signaling.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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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

3 authors.

Victoria B RisbroughCenter of Excellence for Stress and Mental Health, San Diego Veterans Affairs Healthcare System, San Diego, California; Department of Psychiatry, University of California San Diego, San Diego, California. Electronic address: vrisbrough@health.ucsd.edu.
Melonie N VaughnDepartment of Neuroscience, University of California San Diego, San Diego, California.
Samantha F FriendCenter of Excellence for Stress and Mental Health, San Diego Veterans Affairs Healthcare System, San Diego, California; Department of Psychiatry, University of California San Diego, San Diego, California.

Funding

Structural & Network-Function Correlates of Fragmented Early-Life Across SpeciesP50MH096889 · NIMH · UNIVERSITY OF CALIFORNIA-IRVINE · PI SANDMAN, CURT ALAN · 2013 to 2023
$25.4M
Neuronal exosomes to identify biomarkers and pathology of deployment-related TBII01BX004312 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI RISBROUGH, VICTORIA B, RISSMAN, ROBERT · 2019 to 2022
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BLRD VA I01 BX004312CSRD VA IK2 CX002343NIMH NIH HHS P50 MH096889
6 · The paper itself

Abstract

In the past decade, there has been an increasing awareness that traumatic brain injury (TBI) and concussion substantially increase the risk for developing psychiatric disorders. Even mild TBI increases the risk for depression and anxiety disorders such as posttraumatic stress disorder by two- to threefold, predisposing patients to further functional impairment. This strong epidemiological link supports examination of potential mechanisms driving neuropsychiatric symptom development after TBI. One potential mechanism for increased neuropsychiatric symptoms after TBI is via inflammatory processes, as central nervous system inflammation can last years after initial injury. There is emerging preliminary evidence that TBI patients with posttraumatic stress disorder or depression exhibit increased central and peripheral inflammatory markers compared with TBI patients without these comorbidities. Growing evidence has demonstrated that immune signaling in animals plays an integral role in depressive- and anxiety-like behaviors after severe stress or brain injury. In this review, we will 1) discuss current evidence for chronic inflammation after TBI in the development of neuropsychiatric symptoms, 2) highlight potential microglial activation and cytokine signaling contributions, and 3) discuss potential promise and pitfalls for immune-targeted interventions and biomarker strategies to identify and treat TBI patients with immune-related neuropsychiatric symptoms.

Indexed as

Brain ConcussionBrain Injuries, TraumaticStress Disorders, Post-TraumaticAnxiety DisordersHumansInflammationDepressionImmune signalingInflammationPTSDRiskTraumatic brain injury

Identifiers

PMID34955170
PMCPMC12128916

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.