Evidence map›Paper›PMID 41141399›Full record

ArticleNeurotrauma reports2025

Concomitant Traumatic Brain Injury Exacerbates Endotheliopathy in Patients with Spinal Cord Injury.

Shahab Hafezi, Miguel A Ruiz-Cardozo, Sarbani Ghosh, Sravanthi Bandla, Matthew N Montoya Rush, Anand Dharmarajan, Mark H Hoofnagle, Isaiah R Turnbull, Camilo A Molina, Grace M Niziolek

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurotrauma reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. Review
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

10 authors.

Shahab HafeziSection of Acute and Critical Care Surgery, Department of Surgery, Washington University School of Medicine in St. Louis, Saint Louis, Missouri, USA.
Miguel A Ruiz-CardozoDepartment of Neurosurgery, Washington University School of Medicine in St. Louis, Saint Louis, Missouri, USA.
Sarbani GhoshSection of Acute and Critical Care Surgery, Department of Surgery, Washington University School of Medicine in St. Louis, Saint Louis, Missouri, USA.
Sravanthi BandlaSection of Acute and Critical Care Surgery, Department of Surgery, Washington University School of Medicine in St. Louis, Saint Louis, Missouri, USA.
Matthew N Montoya RushSection of Acute and Critical Care Surgery, Department of Surgery, Washington University School of Medicine in St. Louis, Saint Louis, Missouri, USA.
Anand DharmarajanSection of Acute and Critical Care Surgery, Department of Surgery, Washington University School of Medicine in St. Louis, Saint Louis, Missouri, USA.
Mark H HoofnagleSection of Acute and Critical Care Surgery, Department of Surgery, Washington University School of Medicine in St. Louis, Saint Louis, Missouri, USA.
Isaiah R TurnbullSection of Acute and Critical Care Surgery, Department of Surgery, Washington University School of Medicine in St. Louis, Saint Louis, Missouri, USA.
Camilo A MolinaDepartment of Neurosurgery, Washington University School of Medicine in St. Louis, Saint Louis, Missouri, USA.
Grace M NiziolekSection of Acute and Critical Care Surgery, Department of Surgery, Washington University School of Medicine in St. Louis, Saint Louis, Missouri, USA.

Funding

Hematopoietic Stem and Progenitor Cell Dysfunction is an Underlying Mechanism of Injury-Inuced ImmunosuppressionR35GM133756 · NIGMS · WASHINGTON UNIVERSITY · PI TURNBULL, ISAIAH R · 2019 to 2023
$2.0M
NIGMS NIH HHS R35 GM133756
6 · The paper itself

Abstract

Neurotrauma can cause endothelial dysfunction, characterized by neurovascular barrier disruption, tissue edema, neuroinflammation, and coagulation abnormalities, all of which may contribute to secondary injuries and worsened clinical outcomes. Here, we assess the effect of different types of neurotrauma on the local levels of biomarkers of endothelial injury and inflammation. Cerebrospinal fluid (CSF) samples were collected at multiple time points from patients with isolated traumatic spinal cord injury (SCI) and patients with concomitant SCI and traumatic brain injury (TBI). CSF levels of analytes associated with endothelial damage, as well as inflammatory mediators, were measured. Compared with patients with isolated SCI, those with SCI + TBI demonstrated significantly elevated CSF levels of multiple biomarkers linked to endotheliopathy and inflammation. In the presence of TBI, the highest increases in CSF levels of endothelial markers were observed for matrix metalloproteinase 10 (MMP-10), vascular endothelial growth factor A (VEGF-A), and fibroblast growth factor 2 (FGF-2). Among inflammatory factors, thymic stromal lymphopoietin (TSLP) showed the most pronounced difference in CSF content in patients with SCI + TBI compared with those with SCI alone, followed by interferon α2 (IFNα2) and granulocyte-macrophage colony-stimulating factor (GM-CSF). Interestingly, CSF levels of MMP-1, MMP-10, VEGF-A, IFNα2, and TSLP significantly correlated with injury severity score. Our findings indicate that, in the presence of concomitant TBI, patients with SCI exhibit higher CSF levels of biomarkers associated with endotheliopathy, blood-brain barrier breakdown, protease-mediated degradation of endothelial glycocalyx, and neuroinflammation. These results identify potential theranostic biomarkers to stratify high-risk patients and mitigate neurovascular damage, thereby improving clinical outcomes.

Indexed as

biomarkerendotheliopathyinflammationneurotraumaspinal cord injurytraumatic brain injury

Identifiers

PMID41141399
PMCPMC12547390

What OpenQuestion holds

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Registered trials

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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.