Evidence map›Paper›PMID 30086289›Full record

ReviewNeuropharmacology2019

Pathophysiology and treatment of cerebral edema in traumatic brain injury.

Ruchira M Jha, Patrick M Kochanek, J Marc Simard

Registry-linked trialOpen access · hybridAbstract readReview
In one paragraph

Review in Neuropharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07358312 (Traumatic Brain Injury - Efficacy of Steroids in Acute Vasogenic Edema), which is not on this map. Cited by 240 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
240citing papers in PubMed, 6 pooled it
23.3field-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.

NCT07358312 not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Traumatic Brain Injury - Efficacy of Steroids in Acute Vasogenic Edema

TypeobservationalSponsorMeditech FoundationRan2026 to 2029Enrolled280ConditionsTraumatic Brain Injury
3 · Its place in the literature

Who cites it

240 citing papers in PubMed, 6 syntheses or guidelines pooled it, 453 citations in OpenAlex.

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180 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

3 authors at 2 institutions in 1 country.

Ruchira M JhaDepartment of Critical Care Medicine, And Safar Center for Resuscitation Research, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States; Department of Neurology, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States; Department of Neurosurgery, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States; Clinical and Translational Science Institute, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States.
Patrick M KochanekDepartment of Critical Care Medicine, And Safar Center for Resuscitation Research, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States; Clinical and Translational Science Institute, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States; Department of Anesthesiology, University of Pittsburgh, Pittsburgh, PA, United States.
J Marc SimardDepartment of Neurosurgery, School of Medicine, University of Maryland, Baltimore, MD, United States; Department of Pathology, School of Medicine, University of Maryland, Baltimore, MD, United States; Department of Physiology, School of Medicine, University of Maryland, Baltimore, MD, United States. Electronic address: msimard@som.umaryland.edu.
University of Pittsburgh · USUniversity of Maryland, Baltimore · US

Funding

PEDIATRIC NEUROINTENSIVE CARE AND RESUSCITATION RESEARCHT32HD040686 · NICHD · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Robert S B Clark, PATRICK M KOCHANEK · 2000 to 2026
$7.1M
Sulfonylurea receptor 1 (SUR1)- A novel therapeutic target in ischemic strokeR01HL082517 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI SIMARD, J. MARC · 2006 to 2021
$5.6M
Spinal cord injury, progressive hemorrhagic necrosis and the NC(Ca-ATP) channelR01NS060801 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI SIMARD, J. MARC · 2009 to 2018
$3.3M
Fn14, non-canonical NF-kappaB and downstream signaling in neuropathic painR01NS105633 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI SIMARD, J. MARC · 2018 to 2022
$1.9M
Non-canonical NF-kappaB signaling and Sur1-Trpm4 in traumatic brain injuryR01NS102589 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI SIMARD, J. MARC · 2017 to 2021
$1.7M
2,3 cAMP in Traumatic Brain InjuryR01NS087978 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JACKSON, EDWIN KERRY, KOCHANEK, PATRICK M · 2014 to 2018
$1.7M
Translational assessment of sulfonylurea receptor-1 as a biomarker and therapeutic target for cerebral edema in traumatic brain injuryK23NS101036 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JHA, RUCHIRA MENKA · 2017 to 2021
$944k
Brain injury due to transcranial versus transthoracic blast exposureI01BX001629 · VA · BALTIMORE VA MEDICAL CENTER · PI SIMARD, J. MARC · 2013 to 2016
–
Gulf War neurotoxicants and acquired cognitive and neuropsychological dysfunctionI01BX002889 · VA · BALTIMORE VA MEDICAL CENTER · PI SIMARD, J. MARC · 2016 to 2019
–
BLRD VA I01 BX001629BLRD VA I01 BX002889NHLBI NIH HHS R01 HL082517NICHD NIH HHS T32 HD040686NINDS NIH HHS K23 NS101036NINDS NIH HHS R01 NS060801NINDS NIH HHS R01 NS087978NINDS NIH HHS R01 NS102589NINDS NIH HHS R01 NS105633
6 · The paper itself

Abstract

Cerebral edema (CE) and resultant intracranial hypertension are associated with unfavorable prognosis in traumatic brain injury (TBI). CE is a leading cause of in-hospital mortality, occurring in >60% of patients with mass lesions, and ∼15% of those with normal initial computed tomography scans. After treatment of mass lesions in severe TBI, an important focus of acute neurocritical care is evaluating and managing the secondary injury process of CE and resultant intracranial hypertension. This review focuses on a contemporary understanding of various pathophysiologic pathways contributing to CE, with a subsequent description of potential targeted therapies. There is a discussion of identified cellular/cytotoxic contributors to CE, as well as mechanisms that influence blood-brain-barrier (BBB) disruption/vasogenic edema, with the caveat that this distinction may be somewhat artificial since molecular processes contributing to these pathways are interrelated. While an exhaustive discussion of all pathways with putative contributions to CE is beyond the scope of this review, the roles of some key contributors are highlighted, and references are provided for further details. Potential future molecular targets for treating CE are presented based on pathophysiologic mechanisms. We thus aim to provide a translational synopsis of present and future strategies targeting CE after TBI in the context of a paradigm shift towards precision medicine. This article is part of the Special Issue entitled "Novel Treatments for Traumatic Brain Injury".

Indexed as

AnimalsBrain EdemaBrain Injuries, TraumaticHumansNeuroprotective AgentsNeuroprotective AgentsCerebral edemaCytotoxic edemaIonic edemaTraumatic brain injuryVasogenic edema

Identifiers

PMID30086289
PMCPMC6309515
OpenAlexW2886166995

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.