Evidence map›Paper›PMID 21988198›Full record

ReviewJournal of neurotrauma2012

Hemorrhagic progression of a contusion after traumatic brain injury: a review.

David Kurland, Caron Hong, Bizhan Aarabi, Volodymyr Gerzanich, J Marc Simard

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of neurotrauma, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed, 4 pooled it
8.0field-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

136 citing papers in PubMed, 4 syntheses or guidelines pooled it, 333 citations in OpenAlex.

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  20. Pathophysiology of penetrating captive-bolt stunning of horses.Animal welfare (South Mimms, England) · 2025
    Article

76 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

5 authors at 1 institution in 1 country.

David KurlandDepartment of Neurosurgery, University of Maryland School of Medicine, Baltimore, Maryland 21201-1595, USA.
Caron Hong
Bizhan Aarabi
Volodymyr Gerzanich
J Marc Simard
University of Maryland, Baltimore · US

Funding

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
TRPM4 channel in spinal cord injuryR01NS061934 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI GERZANICH, VLADIMIR · 2008 to 2018
$3.3M
Pathological role of the SUR1-regulated NC(Ca-ATP) channel in cortex after subaraR01NS061808 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI SIMARD, J. MARC · 2009 to 2013
$1.6M
Role of TRP channels in secondary injury after brain traumaR01NS072501 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI GERZANICH, VLADIMIR · 2011 to 2014
$1.3M
NHLBI NIH HHS HL082517NINDS NIH HHS NS060801NINDS NIH HHS NS061808NINDS NIH HHS NS061934NINDS NIH HHS R01 NS072501
6 · The paper itself

Abstract

The magnitude of damage to cerebral tissues following head trauma is determined by the primary injury, caused by the kinetic energy delivered at the time of impact, plus numerous secondary injury responses that almost inevitably worsen the primary injury. When head trauma results in a cerebral contusion, the hemorrhagic lesion often progresses during the first several hours after impact, either expanding or developing new, non-contiguous hemorrhagic lesions, a phenomenon termed hemorrhagic progression of a contusion (HPC). Because a hemorrhagic contusion marks tissues with essentially total unrecoverable loss of function, and because blood is one of the most toxic substances to which the brain can be exposed, HPC is one of the most severe types of secondary injury encountered following traumatic brain injury (TBI). Historically, HPC has been attributed to continued bleeding of microvessels fractured at the time of primary injury. This concept has given rise to the notion that continued bleeding might be due to overt or latent coagulopathy, prompting attempts to normalize coagulation with agents such as recombinant factor VIIa. Recently, a novel mechanism was postulated to account for HPC that involves delayed, progressive microvascular failure initiated by the impact. Here we review the topic of HPC, we examine data relevant to the concept of a coagulopathy, and we detail emerging data elucidating the mechanism of progressive microvascular failure that predisposes to HPC after head trauma.

Indexed as

Disease ProgressionBrain InjuriesCerebral Hemorrhage, TraumaticHumans

Identifiers

PMID21988198
PMCPMC3253310
OpenAlexW2101551122

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.