Evidence map›Paper›PMID 27258442›Full record

ReviewJournal of clinical neurophysiology : official publication of the American Electroencephalographic Society2016

Spreading Depolarizations: A Therapeutic Target Against Delayed Cerebral Ischemia After Subarachnoid Hemorrhage.

David Y Chung, Fumiaki Oka, Cenk Ayata

Open access · greenAbstract readReview
In one paragraph

Review in Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 4 pooled it
3.1field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 4 syntheses or guidelines pooled it, 50 citations in OpenAlex.

  1. Pooled it
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  17. Rapid hematoma growth triggers spreading depolarizations in experimental intracortical hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  18. Aneurysmal Subarachnoid Hemorrhage.Neurologic clinics · 2021
    Review
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

David Y Chung*Neurovascular Research Unit, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, U.S.A.; †Stroke Service and Neuroscience Intensive Care Unit, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, U.S.A.; and ‡Department of Neurosurgery, Yamaguchi University School of Medicine, Ube, Japan.
Fumiaki Oka
Cenk Ayata
Massachusetts General Hospital · US

Funding

Targeting ROCK for Neurogliovascular Plasticity & Remodeling After StrokeP01NS055104 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI LO, ENG H. · 2007 to 2018
$13.3M
Neuroscience Resident Research ProgramR25NS065743 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI CASH, SYDNEY S, WILLIAMS, ZIV · 2009 to 2023
$11.8M
Neurology Research Education and Mentorship ProgramR25NS070697 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI KUO, SHENG-HAN · 2010 to 2023
$1.9M
NINDS NIH HHS P01 NS055104NINDS NIH HHS R25 NS065743NINDS NIH HHS R25 NS070697
6 · The paper itself

Abstract

Delayed cerebral ischemia is the most feared cause of secondary injury progression after subarachnoid hemorrhage. Initially thought to be a direct consequence of large artery spasm and territorial ischemia, recent data suggests that delayed cerebral ischemia represents multiple concurrent and synergistic mechanisms, including microcirculatory dysfunction, inflammation, and microthrombosis. Among these mechanisms, spreading depolarizations (SDs) are arguably the most elusive and underappreciated in the clinical setting. Although SDs have been experimentally detected and examined since the late 1970s, their widespread occurrence in human brain was not unequivocally demonstrated until relatively recently. We now know that SDs occur with very high incidence in human brain after ischemic or hemorrhagic stroke and trauma, and worsen outcomes by increasing metabolic demand, decreasing blood supply, predisposing to seizure activity, and possibly worsening brain edema. In this review, we discuss the causes and consequences of SDs in injured brain. Although much of our mechanistic knowledge comes from experimental models of focal cerebral ischemia, clinical data suggest that the same principles apply regardless of the mode of injury (i.e., ischemia, hemorrhage, or trauma). The hope is that a better fundamental understanding of SDs will lead to novel therapeutic interventions to prevent SD occurrence and its adverse consequences contributing to injury progression in subarachnoid hemorrhage and other forms of acute brain injury.

Indexed as

Brain IschemiaCerebral CortexHumansSubarachnoid Hemorrhage

Identifiers

PMID27258442
PMCPMC4894342
OpenAlexW2462639291

What OpenQuestion 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 OpenQuestion graph.