Evidence map›Paper›PMID 20837823›Full record

ReviewArchives of neurology2011

Spreading depolarization: a possible new culprit in the delayed cerebral ischemia of subarachnoid hemorrhage.

Lewis Z Leng, Matthew E Fink, Costantino Iadecola

Abstract readReview
In one paragraph

Review in Archives of neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Guideline
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  15. Spreading depolarizations increase delayed brain injury in a rat model of subarachnoid hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016
    Article
  16. Article
  17. Clinical Development and Implementation of an Institutional Guideline for Prospective EEG Monitoring and Reporting of Delayed Cerebral Ischemia.Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society · 2016
    Review
  18. Article
  19. Article
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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 at 1 institution in 1 country.

Lewis Z LengDepartment of Neurological Surgery, Weill Cornell Medical College, New York Presbyterian Hospital, New York, NY 10065, USA.
Matthew E Fink
Costantino Iadecola
NewYork–Presbyterian Hospital · US

Funding

Radiotelemetry CoreP01HL096571 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI DAVISSON, ROBIN L · 2009 to 2013
$8.8M
NO SYNTHASE GENE EXPRESSION AND CEREBRAL ISCHEMIC DAMAGER01NS034179 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IADECOLA, COSTANTINO · 1995 to 2021
$5.5M
Role of COX-2 Gene Expression in Ischemic Brain DamageR01NS035806 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IADECOLA, COSTANTINO · 1997 to 2010
$3.5M
CHRONIC INTERMITTENT HYPOXIA, NEUROVASCULAR DYSFUNCTION AND STROKER01NS073666 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IADECOLA, COSTANTINO · 2011 to 2015
$1.8M
NO SYNTHASE GENE EXPRESSION AND CEREBRAL ISCHEMIC DAMAGER37NS034179 · NINDS · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI IADECOLA, COSTANTINO · 1999 to 2005
$1.8M
NHLBI NIH HHS HL96571NHLBI NIH HHS P01 HL096571NINDS NIH HHS NS34179NINDS NIH HHS NS35806NINDS NIH HHS R01 NS034179NINDS NIH HHS R01 NS035806NINDS NIH HHS R01 NS073666NINDS NIH HHS R37 NS034179
6 · The paper itself

Abstract

Aneurysmal subarachnoid hemorrhage (SAH) is a devastating disease with a high mortality and morbidity rate. Gradual improvements have been made in the reduction of mortality rates associated with the disease during the last 30 years. However, delayed cerebral ischemia (DCI), the major delayed complication of SAH, remains a significant contributor to mortality and morbidity despite substantial research and clinical efforts. During the last several years, the predominant role of cerebral vasospasm, the long-accepted etiologic factor behind DCI, has been questioned. It is now becoming increasingly clear that the pathophysiology underlying DCI is multifactorial. Cortical spreading depression is emerging as a likely factor in this complex web of pathologic changes after SAH. Understanding its role after SAH and its relationship with the other pathologic processes such as vasospasm, microcirculatory dysfunction, and microemboli will be vital to the development of new therapeutic approaches to reduce DCI and improve the clinical outcome of the disease.

Indexed as

AnimalsBrain IschemiaCortical Spreading DepressionHumansSubarachnoid HemorrhageTime FactorsVasospasm, Intracranial

Identifiers

PMID20837823
PMCPMC3998646
OpenAlexW2046247374

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.