Evidence map›Paper›PMID 21045864›Full record

ReviewJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2011

Clinical relevance of cortical spreading depression in neurological disorders: migraine, malignant stroke, subarachnoid and intracranial hemorrhage, and traumatic brain injury.

Martin Lauritzen, Jens Peter Dreier, Martin Fabricius, Jed A Hartings, Rudolf Graf, Anthony John Strong

Registry-linked trialOpen access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05095857 (S-ketamine for Cortical Spreading Depolarisation in Patients With Severe Acute Brain Injury), which is not on this map. Cited by 394 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
394citing papers in PubMed, 8 pooled it
24.9field-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.

NCT05095857 phase4recruitingnot on this mapstarted 2023, after this paper: background citation

S-ketamine for Cortical Spreading Depolarisation in Patients With Severe Acute Brain Injury

TypeinterventionalSponsorRigshospitalet, DenmarkRan2023 to 2028Enrolled400ConditionsSubarachnoid Hemorrhage, Aneurysmal, Intracerebral Hemorrhage, Traumatic Brain InjuryArmsS-ketamine, Isotonic saline (placebo)
3 · Its place in the literature

Who cites it

394 citing papers in PubMed, 8 syntheses or guidelines pooled it, 778 citations in OpenAlex.

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334 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

6 authors at 5 institutions in 4 countries.

Martin LauritzenDepartment of Clinical Neurophysiology, Glostrup Hospital, Glostrup, Denmark. marlau03@glo.regionh.dk
Jens Peter Dreier
Martin Fabricius
Jed A Hartings
Rudolf Graf
Anthony John Strong
Glostrup Hospital · DKCharité - Universitätsmedizin Berlin · DEKing's College London · GBMax Planck Institute for Metabolism Research · DEUniversity of Cincinnati Medical Center · US

Funding

Wellcome Trust
6 · The paper itself

Abstract

Cortical spreading depression (CSD) and depolarization waves are associated with dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, increased energy metabolism and changes in cerebral blood flow (CBF). There is strong clinical and experimental evidence to suggest that CSD is involved in the mechanism of migraine, stroke, subarachnoid hemorrhage and traumatic brain injury. The implications of these findings are widespread and suggest that intrinsic brain mechanisms have the potential to worsen the outcome of cerebrovascular episodes or brain trauma. The consequences of these intrinsic mechanisms are intimately linked to the composition of the brain extracellular microenvironment and to the level of brain perfusion and in consequence brain energy supply. This paper summarizes the evidence provided by novel invasive techniques, which implicates CSD as a pathophysiological mechanism for this group of acute neurological disorders. The findings have implications for monitoring and treatment of patients with acute brain disorders in the intensive care unit. Drawing on the large body of experimental findings from animal studies of CSD obtained during decades we suggest treatment strategies, which may be used to prevent or attenuate secondary neuronal damage in acutely injured human brain cortex caused by depolarization waves.

Indexed as

Brain InjuriesCerebrovascular CirculationCortical Spreading DepressionElectrophysiological PhenomenaEnergy MetabolismHumansIntracranial HemorrhagesMigraine DisordersNervous System DiseasesStrokeSubarachnoid Hemorrhage

Identifiers

PMID21045864
PMCPMC3049472
OpenAlexW2003509571

What OpenQuestion holds

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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 OpenQuestion graph.