Evidence map›Paper›PMID 28817088›Full record

ReviewInternational journal of molecular sciences2017

The Role of Neurogenic Inflammation in Blood-Brain Barrier Disruption and Development of Cerebral Oedema Following Acute Central Nervous System (CNS) Injury.

Annabel J Sorby-Adams, Amanda M Marcoionni, Eden R Dempsey, Joshua A Woenig, Renée J Turner

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 3 pooled it
7.2field-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

82 citing papers in PubMed, 3 syntheses or guidelines pooled it, 142 citations in OpenAlex.

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22 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.

Annabel J Sorby-AdamsAdelaide Medical School and Adelaide Centre for Neuroscience Research, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide SA 5005, Australia. annabel.sorby-adams@adelaide.edu.au.
Amanda M MarcoionniAdelaide Medical School and Adelaide Centre for Neuroscience Research, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide SA 5005, Australia. amanda.marcoionni@student.adelaide.edu.au.
Eden R DempseyAdelaide Medical School and Adelaide Centre for Neuroscience Research, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide SA 5005, Australia. edendempsey19@gmail.com.
Joshua A WoenigAdelaide Medical School and Adelaide Centre for Neuroscience Research, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide SA 5005, Australia. josh.woenig@adelaide.edu.au.
Renée J TurnerAdelaide Medical School and Adelaide Centre for Neuroscience Research, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide SA 5005, Australia. renee.turner@adelaide.edu.au.
University of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute central nervous system (CNS) injury, encompassing traumatic brain injury (TBI) and stroke, accounts for a significant burden of morbidity and mortality worldwide, largely attributable to the development of cerebral oedema and elevated intracranial pressure (ICP). Despite this, clinical treatments are limited and new therapies are urgently required to improve patient outcomes and survival. Originally characterised in peripheral tissues, such as the skin and lungs as a neurally-elicited inflammatory process that contributes to increased microvascular permeability and tissue swelling, neurogenic inflammation has now been described in acute injury to the brain where it may play a key role in the secondary injury cascades that evolve following both TBI and stroke. In particular, release of the neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP) appear to be critically involved. In particular, increased SP expression is observed in perivascular tissue following acute CNS injury, with the magnitude of SP release being related to both the frequency and degree of the insult. SP release is associated with profound blood-brain barrier disruption and the subsequent development of vasogenic oedema, as well as neuronal injury and poor functional outcomes. Inhibition of SP through use of a neurokinin 1 (NK1) antagonist is highly beneficial following both TBI and ischaemic stroke in pre-clinical models. The role of CGRP is more unclear, especially with respect to TBI, with both elevations and reductions in CGRP levels reported following trauma. However, a beneficial role has been delineated in stroke, given its potent vasodilatory effects. Thus, modulating neuropeptides represents a novel therapeutic target in the treatment of cerebral oedema following acute CNS injury.

Indexed as

AnimalsBlood-Brain BarrierBrain EdemaBrain Injuries, TraumaticCalcitonin Gene-Related PeptideCapillary PermeabilityGene Expression RegulationHumansNeurogenic InflammationNeuronsSubstance PCalcitonin Gene-Related PeptideSubstance Pblood-brain barriercalcitonin gene-related peptidecerebral oedemaneurogenic inflammationneuropeptidesstrokesubstance Ptachykinintraumatic brain injury

Identifiers

PMID28817088
PMCPMC5578176
OpenAlexW2749724913

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.