Evidence map›Paper›PMID 32996580›Full record

ReviewHistology and histopathology2021

Cerebrovascular pathophysiology of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.

Hidenori Suzuki, Hideki Kanamaru, Fumihiro Kawakita, Reona Asada, Masashi Fujimoto, Masato Shiba

Abstract readReview
PubMed Publisher
In one paragraph

Review in Histology and histopathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
9.5field-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.

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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.

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15 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 1 institution in 1 country.

Hidenori SuzukiDepartment of Neurosurgery, Mie University Graduate School of Medicine, Tsu, Japan. suzuki02@clin.medic.mie-u.ac.jp.
Hideki KanamaruDepartment of Neurosurgery, Mie University Graduate School of Medicine, Tsu, Japan.
Fumihiro KawakitaDepartment of Neurosurgery, Mie University Graduate School of Medicine, Tsu, Japan.
Reona AsadaDepartment of Neurosurgery, Mie University Graduate School of Medicine, Tsu, Japan.
Masashi FujimotoDepartment of Neurosurgery, Mie University Graduate School of Medicine, Tsu, Japan.
Masato ShibaDepartment of Neurosurgery, Mie University Graduate School of Medicine, Tsu, Japan.
Mie University · JP

Funding

JSPS KAKENHI JP20K09346JSPS KAKENHI JP20K17963
6 · The paper itself

Abstract

Aneurysmal subarachnoid hemorrhage (SAH) remains a serious cerebrovascular disease. Even if SAH patients survive the initial insults, delayed cerebral ischemia (DCI) may occur at 4 days or later post-SAH. DCI is characteristics of SAH, and is considered to develop by blood breakdown products and inflammatory reactions, or secondary to early brain injury, acute pathophysiological events that occur in the brain within the first 72 hours of aneurysmal SAH. The pathology underlying DCI may involve large artery vasospasm and/or microcirculatory disturbances by microvasospasm, microthrombosis, dysfunction of venous outflow and compression of microvasculature by vasogenic or cytotoxic tissue edema. Recent clinical evidence has shown that large artery vasospasm is not the only cause of DCI, and that both large artery vasospasm-dependent and -independent cerebral infarction causes poor outcome. Animal studies suggest that mechanisms of vasospasm may differ between large artery and arterioles or capillaries, and that many kinds of cells in the vascular wall and brain parenchyma may be involved in the pathogenesis of microcirculatory disturbances. The impairment of the paravascular and glymphatic systems also may play important roles in the development of DCI. As pathological mediators for DCI, glutamate and several matricellular proteins have been investigated in addition to inflammatory molecules. Glutamate is involved in excitotoxicity contributing to cortical spreading ischemia and epileptic activity-related events. Microvascular dysfunction is an attractive mechanism to explain the cause of poor outcomes independently of large cerebral artery vasospasm, but needs more studies to clarify the pathophysiologies or mechanisms and to develop a novel therapeutic strategy.

Indexed as

Cerebrovascular CirculationAnimalsBrainBrain IschemiaCerebral InfarctionEdemaHumansInflammationMiceMicrocirculationRatsSubarachnoid HemorrhageVasospasm, Intracranial

Identifiers

PMID32996580
OpenAlexW3089833726

What Socratic 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 Socratic graph.