Mechanisms of memory impairment in animal models of nontraumatic intracranial hemorrhage: A systematic review of the literature
Peterson C., Umoye AO., Puglisi CH., Waldau B.
Systematic Review on Chronic Inflammation, published in Brain Hemorrhages (2022) — summary generated from the PubMed abstract.
Relatively higher-quality human studies compared with other topics in this database, e.g. multiple RCTs or systematic reviews. This does not mean it is standard or approved care.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Systematic Review
- Journal
- Brain Hemorrhages (2022)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 36093312
- PMCID
- PMC9454327
- DOI
- 10.1016/j.hest.2021.08.002
- Citations
- 2
Abstract (original English)
Mechanisms underlying memory and cognitive dysfunction following spontaneous intracranial hemorrhage are diverse. The aim of this systematic review was to provide a contemporary review of the commonly reported mechanisms responsible for memory impairment following nontraumatic intracranial hemorrhage. PubMed, Embase, and Scopus databases were systematically searched for pre-clinical studies, and results were reported according to PRISMA guidelines. Methodological quality assessment was performed according to the SYRCLE's Risk of Bias tool. Ninety studies met the inclusion criteria. Most of animal studies reported on subarachnoid hemorrhage (48%), followed by intraparenchymal hemorrhage (44%), and intraventricular hemorrhage (8%). Most of subarachnoid hemorrhage studies (30%) reported neuronal apoptosis as a mechanism for memory dysfunction, whereas the most commonly described mechanism following intraparenchymal hemorrhage (40%) and intraventricular hemorrhage (23%) was a proinflammatory response. Based on SYRCLE's Risk of Bias assessment, the average methodological risk of bias of all studies was 56.83 ± 12.77% on a 0-100% scale. There is a great need not only for more preclinical studies with improved methodology, but also for studies reporting negative treatment effects and for multicenter animal studies. In vivo studies on non-rodent animal ICH models can also be helpful.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Relatively higher-quality human studies compared with other topics in this database, e.g. multiple RCTs or systematic reviews. This does not mean it is standard or approved care.
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