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Journal of Neuroinflammation

, 14:108

First Online: 30 May 2017Received: 17 February 2017Accepted: 15 May 2017DOI: 10.1186-s12974-017-0881-y

Cite this article as: Edlmann, E., Giorgi-Coll, S., Whitfield, P.C. et al. J Neuroinflammation 2017 14: 108. doi:10.1186-s12974-017-0881-y

Abstract

Chronic subdural haematoma CSDH is an encapsulated collection of blood and fluid on the surface of the brain. Historically considered a result of head trauma, recent evidence suggests there are more complex processes involved. Trauma may be absent or very minor and does not explain the progressive, chronic course of the condition. This review focuses on several key processes involved in CSDH development: angiogenesis, fibrinolysis and inflammation. The characteristic membrane surrounding the CSDH has been identified as a source of fluid exudation and haemorrhage. Angiogenic stimuli lead to the creation of fragile blood vessels within membrane walls, whilst fibrinolytic processes prevent clot formation resulting in continued haemorrhage. An abundance of inflammatory cells and markers have been identified within the membranes and subdural fluid and are likely to contribute to propagating an inflammatory response which stimulates ongoing membrane growth and fluid accumulation. Currently, the mainstay of treatment for CSDH is surgical drainage, which has associated risks of recurrence requiring repeat surgery. Understanding of the underlying pathophysiological processes has been applied to developing potential drug treatments. Ongoing research is needed to identify if these therapies are successful in controlling the inflammatory and angiogenic disease processes leading to control and resolution of CSDH.

KeywordsAngiogenesis Chronic subdural haematoma Inflammation Head injury Drug therapy AbbreviationsAngAngiopoietin

BBBBlood-brain barrier

CCL-CXCLChemokine ligand

CSDHChronic subdural haematoma

FDPFibrin-fibrinogen degradation product

HIFHypoxia-inducible factor

ILInterleukin

JAK-STATJanus kinase-signal transducer and activator of transcription

JNKc-Jun N-terminal kinase

MAPKMitogen-activated protein kinase

MCPMonocyte chemoattractant protein

MMPMatrix metalloproteinase

NONitric oxide

PGEProstaglandin E

PI3-AktPhosphatidylinositol 3-kinase-serine-threonine kinase

PICPProcollagen type 1

PIIINPProcollagen type 3

TBITraumatic brain injury

TNFTumour necrosis factor

tPATissue plasminogen activator

VEGFVascular endothelial growth factor





Autor: Ellie Edlmann - Susan Giorgi-Coll - Peter C. Whitfield - Keri L. H. Carpenter - Peter J. Hutchinson

Fuente: https://link.springer.com/







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