Citation

Muradashvili N, Lominadze D. Brain Inj. 2013; 27(13-14): 1508-1515.

Affiliation

Department of Physiology and Biophysics, University of Louisville, School of Medicine , Louisville, KY , USA.

Copyright

(Copyright © 2013, Informa - Taylor and Francis Group)

DOI

10.3109/02699052.2013.823562

PMID

24063686

Abstract

Traumatic brain injury (TBI) has been associated with various neurological disorders. However, the role of cerebrovascular dysfunction and its mechanisms associated with TBI are still not well understood. Inflammation is the main cause of vascular dysfunction. It affects properties of blood components and the vascular wall leading to changes in blood flow and in interaction of blood components and vascular endothelium exacerbating microcirculatory complications during inflammatory diseases. One of the markers of inflammation is a plasma adhesion protein, fibrinogen (Fg). At elevated levels, Fg can also cause inflammatory responses. One of the manifestations of inflammatory responses is an increase in microvascular permeability leading to accumulation of plasma proteins in the subendothelial matrix and causing vascular remodelling. This has a most devastating effect on cerebral circulation after TBI that is accompanied with an elevation of plasma level of Fg and with an increased cerebrovascular permeability in injury penumbra impairing the normal healing process. This study reviews cerebrovascular alterations after TBI, considers the consequences of increased blood-brain barrier permeability, defines the role of elevated level of Fg and discusses the potential mechanisms of its action leading to vascular dysfunction, which subsequently can cause impairment in neuronal function. Thus, possible mechanisms of vasculo-neuronal dysfunction after TBI are considered.

Language: en