Inflammation and stroke

Abstract

It is well-known that inflammation plays a major role in the genesis of the atherosclerotic plaque and thus favours the occurrence of stroke. But, inflammation is also involved after an ischaemic event affecting the brain. In this case, one can observe the infiltration of numerous inflammatory cells at the site of the lesion, the activation of the microglia and of pro-inflammatory cytokines, etc. It is usually thought that this poststroke inflammation is rather deleterious, as suggested by the fact that, after an experimentally-induced ischaemic stroke, blockade of the inflammatory response improves the neurological condition of mice. Nevertheless, until now, the application of such experimental treatments in humans has revealed unsuccessful. One of the possible explanations for this phenomenon might be that inflammation also has some beneficial effects, such as clearance of damaged tissue, promotion of angiogenesis, or still tissue remodelling and regeneration. After this first “basic science” part, we will briefly review some clinical aspects of the most significant inflammatory diseases that can cause stroke, i.e., the vasculitis. Among them, Takayasu’s arteritis, giant cell temporal arteritis (Horton’s disease), and primary angiitis of the central nervous system will be discussed. We will also shortly address the question of the antiphospholipid syndrome.