Neuroinflammation in Ischemic Pediatric Stroke

Abstract

Over the last decades, the importance of inflammatory processes in pediatric stroke have become increasingly evident. Ischemia launches a cascade of events: activation and inhibition of inflammation by a large network of cytokines, adhesion and small molecules, protease, and chemokines. There are major differences in the neonatal brain compared to adult brain, but developmental trajectories of the process during childhood are not yet well known. In neonatal stroke ischemia is the leading pathophysiology, but infectious and inflammatory processes have a significant input into the course and degree of tissue damage. In childhood, beside inflammation lanced by ischemia itself, the event of ischemia might be provoked by an underlying inflammatory pathophysiology: transient focal arteriopathy, dissection, sickle cell anemia, Moyamoya and more generalized in meningitides, generalized vasculitis or genetic arteriopathies (as in ADA2). Focal inflammatory reactions tend to be located in the distal part of the carotid artery or the proximal medial arteries, but generalized processes rather tend to affect the small arteries.