Progrediente zerebrale Parenchymschäden durch rezidivierende arterielle Hypotonien

Abstract

To date clinical and experimental investigations have focused on acute strokes and complete infarctions. Histological and immunological staining in animal experiments and improved imaging techniques in patients suggest that selective or incomplete infarction is a common pathomechanism. Incomplete infarction can manifest as laminar necrosis at autopsy and as leukoaraiosis in imaging studies. An important mechanism in the genesis of leukoaraiosis is vascular pathology of the long penetrating arteries of the deep white matter combined with episodes of decreased perfusion pressure or hypotension. We demonstrate that the cumulative effect of repetitive, moderate hypotensive episodes on cognitive performance or cerebral tissue has not been adequately studied and appreciated.