During the last decade much effort has been invested in understanding the events that occur early after SAH. It is now widely accepted that these early events not only participate in the early ischemic injury but also set the stage for the pathogenesis of delayed vasospasm. That early cerebral ischemia occurs after SAH is documented in both experimental SAH and in human autopsy studies; however, angiographic evidence for vasoconstriction early after SAH is lacking and the source of early ischemic injury is therefore unclear. Recently, the cerebral microvasculature has been identified as an early target of SAH. Changes in the anatomical structure of cerebral microvessels, sufficient to cause functional deficits, are found early after experimental SAH. These changes may explain cerebral ischemia in human in the absence of angiographic evidence of large vessel vasoconstriction. This paper summarizes known alterations in cerebral microvasculature during the first 48 h after SAH.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/978-3-7091-0353-1_9 | DOI Listing |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!