Acute SAH from a ruptured intracranial aneurysm contributes for 30% of all hemorrhagic
strokes. The bleeding itself occurs in the subarachnoid space. Nevertheless, injury to the
brain parenchyma occurs as a consequence of the bleeding, directly, via several well-defined
mechanisms and pathways, but also indirectly, or secondarily. This secondary brain injury following
SAH has a variety of causes and possible mechanisms. Amongst others, inflammatory events
have been shown to occur in parallel to, contribute to, or even to initiate programmed cell death
(PCD) within the central nervous system (CNS) in human and animal studies alike.
Mechanisms of secondary brain injury are of utmost interest not only to scientists, but also to
clinicians, as they often provide possibilities for translational approaches as well as distinct time
windows for tailored treatment options.
In this article, we review secondary brain injury due to inflammatory changes, that occur on
cellular, as well as on molecular level in the various different compartments of the CNS: the brain
vessels, the subarachnoid space, and the brain parenchyma itself and hypothesize about possible
signaling mechanisms between these compartments.