Abstract
Intracerebral hemorrhage (ICH) is a major health concern, with high rates of mortality
and morbidity and no highly effective clinical interventions. Basic research in animal
models of ICH has provided insight into its complex pathology, in particular revealing
the role of inflammation in driving neuronal death and neurologic deficits after hemorrhage.
The response to ICH occurs in four distinct phases: (1) initial tissue damage and
local activation of inflammatory factors, (2) inflammation-driven breakdown of the
blood–brain barrier, (3) recruitment of circulating inflammatory cells and subsequent
secondary immunopathology, and (4) engagement of tissue repair responses that promote
tissue repair and restoration of neurologic function. The development of CNS inflammation
occurs over many days after initial hemorrhage and thus may represent an ideal target
for treatment of the disease, but further research is required to identify the mechanisms
that promote engagement of inflammatory versus anti-inflammatory pathways. In this
review, the authors examine how experimental models of ICH have uncovered critical
mediators of pathology in each of the four stages of the inflammatory response, and
focus on the role of the immune system in these processes.
Keywords
intracerebral hemorrhage - stroke - neuroinflammation - neuroimmunology
