Abstract
Intracerebral hemorrhage (ICH) is a deadly subtype of stroke that occurs when an arteriole ruptures and bleeds into the brain parenchyma. There is no specific treatment for ICH and progress has not been made to reduce mortality rates or improve outcomes. The immune response is a key component of secondary injury after ICH and represents an accessible treatment target, as it develops over several days. Initiators of this response include the clotting cascade, complement activation, and toll-like receptor-4 activation. These signaling cascades activate brain resident cells, including microglia, astrocytes, and mast cells, which then secrete pro-inflammatory cytokines, chemokines, and free radicals. This response initiates breakdown of the blood-brain barrier and edema formation. Circulating leukocytes migrate into the brain parenchyma by following chemokine gradients and other signals. Once in the brain, neutrophils, monocytes, and T cells induce secondary injury, but may also be important for phagocytosis of the hematoma and later recovery. This article reviews preclinical literature pertaining to these complex immune responses after ICH and provides clinical correlates when available.
Keywords: Hemorrhagic stroke, inflammation, intracerebral hemorrhage, leukocytes, microglia, stroke.
33
3
2
3