Mechanisms of Damage After Cerebral Hemorrhage

Abstract

The mechanisms triggering brain damage after intracerebral hemorrhage (ICH) are pleiotropic and are in many respects distinct from those contributing to ischemic brain injury. The toxicity of extravasated blood toward all structural components of the neurovascular unit represents a unique feature of ICH-mediated brain damage. Inflammation and oxidative stress appear to play prominent roles in the pathobiology of ICH. The secondary injury after ICH develops over days suggesting the presence of a considerably wide window for therapeutic intervention. Approaches aimed at detoxification of blood-derived noxious components represent a promising target for the treatment of ICH. Pre-clinical animal models provide useful guidance on the pathogenesis of ICH. However, better models to assess re-bleeding (hematoma enlargement) are urgently needed.