title: Molecular pathophysiology of cerebral hemorrhage: secondary brain injury.
abstract: Intracerebral hemorrhage (ICH) is an often fatal type of stroke that kills approximately 30,000 people annually in the United States. If the patient survives the ictus, then the resulting hematoma within brain parenchyma triggers a series of adverse events causing secondary insults and severe neurological deficits. This article discusses selected aspects of secondary brain injury after ICH and outlines key mechanisms associated with hematoma toxicity, oxidative stress, and inflammation. Finally, this review discusses the relevance of hematoma resolution processes as a target for ICH therapy and presents potential clinically relevant molecular targets that could be harnessed to treat secondary injury associated with ICH injury.
authors.affiliation: University of Texas HSC, Medical School, Department of Neurology, 6431 Fannin, Rm 7.210, Houston, TX 77030, USA. J.Aronowski@uth.tmc.edu
authors.forename: Jaroslaw
authors.initials: J
authors.lastname: Aronowski
authors.forename: Xiurong
authors.initials: X
authors.lastname: Zhao
mesh_terms: D001930:Brain Injuries / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology*; D002543:Cerebral Hemorrhage / Q000150:complications* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D006242:Haptoglobins / Q000378:metabolism; D006406:Hematoma / Q000150:complications / Q000503:physiopathology; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism; D006466:Hemopexin / Q000378:metabolism; D006801:Humans; D018384:Oxidative Stress; D047495:PPAR gamma / Q000378:metabolism
chemical_list: D006242:Haptoglobins; D047495:PPAR gamma; D006466:Hemopexin; D006419:Heme Oxygenase (Decyclizing)