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Editorial
September 2014

Targeting the Immune System in Intracerebral Hemorrhage

Author Affiliations
  • 1Division of Neurocritical Care and Emergency Neurology, Department of Neurology, Yale University School of Medicine, New Haven, Connecticut
  • 2Division of Neurocritical Care and Emergency Neurology, Center for Human Genetic Research, Massachusetts General Hospital, Boston
JAMA Neurol. 2014;71(9):1083-1084. doi:10.1001/jamaneurol.2014.1653

Intracerebral hemorrhage (ICH) is the most devastating form of stroke, conferring the highest morbidity and mortality of any stroke subtype.1 To date, most interventions have targeted hematoma expansion. However, ICH expansion occurs early after onset and only in a subset of patients. Therefore, treatments can only be given in the hyperacute setting and, even if successful, will end up benefiting only a minor proportion of patients. In contrast, secondary injury and the development of perihematomal edema (PHE) contribute to further tissue damage and neurologic deterioration over an extended window of hours to days. Therefore, therapies that prevent or reverse such damage could be given more easily and widely.

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