What Causes Hematoma Enlargement in Lobar Intracerebral Hemorrhage?

Abstract

See related article, p 1490. Intracerebral hemorrhage (ICH) accounts for 10% to 15% of all strokes worldwide.1 “Primary” ICH most often results from the rupture of a small penetrating artery, either associated with hypertensive arteriopathy or cerebral amyloid angiopathy (CAA). Whereas CAA-related ICH preferentially affects cortical–subcortical regions, hypertensive bleedings are located in “deep” areas of the brain such as the basal ganglia, thalamus, and brain stem. For both subtypes of ICH, hematoma size on initial brain scan and hematoma enlargement (HE) between the first and second brain imagings are strong and independent predictors of functional outcome.2,3 Hence, the prevention of HE by coagulation activation was recently evaluated as a treatment strategy in acute ICH in a large-scale randomized trial. Although recombinant coagulation factor VII reduced hematoma expansion, a positive effect on functional outcome after 3 months could not be demonstrated.4 One of the reasons for the lack of success of clinical trials so far might be our scarce knowledge regarding the pathophysiology that underlies hematoma growth. Observational studies reported HE to occur in approximately 30% to 40% of all ICH cases depending on the time spans to first and second brain imaging.5 Several predictors of HE have been identified so far, including clinical, laboratory, and radiological parameters.6,7 In this issue of Stroke , Brouwers et al8 identified the apolipoprotein E (APOE) genotype as a new risk factor for HE. APOE was initially characterized for its involvement in Alzheimer disease.9 It is a lipoprotein with …