Abstract
Secondary injury in intracerebral hemorrhage (ICH) is becoming increasingly well characterized and is the subject of intense investigations. After the initial injury caused by tissue disruption and mass effect of the hematoma, products of coagulation, clot retraction, and hemoglobin breakdown initiate a secondary cascade of deleterious events including apoptosis, necrosis, iron-mediated oxidative stress, inflammation, autophagy, and edema formation [1–3]. Tissue swelling, in particular, may contribute to neurological deterioration and disability.
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