Abstract
Intracerebral hemorrhage (ICH) is a perplexing condition with high mortality and no treatment beyond supportive care. A major portion of the injurious process is takes place during the hours following the development of hematoma. This so-called secondary injury is characterized by an inflammatory cascade that involves a variety of cytokines, including tumor necrosis factor (TNF)-α. Several studies in the rodent model of ICH have shown a rapid increase in brain concentrations of TNF-α following hematoma induction. There is a reasonable body of evidence from experimental models of ICH suggesting that upregulation of TNF-α adjacent to the hematoma is associated with increased peri-hematomal edema, and that inhibition of TNF-α attenuates the formation and progression of this edema and ultimately improves outcomes. Unfortunately, efforts to expand upon these findings have interminably stalled at the pre-clinical phase. A robust clinical study to validate serum TNF-α as a marker for secondary injury in ICH patients is yet to materialize.
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Dr. Behrouz (author) has received educational grant from Genentech Inc.
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Behrouz, R. Re-exploring Tumor Necrosis Factor Alpha as a Target for Therapy in Intracerebral Hemorrhage. Transl. Stroke Res. 7, 93–96 (2016). https://doi.org/10.1007/s12975-016-0446-x
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DOI: https://doi.org/10.1007/s12975-016-0446-x