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Blood in the vessels bleeds into the brain parenchyma resulting in the intracerebral hemorrhage (ICH) [1]. The direct mass effect of the rapidly formed hematoma causes the brain damage, which leads to neurologic deficit. Thus, clearing the hematoma may be beneficial to the patient with ICH. However, the Surgical Trial in Intracerebral Hemorrhage (STICH) trial showed no overall benefit from early hematoma evacuation compared to initial conservative treatment [2]. Therefore, the secondary brain injury caused by the metabolic products or the components of hematoma attracted more researchers’ attention [3]. Converging evidence shows that both central and peripheral inflammation play critical roles in the ICH-induced secondary brain injury [3–8]. Previously, most studies concentrated on the downstream inflammatory events, such as proinflammatory cytokines, showed that inflammatory responses contribute to the secondary brain injury after ICH, while no direct clinical effects on targeting these downstream events have been achieved [7]. Hence, it is worth thinking about why this kind of therapeutic strategies has no direct clinical effects and rethinking the roles of inflammation in the ICH.

Rethinking the Roles of Inflammation in the Intracerebral Hemorrhage