Figure 4.

Central fever in the hypothalamus leads to END through three possible mechanisms. First, hyperthermia increases oxygen consumption of neurons, leading to compensatory glycolysis. Lactate accumulation and energy failure lead to cell edema and even necrosis. Second, fever affects blood-brain barrier permeability, increases edema around hematoma, creating conditions for hematoma expansion. Third, activated central immune cells and peripheral immune cells infiltrating through the damaged blood-brain barrier exacerbate the inflammatory response of cerebral hemorrhage, causing further damage to neurons.