Abstract
tereotactic radiosurgery can effectively ablate brain tumors; however, it also has the potential to cause tissue S injury around the tumor site. The acute effects on the brain tissue are usually reversible; they occur <2 months after radiotherapy and result from endothelial cell apoptosis, which causes disruption of the blood-brain barrier and peritumoral edema (20, 22, 33). Acute radiation injury also incites inflammatory pathways, which are accelerated by chronic hypoxia secondary to endothelial remodeling, further setting the stage for “microenvironmental change” (33). If this process continues to evolve, the result is irreversible cerebral radiation necrosis (RN).
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