Peritumoral Edema in Neuro-oncology: Mechanisms, Imaging Biomarkers, and Emerging Therapeutic Methods

Peritumoral edema (PTE) occurs with nearly all intracranial tumors and their treatments. PTE increases mass effect and intracranial pressure. This often causes neurologic decline, worsens function, and complicates treatment planning. At times, emergency care is needed. This review examines current PTE findings and their relevance to neuroimaging and neuro-oncology management. Blood-brain barrier failure results from tumor-induced mechanisms, including angiogenesis, changes in inflammation, alterations in aquaporin-mediated water transport, tight junction failure, pericyte loss, and vesicle signaling. These factors produce various edema types and outcomes. Conventional MRI usually cannot distinguish between these or tell if vasogenic edema is from tumor infiltration or treatment. Thus, this review highlights combined diffusion and perfusion modeling, thermodynamic approaches, AI, radiomics, and anesthetic agents for tracking temporal changes. Corticosteroid treatment for vasogenic edema has risks, such as tapering problems and rebound edema, which offset its benefits. Despite this, corticosteroids remain a first-line therapy. New options, vascular stabilization, changing the microenvironment and edema pathways, and anti-VEGF therapy, are being tested to limit steroid use. This review also covers pre-, intra-, and postoperative care for glioblastoma, meningioma, and brain metastases. Data algorithms now match symptom severity, imaging, and treatment context. Future research should seek biomarker validation, long-term safety, and standard imaging protocols.