title: Radiation necrosis: relevance with respect to treatment of primary and secondary brain tumors.
abstract: Radiation injury to the central nervous system (CNS) manifests in multiple forms and is divided into three categories termed acute, early-delayed, and late-delayed injury patterns. Late-delayed radiation injury, primarily manifesting as leukoencephalopathy or radiation necrosis, is often progressive and may have a negative impact on quality of life. Radiation injury is believed to be a consequence of cell membrane and DNA injury with a pathological expression as vascular injury, depletion of oligodendroglial progenitor cells, and failure of cell-cell interactions that constitute the cellular network of the CNS. In addition, radiation injury results in activation of the inflammatory cascade with perturbation of cytokines, production of reactive oxygen species and vascular endothelial growth factor. Medical treatment of CNS radiation injury and in particular radiation necrosis remains problematic as there is a paucity of clinical trial data to inform treatment decisions, and aside from surgery and corticosteroids only bevacizumab appears to have a compelling therapeutic role.
authors.affiliation: Department of Radiology, University of Washington, St. Louis, MO, USA.
authors.forename: James
authors.initials: J
authors.lastname: Fink
authors.forename: Donald
authors.initials: D
authors.lastname: Born
authors.forename: Marc C
authors.initials: MC
authors.lastname: Chamberlain
mesh_terms: D000818:Animals; D001932:Brain Neoplasms / Q000473:pathology* / Q000556:secondary*; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D009336:Necrosis; D059906:Neuroimaging; D011832:Radiation Injuries / Q000145:classification / Q000150:complications / Q000473:pathology; D017382:Reactive Oxygen Species / Q000378:metabolism; D013997:Time Factors; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D016207:Cytokines; D017382:Reactive Oxygen Species; D042461:Vascular Endothelial Growth Factor A