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.

View details for DOI 10.1007/s11910-012-0258-7

View details for Web of Science ID 000303515500007

View details for PubMedID 22350279