Bevacizumab as a Treatment Option for Radiation-Induced Cerebral Necrosis

Christiane Matuschek, Edwin Boelke, Jens Nawatny, Thomas K. Hoffmann, Matthias Peiper, Klaus Orth, Peter Arne Gerber, Ethelyn Rusnak, Guido Lammering, Wilfried Budach*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

60 Citations (Web of Science)


Radiation necrosis of normal CNS tissue represents one of the main risk factors of brain irradiation, occurring more frequently and earlier at higher total doses and higher doses per fraction. At present, it is believed that the necrosis results due to increasing capillary permeability caused by cytokine release leading to extracellular edema. This process is sustained by endothelial dysfunction, tissue hypoxia, and subsequent necrosis. Consequently, blocking the vascular endothelial growth factor (VEGF) at an early stage could be an option to reduce the development of radiation necrosis by decreasing the vascular permeability. This might help to reverse the pathological mechanisms, improve the symptoms and prevent further progression. A patient with radiationinduced necrosis was treated with an anti-VEGF antibody (bevacizumab), in whom neurologic signs and symptoms improved in accordance with a decrease in T1-weighted fluid-attenuated inversion recovery signals. Our case report together with the current literature suggests bevacizumab as a treatment option for patients with symptoms and radiological signs of cerebral necrosis induced by radiotherapy.
Original languageEnglish
Pages (from-to)135-139
JournalStrahlentherapie Und onkologie
Issue number2
Publication statusPublished - Feb 2011


  • Cerebral radiation necrosis
  • Stereotactic neurosurgery
  • Radiation therapy
  • Bevacizumab
  • Hypoxia

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