Cerebral radiation necrosis refers to necrotic degradation of brain tissue following intracranial or regional radiation either delivered for the treatment of intracranial pathology (e.g. astrocytoma, cerebral arteriovenous malformation) or as a result of irradiation of head and neck tumours (e.g. nasopharyngeal carcinoma).
Although post-radiation treatment effects include pseudoprogression, which seen relatively close to radiation particularly in the setting of concurrent chemotherapy for glioblastoma (Stupp protocol). This article focuses on more delayed effect, generally termed radiation necrosis, which appears months to several years after radiation therapy and involves a space-occupying necrotic lesion with mass effect and neurological dysfunction.
There are numerous potential pathways to radiation necrosis which include:
- vascular injury
- acutely endothelial damage can lead to vasogenic oedema
- chronically fibrosis, hyalinization and stenosis can occur with eventual thrombosis and infarction
- vascular ectasia and telangiectasia are also seen frequently, with capillary telangiectasias and cavernous malformations common findings post whole brain irradiation.
oligodendrocytes and white matter damage
- oligodendrocytes are sensitive to radiation
- loss of white matter accounts for the majority of volume loss
- effects on the fibrinolytic enzyme system
- increase in urokinase plasminogen activator and a simultaneous decrease in tissue plasminogen activator may contribute to cytotoxic oedema and tissue necrosis
- immune mechanisms
T2/FLAIR: white matter high signal
- oedema and mass effect early
- loss of volume later
T1 C+ (Gd)
- white (more common) or grey matter
- single or multiple
- nodular or curvilinear
- "soap-bubble" or "Swiss-cheese" enhancement
- occasionally can be ring enhancing (see MAGIC DR mnemonic)
- MR spectroscopy: typically low choline, creatine, and NAA
- MR perfusion: areas of enhancement and high T2/FLAIR don't show increased rCBV in radiation necrosis or pseudoprogression and could be helpful in distinguishing them from residual lesion or recurrence
- radiation necrosis is usually hypometabolic whereas tumour is hypermetabolic
It has been suggested that involvement of the corpus callosum with the crossing of the midline and multiple lesions or subependymal spread would favour a recurrent tumour over radiation necrosis 2, however, conventional imaging can be misleading, and no individual feature is reliable.
- 1. Kumar AJ, Leeds NE, Fuller GN et-al. Malignant gliomas: MR imaging spectrum of radiation therapy- and chemotherapy-induced necrosis of the brain after treatment. Radiology. 2000;217 (2): 377-84. Radiology (full text) - Pubmed citation
- 2. Mullins ME, Barest GD, Schaefer PW et-al. Radiation necrosis versus glioma recurrence: conventional MR imaging clues to diagnosis. AJNR Am J Neuroradiol. 2005;26 (8): 1967-72. AJNR Am J Neuroradiol (full text) - Pubmed citation
- 3. Brandes AA, Tosoni A, Spagnolli F et-al. Disease progression or pseudoprogression after concomitant radiochemotherapy treatment: pitfalls in neurooncology. Neuro-oncology. 2008;10 (3): 361-7. doi:10.1215/15228517-2008-008 - Free text at pubmed - Pubmed citation
- 4. Brandes AA, Tosoni A, Spagnolli F et-al. Disease progression or pseudoprogression after concomitant radiochemotherapy treatment: pitfalls in neurooncology. Neuro-oncology. 2008;10 (3): 361-7. doi:10.1215/15228517-2008-008 - Free text at pubmed - Pubmed citation