Specific Imaging Findings

Therapy-induced (radiation) cerebral necrosis (TCN) cannot be reliably differentiated from residual/progressive malignancy on CT or conventional MR imaging. TCN appears as an enhancing mass with surrounding vasogenic edema, frequently increasing in size on serial examinations. Internal irregular linear areas of high T1 signal may be found. Typical patterns of contrast enhancement include internal localized specks of bright signal within necrotic areas (“Swiss cheese/soap bubble” – presumably due to contrast leakage into the cavity) and ill-defined feathery peripheral enhancement (“spreading wavefront”). Edema is limited to the white matter without infiltrative gray matter involvement. On perfusion imaging TCN characteristically shows very low relative cerebral blood volume (rCBV), in contrast to malignant neoplasms. The perfusion signal intensity–time curve shows substantially lower signal recovery than in gliomas, reflecting the high degree of contrast leakage within TCN. Necrosis shows higher signal on ADC maps, compared to relatively low ADC values of viable neoplasms. TCN is characterized by decrease of all metabolites on MR spectroscopy and a dominant very high level of lipids, known as “death peak”.

Pertinent Clinical Information

TCN is a serious complication of radiation therapy for intracranial tumors and non-neoplastic conditions. It also occurs following treatment of extracranial diseases, most notably nasopharyngeal carcinoma. Development of TCN is related to the method of radiation delivery, total dose, fraction size, treatment volume, patient age, and administration of chemotherapy. The changes occur from several months to years after treatment, more frequently following high-dose local radiation, such as radiosurgery or brachytherapy.