[en] Radiation has been shown to be an effective therapy for malignant gliomas and metastatic brain tumors. The initial effects of radiation therapy can be confirmed by morphological study including brain CT and MR imaging. However, differentiating tumor recurrence from delayed tissue necrosis is difficult after radiotherapy. Positron emission tomography (PET) with L-[methyl-¹¹C] methionine (MET) and [¹⁸F]-fluoro-3'-deoxy-3'-L-fluoro-thymidine (FLT) provides information about metabolism and cellular proliferation activity of brain tumors. In this study, we evaluate the utility of MET- and FLT-PET to differentiate between radiation necrosis and tumor recurrence in 11 patients with malignant gliomas and 14 patients with metastatic brain tumors. MET-PET demonstrated a significant difference in maximum MET standardized uptake value (SUVmax) between tumor recurrence (3.58±1.08, n=9) and radiation necrosis (2.17±0.56, n=4) in malignant gliomas (P<0.05). However, no significant difference was observed in MET SUVmax between tumor recurrence (3.69±1.55, n=4) and radiation necrosis (2.16±0.38, n=5) in metastatic brain tumors. In FLT-PET, recurrent gliomas had increased FLT SUVmax (1.85±0.63, n=7) and the ratio of tumor tissue to normal brain tissue (T/N ratio) was extremely high (8.29±2.09). Two patients with radiation necrosis exhibited low FLT SUVmax (0.55 and 0.22) and moderate T/N ratio (3.67 and 1.16) in gliomas. In conclusion, MET-PET is a highly sensitive technique to differentiate between tumor recurrence and delayed radiation necrosis following radiotherapy in patients with glioma. On the other hand, significant MET and FLT accumulation is observed in metastatic brain tumors after radiotherapy and a differential diagnosis between the two conditions is difficult. In FLT-PET, kinetic analysis can separate FLT transport (K₁) from tissue retention due to metabolic trapping by phosphorylation (k₃) in tumors. This method may improve the accuracy of differential diagnosis of tumors with moderately increased uptake of tracer. (author)