Radiation injury of the brain.
The clinical, radiologic, and pathologic findings in radiation injury of the brain are reviewed. Late radiation injury is the major, dose-limiting complication of brain irradiation and occurs in two forms, focal and diffuse, which differ significantly in clinical and radiologic features. Focal and diffuse injuries both include a wide spectrum of abnormalities, from subclinical changes detectable only by MR imaging to overt brain necrosis. Asymptomatic focal edema is commonly seen on CT and MR following focal or large-volume irradiation. Focal necrosis has the CT and MR characteristics of a mass lesion, with clinical evidence of focal neurologic abnormality and raised intracranial pressure. Microscopically, the lesion shows characteristic vascular changes and white matter pathology ranging from demyelination to coagulative necrosis. Diffuse radiation injury is characterized by periventricular decrease in attenuation of CT and increased signal on proton-density and T2-weighted MR images. Most patients are asymptomatic. When clinical manifestations occur, impairment of mental function is the most prominent feature. Pathologic findings in focal and diffuse radiation necrosis are similar. Necrotizing leukoencephalopathy is the form of diffuse white matter injury that follows chemotherapy, with or without irradiation. Vascular disease is less prominent and the latent period is shorter than in diffuse radiation injury; radiologic findings and clinical manifestations are similar. Late radiation injury of large arteries is an occasional cause of postradiation cerebral injury, and cerebral atrophy and mineralizing microangiopathy are common radiologic findings of uncertain clinical significance. Functional imaging by positron emission tomography can differentiate recurrent tumor from focal radiation necrosis with positive and negative predictive values for tumor of 80-90%. Positron emission tomography of the blood-brain barrier, glucose metabolism, and blood flow, together with MR imaging, have demonstrated some of the pathophsiology of late radiation necrosis. Focal glucose hypometabolism on positron emissin tomography in irradiated patients may have prognostic significance for subsequent development of clinically evident radiation necrosis.
Valk
P E
PE
Research Medicine and Radiation Biophysics Division, Lawrence Berkeley Laboratory, University of California, CA 94720.
Dillon
W P
WP
D001921:Brain / Q000000981:diagnostic imaging / Q000473:pathology / Q000528:radiation effects*; D001932:Brain Neoplasms / Q000000981:diagnostic imaging / Q000532:radiotherapy; D003937:Diagnosis, Differential; D006801:Humans; D008279:Magnetic Resonance Imaging; D009336:Necrosis; D009364:Neoplasm Recurrence, Local / Q000000981:diagnostic imaging; D011832:Radiation Injuries / Q000150:complications / Q000000981:diagnostic imaging / Q000209:etiology* / Q000473:pathology; D011878:Radiotherapy / Q000009:adverse effects*; D013997:Time Factors; D014055:Tomography, Emission-Computed; D014057:Tomography, X-Ray Computed