Female, 13 years old, with high-grade glioma status post relapse, currently on bevacizumab. Again seen are the sequelae of treated tumor within the left parietal operculum. Encephalomalacia with hemosiderin staining, wispy T1 hyperintensity and minimal if any superimposed enhancement is unchanged. Ill-defined T2 hyperintensity surrounding this lesion has not significantly expanded.Also redemonstrated is evidence of treated recurrent tumor in the left frontal lobe. The parenchyma here is also mildly encephalomalacic with stable ill-defined T2 hyperintensity in the white matter.New from the prior examination is an area of subcortical T2 hyperintensity involving the paramedian left superior frontal gyrus (image 21 series 501). This lesion is nonenhancing and shows no evidence of restricted diffusion. No convincing elevated rCBV is seen, though the area is difficult to evaluate with the presence of sulcal vascularity.T2 hyperintensity within the left genu of corpus callosum is unchanged. Ill-defined nonenhancing signal abnormality spanning the corpus callosum body, however, is more prominent. A few scattered foci of susceptibility within the cerebral hemispheres bilaterally are unchanged and likely reflect the effects of prior therapy. No new enhancing lesions are seen. No evidence of significant new mass effect is detected. Ventricles are stable in size and morphology including ex vacuo dilatation of the left ventricular atrium.
1.Stable treated disease in the left parietal operculum and left anterior frontal lobe.2.New nonenhancing signal abnormality is evident within the paramedian left superior frontal gyrus, and within the body of the corpus callosum. Findings are nonspecific and could represent treatment-related change, but the pattern is similar to that of the patient's prior instance of progression, and as such, continued disease progression is of concern.