Female, 24 years old, with anaplastic astrocytoma currently on Avastin. The left parietal lobe resection cavity is unchanged in size and morphology. Small cystic spaces anterior to the main cavity are not significantly changed in size, though their internal signal no longer suppresses on FLAIR images suggesting a change in the fluid consistency.Ill-defined periventricular T2 hyperintensity surrounding the treatment bed has increased in geographic extent, particularly within the superior parietal lobule. The posterior left thalamus and posterior medial temporal lobe are also affected to a greater degree. Signal abnormality and thickening of the splenium of corpus callosum is grossly unchanged, though signal abnormality within the overlying cingulate white matter has progressed.The previously seen small foci of enhancement anterior to the resection cavity have evolved into a more rim-enhancing, confluent, centrally diffusion restricting lesion. The splenium of the corpus callosum is incorporated in this lesion with new rim enhancement to the right of midline. Ependymal enhancement along the left ventricular atrium has increased. Small foci of periventricular enhancement extending along the left temporal horn appear grossly similar to the prior examination.Ventricular size and morphology are within normal limits. No new abnormal fluid collections are seen. A cavernous malformation with associated developmental venous anomaly in the pons is unchanged. A punctate focus of enhancement within the left IAC is unchanged dating back to 2013, a nonspecific finding but perhaps representing an incidental schwannoma.
Since the prior examination, small enhancing foci anterior to the left parietal lobe cavity have evolved into a more confluent rim-enhancing lesion which incorporates the splenium of corpus callosum. Scattered additional foci of enhancement are stable to slightly more prominent as described above. Ill-defined T2 hyperintensity has progressed in the left cerebral hemisphere and to a lesser degree in the right cerebral hemisphere. While the findings do at least in part reflect posttreatment changes in the context of antiangiogenic therapy, the slowly progressive enhancing components are concerning for persistent tumor growth.