Female, 36 years old, with GBM, presumably IDH wild type, MGMT promotor unmethylated, status post two prior resections and TMZ/RT, PD 2 cycles of IDO pathway inhibitor immunotherapy. Evidence of bilateral frontal craniotomy is seen. A CSF signal intensity cavity is redemonstrated within the left frontal lobe showing no significant interval change. A much smaller resection cavity is also redemonstrated in the right frontal lobe which is similar in size to the prior examination.Extensive abnormal T2/FLAIR signal abnormality is seen affecting the entire right frontal lobe, the insula, basal ganglia, and a small portion of the anterior right temporal lobe. A large portion of the affected right frontal lobe also demonstrates heterogeneous, irregularly marginated enhancement. Although the geographic territory involved with this enhancement has not changed substantially, some individual enhancing lobules are larger, and the intensity of enhancement appears to have increased. Thickening and pathologic enhancement involves the genu of the corpus callosum and does cross to the left frontal lobe.This large lesion induces significant mass effect with effacement of sulci, effacement of the right lateral ventricle, and shift of midline to the left of approximately 10 mm, findings which have progressed.At the site of previously seen T2 FLAIR signal abnormality along the left posterior lateral fourth ventricle, a new 8 mm nodule of enhancement has developed. T2 hyperintensity at this site has progressed and now spreads along the brachium pontis and superiorly into the superior cerebellar peduncle and midbrain.No additional new pathologic enhancement is seen. Scattered foci of nonspecific parenchymal T2 hyperintensity are redemonstrated, at least one of which in the right cerebellum is new.
Since the prior examination, irregular heterogeneous enhancement within the right frontal lobe, along with significant associated mass effect, have progressed. A new enhancing lesion has also developed within the left cerebellum where previously there was only nonenhancing T2/FLAIR signal abnormality. Overall, the findings are concerning for progressive disease, though there could be a minor component of treatment effect as well.