Glioblastoma multiforme. Status post resection followed by chemoradiotherapy. Reresection in October 2015 for relapse. On HSPPC96 vaccine trial. The resection cavity in the left temporal lobe has significantly decreased in size. In the axial plane, it now measures 2.7 cm x 2.5 cm compared to 3.8 cm x 4.8 cm previously. It contains fluid that is now greater is signal on FLAIR, suggesting the presence of blood or protein. The overlying extra-axial collection is significantly thinner.There remains enhancement in the area of the previously suspected post-operative infarct, along the posterolateral inferior surgical margin. This appears slightly less confluent on the early fat saturated postcontrast images and relatively similar in appearance to even minimally increased in confluence with decreased gyriform appearance on the more delayed postcontrast images. Persistence of contrast enhancement at this point is atypical for a bland infarct.Additionally, the contrast enhancement along the surgical margins has progressed since the previous examination with increased thickness of the rind as well as a slightly nodular appearance. This is most prominent along the superior surgical margin from which new lacelike contrast enhancement has extended to involve a significant part of the remaining left temporal lobe, including the mesial temporal lobe. In the axial plane, this new and increasingly confluent contrast enhancement measures maximally 4.0 cm x 3.0 cm (image #46 of series #1201). It is not associated with diffusion restriction or significant hyperperfusion. There is associated progression of nonenhancing T2-hyperintense signal which now spans the length of the left external capsule and most of the posterior limb of the left internal capsule, as well as extending superiorly into the frontoparietal deep white-matter. Overall, there has been only minimal increase in the mass-effect on the posterior body/trigone of the left lateral ventricle despite the progression in the contrast enhancement and associated T2 signal given the retraction of the surgical cavity. There is mild parenchymal expansion involving the remaining left temporal lobe.The remainder of the brain shows no new remote contrast enhancement. Scattered T2/FLAIR-hyperintense foci in the cerebral white-matter reflective of chronic microvascular ischemia are unchanged.The left mastoid air cell T2-hyperintense process persists, but the associated enhancement is minimally improved. The dural venous sinuses and major intracranial arteries are patent. Orbits are notable for previous right cataract surgery.
1.Progressive contrast enhancement along the surgical margins, especially superiorly where it extends into a confluent lace-like pattern into the remaining left temporal lobe but without associated diffusion restriction or hyperperfusion, is nonspecific and may reflect treatment-related effect. However, the presence of viable tumor would be difficult to exclude. Follow-up imaging may better characterize the significance of this finding.2.Enhancement persists in the area of the previously suspected infarct along the inferior posterolateral surgical margin which is atypical for a bland infarct. This is probably involved with the same process described above along the remainder of the surgical margin.3.The associated surrounding nonspecific FLAIR hyperintensity is mildly increased with mild gyral expansion and localized mass effect, and may represent a combination of vasogenic edema, post-treatment changes, and/or tumor. 4.The left temporal resection cavity is smaller but is more FLAIR hyperintense which may reflect the presence of hemorrhage or high protein content. This likely relates to a combination of cavity retraction as well as extrinsic mass effect from the surrounding parenchymal abnormality. 