 Postoperative changes from previous left parietal craniotomy are again seen, with a rounded resection cavity which communicates with the left atrium. Small lateral cystic cavity along the resection cavity margin corresponds to previous biopsy, with persistent susceptibility likely relating to chronic blood products. There is increased susceptibility within the adjacent posterior lateral left thalamic region.Following contrast, there is again progression of areas of somewhat nodular enhancement, with areas of enlarging as well as new enhancement. This is most conspicuous along the medial aspect of the posterior body of the left lateral ventricle, with the area of enhancement now measures 11 mm in greatest thickness on 3/117, previously only 6 mm. Exam also demonstrates more confluent enhancement as compared to a somewhat more peripheral pattern on the prior exam. The previously referenced left periatrial white matter lesion measures 20 x 10 mm on 3/141 as compared to previous 18 x 10 mm, although there are tiny exophytic components not included within the measurement which are now more conspicuous. In addition, there are numerous additional punctate foci of enhancement scattered throughout the left parietal lobe. Several of these are quite remote from the previously seen areas of enhancement, for example near the parietal apex on 3/80 and 3/90. There is also progressive nodular enhancement throughout the left temporal lobe.The extent of FLAIR abnormality is overall similar in distribution compared to the most recent exam, although the component along the right splenium has further increased in thickness. Compared to more remote exams, there is gradual progression of FLAIR abnormality. On diffusion-weighted images, there is punctate mild diffusion restriction along the lateral aspect of the left atrium as well as along the posterior left corona radiata, without definite susceptibility or enhancement in these locations. These are nonspecific but could represent recent punctate foci of ischemia or possibly not yet enhancing hypercellular tumor.There is also redemonstration of a stable heterogeneous lesion in the central pons with central T1 hyperintensity and blooming on susceptibility, consistent with a cavernoma with associated developmental venous anomaly. There is no surrounding abnormal T2 hyperintensity in the pons. The ventricles and sulci are stable. The cisterns remain patent. There is no midline shift or mass effect. No extra-axial fluid collection is identified. Normal flow-voids are demonstrated in the major intracranial vascular structures. The midline structures and craniocervical junction are within normal limits. There is a mucosal retention cyst within the right maxillary sinus. Mild mucosal thickening is noted in the right sphenoid sinus.Perfusion imaging was not performed as this was a concurrent exam with a dynamic liver MRI.
1. Interval progression of areas of nodular enhancement along the resection cavity margins as well as subtle thickening of rightward extension of FLAIR abnormality across the splenium. Increased conspicuity and size of gadolinium punctate foci of more remote enhancement, as well as new foci identified. Findings are again concerning for tumor progression.2. Two punctate foci of mild diffusion restriction along the left periventricular white matter without definite corresponding enhancement. Differential diagnosis includes evolving areas of nonenhancing hypercellular tumor versus trace petechial blood products or punctate infarcts.3. Stable appearance of incidental pontine cavernoma with developmental venous anomaly.