66 years Male (DOB:10/6/1949)Reason: worsening of brain tumor History: lethargy, agitationPROVIDER/ATTENDING NAME: HELENE G RUBEIZ HELENE G RUBEIZ Since the prior exam ill-defined T2 and FLAIR signal hyperintensity involving the left anterior temporal lobe both medial and lateral aspect associated with infiltration into the posterior left thalamus and left insula has progressed and now involves more of the insular cortex and internal capsule as well as the left external capsule and extends into the subcortical and periventricular white matter of the posterior aspect of the frontal lobe and of the anterior aspect of the left parietal lobe. Within the left external capsule there is a 12 x 25 mm axial dimension enhancing focus associated with this lesion. There are associated serpiginous flow-voids within this enhancing lesion. Previously the enhancing component was 3 mm in size.Numerous punctate signal hypointense foci are scattered in the subcortical white matter in both hemispheres as well as the cerebellum. These were also present on the prior exam.Normal vascular flow voids are present in the distal carotid and vertebral arteries, the basilar artery and the proximal anterior, middle and posterior cerebral arteries as well as the internal cerebral veins and superior sagittal sinus.The visualized portions of the paranasal sinuses are clear. The visualized portions of the mastoid air cells are clear. The visualized portions of the orbits are intact.
1.Interval significant progression of left hemispheric lesion known to represent a diffuse astrocytoma as detailed above. Differential consideration includes progression of neoplasm and radiation necrosis.2.Multiple microhemorrhages are scattered throughout both hemispheres of the brain. Differential considerations may include radiation related microhemorrhages. Amyloid angiopathy may have a similar appearance.