Male, 68 years old, with brain lesion for evaluation. The left basal ganglia ring enhancing lesion persists, with perhaps a mild interval decrease in size, now measuring up to 23 mm in diameter, previously up to 25 mm. Internal diffusion restriction seen on prior exams continues to diminish. Subtle developing peripheral T1 hyperintensity is seen aroung this lesion. Some progression of surrounging T2 signal abnormality is seen, particularly at the level of the left caudate body which now shows progressive cystic degeneration. Along the left ventricular atrium, T2 signal abnormality is improved. A separate 4 mm linear focus of enhancement along the left posterior limb of the internal capsule is unchaged. Scattered calcified lesions as represented by areas of T1 hyperintensity and/or susceptibility effect have not changed. Smooth dural thickening and enhancement along the left parietal convexity is also unchanged. No new lesions are seen. Numerous patchy areas of white matter T2 hyperintensity and cortical encephalomalacia are stable. Ventricular size and morphology are unchanged.
1.Persistent ring enhancing lesion in the left basal ganglia with perhaps a mild interval decrease in size. A rim of T1 hyperintensity continues to development around this lesion. 2.Diffusion restriction internal to the above lesion is reduced. Some progression of surrounding T2 signal abnormality is seen, at least along the left caudate body which shows progressive cystic degeneration.3.A separate small enhancing focus in the posterior limb of the left internal capsule is stable. Numerous calcified lesions, and other areas of white matter and cortical injury, are stable. Dural thickening and enhancement along the left parietal convexity is unchaged as well.4.Although no real evidence of progression of the basal ganglia lesion is seen, and some findings would suggest evolution towards chronicity, the findings are still not sufficient to distinguish between infectious and neoplastic etiologies. 