Female, 81 years old, with history of subacute cognitive decline and expressive predominant global aphasia, initial imaging suspicious for pneumatosis versus PRES, status post biopsy with findings of amyloid angiopathy and mild astrocytic proliferation but no clear evidence of inflammation. Since the prior examinations, marked T2 hyperintensity involving the left temporal and occipital lobes, and to a lesser degree the right temporal and occipital lobes, has significantly improved. There is no longer any evidence of edema or mass effect, and the areas of parenchymal signal abnormality which remain demonstrate a more chronic morphology. The previously seen areas of restricted diffusion have resolved and there is no pathologic enhancement.Single voxel spectroscopy performed over the affected left occipital parenchyma shows perhaps a slight reduction of the NAA peak, but otherwise a relatively normal metabolite profile. A broad negative peak at 1.55 ppm is likely artifactual.Sequelae of prior left temporal biopsy are redemonstrated. Numerous scattered foci of periventricular and subcortical ill-defined T2 hyperintensity are again seen without significant interval change. No mass effect is detected. No abnormal extra-axial fluid collections are observed. However, there are numerous scattered punctate foci of susceptibility throughout the cerebral hemispheres, similar to the prior examination.
1.Since the prior examination, areas of marked signal abnormality in the temporal and occipital lobes, left side more than right, have markedly improved. The previously seen edema, mass effect and restricted diffusion have resolved, and there is no pathologic enhancement. Spectroscopic assessment over one of the affected areas shows no evidence to support an aggressive neoplastic process.2.As on the prior examinations, there are numerous scattered foci of subcortical and periventricular ill-defined T2 hyperintensity. Also noted are numerous punctate foci of susceptibility which, given findings on pathology, likely correlate to amyloid angiopathy.3.The differential diagnosis would continue to include a vascular process such as vasculitis or PRES. A rare inflammatory response to amyloid angiopathy can also be considered. An aggressive neoplastic process such as gliomatosis is considered unlikely.