Male, 60 years old, with septic emboli versus watershed ischemia, reevaluate lesions. Scattered relatively discrete foci of bright diffusion signal are seen along the posterior aspect of the cerebral watershed zones bilaterally, appearing relatively similar to the prior examination. These lesions show a very mild corresponding ADC hypointensity. These lesions do not enhance.Very ill-defined diffusion hyperintense signal is seen bilaterally and symmetrically within the periventricular and watershed white matter. The signal is corroborated by the ADC map, and furthermore, it appears more conspicuous than on the prior examination. No associated enhancement is seen.A region of right occipital encephalomalacia is again seen with gyriform T1 hyperintensity, patchy susceptibility artifact and patchy associated enhancement. To a much lesser degree, similar signal abnormality, susceptibility artifact and minimal enhancement are seen within the left occipital lobe.Scattered foci of susceptibility are seen within the cerebellum without significant interval change. No evidence of acute intracranial hemorrhage is seen. There are a few scattered foci of subcortical T2 hyperintensity, some of which correspond to the areas of restricted diffusion as noted above. Ill-defined periventricular T2 hyperintensity is also noted. No significant parenchymal edema or mass effect is seen. The ventricular system remains normal in size and morphology.
1.Scattered discrete foci of diffusion restriction are seen within the posterior cerebral watershed zones bilaterally. There is no associated hemorrhage or enhancement with these lesions, and they appear relatively similar in size and number to the prior examination. These are favored to reflect late acute watershed infarcts.2.A much more ill-defined pattern of mild restricted diffusion is seen within the periventricular and watershed zone white matter of both cerebral hemispheres. This finding has become more conspicuous when compared to the prior examination. This is favored to reflect evolving perfusional or watershed ischemia. A metabolic or toxic process is considered less likely.3.A hemosiderin stained lesion in the right occipital lobe demonstrates imaging features compatible with a late subacute infarct. Scattered foci of susceptibility within the cerebellum are unchanged and likely reflect chronic ischemic lesions.