 There are no foci of restricted diffusion to suggest the presence of acute ischemia. Redemonstrated are multiple scattered punctate foci of susceptibility bilaterally, most prominent in the left temporal and occipital regions, including gyriform susceptibility artifact within the left frontal lobe with intrinsic T1 signal consistent with laminar necrosis in the area of prior infarct. Additional foci of prior infarcts now demonstrate expected encephalomalacia. Confluent areas of T2/FLAIR hyperintensity within the subcortical and periventricular white matter is again noted, consistent with advanced chronic small vessel ischemic disease. Previously demonstrated FLAIR hyperintensity along a left posterior temporal lobe sulcus has resolved and there are no new sulcal foci of FLAIR hyperintensity. There is no mass effect. The ventricles and basal cisterns are unchanged in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. Fluid is again noted within the right mastoid air cells with new fluid within a few left mastoid air cells.
1.There is no restricted diffusion to suggest the presence of acute ischemia.2.Previously demonstrated FLAIR hyperintensity along a left posterior temporal lobe sulcus has resolved and there are no new sulcal foci of FLAIR hyperintensity. 3.Expected evolution of prior infarcts, including cortical laminar necrosis and encephalomalacia within the left frontal lobe.4.Multiple scattered foci of susceptibility bilaterally appearing similar in appearance to prior exam, overall peripheral in distribution and possibly relating to amyloid angiopathy.5.Fluid is again noted within the right mastoid air cells with new fluid within a few left mastoid air cells. 