 MRI:2 punctate foci of mild diffusion hyperintensity with corresponding iso- to mild hypointensity on ADC within the left frontal lobe (306/200 and 306/192) suspicious for subacute infarcts. There is also minimal associated T2 abnormality.Multiple scattered punctate foci of susceptibility bilaterally, most prominent in the left temporal and occipital regions, grossly similar in appearance, however, prior exam was limited by motion. New 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 and resolved cytotoxic edema.Confluent areas of T2/FLAIR hyperintensity within the subcortical and periventricular white matter is again noted, consistent with chronic small vessel ischemic disease. Previous left temporal and occipital sulcal FLAIR hyperintensity, which is felt to be less likely artifactual given focality, is overall no longer appreciated on this exam. However there is minimal residual FLAIR hyperintensity along a left posterior temporal lobe sulcus. There is no mass effect. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The major cerebral flow voids are intact. Post-operative changes noted within the paranasal sinuses with fluid in the right mastoid. The orbits, skull, and scalp soft tissues are grossly unremarkable.MRA:Increased T1 signal is noted within the left caudate along the left frontal lobe area of cortical laminar necrosis, consistent with expected evolution of prior infarct.The intracranial internal carotid arteries are normal in course and caliber. The middle and anterior cerebral arteries are unremarkable. The left vertebral artery is dominant. Mild focal narrowing of the left proximal P2 segment is noted. The basilar artery is normal in course and caliber. There is no evidence of flow-limiting stenosis or aneurysm.
1. 2 foci of mild diffusion restriction in the left frontal lobe suspicious for subacute infarcts. 2. Subtle residual FLAIR abnormality in a left posterior temporal lobe sulcus, with near complete resolution of previously seen more diffuse left temporal lobe FLAIR hyperintensity. Findings could relate to proteinaceous material or blood products. Consider post-contrast imaging for further evaluation.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 grossly similar in appearance to prior exam, overall peripheral in distribution and possibly relating to amyloid angiopathy.5. No evidence of flow-limiting stenosis or aneurysm. Mild left proximal P2 segment narrowing.