 MRI BRAIN: This exam is mildly degraded by motion artifact. Regions of cortical, subcortical, and deep white matter diffusion restriction within the bilateral cerebral hemisphere watershed zones, right more than left, have decreased in size as has the associated T2 hyperintensity. Patchy gyriform enhancement in these areas persists but with developing intrinsic gyriform T1 hyperintensity suggesting laminar necrosis. The dominant region of abnormality within the right occipital, inferior parietal lobule, and posterior temporal regions demonstrates mildly improved diffusion cortical and subcortical restriction and minimally worsened associated T2 hyperintensity that extends to involve the right forceps major. T2 hyperintensity within the posterior medial right thalamus is unchanged. There is increased patchy gyriform enhancement in the regions of signal abnormality compared to the prior exam. The contrast bolus was not of optimal quality, and therefore, the perfusion data may not be entirely reliable. Evidence of largely sulcal elevated rCBV is seen which may reflect vasodilatation and luxury perfusion.There is no evidence of intracranial hemorrhage. 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. There is unchanged fluid within the bilateral mastoid air cells. MR SPECTROSCOPY: The dominant right occipital lesion was interrogated with single voxel spectroscopy performed at multiple TEs. These show a marked lactate peak, significantly decreased NAA, and mildly increased choline relative to the contralateral lobe.
Continued evolution of subacute, possibly watershed, infarcts involving the cerebral hemispheres, right side more than left.Evolving parenchymal abnormality within the right occipital and posterior temporal lobes which is highly likely to represent ischemic injury. This is supported by the distribution which conforms to the PCA territory (including posterior thalamic involvement), as well as MR spectroscopy showing a pronounced lactate presence indicating anaerobic respiration. No findings are seen to suggest an aggressive or highly proliferative process.The underlying etiology for these suspected ischemic lesions is not entirely clear. As above, the high cerebral lesions seem to show a watershed pattern while the right temporo-ccipital lesion appears to be territorial. These could reflect a combination of hypoperfusion and thromboembolic disease. Vasculitis or a PRES-like phenomenon can also be considered. An underlying inflammatory process is felt to be less likely.