Subacute weakness and dysphagia. There are patchy areas of subcortical, deep, and periventricular T2 hyperintensity without restricted diffusion involving the bilateral occipital and parietal lobes, with extension into the temporal lobe and precentral gyrus on the left side. There are also linear T2 hyperintensities along the periventricular white matter of the bilateral frontal horns of the lateral ventricles and patchy and punctate T2 hyperintense areas in the deep and subcortical white matter of the bilateral anterior frontal lobes. There is associated cerebral volume loss, particularly in the left posterior cerebral hemisphere. In addition, there is a small patchy area of high T2 signal involving the medial portion of the left superior cerebellar hemisphere. The brainstem and deep grey matter structures appear to be spared. There is no evidence of intracranial hemorrhage, mass, or acute infarct. There is no abnormal intracranial enhancement. There is no midline shift or herniation. The major cerebral flow voids are intact. The orbits, skull, mastoid air cells, and scalp soft tissues are grossly unremarkable. There is mucosal thickening and fluid in the bilateral sphenoid, right maxillary, and left frontal and anterior ethmoid sinuses.
1. Extensive cerebral white matter disease with brain parenchymal volume loss, as well as a small area of left cerebellar hemisphere white matter abnormality, may represent a neurodegenerative leukoencephalopathy, perhaps related to a mitochondrial disorder or toxic-metabolic process, for example.2. Findings suggestive of acute sinusitis.