65-year-old female history of progressive change in mental status, with symptom onset 1 month ago, and acute worsening overnight. History of DM, HTN, and RA (on weekly Enbrel). Elevated neuronal enolase. Patient motion limits evaluation. There are new confluent areas of increased T2 and decreased T1 signal abnormality especially within the grey and subcortical as well as deep white matter of bilateral occipital lobes and to a lesser extent other bilateral scattered cortex. Additionally, there is restricted diffusion and FLAIR hyperintensity present in the left greater than right caudate nuclei and bilateral putamen (in retrospect, the caudate abnormality may have been present on the prior MRI) with questionable restricted diffusion in bilateral occipital lobes. The left caudate appears mildly enlarged and edematous. There are progressive scattered punctate foci of subcortical white matter T2/FLAIR hyperintensity. There is no evidence of abnormal enhancement.There is asymmetric susceptibility suggested associated with the left dentate nucleus, although no other signal abnormality in this area is appreciated. The ventricles and basal cisterns are normal in size and configuration. There is no evidence of midline shift or mass-effect. The major cerebral flow voids are intact.
New areas of increased T2/FLAIR signal abnormality throughout bilateral occipital lobes, progressive scattered focal subcortical and cortical T2/FLAIR hyperintensity, and FLAIR hyperintensity as well as restricted diffusion within left greater than right caudate nuclei and putamen. No associated enhancement, with questionable susceptibility in left dentate nucleus.The differential diagnosis includes PRES (posterior reversible encephalopathy syndrome) possibly secondary to hypertension and/or from medications. There have been reports of Enbrel resulting in PRES. Other differential considerations should include various encephalitides, metabolic derangements including osmotic demyelination (extrapontine) if clinically appropriate, or the Headenhain variant of CJD given occipital involvement, although subcortical findings would be atypical.