Evaluate for evidence of wernicke or other encephalopathy: reported cirrhosis (EtOH &/or Hepatitis C) and EtOH abuse with concern for high grade Hepatic Encephalopathy likely due to acute alcoholic hepatitis There is no evidence of intracranial hemorrhage, mass, or acute infarct. There are a few scattered foci of cerebral white matter T2 hyperintensity, which are non-specific. There is also foci T2 hyperintensity in the bilateral globi pallidi as well as susceptibility effect and patchy T1 hyperintensity. However, the thalami and mammillary bodies appear to be intact. There is diffuse mild cerebral and cerebellar volume loss. There is no midline shift or herniation. The major cerebral flow voids are intact. The orbits, skull, paranasal sinuses, and scalp soft tissues are grossly unremarkable. However, there appears to be a submucosal T2 hyperintense lesion in the left hard palate that measures up to 12 mm.
1. No evidence of acute intracranial hemorrhage, mass, or acute infarct.2. Abnormality in the bilateral globi pallidi may represent sequela of prior ischemic injury and/or chronic alcoholic encephalopathy, but there are no findings specific for Wernicke encephalopathy or acute hyperammonemic encephalopathy. 3. Diffuse mild cerebral and cerebellar volume loss.4. An apparent submucosal T2 hyperintense lesion in the left hard palate is incompletely characterized, but may represent a reactive or neoplastic process. Further evaluation via an MRI with contrast and otolaryngological examination may be useful.