Female, 63 years old, with worsening altered mental status, hepC cirrhosis with history of hepatic encephalopathy, hyponatremia, head CT today with new hyperattenuation in the pons. An area of susceptibility is seen within the central pons with surrounding T2 hyperintensity which fans up into the cerebral peduncles. A separate smaller focus of susceptibility with no associated T2 hyperintensity is seen within the posterior right frontal lobe.On T1 weighted images, the basal ganglia show mild symmetric intrinsic hyperintensity. No restricted diffusion is seen. Scattered small foci of T2 hyperintensity are present within the subcortical white matter of the cerebral hemispheres but without associated mass effect. Also noted, however, is asymmetric ependymal T2 hyperintensity along the right occipital horn.No pathologic extra-axial fluid collections are detected. Ventricular size is within normal limits.
1. A small pontine hemorrhage is detected, correlating with an abnormality noted on prior CT. This may simply reflect a coagulopathic hemorrhage without any additional underlying process. T2 hyperintensity within the pons may therefore simply reflect edema. However, in the context of rapidly corrected hyponatremia, the possibility of coexisting osmotic demyelination may also be considered.2. A smaller focus of chronic hemorrhage is seen within the right posterior frontal lobe.3. Scattered foci of subcortical T2 hyperintensity are nonspecific.4. Asymmetric ependymal signal abnormality along the right occipital horn could be a variation of normal, though the possibility of an underlying inflammatory or infectious process is not excluded.5. Intrinsic T1 hyperintensity within the basal ganglia is compatible with chronic hepatic encephalopathy. Typical findings for acute hepatic encephalopathy are not clearly present on this examination. Continued follow-up is advised.