Female, 33 years old, with Hashimoto encephalitis and seizure. Some sequences are degraded by motion artifact which slightly limits the evaluation.The previously seen T2 hyperintense signal involving the right parietal, occipital and temporal lobes is largely stable. Extensive bilateral progression of signal abnormality is seen, however, throughout the remaining cerebral hemispheres. There are now patchy areas of new cortical and subcortical T2 hyperintensity with a predominance of findings in the inferior frontal, parietal, occipital and temporal lobes. The basal ganglia are spared, but some involvement of the thalami is seen. Lesions in the midbrain and left cerebellar hemispheres were present previously and have not progressed. Patchy areas of mild cortical restricted diffusion are seen matching the distribution of new disease, though the size of the T2/FLAIR lesions is larger than that of the diffusion lesions.No significant generalized mass effect is seen. No large intracranial hemorrhage or abnormal fluid collection is evident. The ventricular system is stable in size and morphology.
Interval progression of disease is seen with numerous new cortical and subcortical lesions involving both cerebral hemispheres. Mild new cortical restricted diffusion is also seen matching the pattern of new disease but of a lesser magnitude, indicating a minor component of cytotoxic edema.MRA images are motion degraded, but no significant proximal vascular stenosis or occlusion is seen.The constellation of findings would be compatible with progression of an autoimmune encephalitis, as indicated by history, as well as vasculitis. 