Encephalopathy and aphasia. Autoimmune thyroiditis. Assess evolution of brain lesion from prior MRI dated May 8, 2016. The non-territorial swelling and T2 hyperintense signal involving the posterior left cerebral hemisphere including parts of the parietal, occipital and temporal lobes has not changed in overall distribution. The predominantly cortical diffusion restriction is less remarkable than on the prior exam. The smaller superficial inferior right cerebellar lesion shows a similar pattern of evolution. The T2-hyperintense lesion in the posteromedial left thalamus is also unchanged. Mildly increased T2 FLAIR signal centrally within the pons remains unchanged. Single voxel MR spectroscopy with an echo time of 35 ms over the abnormal left parietal lobe shows a prominent lactate doublet peak. The other major metabolite peaks (NAA, Cr, and Cho) are reduced, particularly NAA. Single voxel spectra obtained ovr normal appearing parenchyma, including the basal ganglia, demonstrate normal metabolite peaks with no detectable lactate.
1.The left posterior hemispheric and the smaller right cerebellar and left thalamic abnormalities show interval evolution with slightly decreased diffusion restriction since May 8, 2016. There is no new lesion.2.MR spectroscopy of the left parietal lesion demonstrates findings compatible with failure of energy metabolism and parenchymal injury. Normal appearing regions of the brain show normal MR spectra, which argues against but does not exclude a global metabolic derangement or inborn error of metabolism. 3.Given that the involved parenchyma spans multiple vascular territories, a conventional vascular etiology is felt to be less likely. However, a regional vasculitis could produce lesions with this distribution. Alternatively, direct parenchymal inflammation, such as might be seen with Hashimoto encephalitis, or some other autoimmune process, can also appear similarly.