Female, 13 years old, with seizures and mesial temporal abnormalities on prior imaging. Evaluate by spectroscopy, in particular for lactate expression. Atrophy of the right temporal lobe gyri is again seen. In addition, the right mesial temporal lobe and hippocampal formation are also atrophic and there is abnormal T2 signal corresponding to the amygdala and hippocampal head. The left temporal lobe may also be affected but to a much lesser degree than the right. The gyri recti also seem to be somewhat thinned. The right temporal horn demonstrates mild ex vacuo dilatation. These findings show no significant change from prior exams.Short TE single voxel spectroscopy was performed over the rightamygdala and hippocampal head, at the site of the most conspicuous atrophy and signal abnormality. Artifact compromises the far left end of the spectrum, likely due to poor water suppression. However, the majority of the spectrum is of acceptable quality and shows a uniform reduction in all metabolite peaks. In particular, the NAA peak is not detectable above background noise suggesting significant neuronal loss. No evidence of any lactate is seen. Single voxel spectroscopy of the left mesial temporal lobe shows a reduction in metabolite peaks, but less severe than that seen on the right, and with detectable NAA indicating viable neuronal tissue. A small negative doublet between 1.1 and 1.0 ppm is seen, which does not clearly correspond to any typical metabolite and which may be artifactual.Single voxel spectroscopy was also performed over areas of predominantly gray matter and predominantly white matter in the cerebral cortex. The spectra from these regions are within normal limits. Again, no significant lactate is detected.No evidence of restricted diffusion is seen. No pathologic parenchymal or extra-axial enhancement is observed. The atrophic right mesial temporal lobe shows some intrinsic T1 hyperintensity which may reflect cellular loss and laminar necrosis. No evidence of intracranial hemorrhage is seen. Except as above, the ventricular system is normal in size and morphology.
Again seen is atrophy affecting a large portion of the right temporal lobe with particular volume loss and associated signal abnormality within the mesial temporal structures including the amygdala and hippocampal head. The left temporal lobe and inferior frontal lobes may also be involved, but to a much lesser degree. There has been no significant interval change in these findings.Single voxel spectroscopy performed over the right mesial temporal lobe shows a significant reduction in all major metabolites, particularly NAA which is not detectable above the level of background noise. This pattern is compatible with severe neuronal loss. No evidence of any significant lactate is seen. Spectroscopy of the left mesial temporal lobe shows some reduction in metabolite peaks, but much less severe than on the right, and again no evidence of lactate. Spectroscopy of normal-appearing gray matter and white matter is within normal limits.The above findings are again suggestive of sequelae of a prior encephalitis which could have been infectious/viral or autoimmune/para-neoplastic. Absence of detectable lactate would tend to argue against an ongoing failure of energy metabolism. However, it does not exclude metabolic disease in general as not all metabolic deficiencies are associated with detectable brain lactate.