Female, 15 years old, with left occipital simple partial seizures, right inferior quadrantanopsia, fluctuating area of left T2/FLAIR hyperintensity reported and MRIs. Again seen is ill-defined T2 hyperintensity involving the left paramedian occipital lobe cortex and subcortical white matter. No parenchymal destruction or significant distortion is seen. No associated pathologic enhancement is detected.The extent of this abnormality appears approximately similar to that seen on 08/10/16. It is noted, however, that over the patient's multiple prior examinations, the intensity of the signal has fluctuated. Single and multi voxel short TE spectroscopy was performed over the lesional tissue and compared to areas of normal parenchyma. The lesional tissue demonstrates significant reduction in the NAA peak, very slight elevation of the choline peak, and perhaps minimally elevated lipid relative to normal appearing parenchyma.Redemonstrated is evidence of ex vacuo dilatation of the left frontal horn which largely reflects loss of the caudate nucleus. No other significant areas of signal abnormality or parenchymal lesions are seen. No evidence of intracranial hemorrhage or any abnormal extra-axial fluid collection is detected. Except as above the ventricular system is within normal limits.
Redemonstrated is ill-defined T2 hyperintensity involving the cortex and subcortical white matter of the left paramedian occipital lobe. No focal or masslike lesion is seen. MR spectroscopy demonstrates reduced NAA which generally reflects neuronal injury or loss, as well as a mild elevation of choline and perhaps minimally elevated lipid which are nonspecific findings. There are no features to suggest a high-grade neoplastic process.This type of ill-defined signal abnormality can be seen in parenchyma which has sustained severe prolonged seizure activity. In this scenario, the findings are considered to be the result of the seizure rather than the cause. As to the actual underlying cause, no definite or specific findings are seen. The differential would include inflammation from an infectious, inflammatory or autoimmune etiology; a subtle cortical dysplasia; gliosis from prior insult or injury; or perhaps a very subtle low-grade neoplastic process.Also noted is chronic loss of the left caudate nucleus which results in ex vacuo dilatation of the left frontal horn. This is of uncertain etiology but could indicate a remote ischemic insult, potentially even prenatal or perinatal.