PMC5645159_01
MRI T1 axial view (A) showing rounded hypointense lesion. MRI T1-post (B) showing lesion with minimal abnormal homogenous enhancement. MRI T2 axial view (C) and FLAIR axial view (D) showing rounded hyperintense signal abnormality in the parasagittal right occipital lobe measuring 1.3 cm x 1.0 cm x 1.3 cm.
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MRI demonstrated an abnormal rounded focus of T2 and FLAIR hyperintensity with minimal enhancement in the right superior parasagittal occipital lobe (Fig. 1).
(A) Axial PET scan showing focal increased activity in the right parasagittal occipital lobe with maximum standardized uptake values (SUV) of 22.9 in the occipital lesion, compared to the contralateral side with SUV of 16.7.. (B) Axial PET scan of bilateral temporal lobes showing slightly hypo-metabolic region in the right temporal lobe medially with SUV of 11.2, compared for the left side with SUV of 11.9.
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PET imaging demonstrated a concurrent hypermetabolic focus in the occipital lobe as well as a hypometabolic region within the right temporal lobe (Fig. 2).
(A-D) sEEG recording showing electrographic seizure (red bar) originating (onset marked with black arrows in A) from electrodes inferomedial to (RIM), within (RLM, RUM), and superomedial to (RSM) the occipital lesion.
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Based on the discordant clinical, neurophysiological and imaging data, implantation with intracranial depth electrodes for stereoelectroencephalography (sEEG) was performed, with seven 12-contact depth electrodes "caging" the occipital lesion to best define the boundaries of the seizure-onset zone, and one 12-contact depth electrode per hippocampus/mesial temporal region to assess the extent of the hypothesized epileptic network. sEEG demonstrated innumerable subclinical seizures originating from electrodes within the occipital lesion, and immediately inferior medial, superior medial and inferior lateral to it (Fig. 3).
Hematoxylin and Eosin X40 showing proliferation of Oligodendroglia like cells and neuron without dysplasia. The neurons were negative for CD34 (usually present in DNET in 61% cases). The oligodendroglia like cells had wild type IDH1 and IDH2 genes (by sequencing) and did not show 1p/19q codeletion (by FISH). The Ki-67 proliferation rate was low (< 1%).
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No specific glioneuronal element, adjacent cortical dysplasia or dystrophic calcifications were noted (Fig. 4).