PMC9287778_01
Interictal and ictal EEG: All EEG epochs are displayed in a double-banana montage. Calibration bars are present in each subfigure: horizontal 1 s, vertical 200 muV. 1A. A 15 s epoch showing interictal epileptiform discharges from the left temporal and temporo-occipital regions. Intermittent left temporal slowing is also seen.1B. A 15 s epoch showing electrographic seizure onset from the left hemisphere (arrowhead). 1C. A 60 s epoch showing 6th minute of the seizure. Note prominent the left temporal epileptiform discharges.
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Left temporal slowing and left temporal and temporo-occipital spikes and sharps were present in one recording (see Fig. 1A). EEG features at onset and into the seizure suggested left temporal localization (see Fig. 1 for the EEG features of one seizure).
MRI Brain with coronal oblique T2 images of the temporal lobes from anterior to posterior (a) - (c): There is asymmetric T2 high signal within the left anterior temporal lobe and polar white matter (arrows) consistent with an underlying cortical dysplasia. The hippocampi have a normal appearance. The right temporal lobe myelination is within normal limits for age.
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There was hyperintensity and relatively unmyelinated or poor myelination of the terminal rami within the anterior temporal lobe (see Fig. 2).
Fluorine - 18- fluorodeoxyglucose positron-emission tomography / computed tomography (FDG PET/CT) 3D stereotactic surface projection and normal database comparison (Neurostat): Localized hypometabolism in the left temporal lobe (arrows). Visual cortex hypometabolism related to general anaesthesia.
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A PET scan showed mild diffuse hypometabolism (Fig. 3) involving the anterior and lateral left temporal lobe.
Histopathology. A-C. Medial temporal lobe entorhinal cortex showing neuronal precursors forming a linear band within layer II. A. Low magnification, the asterisk is at a band of neuroblasts (H&E, 40x). B. BCL2 immunohistochemical stain highlighting band-like distribution (asterisk) of neuroblasts (BCL2, 40x). C. High magnification showing clustered neuroblasts in the region of layer II (H&E, 200x). D. Subtotal absence of neurons within cortical layer IV of the distal entorhinal cortex, more than the usual reduction in layer IV neuronal density in this region. This is sufficient for abnormal tangential lamination, or focal cortical dysplasia type 1B by the ILAE classification (NeuN immunohistochemical stain, red lines show position of layer IV, 40x). E. Persistent periventricular neuronal precursors near the temporal horn of the lateral ventricle, with linear extension into the adjacent deep temporal lobe white matter in keeping with an abnormality of neuronal migration (red lines show the distribution of the neuronal precursors, H&E, 100x). F. Increased numbers of single heterotopic neurones within the subcortical and deep white matter of the temporal lobe (asterisk), amounting for to a mild malformation of cortical development (mMCD) (MAP2A immunohistochemistry, 20x). (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
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Focal cortical dysplasia (FCD Type 1b) was seen in the left medial temporal lobe and features of mild malformation of cortical development (mMCD types I and II) were seen in the lateral temporal areas (see Fig. 4).