PMC9062962_01
(Patient 1) (a and b) Oblique views, along with the long axis of the hippocampus, of the magnetic resonance (MR) images with fluid attenuated inversion recovery (FLAIR) sequences, before the left anterior temporal lobectomy at the age of 38, demonstrate a small size of the left calvarium and left entire hemisphere, not just the left temporal lobe. (c) Electroencephalogram (EEG) on day 1 shows lateralized periodic discharges (LPD) at the left fronto-temporal region. (d) Voltage topography of LPD indicates that the maximum amplitude of LPD is located at F7 of International EEG 10-20 system. Blue indicates negativity. (e and f) Axial views of FLAIR images on day 2 depict gliosis in the temporal lobe posterior to the resection cavity (red arrow in e). No definite abnormality is noted at the left frontal lobe (f). Thin chronic subdural hematoma, caused by a fall due to generalized seizure, is also noted on the right side. (g) MR angiography shows increased signals of the peripheries of the left middle and anterior cerebral arteries due to "ictal hyperperfusion" (red arrows). (h and i) On MR angiography of day 9 (h) and day 17 (i), the ictal hyperperfusion is improved. (j and k) Positron emission tomography with fluorodeoxyglucose on day 19 shows rather low metabolism not just in the left temporal lobe, posterior to the resection cavity, but the left entire hemisphere. (l) Intraoperative electrocorticography depicts high-amplitude periodic discharges on the frontal lobe (electrode No 1-10). Asynchronous small-amplitude paroxysms are also recorded on the temporal lobe posterior to the resection cavity (electrode No. 18-22). No paroxysmal discharges are recorded from the medial part of the temporal lobe (electrode No. 24-27). (m) The location and number of the electrodes are indicated on the operative view. Blue trapezoid electrode (No. 24-27) is placed adjoining the medial and basal aspects of the temporal lobe, as described before.[11] Sy: Sylvian veins, RC: Resection cavity at the previous craniotomy. (n and o) Oblique views of FLAIR images, immediately after the operation, showing the resection area (red arrows).
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F1
All clinical findings were typical of MTLE, and the findings of magnetic resonance (MR) images were characterized by a small left calvarium and left entire hemisphere, not just the left temporal lobe [Figures 1a and b]. On the electroencephalogram (EEG), lateralized periodic discharges (LPD) with the maximum amplitude at F7 of the International EEG 10-20 system were recorded in the left frontotemporal region [Figures 1c and d]. MR images showed gliosis in the temporal lobe posterior to the resection cavity [Figure 1e]; however, no definite abnormality was noted in the left frontal lobe [Figure 1f]. In addition, MR angiography (MRA) showed increased signals of the peripheries of the left middle and anterior cerebral arteries due to "ictal hyperperfusion" [Figure 1g]. General anesthesia was maintained with the appearance of a suppression-burst on the EEG monitoring, and the ictal hyperperfusion demonstrated by MRA improved on day 9 [Figure 1h]. On day 17, MRA was performed which did not show ictal hyperperfusion [Figure 1i], and positron emission tomography with fluorodeoxyglucose (FDG-PET) on day 19 showed rather low metabolism in the entire left hemisphere [Figures 1j and k]. Asynchronous small-amplitude paroxysms were also recorded in the temporal lobe posterior to the resection cavity [Figures 1l and m]. These areas were resected [Figures 1n and o].
PMC9062962_02
(Patient 2) (a) Electroencephalogram (EEG) at the 1st super-refractory status epilepticus depicts ictal discharges with evolution continued on the medial part of the left frontal region at the C3 and Cz (red arrows). (b and c) T1-weighted images with gadolinium enhancement fail to reveal the tumor recurrence in the left frontal lobe. (d) Fluid attenuated inversion recovery (FLAIR) image shows gliosis at the interhemispheric cortex medial to the resection cavity (red arrow), in addition to the frontal white matter posterior to the resection cavity (blue arrow). (e) Diffusion-weighted images depict a strong hyperintensity at the medial part of the resection cavity in the left frontal lobe (red arrow) and laminar hyperintensity along with the cortex in the left parietal lobe (white arrows). (f and g) Axial (f) and sagittal views (g) of the fusion images of positron emission tomography with fluorodeoxy glucose (FDG-PET) and FLAIR images demonstrate a strong accumulation at the interhemispheric cortex, medial to the resection cavity in the left frontal lobe (red arrows). (h and i) Intraoperative electrocorticography shows frequent paroxysmal discharges on the interhemispherical surface, medial to the surgical defect in the left frontal lobe. The location and number of the electrodes are indicated on the schematic drawing of the interhemispheric surface. (j and k) Axial (j) and sagittal views (k) of FLAIR images, immediately after the operation, show the resection area, which is identical to the high accumulation area on FDG-PET.
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F2
EEG revealed ictal discharges with evolution continued on the medial part of the left frontal region [Figure 2a], which occasionally propagated to the surroundings. Subsequent MR images failed to reveal tumor recurrence [Figures 2b and c]; however, gliosis was noted medial and posterior to the resection cavity [Figure 2d]. Diffusion-weighted images (DWI) showed a strong hyperintensity at the medial part of the resection cavity in the left frontal lobe and laminar hyperintensity along with the cortex, named "cortical hyperintensity," in the left parietal lobe [Figure 2e]. In addition, FDG-PET showed a strong accumulation in the medial part of the resection cavity [Figures 2f and g]. Intraoperative ECoG showed frequent paroxysmal discharges on the interhemispheric surface, medial to the surgical defect in the left frontal lobe [Figures 2h and i], and the area was resected [Figures 2j and k].