PMC6879674_01
Representative magnetic resonance images from case 2. (A) Diffusion weighted imaging at day 5 following onset of left-sided convulsion revealed high signals in subcortical areas in the right hemisphere. (B) T1-weighted imaging 2 years following onset revealed right hemispheric atrophy. (C) Arterial spin labeling at the same time revealed hypoperfusion in the right hemisphere.
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F1
Brain DWI showed reduced diffusivity in the cortex and subcortical white matter in the right hemisphere, at 5 days after the occurrence (Figure 1A). ASL (Figures 1B,C). At the age of 59 months, he underwent right hemispherotomy. The histopathological examination with hematoxylin-eosin staining revealed an excessive number of neurons and glia cells in the white matter with intact cortical architecture and absence of aberrant cells, corresponding to FCD type IIId, in the cerebral tissues of the tip of the right temporal lobe (Supplementary Figures 1C,D) and adjacent to the right hippocampus.
Representative pathological findings with hematoxylin-eosin staining of the left lateral temporal lobe (A-C) and left amygdala (D) from case 3. (A) Normal architecture of cortical and subcortical white matter (x100). (B) Excessive number of neurons in the white matter (x200, arrowheads). (C) Neurons with increased nuclear/cytoplasmic ratio in the cortex (x200). (D) Clustered immature neurons (x200).
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F2
The histopathological examination with hematoxylin-eosin staining revealed immature-like neurons with large nuclei in the cerebral cortex of the tip of the left temporal lobe (Supplementary Figure 2B). An excessive number of neurons and glial cells was observed in the white matter of the same region, corresponding to FCD type IIId (Figures 2A-C). Clustering of immature-like neurons was observed in the left amygdala (Figure 2D) and gliosis was observed in the right hippocampus.
PMC6879674_02
Representative magnetic resonance images from case 2. (A) Diffusion weighted imaging at day 5 following onset of left-sided convulsion revealed high signals in subcortical areas in the right hemisphere. (B) T1-weighted imaging 2 years following onset revealed right hemispheric atrophy. (C) Arterial spin labeling at the same time revealed hypoperfusion in the right hemisphere.
fneur-10-01233-g0001.jpg
PMC6879674_02_fneur-10-01233-g0001.jpg
F1
Brain DWI showed reduced diffusivity in the cortex and subcortical white matter in the right hemisphere, at 5 days after the occurrence (Figure 1A). ASL (Figures 1B,C). At the age of 59 months, he underwent right hemispherotomy. The histopathological examination with hematoxylin-eosin staining revealed an excessive number of neurons and glia cells in the white matter with intact cortical architecture and absence of aberrant cells, corresponding to FCD type IIId, in the cerebral tissues of the tip of the right temporal lobe (Supplementary Figures 1C,D) and adjacent to the right hippocampus.
PMC6879674_03
Representative pathological findings with hematoxylin-eosin staining of the left lateral temporal lobe (A-C) and left amygdala (D) from case 3. (A) Normal architecture of cortical and subcortical white matter (x100). (B) Excessive number of neurons in the white matter (x200, arrowheads). (C) Neurons with increased nuclear/cytoplasmic ratio in the cortex (x200). (D) Clustered immature neurons (x200).
fneur-10-01233-g0002.jpg
PMC6879674_03_fneur-10-01233-g0002.jpg
F2
The histopathological examination with hematoxylin-eosin staining revealed immature-like neurons with large nuclei in the cerebral cortex of the tip of the left temporal lobe (Supplementary Figure 2B). An excessive number of neurons and glial cells was observed in the white matter of the same region, corresponding to FCD type IIId (Figures 2A-C). Clustering of immature-like neurons was observed in the left amygdala (Figure 2D) and gliosis was observed in the right hippocampus.