PMC7827503_01
(a and b) Preoperative magnetic resonance (MR) images. (a) T1-weighted MR image with gadolinium-DTPA enhancement demonstrates a large parasagittal meningioma in the right frontal region extending to the left side. (b) On MR image with fluid-attenuated inversion recovery sequence (FLAIR), mild atrophy of the cerebrum including the hippocampus is noted. (c and d) FLAIR images immediately after the surgery confirm the total removal of the meningioma through a right frontal craniotomy, without causing damage to the underlying cortex. (e and f) FLAIR images 3 months postoperatively reveal a subdural hematoma on the left side and marked ventricular enlargement. Bilateral hippocampal atrophy is more evident than that before tumor surgery. In particular, the right hippocampus is markedly atrophied, with marked enlargement of the right inferior horn. Periventricular hyperintensity, especially on the right side, is also observed. (g and h) Computed tomography image 6 months postoperatively shows progressive ventriculomegaly, while the left subdural hematoma is decreased in size. White arrows indicate the ventriculoperitoneal (VP) shunt. (i and j) FLAIR images, after changing the setting pressure of the VP shunt system, show that the ventricular size is well controlled. Atrophy of the cerebrum, including the hippocampus, and periventricular hyperintensity, predominantly on the right side, are apparent. White arrows indicate artifacts caused by the VP shunt system. (k and l) Perfusion MR with arterial spin labeling demonstrates a markedly decreased signal in the right cerebral cortex. White arrows indicate artifacts caused by the VP shunt system.
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F1
Magnetic resonance imaging (MRI) demonstrated a large parasagittal meningioma in the right frontal region extending to the left side [Figure 1a]. Mild atrophy of the cerebrum, including the hippocampus, was noted, but was estimated to be age appropriate [Figure 1b]. She underwent total removal of the tumor (histologically microcystic meningioma) through a right frontal craniotomy, without causing damage to the underlying cortex [Figure 1c and d]. MRI revealed ventriculomegaly and a subdural hematoma on the left side [Figure 1e]. In particular, the right hippocampus was markedly atrophied, with enlargement of the right inferior horn [Figure 1f]. Computed tomography showed progressive ventricular enlargement [Figure 1g and h], and EEG revealed reappearance of repetitive paroxysmal discharges in the right frontal region. Although the ventricular size was controlled by changing the setting pressure of the VP shunt system [Figure 1i and j], her clinical and EEG findings did not change. Perfusion MRI with arterial spin labeling (ASL) demonstrated a markedly decreased signal in the right cerebral cortex [Figure 1k and l].
(a) Electroencephalography (EEG) 3 months postoperatively reveals repetitive paroxysmal discharges in the right frontal region (F4 of the International EEG 10-20 System). (b) Continuous EEG monitoring during barbiturate coma therapy, 6 months after tumor removal, demonstrates periodic paroxysmal discharges, especially in the right frontal region. (c-f) Intraoperative findings during epilepsy surgery. (c) Three-dimensional reconstruction of the computed tomography scan demonstrates the extent of the craniotomy. (d) The position and number of the subdural electrodes are placed on the intraoperative photographs, shown in an orientation matched with (c). (e) Intraoperative electrocorticography (ECoG) reveals periodic paroxysmal discharges with the maximal amplitude of electrode No. 7. Fast-wave activities ride on the descending phase of these paroxysmal activities. (f) Beta and gamma activities are determined by time-frequency analysis of the paroxysmal ECoG activities recorded from electrode No. 7.
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F2
Barbiturate coma therapy with thiamylal sodium was administered; however, continuous EEG monitoring demonstrated periodic paroxysmal discharges, especially in the right frontal region [Figure 2a and b]. Through reopening of the right frontal craniotomy [Figure 2c], the frontal convexity was exposed [Figure 2d]. ECoG revealed periodic paroxysmal discharges in the neighboring cortex where the meningioma was located [Figure 2e]. Beta and gamma activities were determined by time-frequency analysis of these paroxysmal activities [Figure 2f].
Histopathological findings of the resected paroxysmal foci. (a and b) Numerous senile plaques associated with the amyloid core (black arrows) are noted in the cortex. Rarefaction of white matter was focally prominent. (c and d) Amyloid beta immunopositive senile plaques are located mainly in the cortex. Amyloid beta deposition is also observed in some of the meningeal and cortical blood vessels. (e) The amyloid core of the senile plaque tested positive for Dylon staining (arrow heads). Amyloid beta deposition was also observed in the cortical blood vessels (arrows). (f) Phosphorylated tau immunopositive neurofibrillary tangles and numerous neuropil threads are observed. (g) Immunostaining for glial fibrillary acidic protein demonstrates severe gliosis in the white matter and prominent astrocytic reaction against senile plaques in the cortex.
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F3
Histologically, in the resected cortex, there were numerous senile plaques [Figure 3a and b], which tested immunopositive for amyloid beta [Figure 3c and d] and positive for Congo red and Dylon staining [Figure 3e], as well as phosphorylated tau-immunopositive neurofibrillary tangles (NFTs) and neuropil threads [Figure 3f]. Amyloid beta deposition was also observed in some of the meningeal and cortical blood vessels [Figure 3c]. Rarefaction of the white matter was focally prominent [Figure 3a], in which phosphorylated neurofilament immunostaining revealed axonal degeneration. Immunostaining for glial fibrillary acidic protein demonstrated severe gliosis in the white matter and prominent astrocytic reaction against senile plaques in the cortex [Figure 3g].