PMC6742723_01
MRI in November 2013. An abnormal signal was confined to left frontal lobe. It was not obvious on the T1-weighted image (A) and hyperintense on the T2-weighted-Fluid-Attenuated Inversion Recovery (T2-FLAIR) image (B) in the absence of enhancement (C). The T2-weighted image was unavailable.
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F1
In November 2013, he underwent a magnetic resonance imaging (MRI) scan that was unremarkable, except for the presence of small patchy areas in the left frontal lobe (Figure 1).
MRI in October 2017. There was a cystic lesion in the left frontal lobe that presented as hypointense on the T1-weighted image (A), hyperintense on the T2/T2-FLAIR/Apparent diffusion coefficient (ADC) image (B,C,E) and hypointense on the diffusion weighted imaging (DWI, D), with surrounding edema and rim enhancement (F).
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F2
He underwent another MRI scan, revealing a cystic lesion with rim enhancement at the same location (Figure 2).
Fluorodeoxyglucose-positron emission tomography-computed tomography (FDG-PET-CT) in October 2017. FDG-PET-CT indicated low glucose metabolism of left frontal-parietal lobe, which was suggestive of an intracranial primary benign lesion.
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F3
Fluorodeoxyglucose-positron emission tomography-computed tomography (FDG-PET-CT) showed low metabolism (Figure 3), and coupled with the patient's raw food diet, a diagnosis of parasitosis was made.
MRI in September 2018. The cystic lesion in left frontal lobe was enlarged. The lesion showed the same characteristics as the MRI scan performed in 2017. [(A-F) Represents T2-weighted image, FLAIR, DWI, ADC, axial and sagittal post-contrast T1-weighted image, respectively. The pre-contrast T1-weighted image was unavailable].
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F4
MRI scan revealed further enlargement of the lesion (Figure 4), and magnetic resonance spectroscopy (MRS, Figure 5A) and diffusion tensor imaging (DTI, Figure 5B) were scheduled. MRS detected a significantly heightened choline (Cho) peak and a weakened N-acetylaspartate (NAA) peak.
(A) Magnetic resonance spectroscopy (MRS) in September 2018. MRS of peri-enhancement area detected a significantly heightened choline (Cho) peak at 3.2 ppm, and a weakened N-acetylaspartate (NAA) peak at 2.0 ppm. Resonance peak integral of Cho and NAA were 1.96 and 0.40, respectively. The Cho/NAA ratio was 4.9. (B) Diffusion tensor imaging (DTI) in September 2018. Three-dimensional reconstruction images showed an invasion of the lesion into the left pyramidal tract.
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F5
MRI scan revealed further enlargement of the lesion (Figure 4), and magnetic resonance spectroscopy (MRS, Figure 5A) and diffusion tensor imaging (DTI, Figure 5B) were scheduled. MRS detected a significantly heightened choline (Cho) peak and a weakened N-acetylaspartate (NAA) peak.
(A) Use of an intraoperative electrophysiological monitor during surgery. Electrodes were placed on the surface of the brain to identify the functional area. (B) The pale-yellow cystic fluid suctioned by the needle. (C) The cyst wall exposed after removing the cystic fluid. It was soft and dark red in appearance.
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F6
We performed lesion resection under an intraoperative electrophysiological monitor to protect the adjoining precentral gyrus (Figure 6A). Beneath the cortex, there was a solid-cystic lesion containing pale-yellow cystic fluid (Figure 6B). The cyst wall was soft and dark red in appearance (Figure 6C).
Histological analysis. The pathological report gave a diagnosis of glioblastoma, WHO IV, without mutation of the isocitrate dehydrogenase 1 (IDH1) gene.
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F7
Health Organization (WHO) Classification of Tumors of the Central Nervous System. Histological analysis showed an absence of mutation of the isocitrate dehydrogenase 1 (IDH1) gene (Figure 7).