PMC8696155_01
The top row (A1-G1) displays magnetic resonance (MR) images from the initial study during the first admission, and the bottom row (A2-G2) displays the corresponding images during the relapse 2 months later. The lesion (A1,A2) returns an isointense signal on T1-weighted images and (B1,B2) demonstrates enhancement on post-contrast images. (C2) High T2-signal cystic lesions are seen along the leptomeningeal surface that increased in size and number during the relapse. (D2) The internal signal of these cystic lesions is not entirely suppressed on fluid attenuation inversion recovery (FLAIR) sequence. (E1,E2) No blooming artifacts seen on gradient echo (GRE) sequence. (F1,G1;F2,G2) Restricted diffusion is not demonstrated in both studies.
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F1
Magnetic resonance imaging of the brain revealed diffuse enhancing nodular leptomeningeal thickening, especially at the basal cisterns (Figure 1). The follow-up MR brain study revealed exuberant nodular leptomeningeal enhancement that was more extensive than the initial study (Figure 1).
The top row (A1-C1) displays MR images from the initial study during the first admission, and the bottom row (A2-C2) displays the corresponding images during the relapse 2 months later. (A1,A2) There were cystic lesions with high T2 signal along the leptomeningeal surface. These initially small non-enhancing cystic lesions [white arrows, (B1)] increased in size and number in the follow-up scan [white arrows, (B2)]. (A2) Brain tissue was seen herniating through a Burr hole from a previous external ventricular shunt site, indicating that there was increased intracranial pressure. (C1,C2) Coronal post-contrast T1 images demonstrate the predominantly basal cisternal location of the nodular leptomeningeal thickening.
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F2
Small non-enhancing cystic lesions were seen along the leptomeningeal surface (Figure 2B1), and no restricted diffusion was depicted. Also, the previously seen cystic lesions have increased in size and number (Figures 2B2,C).
MR spectroscopy (TE/TR = 144 ms/2,000 ms) findings of elevated choline:creatine ratio (4.34) suggesting high cell turnover in favor of malignancy. The absence of a singlet peak at 3.8 ppm makes tuberculoma less likely.
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F3
MR spectroscopy (single voxel placed at the thickened tentorium cerebelli) showed a markedly elevated choline:creatine ratio of 4.34 and absence of a singlet peak at 3.8 ppm (Figure 3).
(A) The lesion showed moderate neoplastic cells with background desmoplastic and myxoid changes. (H&E, original magnification x20). (B) The cells were fairly monomorphic with mild nuclear pleomorphism displaying enlarged round to oval nuclei with fine nuclear chromatin and inconspicuous nucleoli hematoxylin and eosin (H&E), original magnification x40). (C) Occasional mitosis was seen (arrow) (H&E, original magnification x40). (D) High Ki-67 proliferation rate of the neoplastic cells (immunohistochemical (IHC) Ki-67, original magnification x20). (E) The neoplastic cells were positive for S100 (IHC S100, original magnification x20). (F) The cells showed positivity toward synaptophysin immunostain (IHC synaptophysin, original magnification x40).
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Histopathological examination (HPE) revealed a moderately cellular neoplastic proliferation with background desmoplastic and myxoid changes seen from the hematoxylin and eosin (H&E) stain slides (Figure 4A). The cells were fairly monomorphic with mild nuclear pleomorphism displaying enlarged round to oval nuclei with fine chromatin and inconspicuous nucleoli (Figure 4B). Occasional mitosis was seen (Figure 4C). The Ki-67 proliferation rate was high, accounting for about 80% (Figure 4D). Immunohistochemical (IHC) studies showed that the tumor cells were positive for S100 and synaptophysin (Figures 4E,F).