PMC10159325_01
Magnetic resonance imaging (MRI) on admission (a-c). An extra-axial tumor on the left frontal lobe is hypointense on T1-weighted image (a) and hyperintense without peritumoral edema on T2-weighted image (b). Gadolinium-enhanced T1-weighted image shows a homogenously enhanced tumor with leptomeningeal enhancement around the tumor.
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F1
On brain magnetic resonance imaging (MRI), the tumor appeared hypointense on T1-weighted images [Figure 1a], and hyperintense on T2-weighted images [Figure 1b] without peritumoral edema. Gadolinium-enhanced T1-weighted images demonstrated a homogenously enhanced extra-axial tumor with peritumoral leptomeningeal enhancement [Figure 1c].
Magnetic resonance imaging on admission (a) and 1 month later (b and c). Gadolinium-enhanced T1-weighted sagittal image on admission shows leptomeningeal enhancement around the tumor (a), which is markedly enlarged 1 month later ([b], sagittal image; [c], axial image).
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F2
One-month post-admission MRI revealed that the tumor size was unchanged, but peritumoral leptomeningeal gadolinium enhancement was significantly expanded [Figures 2a-c].
Intraoperative findings (a-c) and postoperative magnetic resonance imaging (MRI) (d-e). The tumor is soft and reddish (a). The subarachnoid space is broadly filled with yellowish semisolid materials (b), which are biopsied (c). Postoperative MRIs at 1 week (d, upper panel) and 3 years later (d, lower panel) demonstrate a rapid improvement of leptomeningeal enhancement and no recurrence of it.
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F3
When the dura mater was incised and turned over, a soft and reddish tumor was exposed [Figure 3a]. Peritumoral subarachnoid space was filled with yellowish semisolid substances [Figure 3b]. Most of the tumor was excised, but the semisolid substances in the subarachnoid space were only biopsied to avoid brain damage due to the removal [Figure 3c]. Postoperatively, seizures resolved, and 1-week postsurgery MRI revealed remarkable attenuation of the leptomeningeal enhancement [Figure 3d, upper panel]. The patient has passed more than 3 years without recurrence of seizures, leptomeningitis [Figure 3d, lower panel], meningioma, and breast cancer.
Histopathological (hematoxylin and eosin stain; [a-e]) and immunohistochemical (f-u) findings. The convexity dural-based tumor consists of angiomatous components with numerous small to medium-sized vascular channels (a, low-magnification, and b) and microcystic components with microcysts and cobweb-like background (c). Inflammatory infiltrates exist in the border zone between the tumor and the dura mater (d), and mainly consist of lymphocytes (insert of d). The lesion in the subarachnoid space consists of a cluster of neutrophils (insert of e) with fibrinous exudates (e). The tumor cells are reactive for vimentin (f) and slightly reactive for epithelial membrane antigen (g). Vascular endothelial cells were positive for CD34. MIB-1 index is <1%. Inflammatory infiltrates in the border zone between the tumor and the dura mater are reactive for CD3 (j) and CD20 (k), but almost non-reactive for CD15 (l), while those around lymph follicles are positive for CD68 (m) and CD138 (n). The inflammatory cells in the border zone are also broadly reactive for IgG, but those of <10% are reactive for IgG4. In contrast, inflammatory infiltrates in the subarachnoid space are reactive for CD15 (q) and not for CD68 (r), CD45 (s), CD20 (t), and CD138 (u). Bar = 0.5 mm (a), 100 mum (b-g and m-u), 12.5 mum (insert of d), 25 mum (insert of e), 200 mum (h and i), and 50 mum (j-l).
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F4
The convexity dural-based tumor [Figure 4a] consisted of angiomatous components with numerous small to medium-sized vascular channels [Figure 4b], and microcystic components with microcysts and cobweb-like background [Figure 4c], associated with some meningothelial cells. In the border zone between the convexity dural-based tumor and the dura mater, however, there were inflammatory infiltrates and formation of some lymph follicles [Figure 4d]. Infiltration of numerous neutrophils and fibrinous exudates was also observed in the subarachnoid space [Figure 4e]. Tucson, AZ, USA) and the used antibodies were listed in Table 1. Tumor cells were positive for vimentin [Figure 4f] and slightly positive for epithelial membrane antigen [Figure 4g], and vascular endothelial cells were positive for CD34 [Figure 4h]. Glial fibrillary acidic protein was negative, and MIB-1 index [Figure 4i] was <1% in the convexity dural-based tumor. On the other hand, inflammatory cells infiltrating into the border zone between the tumor and the dura mater were positive for CD3 (T-cell-associated antigen; Figure 4j) and CD20 (B-cell-associated antigen; Figure 4k), and negative for CD15 (neutrophil-associated antigen; Figure 4l); and those around lymph follicles were positive for CD68 (histocyte-associated antigen; Figure 4m) and CD138 (plasma cell-associated antigen; Figure 4n). IgG4 positive [Figure 4p]. In contrast, almost all inflammatory cells infiltrating into the subarachnoid space were positive for CD15 [Figure 4q], while almost no cells were positive for CD68 [Figure 4r], CD45 (lymphocyte-associated antigen; Figure 4s), CD20 [Figure 4t], and CD138 [Figure 4u].