PMC6720354_01
CT imaging revealed hydrocephalus and an iso-density mass lesion at the left thalamus (A). MRI revealed imaging revealed a poorly circumscribed mass lesion in the left thalamus, extending to both the midbrain and the right thalamus. The signal patterns were T1-low (B), T2-high (C), T2*-high (D), diffusion weighted image-slight high (E), T1 Gadrinium-nonenhanced (F), and fluid attenuation inversion recovery-high (G; axial, H; coronal, I; sagittal), respectively. MRA showed no obvious vascular abnormalities (H).
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Computed tomography (CT) revealed hydrocephalus and an iso-density mass lesion in the left thalamus (Figure 1(A)), and the patient was transported to our hospital. Magnetic resonance imaging (MRI) revealed a poorly circumscribed mass lesion extending to both the midbrain and the right thalamus from the left thalamus (Figures 1(B)-1(I)) and magnetic resonance angiography (MRA) detected no vascular abnormalities such as aneurysms, arterio-venous malformation or moya-moya disease (Figure 1(H)).
Hematoxylin-Eosin (H&E) staining revealed proliferation of various palisading cells with bipolar nature and no obvious findings of Rosenthal fiber (A, B). The immunohistochemical status of IDH1 showed wildtype IDH1 (C) and the Ki-67 labeling index was approximately 4% (D). CD34 staining suggested low microvascular proliferation (E). The optical magnification ratio of photomicrographs is 200-fold except for (B) (400-fold). The histone H3-K27M mutation was detected by Sanger sequencing (F).
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Routine pathological examination of cell morphology suggested anaplastic astrocytoma, but the lack of necrosis or hypervascularity also suggested the possibility of diffuse astrocytoma or pilocytic astrocytoma with degeneration (Figures 2(A)-2(B)). Immunohistochemical isocitrate dehydrogenase 1 (IDH1) analysis suggested wildtype IDH1 status (Figure 2(C)). Moreover, immunohistochemical Ki-67 staining suggested low rate of cell proliferation (Figure 2(D)) and CD34 staining suggested low microvascular proliferation (Figure 2(E)). We therefore consulted another institution for definitive diagnosis and finally got the report that the H3-K27M mutation had been confirmed by Sanger sequencing (Figure 2(F)).
Follow-up MRIs conducted every 4 weeks revealed fluid attenuation inversion recovery and no change in tumor size and pattern of intensity ((A); shortly after surgery, (B); 4 weeks later, (C); 8 weeks later).
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Follow-up MRIs conducted every 4 weeks showed no change in tumor size or intensity pattern (Figures 3(A)-3(C)).
The emergency head CT on postpartum day 2 revealed cerebral herniation due to massive intratumoral hemorrhage ((A); axial view, (B); coronal view).
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An emergency head CT performed after resuscitation revealed cerebral herniation due to massive intratumoral hemorrhage (Figures 4(A)-4(B)), and the patient died 3 weeks after the hemorrhage.