PMC8293275_01
Computed tomography (CT) and contrast-enhanced magnetic resonance imaging (MRI) were performed in June 2018 (A-E). CT images of brain window images demonstrated a well-demarcated mass with fat density in the left temporal lobe and cerebellar vermis with calcification (A,B). MRI revealed a hyper- and isointense mixed mass on T1-weighted image (C) and iso- and hyperintense mixed mass on T2-weighted image (D). Gadolinium-enhanced T1-weighted image showed heterogeneous enhancement (E). The lesion in the cerebellum compressed the fourth ventricle (E) and caused supratentorial obstructive hydrocephalus (F). In 2013, the cerebellum lesion was relatively small (G) and did not cause obstructive hydrocephalus (H). Postoperative MRI indicated the cerebellar mass was near-totally removed (I).
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F1
CT revealed a large heterogeneous mass (5 cm * 3.4 cm) in the temporal lobe with curvilinear calcification (Figure 1A), and a small hypodense lesion (3.6 * 2.8 * 3 cm) in the cerebellar vermis with predominantly fatty density and ill-defined margin caused compression of ambient cisterns. The bone window showed the mild compression of perilesional cranial bones (Figure 1B). The lesions were hyperintense on T1-weighted images (WI) (Figure 1C) and iso-to hyperintense on T2WI (Figure 1D), indicating the lipomatous component of the lesion. T1WI revealed obvious heterogeneous enhancement, particularly in the cerebellar vermis (Figure 1E). The cerebellar lesion extended through the tentorium cerebelli and caused obstructive hydrocephalus (Figure 1F). Back then, the cerebellar lesion was relatively small (6.4 * 4.3 * 4.6 cm) (Figure 1G) without any sign of obstructive hydrocephalus (Figure 1H). Postoperative MRI indicated the cerebellar mass was removed near-total (Figure 1I).
Histological images (A,B) and immunohistochemical staining images (C-E). (A) The tumor consisted of uniform round cells with small, round, or oval nuclei with finely speckled chromatin and large lipid vacuoles (hematoxylin and eosin staining; original magnification: x400). (B) The tumor cells were accompanied by a large number of vascular hyperplasia and papillary structure. There were scattered adipose tissue and lymphatic structures in the tumor (hematoxylin and eosin staining; original magnification: x200). (C) Strong NeuN immunopositivity of neoplastic cells. (D) GFAP-positive component and immunonegative neurocytic fields. (E) The Ki-67 proliferation index was 5-10%.
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F2
Microscopic examination showed a glioneuronal tumor with dense and diverse tumor cells, accompanied by extensive vascular hyperplasia, and papillary structures along with scattered adipose tissue and lymphatic structures in excised tumor mass (Figures 2A,B). Immunohistochemical staining showed the tumor cells had a positive expression for NeuN (Figure 2C), GFAP (Figure 2D), CD56, ATRX, Olig-2, and negative expression for CD45 (LCA), CD20, EMA. The Ki-67 proliferation index was low (5-10%) in tumor cells (Figure 2E).