PMC7332709_01
Magnetic resonance imaging (MRI) at the first visit showing an incidentally found sellar tumor. The posterior pituitary gland was located superoposterior to the tumor (open arrowhead in a). The pituitary gland seemed to be on top of the tumor (arrows in c and d). Cavernous sinus invasion is indicated by arrowheads (b and d) (a) Sagittal T1-weighted image (WI). (b) Coronal T1WI. (c) Sagittal gadolinium-enhanced image (GEI). (d) Coronal GEI.
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F1
Magnetic resonance imaging (MRI) found a sellar lesion with a diameter of 18 mm invading into the bilateral cavernous sinus [Figure 1].
A magnetic resonance imaging (MRI) study for 6 years after the first visit demonstrated an extensively grown tumor occupying the sellar and wide juxtasellar regions (a-d). The white arrow indicates a relatively well-enhanced area, supposed to be the pituitary gland, on top of the tumor (d). The black arrow indicates an invasion of the front of the tumor into the clivus (c and d). (a) Coronal T1WI, (b) sagittal T2WI, (c) sagittal GEI, (d) coronal GEI.
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F2
MRI showed a large tumor with a maximal diameter of 56 mm, involving the sellar, suprasellar, retroclival, and bilateral cavernous sinus regions and strongly compressing the optic nerve and optic chiasm [Figure 2].
A sagittal computed tomography (CT) scan the tumor was isodense to the brain parenchyma (a). The sellar floor was extensively thickened (arrows in a and b). (a) Brain window. (b) Bone window.
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F3
A computed tomography (CT) scan showed that the tumor was slightly hyperdense [Figure 3].
A magnetic resonance imaging (MRI) scan immediately after the surgery showing sufficient decompression of the optic chiasma. The pituitary gland was well preserved (arrows in a and b). (a) Sagittal GEI and (b) coronal GEI.
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F4
Postoperative MRI demonstrated the sufficient decompression of the optic chiasm and an intact pituitary gland [Figure 4].
Histologic features of the specimen obtained by transsphenoidal surgery. The tumor was composed of neoplastic cells with scant to moderate cytoplasm and chromatin-rich oval or short rod-like nuclei. The neoplastic cells partly formed a lobular arrangement (x200, a). A few ganglion-like cells were seen (x600, b). On immunohistochemistry, the tumor was diffusely positive for synaptophysin (x200, c), neurofilament protein (x200, d), NeuN (x200, e), chromogranin A (x200, f), and arginine vasopressin (x400, g). S-100 protein was positive mainly in the spindle cells surrounding a fibrovascular stroma (x200, h). Bar = 100 mum.
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F5
Pathologically, the tumor was composed of a proliferation of round to oval neoplastic cells with scant to moderate cytoplasm and chromatin-rich short rod-like nuclei against a background of intercellular neuropil-like fibrillary matrix [Figure 5a]. These cells were partly packed, showing a lobular arrangement separated by a fibrovascular stroma [Figure 5b]. The neoplastic cells and fibrillary matrix were immunohistochemically positive for neuronal markers, including synaptophysin [Figure 5c], neurofilament protein [Figure 5d], neuron-specific enolase, and NeuN [Figure 5e] chromogranin A [Figure 5f]. The neoplastic cells were also positive for arginine vasopressin (AVP) [Figure 5g]. The S-100 protein [Figure 5h] and vimentin were positive, mainly in spindle cells surrounding the fibrovascular stroma.
A magnetic resonance imaging (MRI) scan studied at 34 months after the surgery showed the control of the tumor growth. The surgically debulked area was occupied by fibrous tissues (* in a and b) (a) sagittal GEI. (b) Coronal GEI.
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F6
She underwent 50-Gy of intensity-modulated radiation therapy to the residual tumor due to hospital's standard operating procedure, which has controlled its growth for the 3 years [Figure 6].