A gangliocytoma/ganglioglioma with no atypical or malignant features was subtotally resected from the right temporal lobe of a 16-year-old woman. A second resection was performed 8 years later to treat a locally recurrent lesion with increased cellularity that was diagnosed as a World Health Organization Grade II ganglioglioma on the basis of neuropathological examination. Molecular analysis of the recurrent tumor revealed a TP53 gene mutation, but no amplification of the epidermal growth factor receptor (EGFR) gene. Radiotherapy (60 Gy) was administered after the second resection. The patient returned 1 year later with a second focal recurrence. The specimen obtained during the third resection of tumor exhibited exclusively astrocytic differentiation, cellular pleomorphism with multinucleated cells, high mitotic activity, and endothelial proliferation. Therefore, the tumor was diagnosed to be a glioblastoma multiforme (GBM). Molecular analysis of tumor DNA from the second recurrent tumor demonstrated the presence of the TP53 mutation, which previously had been observed in the first recurrent tumor, but again no evidence of EGFR amplification. Findings demonstrate that the presence of TP53 mutation in progressed gangliogliomas should be interpreted as a progression-associated mutation rather than a consequence of treatment. This is the first report to indicate that the molecular pathways of gangliocytomas/gangliogliomas progressing to become GBMs may parallel those of diffuse astrocytomas progressing to become GBMs.
4Results. All nine patients had complete or substantial resolution of their formerly intractable headache after TSS. Headaches consisted of ocular pain ipsilateral to the adenoma localization within the sella in four cases and bifrontal headache in five.Magnetic resonance imaging of these patients revealed small diaphragmatic foramen, which were so narrow that only the pituitary stalk could pass. Computed tomography scans showed ossification beneath the sellar floor in the sphenoid sinus, presellar type in six cases, and choncal type in three. The adenomas included cysts in seven cases.There was no cavernous sinus invasion. Intrasellar pressure measurements averaged 41.5 ± 8.5 mmHg, range 34-59, significantly higher than in control patients without headache (n = 12), namely 22.2 ± 10.6 mmHg (16-30).Conclusion. In this study, the authors demonstrated the validity of TSS in the treatment of intractable headache associated with pituitary adenoma. The presence of ocular pain, especially ipsilateral to the adenoma, integrity of the diaphragm sella, and ossification in the sphenoid sinus, cyst or hemorrhage and the absence of cavernous sinus invasion were the indications for TSS for patients complaining of intractable headache and having pituitary adenomas.
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A novel method for the simulation of the clipping position for cerebral aneurysms based on threedimensional computed tomography (3D CT) angiography was evaluated. Rotating the regional 3D CT angiography images including the aneurysm provided the virtual intraoperative views of 36 cerebral aneurysms that were eligible for clipping through a pterional approach with a perpendicularly applied straight clip. The cut-along-trace function of the 3D CT workstation was used to simulate the clipping position. The presence or absence of aneurysm remnants was preoperatively evaluated by observing the clipping simulation image. Intraoperative endoscopy and postoperative cerebral angiography were routinely performed to confirm the completeness of obliterations. Nineteen of 21 aneurysms for which complete obliteration was preoperatively expected were confirmed to have no aneurysm remnant. Nine of 15 aneurysms which were expected to have aneurysm remnant were confirmed to persist. The clipping simulation images could correctly predict aneurysm remnant after the initial clipping with a sensitivity of 90.5% and specificity of 60%. The present simulation method can predict aneurysm remnants and improve the likelihood of complete obliteration by clipping.
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