Presentation
Abnormal behavior for 2 weeks.
Patient Data
A well-defined mass of altered signal intensity that is T2/FLAIR hyperintense, T1 hypointense with necrotic areas, with no restricted diffusion, in the left frontoparietal lobe, deep white matter, and gangliocapsular region. It is associated with surrounding T2/FLAIR hyperintensity extending in the white matter of the frontal parietal temporal lobe, internal capsule, and midbrain, likely vasogenic edema. Post-contrast imaging shows enhancement in solid components and periphery.
A few foci of SWAN blooming within the mass are suggestive of hemorrhages. Mass effect in the form of effacement of the underlying left lateral ventricle and a midline shift of 5 mm.
Case Discussion
The patient underwent a left frontoparietal craniotomy and endoscopic-assisted gross tumor excision.
On histopathology, microscopic examination showed high-grade glioma with vascular proliferation and necrosis. IHC spindle cells are positive for vimentin and negative for GFAP, OLIG2, IDH1, EMA, and CK. Gemistocytic cells are positive for GFAP and OLIG2. CD34 expression is focal. Ki67 ~ 20% and P53 mutant. Final diagnosis of gliosarcoma: IDH wild type, grade IV.
The current WHO classification of CNS cancers (2021) recognizes gliosarcoma as a classic variety of glioblastoma and classifies it as a variant of glioblastoma. These are primary intra-axial neoplasms that are both glial and mesenchymal, and they are classified as extremely malignant (WHO grade 4).
MRI signal characteristics of these tumors show heterogeneous hyperintense mass on T1, heterogeneous signal due to hemorrhage, and necrotic components on T2 with thick irregular rim of enhancement on post-contrast images.
These tumors carry a very poor prognosis.
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