Contributed by Gustavo Sevlever, MD, PhD1,2; Naomi Arakaki, MD1; María Asunción Beña, MD5; Andrés Cervio, MD3; Miguel A. Riudavets, MD1,4
Departments of 1Neuropathology, 2Research, and 3Neurosurgery.
Institute for Neurological Research, FLENI. Buenos Aires, Argentina.
4Laboratory of Histopathology, OCME. Buenos Aires, Argentina.
5Laboratory of Histopathology, Hospital Milstein. Buenos Aires, Argentina
CLINICAL HISTORY
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A 56-year old man with past medical history of surgery for congenital pulmonary valve disease, transient ischemic attack without sequelae, meningitis with brain abscess, hyperuricaemia and atrial fibrillation presented with recently increased tiredness, loss of strength and headache. Physical examination revealed dysarthria, and paresthesia in the left hand. No lymphadenopathies, fever, or weight loss were detected. CT-scan of the chest, abdomen and pelvis revealed no abnormalities, and HIV test was negative. On MRI, two intra-axial masses, hyperintense on T1, with contrast ring enhancement in right thalamo-capsular area, and frontal convexity, were visualized (Fig 1). A stereotactic biopsy of the thalamic lesion was performed. Three weeks later, a grayish, soft mass was resected from the frontal lesion through a right fronto-parietal craniotomy.
GROSS AND MICROSCOPIC PATHOLOGY
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Macroscopically, the resected lesion consisted of multiple white fragments measuring 0.7 x 0.5 x 0.2 cm. Intraoperative pathology examination revealed pleomorphic cells with occasional processes distributed in sheets with eosinophilic, granular cytoplasm, and vesicular nuclei with prominent nucleoli (Fig 2). An intraoperative diagnosis of glioma was reached. Permanent sections of both biopsies showed a neoplasm composed of round, eosinophilic cells with granular cytoplasm, and round, occasionally clear nuclei with prominent nucleoli (Fig 3). No necrosis, vascular hyperplasia or increased mitotic index were appreciated in the area of material submitted for sampling. Tumor cells were immunoreactive for glial fibrillary acidic protein (GFAP) and CD68 (Figs 4, 5, respectively), but not for pancytokeratin marker (AE1-AE3). Ki-67 labeling was around 9%. What is your diagnosis?
International Society of Neuropathology