Brain Pathology Case of the Month - October 2019

Contributed by Jawale P M, MD1, Gulwani Hanna V, DNB MNAMS2
1Senior Resident. 2Assistant Professor Department of Pathology, Bhopal Memorial Hospital and Research Centre, Bhopal, India.


A 58-year old man presented with recent onset headache, speech disturbances and vomiting for last 3 days. On examination, he was conscious with stable vital parameters. There was no other significant neurological deficit. Since his routine investigations and systemic examination was largely within normal limits, he underwent neuroimaging studies. MRI study (Axial, sagittal, coronal, contrast and noncontrast sections) demonstrated a fairly well-defined solid-cystic lesion of size 43.2cm in the left temporo-parietal region involving gray and white matter. The mass showed heterogenous enhancement and was predominantly hypointense on T1W image (Fig. 1a). Post-contrast imaging showed a solid component with diffuse enhancement and a cystic area at periphery (Figs. 1b, 1c). Perilesional edema was observed resulting in effacement of adjacent sulci and temporal horn of left lateral ventricle. Patient underwent left temporo-parietal craniotomy with resection of tumor.


Histopathology examination of the tumor tissue bits submitted revealed a piloid neoplasm with variable cellularity (Fig.1d).The tumor cells were predominantly bipolar and rather monomorphous in appearance in loosely cellular areas (Fig. 1e). Background showed prominent mucoid or myxoid change with microcysts formation (Fig.1e) that were highlighted by alcian blue stain (Fig.1f). Some of the tumor cells were arranged in angiocentric arrangement whereas in other places intricate vascular pattern was observed (Fig.1g). Nearly 25-30 % of tumor was hypercellular with presence of mildly enlarged pleomorphic nuclei with chromatin clumping and irregular nuclear margins (Fig. 1h). Increased mitotic activity (7-8 mitoses per 10 high power fields) was observed in the tumor (arrows, Fig. 1h). Periphery of lesion showed reactive gemistocytes and glomeruloid vasculature with tumor infiltration in adjacent brain tissue (Fig. 1i). There was absence of biphasic pattern, eosinophilic granular bodies, Rosenthal fibers, calcification, necrosis, or endothelial proliferation. Strong diffuse immunoreactivity was observed in bipolar neoplastic cells for Glial fibrillary acidic protein (GFAP) (Fig. 1j), S100 (Fig. 1k) and synaptophysin. Epithelial membrane antigen (EMA) was negative. In hypercellular areas, Ki-67 proliferation index was 20-25%. What is your diagnosis?


International Society of Neuropathology