Contributed by 1Brian H Le, MD and 2Matthew Sandusky, MD
1Department of Pathology, Reading Hospital and Medical Center, West Reading, PA
2Department of Diagnostic Imaging, Brown University, Providence, RI
An 81 year-old male with a clinical history of hypertension and hyperlipidemia presented with weakness, confusion, aphasia, and short-term amnesia. Five months prior to presentation he had sustained a stroke involving the left middle cerebral artery. Current imaging by CT scan reveals worsening edema in the vascular territorial distribution of the left middle cerebral artery accompanied an ovoid, mass-like lesion in the left temporal-parietal region. Follow-up MRI revealed, in the anterior aspect of the left temporal lobe and extending into the insula and basal ganglia, a 5.0 x 4.6 x 3.2 cm mass with serpiginous border enhancement. Foci devoid of enhancement were also observed, suggestive of necrosis. The patient subsequently underwent a craniotomy with attempt at gross total resection, yielding an approximate 20 mL aggregate of tissue.
Histologic examination of the tumor shows biphasic histology. The less dominant morphologic pattern consists of a hypercellular proliferation of pleomorphic cells, with occasional giant cells, present within a gliofibrillary background (figure 1). Foci of microvascular proliferation are observed (figure 2). Cellular elements within this component show reactivity for glial fibrillary acidic protein (GFAP), vimentin, and S-100 protein.
The second, more prominent component is composed of cells with large nuclei, present within a background of extensive necrosis (figure 3). High power magnification is notable for nuclear molding and an elevated mitotic index (figures 4 and 5). Cellular constituents comprising this component show faint immunoreactivity for S-100 and neurofilament, but more prominent reactivity for synaptophysin (figure 6), and neuron-specific enolase (NSE) (figure 7).