Brain Pathology Case of the Month - November 2006

Contributed by Christopher A. Robinson, MD
Department of Pathology, Royal University Hospital and Saskatoon Health Region, Saskatoon, Saskatchewan, Canada
Published on line in November 2006


A 39-year-old man presented to a small local hospital in northern Saskatchewan following new-onset seizure activity. A single seizure began focally in the left arm and subsequently became secondarily generalized. He was observed in hospital for two days, during which there were no further seizures. He was released after arrangements had been made for him to follow-up with a neurologist, an appointment which he did not keep. Two months later he presented to our institution after having had three similar seizures in short succession. On examination, he was alert and oriented, but drowsy. There was a mild dysphasia, and a partial right-sided visual field defect. Physical examination was otherwise relatively unremarkable. There was no history of headache, nausea, vomiting, weakness, altered sensation, or fever. There were no significant past medical or surgical histories. The patient occasionally smoked cigarettes, had previously abused alcohol, and had previously been exposed to tuberculosis.

A CT scan of the head revealed a 3 x 2.7 x 2.2 cm mass in the left temporoparietal region, with a slightly thickened, rim-enhancing wall following administration of contrast media (Figure 1). There was prominent surrounding edema, with left hemispheric sulcal effacement, compression of the left lateral ventricular frontal and occipital horns, and approximately 0.6 cm of left-to-right shift of mid-line structures.

Routine pre-operative investigations, including bloodwork and chest x-ray, were unremarkable, and a pre-operative diagnosis of left temporoparietal brain tumor, most likely a high grade glioma, was made. The patient was started on Decadron and Dilantin, and was subsequently taken to the operating theatre where a left temporoparietal craniotomy was performed for resection of this mass. During the operation, the mass was found to have a fairly hard and somewhat rubbery consistency, with a well demarcated plane of resection between it and the surrounding edematous brain parenchyma. A gross total resection was performed, and the specimen was submitted for pathological evaluation and microbiological studies.


Grossly, the resection specimen consisted of several fragments of firm, rubbery grayish-tan tissue, the largest of which measured 3.5 x 2.8 x 1.5 cm in greatest dimensions.

Microscopic examination revealed prominent central necrosis surrounded by a comparatively thin hypercellular zone of inflammation containing numerous small granulomata, which were well visualized with Masson trichrome staining (Figure 2). Prominent but variable collagen (Figure 3) and reticulin (Figure 4) deposition was present within both the central necrotic zone and its surrounding rim of granulomatous tissue, where it was present between, but generally not within, granulomata. A variably thick band of karyorrhectic debris was often found at the transition between the central necrotic zone and the surrounding granulomatous tissue (Figure 5). The granulomata consisted of a central collection of epithelioid macrophages surrounded by a prominent, but somewhat variable, inflammatory infiltrate (Figure 6) consisting predominantly of both CD4 and CD8 (Figure 7) immunopositive T lymphocytes, along with lesser numbers of plasma cells and macrophages. Both neutrophils and eosinophils were inconspicuous. Many granulomata contained centrally-situated giant cells, some of the Langhans type (Figure 8), or small areas of caseous necrosis (Figure 9). Many blood vessels within the central necrotic zone showed luminal fibrous occlusion (Figure 10). Occasional blood vessels in the granulomatous tissue and surrounding brain parenchyma showed prominent perivascular and intramural collections of lymphocytes and plasma cells (Figure 11). Brain parenchyma surrounding the main lesion showed prominent astrocytic gliosis, but only occasional astrocytes and their processes were seen within the lesion itself with GFAP immunohistochemistry (Figure 12). Microorganisms were not identified with special stains, including those for acid-fast bacilli and fungi.


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