Case 785 -- A 78-year-old male patient with a right occipital lesion

Contributed by Marco Gessi MD1, Udo Kellner MD2, Harald Stein MD3, Torsten Pietsch MD1
1Inst. of Neuropathology, University of Bonn Medical Center, Bonn Germany
2Inst. of Pathology, Klinikum Minden, Minden, Germany
3Pathodiagnostik, Berlin, Germany


CLINICAL AND RADIOLOGICAL FINDINGS

A 78-year-old male patient developed gait disturbances, increasing left hemianopsia and left visual impairment for several weeks. The patient did not present clinical or anamnestic evidence of systemic disease. The MRI examination revealed a 3 cm contrast enhancing, right parieto-occipital lesion with marked edema and involvement of the posterior horn of the lateral right ventricle as well as infiltration of the splenium of the corpus callosum (Figs. 1, 2 and 3). The neuroradiological features were suspicious of a high grade glioma. The patient underwent surgical operation through an occipital craniotomy. The lesion was completely resected.

HISTOPATHOLOGICAL AND MOLECULAR FINDINGS

Histologically, the specimen consisted of necrotic and hemorrhagic brain tissue in which polymorphic, medium to large sized atypical lymphocyte-like cells (Figs. 4 and 5) were accompanied by plasma cells, neutrophils and macrophages, with active phagocytosis of cellular debris. Apoptosis could be also easily detected. The reticulin stain illustrated that the lymphocyte-like cells presented focally an angiocentric growth pattern (Fig. 6). Features of an intravascular growth were absent. The Gram and Grocott stains were negative. The atypical lymphocyte-like cells were positively labelled with antibodies against CD30, CD56 (Figs. 7 and 8, respectively), Perforin and showed a cytoplasmic positivity with CD3. However, CD20, CD4, CD5 and ALK-1 were negative. The proliferation index evaluated with antibody against Ki67 antigen (MIB-1) reached a value of 70% (Fig. 9). The immunohistochemical staining with antibody against EBV-LMP1 protein was positive in the atypical cells. The molecular PCR-based analysis revealed a clonal rearrangement of T-cell receptor (TCR) (rearrangement type Vγ 4-jI).

FINAL DIAGNOSIS


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