Brain Pathology Case of the Month - June 2006

Contributed by 1Silke Vogelgesang, 2Andre Hippe, 2 Christof Kessler, 1Rolf W. Warzok
1Department of Neuropathology, 2Clinic of Neurology, University of Greifswald, Germany
Published on line in June 2006


An 80-year-old female was referred to hospital because of acute deterioration of memory and orientation. Additionally, there was weakness in the left leg. During hospitalization she developed severe neuropsychiatric deficits with auditory and visual hallucinations. Her past medical history was uneventful.

Cranial magnetic resonance imaging was atypical and showed a small number of patchy, periventricular lesions as well as small areas of abnormally increased T2 signal intensity in the temporo-occipital region of the right hemisphere. The EEG revealed impairment of vigilance with subcortical disturbances. No stenosis of cerebral vessels was evident by Doppler and duplex ultrasound.

The cerebrospinal fluid showed evidence of a breakdown in the integrity of the blood brain barrier, with elevated protein levels and slight pleocytosis. There were no skin changes. Clinically, viral encephalitis was suspected. During hospitalization, the patient developed thrombosis and died of a massive pulmonary thromboembolism.


Autopsy revealed a slight edema of the cerebrum without macroscopically detectable foci. Microscopic examination demonstrated accumulations of large cells with vesicular nuclei and prominent nucleoli within the blood vessels of the brain and spinal cord that sometimes invaded the vascular wall (Fig. 1A). Occasionally, the tumor cells occluded the vascular lumen, resulting in small infarcts within the adjacent brain tissue. Immunohistochemically, tumor cells expressed pan-B markers such as CD79a and CD20 (Fig. 1B). Ki-1 labelling showed a high proliferative activity of 80% (Fig. 1C).

Additionally, the leptomeningeal and cerebral small to medium sized vessels showed massive, homogeneous eosinophilic thickening of their walls. These vessels occasionally were accompanied by small, parenchymal bleeds with necrosis; affected vascular walls were birefringent with Congo red and immunolabeled with antibodies against beta-amyloid (Fig. 1D). Light chain deposits (kappa or lambda) were not detectable. There were only infrequent senile plaques within the brain parenchyma.


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