Contributed by Stefanie Scheil1, Torsten Horn2, Ulrich Kunz3, Andreas Gabelmann4, Anna-Leena Sirén5, Rüdiger Klein6, Christoph Schindler7, Peter Möller1, and Clemens Sommer1*
1Institute of Pathology, *Laboratory of Neuropathology, University Hospitals of Ulm, Ulm, Germany
2Department of Pediatrics, University Hospitals of Ulm, Germany
3Department of Neurosurgery, Armed Forces Military Hospital, Ulm, Germany
4Department of Radiology, University Hospitals of Ulm, Germany
5Max-Planck-Institute of Experimental Medicine, Göttingen, Germany
6Department of Neuropathology, University of Würzburg, Würzburg, Germany
7Department of Pathology, Nuremberg City Hospital, Nuremberg, Germany
Published on line in May, 2004
In the 35th week of gestation a fetal sonography was performed which showed a parietal mass. Anamnestic examination of the African mother revealed a history of minor abdominal trauma. In the 28th week of gestation she had slipped on a wet floor, but had not experienced any subsequent hematoma or vaginal bleeding. She was otherwise well and had no signs of infectious disease; in particular, anti-HIV-antibodies were negative. She had lived in Germany throughout her pregnancy. In the 38th week of gestation the diameter of the parietal mass was about 5 cm. A Caesarian section was performed at this stage. Laboratory investigations were normal, apart from reduced prothrombin time (PT) (Normalized Ratio 0.11; normal range 0.9-1.2) and the mother had no abnormal coagulation. After vitamin K substitution and application of fresh frozen plasma, the PT was within normal range. No jaundice or swelling of lymph nodes was observed. Both the neonate and his mother had the identical blood group, B positive. No macroscopic abnormalities of the placenta or umbilical cord were observed. The entire mass was removed at surgery. Postoperatively, the boy recovered well. Neurological examination showed slightly reduced spontaneous movement of the right side. Two weeks later, both mother and son were discharged from hospital.
GROSS AND MICROSCOPIC PATHOLOGY:
Macroscopically, the material removed (weight 20 g) had the appearance of an old hematoma surrounded by sparse membranous firm tissue.
Microscopic examination revealed large amounts of blood surrounded by a thin membrane and brain parenchyma with reactive changes (Fig 1, Fig 2). There were numerous macrophages, siderophages, hemosiderin deposits in the brain and associated leptomeninges (Fig. 3). The surrounding brain showed dystrophic mineralization (Fig. 4) as well as reactive gliosis (Fig. 5) confirmed by GFAP immunostaining (Fig. 6). In some of these areas were numerous clusters and nests of cells with scant cytoplasm and dense chromatin (Fig 7, Fig 8, Fig 9), which were synaptophysin- and GFAP-negative (Fig. 10). These cells had a high proliferation rate as demonstrated by Ki-67 (Fig. 11). The cells were chloracetatesterase-negative, but positive for glycophorin A (Fig. 12). They were negative for CD34 (Fig. 13), CD20 and CD3. We did not find any morphologic signs or positive immunoreactivity for toxoplasma gondii or cytomegalovirus (not shown). The noninvolved cerebral cortex appeared normal (Fig. 14).