Contributed by Matthias Reitz (1), Jozef Zustin (2), Jakob Matschke (3), Nils Ole Schmidt (1), Manfred Westphal (1)
(1) Department of Neurological Surgery, (2) Department of Pathology, (3) Institute of Neuropathology
University Medical Center Hamburg-Eppendorf, Hamburg, Germany
A 56-year-old female patient was admitted to the department of neurological surgery of the University Hospital Hamburg Eppendorf because of a chronic, severe left-sided headache. The neurological examination did not reveal any pathological findings. Further medical history included idiopathic arterial hypertension and hypercholesteremia. A cranial CT scan showed an osteolytic lesion (~1,5cm) within the lateral wing of the left sphenoid bone (Fig. 1). Further diagnostic work-up with a cranial MRI scan revealed a 2 x 1,5 x 1,3cm contrast-enhancing, extradural tumor eroding the left wing of the sphenoid bone without apparent infiltration or substantial compression of the cerebrum (Figs. 2, 3; T1 sequence with contrast). A gross total resection of the tumor along with some adjacent bone was performed. The resulting bone defect was reconstructed using bone cement. Intraoperatively, dural infiltration of the tumor was not seen. The patient went through an uneventful postoperative period. No neurological deficits occurred. The headache ameliorated, wound-healing was without any signs of infection or other disturbances. The patient was recurrence-free on a 12 month follow-up.
The resected tissue fragments had a total volume of about 3 cc. They were gray-white and had a firm-to-hard consistency. Histopathological features of the tumor included a lobulated pattern with a hypocellular centre (Fig. 4). The tumor contained spindle and stellate-shaped cells in a sieve-like pattern (Fig. 5) with areas of cartilaginous matrix (Fig. 6). Increased cellularity and scattered multinucleated giant cells were found predominately at the periphery of the tumor (Fig. 7). Diffuse or grungy calcifications were observed focally throughout the tumor mass (Fig. 8). Analysis of serial tumor sections revealed two areas of relatively more compact calcifications (Fig. 9). Immunohistochemically, the tumor cells showed positivity for vimentin but no immunoreaction against S100-protein, cytokeratins, actin and desmin (not shown). The proliferative activity as determined in the Ki67-labeling index was less than 1 % (not shown).