Neuroradiology case of the day

ing prolonged posterior nasal packing. His past medical his- tory had been unremarkable except for a 2-year history of nasal obstruction. A physical examination revealed a large mass in the posterior nasal cavity and nasopharynx, and in view of his age and history of hemorrhage, an initial diagnosis of juvenile nasopharyngeal angiofibroma was considered. CT and MR studies, however, failed to show a mass centered at the classic location of angiofibroma; there was no significant retroantral extension into the pterygopalatine fossa (Figs. 1A- 1C). T2-weighted MR images clearly differentiated tumor from edematous mucosal changes, a distinction not readily made on Ti -weighted MR images or CT scans. All studies revealed serous otitis media caused by eustachian tube obstruction. Angiographic studies (not shown) revealed a hypervascular blush fed by the internal maxillary branches of both external carotid arteries. The blush was not as dense as that usually seen with angiofibroma. In addition, there were bilateral intra- canalicular masses consistent with acoustic neuromas. Pre- operative embolization of the nasal mass and subsequent surgical resection of tumor resulted in complete extirpation. Histologic examination revealed a typical meningioma, with numerous psammomatous calcifications and whorl formation. Meningiomas account for approximately 15% of all primary brain tumors. These neoplasms are derived from arachnoidal cells, which may be found in ectopic locations. Patients with type II or central neurofibromatosis are susceptible to the development of tumors of the neuraxis, such as meningioma and neurogenic tumors. Patients with neurofibromatosis II are thought to have a defect on chromosome 22, which would account for the dominant transmission of the disease. Pa- tients with neurofibromatosis I have cutaneous manifestations that are absent in neurofibromatosis II, and a chromosome- 17 abnormality. Neurofibromatosis II is far less common than