Olfaction preservation in anterior cranial base approaches: an anatomic study.

OBJECTIVE: To study the anatomic basis for olfaction-sparing anterior cranial base approaches. METHODS: The medial anterior skull base containing the olfactory unit and delimited by the inner table of the frontal sinus, the lesser wing of the sphenoid bone, and the medial orbital walls was removed from six cadaveric specimens. Histological methods were used to investigate the location, distribution, and depth of penetration of olfactory nerves. Hematoxylin and eosin and Gomori trichrome staining were used to visualize landmarks and architecture. S-100 neurofilament protein immunostaining was used to identify nerve fascicles and axons. In three cadaveric head specimens, olfaction-sparing craniofacial approaches were performed and the excised olfactory units were evaluated histologically. RESULTS: Bundles of olfactory nerves were identified primarily in the nasal septum; relatively fewer bundles could be identified in the middle turbinate. Olfactory nerve endings were identified up to 20 mm below the cribriform plate (range, 7-20 mm). The superior and middle nasal meatus were most innervated; olfactory innervation was virtually absent in the inferior nasal meatus. Histological evaluation of the olfactory unit elevated during olfaction-sparing techniques routinely revealed transection of olfactory nerves that exited the skull base. CONCLUSION: In olfaction-sparing anterior cranial base approaches, the olfactory nerves are inevitably transected. The clinical significance of olfactory nerve transection for postoperative functional recovery of olfaction remains to be analyzed.

Correlation of endothelin-1 and transforming growth factor beta 1 with malignancy and vascularity in human gliomas.

Because the prominent neovascularization characteristic of high grade primary brain tumors is composed mostly of vascular smooth muscle cells (VSMC), we studied the expression of the potent smooth muscle mitogen endothelin-1 (ET-1) and one of its secretagogues, transforming growth factor beta 1 (TGF-beta 1) in a series of astrocytic tumors. TGF-beta 1 is also of interest due to its known activity as an angiogenic factor. Using immunohistochemical methods, we examined 30 surgical cases: 10 glioblastoma multiforme, 10 anaplastic astrocytomas, and 10 low-grade astrocytomas. Using a monoclonal antibody to TGF-beta 1 and a polyclonal antibody to ET-1, we detected both growth factors in all cases of glioblastoma examined. In cases of anaplastic astrocytoma, 4 tumors were positive for both factors; 2 contained only ET-1; 2 contained only TGF-beta 1; and 2 exhibited no tumor cell immunoreactivity for either factor. In low-grade astrocytoma, 4 of 10 tumors showed weak ET-1 immunoreactivity; 2 of those contained TGF-beta 1 immunopositive tumor astrocytes: 6 tumors were negative for both factors. In all tumors that expressed both factors, serial sections showed that regions of ET-1 immunopositivity also tended to be positive for TGF-beta 1. Endothelial cells within all tumors were positive for ET-1. ET-1 and TGF-beta 1 are present in human astrocytomas and their expression correlates with tumor vascularity and malignancy. These results suggest roles for both ET-1 and TGF-beta 1 in the growth and progressive angiogenesis of the human glioma.