ABSTRACT
Introduction Schwannoma of the olfactory groove is an extremely rare tumor that can share a differential diagnosis with meningioma or neuroblastoma. Objectives The authors present a case of giant schwannoma involving the anterior cranial fossa and ethmoid sinuses. Case Report The patient presented with a 30-month history of left nasal obstruction, anosmia, and sporadic ipsilateral bleeding. Computed tomography of the paranasal sinuses revealed expansive lesion on the left nasal cavity extending to nasopharynx up to ethmoid and sphenoid sinuses bilaterally with intraorbital and parasellar extension to the skull base. Magnetic resonance imaging scan confirmed the expansive tumor without dural penetration. Biopsy revealed no evidence of malignancy and probable neural cell. Bifrontal craniotomy was performed combined with lateral rhinotomy (Weber-Ferguson approach), and the lesion was totally removed. The tumor measured 8.0 4.3 3.7 cm and microscopically appeared as a schwannoma composed of interwoven bundles of elongated cells (Antoni A regions)mixed with less cellular regions (Antoni B). Immunohistochemical study stained intensively for vimentin and S-100. Conclusion Schwannomas of the olfactory groove are extremely rare, and the findings of origin of this tumor is still uncertain but recent studies point most probably to the meningeal branches of trigeminal nerve or anterior ethmoidal nerves. .
Subject(s)
Animals , Female , Male , Mice , Cell Membrane Permeability/physiology , Hair Cells, Auditory/physiology , Ion Channels/physiology , Mechanotransduction, Cellular/physiology , Animals, Newborn , Cadherins/genetics , Cell Membrane Permeability/genetics , Chelating Agents/pharmacology , Dihydrostreptomycin Sulfate/pharmacology , Embryo, Mammalian , Egtazic Acid/analogs & derivatives , Egtazic Acid/pharmacology , Hair Cells, Auditory/cytology , Hair Cells, Auditory/drug effects , In Vitro Techniques , Ion Channels/drug effects , Mice, Transgenic , Mechanotransduction, Cellular/drug effects , Mechanotransduction, Cellular/genetics , Membrane Potentials/drug effects , Membrane Potentials/genetics , Myosins/genetics , Organ of Corti/cytology , Protein Precursors/geneticsABSTRACT
Estrogen replacement therapy in postmenopausal women may reduce the risk of Alzheimer's disease, possibly by ameliorating neuronal degeneration. In the present study, we examined the neuroprotective spectrum of estrogen against excitotoxicity, oxidative stress, and serum-deprivation-induced apoptosis of neurons in mouse cortical cultures. 17beta-estradiol as well as 17alpha-estradiol and estrone attenuated oxidative neuronal death induced by 24 hr exposure to 100 microM FeCl2, excitotoxic neuronal death induced by 24 hr of exposure to 30 microM N-methyl-D-aspartate (NMDA) and serum-deprivation induced neuronal apoptosis. Furthermore, estradiol attenuated neuronal death induced by Abeta25-35. However, all these neuroprotective effects were mediated by the anti-oxidative action of estrogens. When oxidative stress was blocked by an antioxidant trolox, estrogens did not show any additional protection. Addition of a specific estrogen receptor antagonist ICI182,780 did not reverse the protection offered by estrogens. These findings suggest that high concentrations of estrogen protect against various neuronal injuries mainly by its anti-oxidative effects as previously shown by Behl et al. Our results do not support the view that classical estrogen receptors mediate neuroprotection.
Subject(s)
Mice , Amyloid beta-Peptides/pharmacology , Animals , Antioxidants/pharmacology , Antioxidants/metabolism , Apoptosis/drug effects , Cells, Cultured , Chelating Agents/pharmacology , Chromans/pharmacology , Estradiol/pharmacology , Estrogens/pharmacology , Estrogens/metabolism , Estrone/pharmacology , Ethylenediamines/pharmacology , Excitatory Amino Acid Agonists/pharmacology , Ferric Compounds/pharmacology , L-Lactate Dehydrogenase/analysis , N-Methylaspartate/pharmacology , Neurons/metabolism , Neurons/drug effects , Neurons/cytology , Organ of Corti/cytology , Peptide Fragments/pharmacology , Staurosporine/pharmacologyABSTRACT
Estrogen replacement therapy in postmenopausal women may reduce the risk of Alzheimer's disease, possibly by ameliorating neuronal degeneration. In the present study, we examined the neuroprotective spectrum of estrogen against excitotoxicity, oxidative stress, and serum-deprivation-induced apoptosis of neurons in mouse cortical cultures. 17beta-estradiol as well as 17alpha-estradiol and estrone attenuated oxidative neuronal death induced by 24 hr exposure to 100 microM FeCl2, excitotoxic neuronal death induced by 24 hr of exposure to 30 microM N-methyl-D-aspartate (NMDA) and serum-deprivation induced neuronal apoptosis. Furthermore, estradiol attenuated neuronal death induced by Abeta25-35. However, all these neuroprotective effects were mediated by the anti-oxidative action of estrogens. When oxidative stress was blocked by an antioxidant trolox, estrogens did not show any additional protection. Addition of a specific estrogen receptor antagonist ICI182,780 did not reverse the protection offered by estrogens. These findings suggest that high concentrations of estrogen protect against various neuronal injuries mainly by its anti-oxidative effects as previously shown by Behl et al. Our results do not support the view that classical estrogen receptors mediate neuroprotection.