Otology & Neurotology 35:895Y898 Ó 2014, Otology & Neurotology, Inc.
Small Vestibular Schwannomas Presenting with Facial Nerve Palsy *Mana Espahbodi, *Matthew L. Carlson, *Te-Yung Fang, *†Reid C. Thompson, and *†David S. Haynes *Departments of OtolaryngologyYHead and Neck Surgery, and ÞNeurologic Surgery, Vanderbilt University, Nashville, TN
Objective: To describe the surgical management and convalescence of two patients presenting with severe facial nerve weakness associated with small intracanalicular vestibular schwannomas (VS). Study Design: Retrospective review. Patients: Two adult female patients presenting with audiovestibular symptoms and subacute facial nerve paralysis (House-Brackmann Grade IV and V). In both cases, post-contrast T1-weighted magnetic resonance imaging revealed an enhancing lesion within the internal auditory canal without lateral extension beyond the fundus. Intervention(s) and Results: Translabyrinthine exploration demonstrated vestibular nerve origin of tumor, extrinsic to the facial nerve, and frozen section pathology confirmed schwannoma. Gross total tumor resection with VIIth cranial nerve preservation and de-
compression of the labyrinthine segment of the facial nerve was performed. Both patients recovered full motor function between 6 and 8 months after surgery. Conclusion: Although rare, small VS may cause severe facial neuropathy, mimicking the presentation of facial nerve schwannomas and other less common pathologies. In the absence of labyrinthine extension on MRI, surgical exploration is the only reliable means of establishing a diagnosis. In the case of confirmed VS, early gross total resection with facial nerve preservation and labyrinthine segment decompression may afford full motor recoveryVan outcome that cannot be achieved with facial nerve grafting. Key Words: Acoustic neuromaVFacial nerveVParalysisVVestibular schwannoma. Otol Neurotol 35:895Y898, 2014.
Vestibular schwannomas (VS) are benign slow-growing tumors arising from the Schwann cells of the VIIIth cranial nerve and commonly manifest with hearing loss, tinnitus, and disequilibrium. Overall, they comprise 10% of all intracranial tumors and over 80% of cerebellopontine angle lesions. Although facial nerve outcomes among patients with normal preoperative function have been extensively studied, subjects presenting with severe facial paresis are commonly excluded from analysis. Clinically apparent preoperative facial nerve weakness is rare, occurring in less than 5% of VS (1). As such, rapidly progressive and severe preoperative paresis, particularly in the setting of a small tumor, raises suspicion for a facial nerve schwannoma (FNS), meningioma, or other less common pathologies (2Y4). Herein, we report our experience managing two such cases that were recently evaluated at the authors’ institution.
CASE DESCRIPTIONS Patient 1 An otherwise healthy 53-year-old female patient presented with an 8-week history of right-sided hearing loss, disequilibrium, and facial nerve weakness. The patient was initially managed at an outside facility with a high-dose prednisone taper. Physical examination revealed HouseBrackmann (HB) Grade IV facial nerve function and audiometric testing yielded nonserviceable hearing (AAOHNS Class D). Gadolinium-enhanced magnetic resonance imaging (MRI) demonstrated a 1.3-cm intracanalicular lesion without enhancement extending beyond the fundus (Fig. 1, A and B). Management options were reviewed, and given the atypical presentation of rapidly progressive facial paresis, the patient elected to undergo microsurgical resection via a translabyrinthine approach. Intraoperative facial nerve stimulation at the root exit zone yielded electrically evoked potentials at 0.05 mA. During tumor dissection, it became evident that the tumor was intrinsic to the vestibular portion of VIIIth cranial nerve and clearly arose separate from the facial nerve. Gross total resection with facial nerve preservation was achieved and the labyrinthine segment of the
Address correspondence and reprint requests to David S. Haynes, M.D., Department of OtolaryngologyYHead and Neck Surgery, The Bill Wilkerson Center for Otolaryngology & Communication Sciences, 7209 Medical Center East, South Tower 1215 21st Avenue South, Nashville, Tennessee 37232-8605; E-mail: [email protected] The authors disclose no conflicts of interest.
895
Copyright © 2014 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited.
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M. ESPAHBODI ET AL.
facial nerve was decompressed. Final pathologic findings confirmed the diagnosis of schwannoma. Within 8 months after surgery, normal function was recovered. Patient 2 A 53-year-old female patient presented with a 2-year progressive right-sided hearing loss and tinnitus with a 2-month history of acute onset facial nerve paralysis. As revealed by a physical examination, the patient exhibited HB Grade II function and audiometric testing revealed AAO-HNS class D hearing. Subsequent contrast-enhanced MRI demonstrated a 1.4-cm intracanalicular tumor (Fig. 1, C and D). The patient was treated with oral glucocorticoid therapy but despite this progressed to HB Grade V function within 1 week. Options were reviewed, and given the progression of facial nerve weakness, she elected to undergo microsurgical
resection. Within 3 months after onset of facial paralysis, the patient underwent a translabyrinthine approach. Intraoperatively, it was determined that the tumor was of vestibular nerve origin, extrinsic to the VIIth cranial nerve. Gross total resection with decompression of the labyrinthine segment of the facial nerve was achieved, and at the conclusion of dissection, the proximal facial nerve was stimulated at 0.05 mA. Intraoperative frozen section pathology confirmed schwannoma. Within 6 months after surgery, the patient recovered normal facial nerve function. DISCUSSION Vestibular schwannomas commonly present with sensorineural hearing loss, tinnitus, and vestibulopathy. Clinically apparent facial weakness occurs in approximately 3% of tumors and is usually associated with late disease (1).
FIG. 1. Coronal (A) and axial (B) T1-weighted magnetic resonance imaging (MRI) with gadolinium demonstrating a 1.3-cm enhancing intracanalicular lesion. Post-contrast coronal (C) and axial (D) T1-weighted MRI revealing a 1.4-cm enhancing lesion with minimal cerebellopontine angle extension. Notably, both lesions do not appear to extend laterally beyond the confines of the internal auditory canal, and there is no perigeniculate enhancement seen. Otology & Neurotology, Vol. 35, No. 5, 2014
Copyright © 2014 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited.
SMALL VS PRESENTING WITH FACIAL PALSY Matthies and Samii examined the presenting symptoms of 1,000 VS and found that among the small group of patients presenting with facial paresis, only 1% had tumors confined to the internal auditory canal (5). Sudden onset or severe facial paresis is an exceedingly rare presentation for intracanalicular VS and generally indicates involvement of a primary VIIth cranial nerve tumor, meningioma, malignancy, or other less common lesions (1Y4). In most cases, the diagnosis of FNS can be established preoperatively, with MRI demonstrating tumor extension beyond the fundus into the proximal fallopian canal. When confined to the internal auditory canal and cerebellopontine angle, there are no dependable radiologic features or diagnostic tests that distinguish these pathologies, and surgical exploration remains the only definitive method for establishing a diagnosis (2,3). Several series have reviewed cases of presumed VS, presenting with normal facial nerve function and without radiographic involvement of the fallopian canal, that were discovered to be FNSs during surgery (6Y8). In the current study, the authors review the opposite scenario; two patients presented with symptoms suspicious for FNS, namely severe facial paralysis with small intracanalicular lesions, who were ultimately found to have VS during surgical exploration. To the best of our knowledge, only one previous case report has specifically addressed this uncommon presentation (1). The surgical management of small VS manifesting with facial paralysis presents the surgeon with an unfamiliar quandary. Should the patient undergo same-surgery facial nerve reinnervation, either using an interposition graft spanning the involved segment or facial-hypoglossal anastomosis? Or should the facial nerve be preserved, trusting that the patient will recover HB Grade III function or better? With very few cases available to draw information from, it may be useful to extrapolate from other more common conditions. In general terms, the management of the facial nerve is influenced by the underlying pathology (e.g., infection, trauma, benign tumors, or malignancy), presenting facial nerve function, duration of paralysis, and the status of the facial nerve-tumor interface. As a guiding principle when approaching benign tumors of the lateral skull base, the anatomical continuity of the facial nerve should be preserved in patients with good preoperative function even at the expense of complete resection; facial nerve sacrifice with reinnervation is often considered in subjects with moderate to severe paresis, understanding that facial nerve grafting commonly restores HB Grade III or IV function (9). One of the most critical aspects influencing facial nerve outcome is the duration of paralysis. Paralleling idiopathic (Bell’s) palsy and facial paralysis from temporal bone trauma, surgical outcomes for benign temporal bone lesions appear to be strongly linked with the timing of intervention (10,11). Ikeda et al. found that in patients with facial paralysis associated with unoperated aural cholesteatoma, early surgical treatment within 2 months resulted in statistically significantly better outcomes (12). Wexler et al. reported one case of sudden complete facial nerve paralysis
897
in a patient with a surgically confirmed intracanalicular VS (1). The patient was evaluated 3 months after initial onset and underwent a translabyrinthine approach with complete tumor resection and facial nerve preservation. At only 3 months after surgery, the patient demonstrated partial recovery with near complete eye closure; information regarding definitive facial function was not reported. Similarly, the two currently presented patients underwent tumor resection and labyrinthine facial nerve decompression within 3 months of paralysis and experienced significant clinical improvement. With VS, facial paralysis is presumably from direct compression of the tumor, local ischemia from vascular compromise, or tracking neural edema with compression focusing at the labyrinthine segment of the facial nerve. In contrast to FNS, meningiomas, paragangliomas, and malignancy, facial paralysis with VS does not appear to be linked with infiltrative growth (2,13). In the two presented cases, as well as the report by Wexler et al., the tumor could be readily separated from the facial nerve (1). This important difference further supports the argument for facial nerve preservation, even in the setting of subacute moderate to severe weakness. Given the rarity of the studied condition, we cannot make any definitive statements regarding optimal management of VS causing advanced paralysis. However, these two index cases demonstrate several important points. First, the finding of acute onset facial paresis in an intracanalicular tumor does not exclude the possibility of VS. Second, even in the setting of severe facial nerve weakness, careful exploration should be performed to determine the nerve of origin before considering facial nerve sacrifice. Finally, tumor resection combined with labyrinthine segment facial nerve decompression may offer the chance of full recovery in the setting of subacute paralysis. CONCLUSION Rarely do small primary VS manifest with facial weakness. Intracanalicular tumors presenting with rapidly progressive, severe facial palsy suggest the diagnosis of FNS, meningioma, malignancy, or other less common pathologies. When the diagnosis remains uncertain, early microsurgical exploration should be considered to establish diagnosis and guide treatment. Preoperative facial nerve function, the status of the facial nerve-tumor interface, and intraoperative frozen section pathology can assist in determining optimal management. In cases of confirmed VS with recent onset facial nerve paralysis, tumor resection with facial nerve preservation should be considered regardless of the severity of preoperative paresis. Gross total tumor resection with labyrinthine segment decompression may allow for full recovery, a result unattainable with facial nerve grafting. REFERENCES 1. Wexler DB, Fetter TW, Gantz BJ. Vestibular schwannoma presenting with sudden facial paralysis. Arch Otolaryngol Head Neck Surg 1990;116:483Y5. Otology & Neurotology, Vol. 35, No. 5, 2014
Copyright © 2014 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited.
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M. ESPAHBODI ET AL.
2. Asaoka K, Barrs DM, Sampson JH, et al. Intracanalicular meningioma mimicking vestibular schwannoma. AJNR Am J Neuroradiol 2002;23:1493Y6. 3. Park HY, Kim SH, Son EJ, et al. Intracanalicular facial nerve schwannoma. Otol Neurotol 2007;28:376Y80. 4. Hilton MP, Kaplan DM, Ang L, et al. Facial nerve paralysis and meningioma of the internal auditory canal. J Laryngol Otol 2002;116:132Y4. 5. Matthies C, Samii M. Management of 1000 vestibular schwannomas (acoustic neuromas): clinical presentation. Neurosurgery 1997;40:1Y9; discussion 10. 6. Jacob JT, Driscoll CL, Link MJ. Facial nerve schwannomas of the cerebellopontine angle: the Mayo Clinic experience. J Neurol Surg B Skull Base 2012;73:230Y5. 7. McMenomey SO, Glasscock ME 3rd, Minor LB, et al. Facial nerve neuromas presenting as acoustic tumors. Am J Otol 1994;15:307Y12.
8. Mowry S, Hansen M, Gantz B. Surgical management of internal auditory canal and cerebellopontine angle facial nerve schwannoma. Otol Neurotol 2012;33:1071Y6. 9. Ozmen OA, Falcioni M, Lauda L, et al. Outcomes of facial nerve grafting in 155 cases: predictive value of history and preoperative function. Otol Neurotol 2011;32:1341Y6. 10. Gantz BJ, Rubinstein JT, Gidley P, et al. Surgical management of Bell’s palsy. Laryngoscope 1999;109:1177Y88. 11. Chang CY, Cass SP. Management of facial nerve injury due to temporal bone trauma. Am J Otol 1999;20:96Y114. 12. Ikeda M, Nakazato H, Onoda K, et al. Facial nerve paralysis caused by middle ear cholesteatoma and effects of surgical intervention. Acta Otolaryngol 2006;126:95Y100. 13. Leonetti JP, Anderson DE, Marzo SJ, et al. Facial paralysis associated with glomus jugulare tumors. Otol Neurotol 2007;28:104Y6.
Otology & Neurotology, Vol. 35, No. 5, 2014
Copyright © 2014 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited.
Small Vestibular Schwannomas Presenting with Facial Nerve Palsy *Mana Espahbodi, *Matthew L. Carlson, *Te-Yung Fang, *†Reid C. Thompson, and *†David S. Haynes *Departments of OtolaryngologyYHead and Neck Surgery, and ÞNeurologic Surgery, Vanderbilt University, Nashville, TN
Objective: To describe the surgical management and convalescence of two patients presenting with severe facial nerve weakness associated with small intracanalicular vestibular schwannomas (VS). Study Design: Retrospective review. Patients: Two adult female patients presenting with audiovestibular symptoms and subacute facial nerve paralysis (House-Brackmann Grade IV and V). In both cases, post-contrast T1-weighted magnetic resonance imaging revealed an enhancing lesion within the internal auditory canal without lateral extension beyond the fundus. Intervention(s) and Results: Translabyrinthine exploration demonstrated vestibular nerve origin of tumor, extrinsic to the facial nerve, and frozen section pathology confirmed schwannoma. Gross total tumor resection with VIIth cranial nerve preservation and de-
compression of the labyrinthine segment of the facial nerve was performed. Both patients recovered full motor function between 6 and 8 months after surgery. Conclusion: Although rare, small VS may cause severe facial neuropathy, mimicking the presentation of facial nerve schwannomas and other less common pathologies. In the absence of labyrinthine extension on MRI, surgical exploration is the only reliable means of establishing a diagnosis. In the case of confirmed VS, early gross total resection with facial nerve preservation and labyrinthine segment decompression may afford full motor recoveryVan outcome that cannot be achieved with facial nerve grafting. Key Words: Acoustic neuromaVFacial nerveVParalysisVVestibular schwannoma. Otol Neurotol 35:895Y898, 2014.
Vestibular schwannomas (VS) are benign slow-growing tumors arising from the Schwann cells of the VIIIth cranial nerve and commonly manifest with hearing loss, tinnitus, and disequilibrium. Overall, they comprise 10% of all intracranial tumors and over 80% of cerebellopontine angle lesions. Although facial nerve outcomes among patients with normal preoperative function have been extensively studied, subjects presenting with severe facial paresis are commonly excluded from analysis. Clinically apparent preoperative facial nerve weakness is rare, occurring in less than 5% of VS (1). As such, rapidly progressive and severe preoperative paresis, particularly in the setting of a small tumor, raises suspicion for a facial nerve schwannoma (FNS), meningioma, or other less common pathologies (2Y4). Herein, we report our experience managing two such cases that were recently evaluated at the authors’ institution.
CASE DESCRIPTIONS Patient 1 An otherwise healthy 53-year-old female patient presented with an 8-week history of right-sided hearing loss, disequilibrium, and facial nerve weakness. The patient was initially managed at an outside facility with a high-dose prednisone taper. Physical examination revealed HouseBrackmann (HB) Grade IV facial nerve function and audiometric testing yielded nonserviceable hearing (AAOHNS Class D). Gadolinium-enhanced magnetic resonance imaging (MRI) demonstrated a 1.3-cm intracanalicular lesion without enhancement extending beyond the fundus (Fig. 1, A and B). Management options were reviewed, and given the atypical presentation of rapidly progressive facial paresis, the patient elected to undergo microsurgical resection via a translabyrinthine approach. Intraoperative facial nerve stimulation at the root exit zone yielded electrically evoked potentials at 0.05 mA. During tumor dissection, it became evident that the tumor was intrinsic to the vestibular portion of VIIIth cranial nerve and clearly arose separate from the facial nerve. Gross total resection with facial nerve preservation was achieved and the labyrinthine segment of the
Address correspondence and reprint requests to David S. Haynes, M.D., Department of OtolaryngologyYHead and Neck Surgery, The Bill Wilkerson Center for Otolaryngology & Communication Sciences, 7209 Medical Center East, South Tower 1215 21st Avenue South, Nashville, Tennessee 37232-8605; E-mail: [email protected] The authors disclose no conflicts of interest.
895
Copyright © 2014 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited.
896
M. ESPAHBODI ET AL.
facial nerve was decompressed. Final pathologic findings confirmed the diagnosis of schwannoma. Within 8 months after surgery, normal function was recovered. Patient 2 A 53-year-old female patient presented with a 2-year progressive right-sided hearing loss and tinnitus with a 2-month history of acute onset facial nerve paralysis. As revealed by a physical examination, the patient exhibited HB Grade II function and audiometric testing revealed AAO-HNS class D hearing. Subsequent contrast-enhanced MRI demonstrated a 1.4-cm intracanalicular tumor (Fig. 1, C and D). The patient was treated with oral glucocorticoid therapy but despite this progressed to HB Grade V function within 1 week. Options were reviewed, and given the progression of facial nerve weakness, she elected to undergo microsurgical
resection. Within 3 months after onset of facial paralysis, the patient underwent a translabyrinthine approach. Intraoperatively, it was determined that the tumor was of vestibular nerve origin, extrinsic to the VIIth cranial nerve. Gross total resection with decompression of the labyrinthine segment of the facial nerve was achieved, and at the conclusion of dissection, the proximal facial nerve was stimulated at 0.05 mA. Intraoperative frozen section pathology confirmed schwannoma. Within 6 months after surgery, the patient recovered normal facial nerve function. DISCUSSION Vestibular schwannomas commonly present with sensorineural hearing loss, tinnitus, and vestibulopathy. Clinically apparent facial weakness occurs in approximately 3% of tumors and is usually associated with late disease (1).
FIG. 1. Coronal (A) and axial (B) T1-weighted magnetic resonance imaging (MRI) with gadolinium demonstrating a 1.3-cm enhancing intracanalicular lesion. Post-contrast coronal (C) and axial (D) T1-weighted MRI revealing a 1.4-cm enhancing lesion with minimal cerebellopontine angle extension. Notably, both lesions do not appear to extend laterally beyond the confines of the internal auditory canal, and there is no perigeniculate enhancement seen. Otology & Neurotology, Vol. 35, No. 5, 2014
Copyright © 2014 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited.
SMALL VS PRESENTING WITH FACIAL PALSY Matthies and Samii examined the presenting symptoms of 1,000 VS and found that among the small group of patients presenting with facial paresis, only 1% had tumors confined to the internal auditory canal (5). Sudden onset or severe facial paresis is an exceedingly rare presentation for intracanalicular VS and generally indicates involvement of a primary VIIth cranial nerve tumor, meningioma, malignancy, or other less common lesions (1Y4). In most cases, the diagnosis of FNS can be established preoperatively, with MRI demonstrating tumor extension beyond the fundus into the proximal fallopian canal. When confined to the internal auditory canal and cerebellopontine angle, there are no dependable radiologic features or diagnostic tests that distinguish these pathologies, and surgical exploration remains the only definitive method for establishing a diagnosis (2,3). Several series have reviewed cases of presumed VS, presenting with normal facial nerve function and without radiographic involvement of the fallopian canal, that were discovered to be FNSs during surgery (6Y8). In the current study, the authors review the opposite scenario; two patients presented with symptoms suspicious for FNS, namely severe facial paralysis with small intracanalicular lesions, who were ultimately found to have VS during surgical exploration. To the best of our knowledge, only one previous case report has specifically addressed this uncommon presentation (1). The surgical management of small VS manifesting with facial paralysis presents the surgeon with an unfamiliar quandary. Should the patient undergo same-surgery facial nerve reinnervation, either using an interposition graft spanning the involved segment or facial-hypoglossal anastomosis? Or should the facial nerve be preserved, trusting that the patient will recover HB Grade III function or better? With very few cases available to draw information from, it may be useful to extrapolate from other more common conditions. In general terms, the management of the facial nerve is influenced by the underlying pathology (e.g., infection, trauma, benign tumors, or malignancy), presenting facial nerve function, duration of paralysis, and the status of the facial nerve-tumor interface. As a guiding principle when approaching benign tumors of the lateral skull base, the anatomical continuity of the facial nerve should be preserved in patients with good preoperative function even at the expense of complete resection; facial nerve sacrifice with reinnervation is often considered in subjects with moderate to severe paresis, understanding that facial nerve grafting commonly restores HB Grade III or IV function (9). One of the most critical aspects influencing facial nerve outcome is the duration of paralysis. Paralleling idiopathic (Bell’s) palsy and facial paralysis from temporal bone trauma, surgical outcomes for benign temporal bone lesions appear to be strongly linked with the timing of intervention (10,11). Ikeda et al. found that in patients with facial paralysis associated with unoperated aural cholesteatoma, early surgical treatment within 2 months resulted in statistically significantly better outcomes (12). Wexler et al. reported one case of sudden complete facial nerve paralysis
897
in a patient with a surgically confirmed intracanalicular VS (1). The patient was evaluated 3 months after initial onset and underwent a translabyrinthine approach with complete tumor resection and facial nerve preservation. At only 3 months after surgery, the patient demonstrated partial recovery with near complete eye closure; information regarding definitive facial function was not reported. Similarly, the two currently presented patients underwent tumor resection and labyrinthine facial nerve decompression within 3 months of paralysis and experienced significant clinical improvement. With VS, facial paralysis is presumably from direct compression of the tumor, local ischemia from vascular compromise, or tracking neural edema with compression focusing at the labyrinthine segment of the facial nerve. In contrast to FNS, meningiomas, paragangliomas, and malignancy, facial paralysis with VS does not appear to be linked with infiltrative growth (2,13). In the two presented cases, as well as the report by Wexler et al., the tumor could be readily separated from the facial nerve (1). This important difference further supports the argument for facial nerve preservation, even in the setting of subacute moderate to severe weakness. Given the rarity of the studied condition, we cannot make any definitive statements regarding optimal management of VS causing advanced paralysis. However, these two index cases demonstrate several important points. First, the finding of acute onset facial paresis in an intracanalicular tumor does not exclude the possibility of VS. Second, even in the setting of severe facial nerve weakness, careful exploration should be performed to determine the nerve of origin before considering facial nerve sacrifice. Finally, tumor resection combined with labyrinthine segment facial nerve decompression may offer the chance of full recovery in the setting of subacute paralysis. CONCLUSION Rarely do small primary VS manifest with facial weakness. Intracanalicular tumors presenting with rapidly progressive, severe facial palsy suggest the diagnosis of FNS, meningioma, malignancy, or other less common pathologies. When the diagnosis remains uncertain, early microsurgical exploration should be considered to establish diagnosis and guide treatment. Preoperative facial nerve function, the status of the facial nerve-tumor interface, and intraoperative frozen section pathology can assist in determining optimal management. In cases of confirmed VS with recent onset facial nerve paralysis, tumor resection with facial nerve preservation should be considered regardless of the severity of preoperative paresis. Gross total tumor resection with labyrinthine segment decompression may allow for full recovery, a result unattainable with facial nerve grafting. REFERENCES 1. Wexler DB, Fetter TW, Gantz BJ. Vestibular schwannoma presenting with sudden facial paralysis. Arch Otolaryngol Head Neck Surg 1990;116:483Y5. Otology & Neurotology, Vol. 35, No. 5, 2014
Copyright © 2014 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited.
898
M. ESPAHBODI ET AL.
2. Asaoka K, Barrs DM, Sampson JH, et al. Intracanalicular meningioma mimicking vestibular schwannoma. AJNR Am J Neuroradiol 2002;23:1493Y6. 3. Park HY, Kim SH, Son EJ, et al. Intracanalicular facial nerve schwannoma. Otol Neurotol 2007;28:376Y80. 4. Hilton MP, Kaplan DM, Ang L, et al. Facial nerve paralysis and meningioma of the internal auditory canal. J Laryngol Otol 2002;116:132Y4. 5. Matthies C, Samii M. Management of 1000 vestibular schwannomas (acoustic neuromas): clinical presentation. Neurosurgery 1997;40:1Y9; discussion 10. 6. Jacob JT, Driscoll CL, Link MJ. Facial nerve schwannomas of the cerebellopontine angle: the Mayo Clinic experience. J Neurol Surg B Skull Base 2012;73:230Y5. 7. McMenomey SO, Glasscock ME 3rd, Minor LB, et al. Facial nerve neuromas presenting as acoustic tumors. Am J Otol 1994;15:307Y12.
8. Mowry S, Hansen M, Gantz B. Surgical management of internal auditory canal and cerebellopontine angle facial nerve schwannoma. Otol Neurotol 2012;33:1071Y6. 9. Ozmen OA, Falcioni M, Lauda L, et al. Outcomes of facial nerve grafting in 155 cases: predictive value of history and preoperative function. Otol Neurotol 2011;32:1341Y6. 10. Gantz BJ, Rubinstein JT, Gidley P, et al. Surgical management of Bell’s palsy. Laryngoscope 1999;109:1177Y88. 11. Chang CY, Cass SP. Management of facial nerve injury due to temporal bone trauma. Am J Otol 1999;20:96Y114. 12. Ikeda M, Nakazato H, Onoda K, et al. Facial nerve paralysis caused by middle ear cholesteatoma and effects of surgical intervention. Acta Otolaryngol 2006;126:95Y100. 13. Leonetti JP, Anderson DE, Marzo SJ, et al. Facial paralysis associated with glomus jugulare tumors. Otol Neurotol 2007;28:104Y6.
Otology & Neurotology, Vol. 35, No. 5, 2014
Copyright © 2014 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited.
