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Andrew Coughlin, MD Faculty Advisor: Tomoko Makishima, MD, PhD The University of Texas Medical Branch Department of Otolaryngology Grand Rounds Presentation September 30, 2010 History of CPA tumors Discuss Relevant Anatomy Epidemiology and Tumor Biology Signs/Symptoms of CPA tumors Brief overview of other CPA tumors Treatment options Present a case presentation Represent 10% of all intracranial tumors Vestibular Schwannomas/Acoustic Neuroma represent 78% of these tumors (1) Differential Meningiomas Epidermoids Other Cranial Nerve Schwannomas Dermoid Tumors ( Chordomas, Teratomas) Arachnoid Cysts Lipomas Metastatic Tumors Vascular Tumors (Hemangioma/Glomus Tumor) Sir Charles Balance (2,3) 1894 First successful removal of Vestibular Schwannoma 1907 Patient still alive but had CN VII paresis Harvey Cushing 1917 Monograph described CPA syndrome Pioneered subtotal resection through bilateral suboccipital craniectomy Walter Dandy (5) Advocated debulking with capsule removal and decreased operative mortality to 10% William House (6-8) Advocated Translabyrinthine approach 1960’s Introduced the microscope and dental drill to identify the facial nerve Introduced middle cranial fossa approach Ipsilateral Hearing Loss Facial Hypesthesia Hydrocephalus Respiratory Failure and Death Autopsy series have shown incidence of 1.7 to 2.7% (9,10) MRI of 10,000 patients seen for non-otologic reasons showed 7 positive cases or 0.07% (11) Denmark reports of 1.3 per 100,000 population (12) 1. They are not Neuromas 2. They rarely are found on the acoustic portion of the nerve *Involvement of the acoustic portion of the nerve often leads to erosion of the cochlea. Arise from Schwann cells within the IAC (1) Equal frequency between inferior and superior divisions of the vestibular nerve. Arise from Scarpa Ganglion instead of Obersteiner-Redlich zone. Scarpa’s ganglion has highest density of schwann cells NF 2 Gene found at 22q12 Sporadic Variety (95%) (13) Tumor suppressor gene preventing schwann cell proliferation Hypothesized that there are two hits to the normal NF gene Neurofibromatosis type II Autosomal Dominant Inherit one abnormal and one normal gene with one hit to the normal allele. Blood tests available to screen family members. 1. Neuregulin Expressed by schwann cells to control proliferation and survival of schwann cells 2. Chemokines 3. FGF, TGF-β, VEGF, PDGF (14-17) Sex Hormones (18) Previous studies showed increased growth in pregnancy Recent studies have not shown growth modulation or receptors for sex hormones History and Physical Exam Audiologic testing Vestibular Testing Imaging Intracanalicular tumors 1. 2. 3. CPA extension 1. Hearing Loss Tinnitus Vestibular dysfunction/Vertigo Disequilibrium/Ataxia Brainstem Extension 1. 2. 3. Midface Hypesthesia Hydrocephalus (vision loss and headache) Other Cranial Neuropathies *SNHL>tinnitus>disequilibrium>facial hypesthesia (13) Present in >85% of patients (19) 5% of patients with VS have no associated hearing loss (20) Speech discrimination out of proportion to HL Many notice difficulty on the telephone Occurs in up to 20% of patients (13) 1% of patients with SSNHL have a vestibular schwannoma (21) 48% of patients with SSNHL will have some recovery of hearing (21) Don’t rule out VS if they recover 2nd most common presenting sign Often precedes hearing loss Can be present without hearing loss Can be high pitch, hissing, or a roar Can localize to the opposite ear Unilateral tinnitus should be evaluated 36-50% of patients describe disequilibrium (1) Vague, transient lightheadedness Acute vertigo is presenting symptom in 27% of patients but is associated with smaller tumors. Presenting symptom in 4% of patients Larger tumors >2cm Maxillary division 1st Corneal reflex is the first to go Facial weakness is rare If present should assume a different type of tumor. Rare Loss of corneal reflex Nystagmus (toward affected side) Diplopia Involvement of CN VI Blurry vision Papilledema and optic atrophy from compression Hitselberger Sign Decreased sensation of EAC Sensory VII more sensitive than Motor VII Absent corneal reflex, nystagmus Hypesthesia to pinprick and touch Weakness of Temporalis/Masseter muscles Other cranial neuropathy’s Gait disturbances or difficulty with finger to nose testing Downsloping high frequency SNHL 65% (22) 5% of patients show no hearing loss (23) Rollover: Speech discrimination worse than expected and worse with increased sound intensities Retrocochlear losses more common than cochlear AAO-HNS classification Class Pure tone average (0.5, 1, Speech discrimination 2, 3 kHz measured in dB score (%) HL) A 0–30 70–100 B 31–50 50–100 C >50 50–100 D Any <50 Gardner-Robertson Classification Class Pure Tone/Speech Speech Discrimination Reception Threshold (dB Score (%) HL) 1 0–30 70–100 2 31–50 50–69 3 51–90 5–49 4 >90 1–4 Word Recognition Scores Class Word Recognition Score (%) I 70–100 II 50–69 III 1–50 IV 0% **Positive test has 85% sensitivity for identifying retrocochlear problem Acoustic Reflex Threshold Increased (compared with cochlear norms) or absent if retrocochlear process Sensitivity of 85 to 90% (25) False Positive rate 10% False Negative rate 18-30% for intracanalicular tumors Number larger than in the past Five waveforms are produced with the most common being a latency in wave V compared to the normal ear of >0.2msec. Recommended as a screening test for those with low suspicion of vestibular schwannoma. 70-90% of patients will show some abnormality (26) 50% of small tumors produce no abnormalities (27) Caloric testing is commonly the only abnormality Inferior vestibular nerve tumors may be missed Superior nerve showed decrease in 98% Inferior nerve shows decrease in only 60% (28) Therefore not used as a screening test 90% of vestibular schwannomas will enhance with contrast Frequently misses tumors that are not intracanalicular and do not extend >5mm to the CPA. 63% accuracy at diagnosis (29) Gold Standard for Vestibular Schwannomas Gadolinium is preferentially taken up by tumor Hyperintense on T1 and T2 studies Non-contrasted studies Better visualization of small tumors Gadolinium enhanced studies Can identify tumors as small as 3mm (30) Hypointense T1, Isointense on T2 Some recommend T2 fast spin-echo MRI as screening test but most will likely require at thin slice MRI if abnormalities are found (31) VESTIBULAR SCHWANNOMA Centered on IAC Globular appearance Ice cream cone appearance in IAC Bony erosion of IAC Cystic degeneration or hemorrhage may be present MENINGIOMA Extend along petrous ridge Sessile appearance “Dural Tail” at periphery Iso/Hypointense on T1 Hypo to Hyperintense on T2 3% of all CPA tumors (13) Do not metastasize but do recur due to bony invasion Are formed from cap cells around arachnoid villi near dural sinus’ and where CN’s enter their foramina Generally are not intracanalicular so must be larger to cause hearing concerns Signs and Symptoms (32) Usually cause spontaneous nystagmus, facial hypesthesia, and gait ataxia If inferior can cause hoarseness, dysphagia, tongue atrophy If within the IAC can produce similar symptoms as Vestibular Schwannoma Hearing tests will show retrocochlear process if large enough, and 25% will have normal ABR’s (33) Treatment Surgical Excision Must remove rim of normal dura and possibly bone Poor hearing Translabyrinthine approach Good hearing Suboccipital or Middle Fossa Approach Middle Fossa is better for more superiorly based tumors. Identical to cholesteatoma Develop from epithelial rest cells Slow growing Commonly don’t present until 20-30’s Arise adjacent to brainstem and infiltrate areas of least resistance Can have irregular shape and infiltrate widely Signs/Symptoms Facial twitching is commonly described Can become quite large before causing symptoms Progressive facial paralysis more common than schwannomas Audio/ABR/Speech discrimination consistent with other retrocochlear losses Treatment is surgical excision T1 post Gadolinium T1 post Gadolinium T2 T1 Flair T1 T2 T1 T1 Histologically identical to Vestibular Schwannomas Characteristics Rarely restricted to IAC Commonly have skip lesions Generally involve part of geniculate ganglion Signs/Symptoms Unilateral hearing loss Tinnitus Vertigo Aural fullness (if distal to geniculate) Facial weakness is rare unless very large Hearing tests show retrocochlear process but impedance testing can show ipsilateral absent acoustic reflex Treatment is observation If growth or facial nerve dysfunction Resection of nerve with cable grafting Translabyrinthine approach most commonly used Facial nerve decompression can be used if paresis is developing Glomus Tumors Hemangiomas Bright on T1 and T2, Drained via infralabyrinthine approach Embryonic tumors (Dermoids, teratomas, chordomas) Treatment is drainage Cholesterol Granulomas Centered on geniculate, slow progressive facial weakness, surgical excision with facial nerve grafting Arachnoid Cysts Jugular Foramen Syndrome (IX,X,XI), Surgical excision Excision with dysfunction Primary Axial Tumors of CNS (glioma, hemangioblastoma, medulloblastoma) Surgical excision +/- radiation therapy Observation Surgery Stereotactic Radiosurgery Radiation Therapy **Generally tumors <3cm can be treated with stereotactic radiosurgery but microsurgery is the treatment of choice Growth rates vary from 0 to 2cm per year with an average of 2mm (34) 38.9-82% have some growth at ≥38 months (24) 14 to 24% of patients watched will go on to have some treatment (12) Age should not be determining factor 1. 2. 3. Single MRI is not adequate Young patient with small tumor Older patient with large tumor Older patient with small tumor Repeat at 6 months and then again yearly Longstanding hearing loss may represent a slow growing tumor (35) First Introduced Leskell in 1969 Gamma Knife LINAC Uses multiple beams from a linear accelerator One session Fractionated Radiotherapy Uses 201 ionizing beams of gamma rays from cobalt 60 source One session Newer therapy to eradicate cells in different cell cycle stages Multiple sessions Goal is to stop tumor growth, not shrink or remove tumor Local control = not requiring salvage therapy 87 to 100% local control rates all three combined 23% of cases have transient increase tumor volume due to central necrosis 6mo to 5yr to disappear Therefore some patients receive unnecessary salvage therapy Hasegawa et al. 2005 (36) 317 patients Median follow up 7.8 years 10 yr local control >92% Partial or complete radiographic response 62% Progression free survival 96% if <15cm3 vs 57% if >15cm3 p<0.001 Better with no brainstem compression/4th ventricle obstruction p<0.001 Most tumor progression within 3 years Freidman et al. 2006 (37) 390 patients Median follow up 40 months Median dose of 12.5 Gy 5- and 10-year local control 90% Only 1% of patients required surgery for treatment failure Many different regimens studied Dose 15-57.6 Gy/3-32fx Median Follow ups of 48 months 5- year local control of >90% **Relatively new idea so no long term outcomes available Tumor Control 73.8 to 100% for Radiosurgery 91.4 to 100% for FSRT Tumor Shrinkage 38 to 76.2% for Radiosurgery with single dose 34 to 76% for FSRT Tumor Growth 0-26.2% for Radiosurgery 0-12.5% for FSRT Hearing Preservation 47-71% for Radiosurgery 57-100%for FSRT Defined as G-R class I/II Early studies 16Gy = 46% Later Studies 12-13Gy = 68-78% with no change in control (24) Prasad et al. (39) 153 patients Median follow up of 4.2 years Useful hearing preservation rate of 58% Size matters <1cm3 = 75% hearing preservation >1cm3 = 57% hearing preservation GK vs FSRT Andrews et al. 2001 (40) 109 patients 63 GK at 12Gy 46 FSRT at 50Gy/25fx Follow up was 3 years 33% vs 81% hearing preservation (GK/FSRT) 98% vs 97% local control (GK/FSRT) Thought is that lower dose in multiple fractions leads to decreased late normal tissue damage GK dose decrease from 16Gy to 12-13Gy decreased rates from 15% to 0% (41) LINAC dose decrease of 16Gy to 12.5Gy showed drop in neuropathy from 4.4% to 0.7% (37) RS vs FSRT ranges of 0-52% vs 0-4%(38) GK dose decrease from 16Gy to 12-13Gy decreased rates from 16% to 4.4% (41) LINAC dose decrease of 16Gy to 12.5Gy showed drop in neuropathy from 3.7% to 0.7% (37) RS vs FSRT ranges of 2.4-29% vs 0-16% (38) Hydrocepahlus Tinnitus 3.6% Malignant transformation 1.4 to 1.7% Peritumoral cyst formation 1.4 to 3.6% Vertigo 0.2 to 5% Ataxia 0-11% (24), with highest rates in FSRT 0 to 0.3% 3 cases in all studies reviewed with time to presentation of 5, 7.5, and 18 yrs post therapy Disequilibrium 33% likely due to weaker central compensation (42) 1. 2. 3. Translabyrinthine Approach Middle Cranial Fossa Approach Retrosigmoid-Suboccipital Approach **All will require discussion/collaboration with Neurosurgery ADVANTAGES Least cerebellar retraction Wide exposure of posterior fossa No size limit for resection Facial nerve easily identified throughout Ease of facial nerve repair if damaged/resected during removal Low recurrence Low headaches DISADVANTAGES Residual hearing is sacrificed Requires abdominal fat graft ADVANTAGES Best hearing preservation <30db PTA >70% speech discrimination Good exposure of lateral IAC, CPA, and clivus Drilling is extradural decreasing morbidity DISADVANTAGES Limited to tumors <2cm in greatest dimension Temporal lobe retraction Must dissect around facial nerve due to its superior position Limited posterior fossa exposure ADVANTAGES Can attack any size tumor Hearing preservation possible Wide exposure of brainstem and lower cranial nerves Neurosurgeon familiarity Consistent facial nerve identification DISADVANTAGES Must be medially located with <2cm CPA extension Lateral tumors risk injury to endolymphatic sac and vestibular labyrinth Cerebellar retraction occulomotor abnormalities and postop disequilibrium Increased air embolism risk (Sitting vs Park Bench position) Translabyrinthine Total Resection 99.5 to 99.7% (44-45) Near total resection (<25mm2 or 2mm thick) Visible on MRI in 50% of patients with 3% risk of recurrence (46-47) Middle Cranial Fossa Total Resection 98% (48) Retrosigmoid Total resection 95% (49) Serviceable hearing defined as class A/B or 1/2 (24) Middle cranial fossa 51% Retrosigmoid 31% Meyer et al. 2006 (50) 162 consecutive patients via MCF approach Class A/B hearing preserved in 41% 56/113 (50%) with WR >70% preoperatively maintained that level. Tumor 0.2-1.0cm = 59% Tumor 1.1-1.4cm = 39% Tumor 1.5-2.5cm = 33% Reporting function at 6-12 month point is gold standard Preserved = Grade I/II (24) Retrosigmoid 91% Middle Cranial Fossa 88% Translabyrinthine 77% Delayed paralysis (>72hrs after surgery) Described by Grant et al. 2002 Incidence 5% (51) 79% regain postoperative function by 1 yr Pooled data from 19 studies 360/4297 (8%) rate (52) MCF approach 6% TL approach 8% RS approach 11% Occurs at two different time points POD 2-3 (Early) POD 10-14 (Late) Occurs roughly 10% of patients >3 months postop (52) RS approach 21% MCF approach 8% TL approach 3% Mechanisms 1. 2. 3. 4. Bone dust contacting CSF/Meninges Aseptic Meningitis Occipital nerve entrapment Scarred neck muscles and dura Migraine Mortality 1% due to neurovascular injury Meningitis 1-8% Aseptic more common than bacterial (bone dust/inflammation) S. aureus most common pathogen Tinnitus Balance abnormalities 50% with preop tinnitus will have resolution postop Occurs in most patients but gone by 6-9 months Seizure/Hydrocephalus/Stroke (24) Rare and <2% of cases Myrseth et al 2005 (53) Retrospective review 189 patients tumors ≤3cm 86 by microsurgery vs. 103 by GK 5.9 year mean follow up Local control rates of 89.2% Surgery vs 94.2% GK HB 1-2 in 79.8% Surgery vs 94.8% GK p=0.0026 Quality of life significantly lower in surgery group compared to gamma knife group *MCF approach was not utilized Pollock et al. 2006 (54) Prospective cohort of 82 patients unilateral VS <3cm 36 Surgery vs 46 GK Average follow up of 42 months Local control 96% Surgery vs 100% GK p= 0.50 HB 1/2 in 75% Surgery vs 96% GK p<0.01 Hearing Preserved 5% Surgery vs 63% GK p<0.001 Quality of life all statistically better for GK Physical functioning Bodily pain scores Dizziness Handicap Inventory Vestibular schwannomas are the most common CPA tumor Unilateral Tinnitus or SNHL must be evaluated Tumors <3cm in size treated with radiosurgery GK or LINAC have comparable results FSRT may prove more beneficial but requires more than 1 day of treatment For patients with no serviceable preoperative hearing, translabyrinthine approach is best choice For Hearing Preservation options the middle cranial fossa approach appears to be slightly better than the retrosigmoid approach due to decreased rates of complications. 55 y/o female with 2 year history of falls and disequilibrium Falls are now progressive and daily Denies true vertigo just imbalanced Also has tinnitus, neck spasms, and migraines She denies any hearing loss but family feels otherwise PMHx: PSHx: HCTZ, metoprolol, sydol prn, soma, and ambien prn Allergies: 45pack year history of smoking, -EtOH Medications: Noncontributory SHx: Partial hysterectomy and R thyroid lobectomy FHx: HTN, Hypothyroidism Sulfa ROS: Otherwise negative. No vision or constitutional problems General: NAD oriented x3 Head: NCAT Eyes: No nystagmus, PERRLA, EOMI ENT: TM’s intact, Tuning forks normal Neck: No masses or lymphadenopathy Neuro: CN II-XII intact, unsteady Romberg, tandem gait falling to the left, and left finger to nose ataxia Audiogram Normal hearing with mild high frequency SNHL at 4000Hz bilaterally ENG Decreased accuracy on horizontal smooth pursuit 54% weakness on left air caloric testing MRI 1.5 to 2cm lesion closely associated with CN VII/VIII. It is intracanalicular with extension into CPA. No evidence of brainstem compression or ventricular obstruction 1. 2. 3. 4. Finger to nose and gait ataxia Essentially normal hearing ENG positive for left lateral canal weakness 2cm tumor, no hydrocephalus Patient had previous MRI 2005 showing no tumor Therefore it is decided that we perform suboccipital craniotomy for excision of tumor Tumor Tentorium Cerebelli Retracted Cerebellum CN VII/VIII Complex Tumor Tentorium Cerebelli Retracted Cerebellum CN VII/VIII Complex Tumor Tentorium Cerebelli AICA CN V Retracted Cerebellum CN VII/VIII Complex Tumor CN VI Tentorium Cerebelli AICA CN V Retracted Cerebellum Final Pathology: Meningioma No complications at this point Tuning forks 256hz and 512hz normal HB I immediately and 72 hours postoperatively 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. Baileys. House WF. A history of acoustic tumor surgery: 1800–1900, early history. In: House WF, Luetje CM, eds. Acoustic tumors Vol. 1. Baltimore: University Park Press, 1979:3–8. Rosenberg SI. Natural history of acoustic neuromas. Laryngoscope 2000;110:497–508. Cushing H. Tumors of the nervus acusticus and the syndrome of the cerebellopontine angle (Reprint of the 1917 edition.) New York: Hafner, 1963. Dandy WE. An operation for the total removal of cerebellopontine (acoustic) tumors. Surg Gynecol Obstet 1925;41:129–148. House WF. Report of cases: monographtranstemporal bone microsurgical removal of acoustic neuromas. Arch Otolaryngol 1964;80:617–667. Glasscock ME III, Steenerson RL. A history of acoustic tumor surgery: 1961–present. In: House WF, Luetje CM, eds. Acoustic tumors Vol. 1. Baltimore: University Park Press, 1979:33–41. House WF. Exposure of the internal auditory canal and its contents through the middle cranial fossa. Laryngoscope 1961;71:1363–1385. Hardy M, Crowe SJ. Early asymptomatic acoustic tumor: report of 6 cases. Arch Surg 1936;32:292–301. Eckermeier LS, Sorenson GD, McGavran MH. Histopathology of 30 non-operated acoustic schwannomas. Arch Otorhinolaryngol 1979;222:1. Anderson TD, Loevner LA, Bigelow DC, et al. Prevalence of unsuspected acoustic neuroma found by magnetic resonance imaging. Otolaryngol Head Neck Surg 2000;122:643– 646. Tos M, Stangerup S, Caye-Thomasen P, et al. What is the real incidence of vestibular schwannoma? Arch Otolarygol Head Neck Surg 2004;130:216–220. Cummings Murphy PR, Myal Y, Sato Y, et al. Elevated expression of basic fibroblast growth factor messenger ribonucleic acid in acoustic neuromas. Mol Endocrinol 1989;3:225–231. Diensthuber M, Brandis A, Lenarz T, et al. Co-expression of transforming growth factor-β1 and glial cell line derived neurotrophic factor in vestibular schwannomas. Otol Neurotol 2004;25:359–365. Cayé-Thomasen P, Baandrup L, Jacobsen GK, et al. Immunohistochemical demonstration of vascular endothelial growth factor in vestibular schwannomas correlates to tumor growth rate. Laryngoscope 2003;113:2129–2134. Brieger J, Bedavanija A, Lehr H, et al. Expression of angiogenic growth factors in acoustic neuroma. Acta Otolaryngol 2003;123: 1040–1045. Beatty CW, Scheithauer BW, Katzmann JA, et al. Acoustic schwannoma and pregnancy: a DNA flow cytometric, steroid hormone receptor, and proliferation marker study. Laryngoscope 1995;105:693–700. Selesnick SH, Jackler RK, Pitts LW. The changing clinical presentation of acoustic tumors in the MRI era. Laryngoscope 1993;103:431–436. Sataloff RT, Davies B, Myers DL: Acoustic neuromas presenting as sudden deafness. Am J Otol 1985; 6:349. Friedman RA, Kesser BW, Slattery WH, et al. Hearing preservation in patients with vestibular schwannomas with sudden sensorineural hearing loss. Otolaryngol Head Neck Surg 2001;125:544–551. Johnson EW. Results of auditory tests in acoustic tumor patients. In: House WF, Luetje CM, eds. Acoustic tumors Vol. 1. Baltimore: University Park Press, 1979:209–224. Beatty CW, Ebersold MJ, Harner SG: Residual and recurrent acoustic neuromas. Laryngoscope 1987; 97:1168. Backous DD, Pham HT: Guiding patients through the choices for treating vestibular schwannomas: Balancing options and ensuring informed consent. Otolaryngol Clin N Am 2007; 40: 521-540. Wilson DF, Hodgson RS, Gustafson MF, et al. The sensitivity of auditory brainstem response testing in small acoustic neuromas. Laryngoscope 1992;102:961–964. Jenkins HA. Long-term adaptive changes of the vestibulo-ocular reflex in patients following acoustic neuroma surgery. Laryngoscope 1985;95:1224–1234 Nedzelski JM, Schessel DA, Pfleiderer A, et al. Conservative management of acoustic neuromas. Otolaryngol Clin North Am 1992;25:691–705. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47. 48. 49. 50. 51. 52. 53. 54. Linthicum FH. Electronystagmography findings in patients with acoustic tumors. Semin Hear 1983;4:47–53. Welling DB, Glasscock ME III, Woods CI, et al. Acoustic neuroma: a cost-effective approach. Otolaryngol Head Neck Surg 1990;103:364–370. Press GA, Hesselink JR: MR imaging of cerebellopontine angle and internal auditory canal lesions at 1.5T. AJR Am J Roentgenol 1988; 150:1371. Shelton C, Harnsberger HR, Allen R, et al. Fast spin echo magnetic resonance imaging: clinical application in screening for acoustic neuroma. Otolaryngol Head Neck Surg 1996;114:71–76. Granick MS, Martuza RL, Parker SW, et al. Cerebellopontine angle meningiomas: clinical manifestations and diagnosis. Ann Otol Rhinol Laryngol 1985;94:34–38. Selters WA, Brackmann DE. Acoustic tumor detection with brain stem electric response audiometry. Arch Otolaryngol 1977;103:181–187. House WF: Translabyrinthine approach. In: House WF, Leutje CM, Doyle KJ, ed. Acoustic Tumors, San Diego: Singular Publishing; 1997:171-176. Charabi S, Thomsen J, Mantoni M, et al. Acoustic neuroma (vestibular schwannoma): growth and surgical and nonsurgical consequences of the wait-and-see policy. Otolaryngol Head Neck Surg 1995;113:5–14. Hasegawa T., Fujutani S., Katsumata S., et al: Stereotactic radiosurgery for vestibular schwannomas: analysis of 317 patients followed more than 5 years. Neurosurgery 57. 257-265.2005 Friedman W.A., Bradshaw P., Myers A., et al: Linear accelerator radiosurgery for vestibular schwannomas. J Neurosurg 105. 657-661.2006. Likterov I, Allbright RM, Selesnick SH: LINAC radiosurgery and radiotherapy treatment of acoustic neuroma. Otolaryngol Clin N Am 2007; 40: 541-570. Prasad D., Steiner M., Steiner L.: Gamma surgery for vestibular schwannoma. J Neurosurg 92. 745-759.2000. Andrews D.W., Suarez O., Goldman W., et al: Stereotactic radiosurgery and fractionated stereotactic radiotherapy for the treatment of acoustic schwannomas: comparative observations of 125 patients treated at one institution. Int J Radiat Oncol Biol Phys 50. (5): 1265-1278.2001. Kondziolka D., Lunsford D., McLaughlin , et al: Long-term outcomes after radiosurgery for acoustic neuromas. N Engl J Med 1998, 339: 1426-1433. Roland PS, Eston D. Stereotactic radiosurgery for acoustic tumors. Otolaryngol Clin North Am 2002;35:343–355. Bennett M, Haynes DS: Surgical approaches and complications in the removal of vestibular schwannomas. Otolaryngol Clin N Am 2007; 40: 589-609. Shelton C. Unilateral acoustic tumors: how often do theyrecur after translabyrinthine removal? Laryngoscope 1995;105:958–966. Thedinger BA, Glasscock ME III, Cueva RA, et al. Postoperative radiographic evaluation after acoustic neuroma and glomus jugulare tumor removal. Laryngoscope 1992;102:261–266. Pace-Balzan A, Ley RH, Ramsden RT, et al. Growth characteristics of acoustic neuromas with particular reference to the fate of capsule fragments remaining after tumor removal: implications for patient management. In: Tos M, Thomsen J, eds. Proceedings of the first international conference on acoustic neuroma Amsterdam:Kugler. 1992:701–703. Bloch D, Oghalai JS, Jackler RK, et al. The role of less than complete resection of acoustic neuroma. Otolaryngol Head Neck Surg 2004;130:104–112. Friedman RA, Kesser B, Brackmann DE, et al. Long-term hearing preservation after middle fossa removal of vestibular schwannoma. Otolaryngol Head Neck Surg 2003;129:660–665. 99. Ebersold MJ, Harner SG, Beatty CW, et al. Current results of the retrosigmoid approach to acoustic neurinoma. J Neurosurg 1992;76:901–909. Meyer T.A., Canty P.A., Wilkinson E.P., et al: Small acoustic neuromas: surgical outcomes versus observation or radiation. Otol Neurotol 2006, 27(3): 380-392. Grant GA, Rostomily RR, Kim K, et al. Delayed facial palsy after resection of vestibular schwannoma. J Neurosurg 2002;97:93–96. Harsha W.J., Backous D.D.: Counseling patients on surgical options for treating acoustic neuroma. Otolaryngol Clin North Am 2005, 38(4): 643-652. Myrseth E., Moller P., Pederson P.H., et al: Vestibular schwannomas: clinical results of quality of life after microsurgery or gamma knife radiosurgery. Neurosurgery 2005, 56(5): 927-935. Pollock B.E., Discoll C.L.W., Foote R.L., et al: Patient outcomes after vestibular schwannoma management: a prospective comparison of microsurgical resection and stereotactic radiosurgery. Neurosurgery 2006, 59(1): 77-85.