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Dive into the research topics where Thomas O. Willcox is active.

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Featured researches published by Thomas O. Willcox.


Otology & Neurotology | 2002

Temporal bone hemangiomas involving the facial nerve.

Oren Friedman; Brian A. Neff; Thomas O. Willcox; Lawrence C. Kenyon; Robert T. Sataloff

Objective Hemangiomas of the facial nerve are rare tumors that can mimic more common temporal bone tumors such as vestibular schwannomas and facial nerve schwannomas. This article reviews the diagnostic challenges in the surgical treatment of facial nerve hemangiomas. Study Design Two case reports and literature review. Results Early diagnosis and surgical excision of facial nerve hemangiomas can sometimes allow tumor removal with facial nerve preservation. In patients in whom the facial nerve needs to be resected to remove the hemangioma, primary anastomosis or cable nerve grafting can yield House-Brackmann Grade III/VI postoperative facial nerve function. Conclusion Complete surgical excision of facial nerve hemangiomas with primary facial nerve repair (when necessary) is the treatment of choice for these lesions.


International Journal of Radiation Oncology Biology Physics | 2009

Toward dose optimization for fractionated stereotactic radiotherapy for acoustic neuromas: comparison of two dose cohorts.

David W. Andrews; Maria Werner-Wasik; Robert B. Den; Sun Ha Paek; Beverly Downes-Phillips; Thomas O. Willcox; Greg Bednarz; Mitchell Maltenfort; James J. Evans; Walter J. Curran

PURPOSE To describe our initial experience of fractionated stereotactic radiotherapy dose reduction comparing two dose cohorts with examination of tumor control rates and serviceable hearing preservation rates. METHODS AND MATERIALS After institutional review board approval, we initiated a retrospective chart review to study the hearing outcomes and tumor control rates. All data were entered into a JMP, version 7.01, statistical spreadsheet for analysis. RESULTS A total of 89 patients with serviceable hearing had complete serial audiometric data available for analysis. The higher dose cohort included 43 patients treated to 50.4 Gy with a median follow-up (latest audiogram) of 53 weeks and the lower dose cohort included 46 patients treated to 46.8 Gy with a median follow-up of 65 weeks. The tumor control rate was 100% in both cohorts, and the pure tone average was significantly improved in the low-dose cohort (33 dB vs. 40 dB, p = 0.023, chi-square). When the patient data were analyzed at comparable follow-up points, the actuarial hearing preservation rate was significantly longer for the low-dose cohort than for the high-dose cohort (165 weeks vs. 79 weeks, p = .0318, log-rank). Multivariate analysis revealed the dose cohort (p = 0.0282) and pretreatment Gardner-Robertson class (p = 0.0215) to be highly significant variables affecting the hearing outcome. CONCLUSION A lower total dose at 46.8 Gy was associated with a 100% local control tumor rate and a greater hearing preservation rate. An additional dose reduction is justified to achieve the optimal dose that will yield the greatest hearing preservation rate without compromising tumor control for these patients.


Otolaryngology-Head and Neck Surgery | 1993

A Comparison of Growth Rates of Acoustic Neuromas: Nonsurgical Patients vs. Subtotal Resection:

Seth I. Rosenberg; Herbert Silverstein; Michael A. Gordon; John M. Flanzer; Thomas O. Willcox; Julie Silverstein

A conservative approach to the management of acoustic neuromas in elderly patients has been used since 1971. Elderly patients without symptoms of brain stem compression are initially treated by observation and yearly radiographic imaging. A translabyrinthine radical-subtotal resection is performed if brain stem compression is present or if tumor is growing rapidly. Twenty-three patients, ages 65 to 86 years, had initial nonsurgical management of their tumors. Growth rates could be determined for 16 patients. Thirteen patients not requiring surgery had an average tumor growth rate of 0.6 mm/yr. Three patients with an average growth rate of 6.8 mm/yr eventually required surgery. No patient whose tumor was < 15 mm at initial evaluation has experienced brain stem symptoms or demonstrated rapid tumor growth. Twenty-four patients ages 65 to 86 years underwent planned subtotal tumor excision. Eighteen patients followed postoperatively for more than 1 year demonstrated an average rate of regrowth of tumor of 0.7 mm/yr. (OTOLARYNGOL HEAD NECK SURG 1993;109:482-7.)


Otolaryngology-Head and Neck Surgery | 2000

Endoscopic repair of cerebrospinal fluid rhinorrhea.

Vivian Mao; William M. Keane; Joseph P. Atkins; Joseph R. Spiegel; Thomas O. Willcox; Marc Rosen; David W. Andrews; David Zwillenberg

Endoscopic repair of cerebrospinal fluid rhinorrhea is a promising alternative to traditional repair techniques. This article reports our experience with 21 cases (10 spontaneous, 8 iatrogenic, and 3 traumatic). Various diagnostic radiographic modalities were used, including computer-aided techniques. Most repairs were accomplished with a free fascial graft positioned in the epidural space. Postoperative lumbar drainage was used in 15 cases. Initial repair was successful in 18 cases (85.7%). In all 3 failures, the surgeon had difficulty with proper graft placement. Additionally, 2 of these cases were confounded by early inadvertent removal of the lumbar drain. All patients in whom the procedure failed underwent a second successful endoscopic repair. There were no major complications. In our experience endoscopic repair of cerebrospinal fluid rhinorrhea is a safe and effective approach that can be improved with computer-aided localization devices. Proper graft placement is critical, and lumbar drainage is an important adjunct in selected cases. (Otolaryngol Head Neck Surg 2000;122:56–60.)


Neurosurgical Focus | 2012

Surgical management of temporal meningoencephaloceles, cerebrospinal fluid leaks, and intracranial hypertension: treatment paradigm and outcomes.

Tyler J. Kenning; Thomas O. Willcox; Gregory J. Artz; Paul Schiffmacher; Christopher J. Farrell; James J. Evans

OBJECT Thinning of the tegmen tympani and mastoideum components of the temporal bone may predispose to the development of meningoencephaloceles and spontaneous CSF leaks. Surgical repair of these bony defects and associated meningoencephaloceles aids in the prevention of progression and meningitis. Intracranial hypertension may be a contributing factor to this disorder and must be fully evaluated and treated when present. The purpose of this study was to establish a treatment paradigm for tegmen defects and elucidate causative factors. METHODS The authors conducted a retrospective review of 23 patients undergoing a combined mastoidectomy and middle cranial fossa craniotomy for the treatment of a tegmen defect. RESULTS The average body mass index (BMI) among all patients was 33.2 ± 7.2 kg/m(2). Sixty-five percent of the patients (15 of 23) were obese (BMI > 30 kg/m(2)). Preoperative intracranial pressures (ICPs) averaged 21.8 ± 6.0 cm H(2)O, with 10 patients (43%) demonstrating an ICP > 20 cm H(2)O. Twenty-two patients (96%) had associated encephaloceles. Five patients underwent postoperative ventriculoperitoneal shunting. Twenty-two CSF leaks (96%) were successfully repaired at the first attempt (average follow-up 10.4 months). CONCLUSIONS Among all etiologies for CSF leaks, those occurring spontaneously have the highest rate of recurrence. The surgical treatment of temporal bone defects, as well as the recognition and treatment of accompanying intracranial hypertension, provides the greatest success rate in preventing recurrence. After tegmen dehiscence repair, ventriculoperitoneal shunting should be considered for patients with any combination of the following high-risk factors for recurrence: spontaneous CSF leak not caused by another predisposing condition (that is, trauma, chronic infections, or prior surgery), high-volume leaks, CSF opening pressure > 20 cm H(2)O, BMI > 30 kg/m(2), preoperative imaging demonstrating additional cranial base cortical defects (that is, contralateral tegmen or anterior cranial base) and/or an empty sella turcica, and any history of an event that leads to inflammation of the arachnoid granulations and impairment of CSF absorption (that is, meningitis, intracranial hemorrhage, significant closed head injury, and so forth).


Otology & Neurotology | 2009

Clinical, radiographic, and audiometric predictors in conservative management of vestibular schwannoma.

Prashant S. Malhotra; Pranav Sharma; Michael A. Fishman; F. Lawson Grumbine; Renee Tholey; Vincent Q. Dam; Abhijit Dasgupta; Edward Pequignot; Thomas O. Willcox

Objective: Vestibular schwannomas (VS) can be managed by observation. The goals were to examine clinical, radiographic, and audiometric variables at presentation and during observation that may predict which patients fail conservative management. Methods: A retrospective chart review was performed of 202 patients who elected observation primarily. Data collection included presenting symptoms, symptom progression, tumor size, audiologic measures, and global clinical outcomes. Univariate and multivariate analyses were performed. Results: Follow-up ranged from 1 month to 16 years (mean, 2.48 yr). Nineteen patients (9.4%) in the study group failed. Disequilibrium as a presenting symptom appeared more often in patients who failed observation (58% versus 32%; p = 0.039), as did new-onset disequilibrium. Presenting tumor size differed for patients who failed conservative management, with a mean of 14.0 versus 8.4 mm (p = 0.0006). Neurotologic complications compared favorably to those treated with primary surgery or radiotherapy. Conclusion: Patients with subjective disequilibrium at presentation and subjective disequilibrium developed during observation may be more likely to fail conservative management. Increased tumor size at presentation also may indicate the same, although no threshold could be achieved.


American Journal of Otolaryngology | 2017

Rate of tympanic membrane perforation after intratympanic steroid injection

Michael C. Topf; David Hsu; Douglas R. Adams; Tingting Zhan; Stanley Pelosi; Thomas O. Willcox; Brian McGettigan; Kyle W. Fisher

PURPOSE To determine the rate of persistent tympanic membrane perforation after intratympanic steroid injection. To determine which comorbid conditions and risk factors are associated with prolonged time to perforation closure following intratympanic steroid injection. MATERIALS AND METHODS Clinical data were gathered for patients who had undergone intratympanic steroid injection to treat sudden sensorineural hearing loss or Ménières disease. Primary outcomes analysis included rate of persistent tympanic membrane perforation, defined as perforation at least 90days following last injection, and time to perforation healing. Age, sex, number of injections, smoking status, diabetes mellitus, previous head and neck irradiation, and concurrent oral steroids, were analyzed as potential predictors of persistent perforation. RESULTS One hundred ninety two patients were included in this study. Three patients (1.6%) had persistent tympanic membrane perforations. All three patients received multiple injections. One patient underwent tympanoplasty for repair of persistent perforation. The median time to perforation healing was 18days. There was no statistically significant variable associated with time to perforation healing. However, patients with prior history of head and neck radiation averaged 36.5days for perforation healing compared to 17.5days with no prior history of radiation and this approached statistical significance (p=0.078). CONCLUSIONS The rate of persistent tympanic membrane perforation following intratympanic steroid injection is low. Patients with a history of radiation to the head and neck may be at increased risk for prolonged time for closure of perforation.


Laryngoscope | 2006

Retropharyngeal pseudomeningocele presenting as dysphagia after atlantooccipital dislocation.

David Cognetti; W Scott Enochs; Thomas O. Willcox

Educational Objective: At the conclusion of this paper, the readers should be able to recognize a retropharyngeal pseudomeningocele as a potential complication of atlanto occipital dislocation.


Otolaryngology-Head and Neck Surgery | 2007

Malignant Melanoma of the Middle Ear

Joseph Curry; Brain C. Kung; Thomas O. Willcox

A 60-year-old man with a history of renal cell carcinoma presented to a local otolaryngologist with a left aural fullness. Examination revealed only serous otitis media. Audiometry showed a mild mixed left hearing loss. On follow-up, his symptoms had not resolved and a dark blue mass was noted behind the tympanic membrane. Computed tomography (CT) identified a 10 6 mm mass in the superior mesotympanum and epitympanum. No bony erosion was evident, and the jugular bulb and ossicles were intact. The eustachian tube orifice was clear. The facial nerve was not involved. Magnetic resonance imaging (MRI) revealed a mass with variegated, intermediate intensity signal on T1 and T2 sequences (Fig 1). Subsequently, the patient underwent attempted middle ear exploration. However, shortly after the procedure was started, it was abandoned because of profuse bleeding. Biopsies were nondiagnostic. The patient was then referred to our care. After reviewing the case and images, glomus tympanicum was suspected, and the patient was scheduled for tumor resection. Intraoperatively, the mass was far more extensive than the imaging revealed. A dark blue mass filled the mesotympanum and extended into the epitympanum (Fig 2A, see online supplemental material for Fig 2B: www.http://journal.entnet.org). The tumor eroded the lenticular process and did not appear to originate from the promontory. Gross tumor was removed from the middle ear, and mastoidectomy was performed. Frozen sections were inconclusive. Because no diagnosis was yet established, the head of the maleus and stapes superstructure were left in place. Histologic findings showed pleomorphic cells and abundant pigment granules. On immunopathologic examination, the specimen was positive for S-100, HMB-45, and Melan A, and resulted in a diagnosis of malignant melanoma. The patient was referred to medical oncology, radiation


Otolaryngology-Head and Neck Surgery | 1999

Unusual otolaryngic presentations of ameloblastoma.

Richard R. Schmidt; Ron L. Moses; Daniel Loggi; Joseph V. Puzzi; Ritu Malhotra; Thomas O. Willcox; William M. Keane

both pathologists and surgeons: to pathologists because of their variable histologic appearance and to surgeons for their unrelenting ability to recur. Much of the literature has centered around discussions of origin, behavior, various classification systems, and surgical treatments for ameloblastomas. Controversy exists concerning the cell of origin of the ameloblastoma, resulting in the appearance of more than 50 names for this tumor in the literature. Amelois old French for enamel, although this tumor contains no enamel. It is thought to originate from tissue that differentiates into the enamel organ. Blastoma,meaning tumor of one type, is an oversimplification of this histologically diverse tumor. The World Health Organization in 1971 defined ameloblastomas as benign but locally invasive neoplasms consisting of proliferating odontogenic epithelium lying in a fibrous stroma. However, cases of both ameloblastic carcinoma and metastasizing ameloblastoma have been reported. Gold 1 defined ameloblastomas as low-grade malignant basaloid neoplasms with a variable range of histologic patterns, clinical forms, and behavior. He also compared ameloblastomas to basal cell carcinomas with regard to their biologic behavior. Ameloblastomas are the most common odontogenic neoplasm and yet comprise only 1% of all tumors of the maxilla and mandible. 2 Males and females are affected equally, with most presenting during the fourth decade of life. 3,4 The mandible is the site of origin in 80% of cases, whereas approximately 20% arise in the maxilla. 4

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Gregory J. Artz

Thomas Jefferson University Hospital

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James J. Evans

Thomas Jefferson University

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William M. Keane

Thomas Jefferson University

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David W. Andrews

Thomas Jefferson University

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John M. Lasak

Thomas Jefferson University

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Marc Rosen

Thomas Jefferson University

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Vijay M. Rao

Thomas Jefferson University Hospital

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