- •Preface
- •Contents
- •Contributors
- •1 Primary Orbital Cancers in Adults
- •1.1 Lymphoproliferative Disorders
- •1.1.1 Presenting Signs and Symptoms, Histopathologic and Molecular Genetic Characteristics, and Diagnosis
- •1.1.2 Treatment
- •1.1.3 Follow-up
- •1.2 Mesenchymal Tumors
- •1.2.1 Fibrous Histiocytoma
- •1.2.2 Solitary Fibrous Tumor
- •1.2.3 Hemangiopericytoma
- •1.2.4 Other Mesenchymal Tumors
- •1.3 Lacrimal Gland Tumors
- •References
- •2 Nonmalignant Tumors of the Orbit
- •2.1 Presentation
- •2.2 Cystic Lesions
- •2.3 Vascular Tumors
- •2.4 Lymphoproliferative Masses
- •2.6 Mesenchymal Tumors
- •2.7 Neurogenic Tumors
- •2.8 Lacrimal Gland Tumors
- •References
- •3 Pediatric Orbital Tumors
- •3.1 Introduction
- •3.2 Cystic Lesions
- •3.2.1 Dermoid Cyst
- •3.2.1.1 Clinical Presentation
- •3.2.1.2 Imaging
- •3.2.1.3 Histopathology
- •3.2.1.4 Treatment
- •3.2.1.5 Prognosis
- •3.2.2 Teratoma
- •3.2.2.1 Clinical Presentation
- •3.2.2.2 Imaging
- •3.2.2.3 Histopathology
- •3.2.2.4 Treatment
- •3.2.2.5 Prognosis
- •3.3 Vascular Tumors
- •3.3.1 Capillary Hemangioma
- •3.3.1.1 Clinical Presentation
- •3.3.1.2 Imaging
- •3.3.1.3 Histopathology
- •3.3.1.4 Treatment
- •3.3.1.5 Prognosis
- •3.3.2 Lymphangioma
- •3.3.2.1 Clinical Presentation
- •3.3.2.2 Imaging
- •3.3.2.3 Histopathology
- •3.3.2.4 Treatment
- •3.3.2.5 Prognosis
- •3.4 Histiocytic Lesions
- •3.4.1 Eosinophilic Granuloma
- •3.4.1.1 Clinical Presentation
- •3.4.1.2 Imaging
- •3.4.1.3 Histopathology
- •3.4.1.4 Treatment
- •3.4.1.5 Prognosis
- •3.5 Neural Tumors
- •3.5.1 Optic Nerve Glioma
- •3.5.1.1 Clinical Presentation
- •3.5.1.2 Imaging
- •3.5.1.3 Histopathology
- •3.5.1.4 Treatment
- •3.5.1.5 Prognosis
- •3.5.2.1 Clinical Presentation
- •3.5.2.2 Imaging
- •3.5.2.3 Histopathology
- •3.5.2.4 Treatment
- •3.5.2.5 Prognosis
- •3.6 Malignant Lesions
- •3.6.1 Ewing Sarcoma
- •3.6.1.1 Clinical Presentation
- •3.6.1.2 Imaging
- •3.6.1.3 Histopathology
- •3.6.1.4 Treatment
- •3.6.1.5 Prognosis
- •3.6.2 Neuroblastoma
- •3.6.2.1 Clinical Presentation
- •3.6.2.2 Imaging
- •3.6.2.3 Histopathology
- •3.6.2.4 Treatment
- •3.6.2.5 Prognosis
- •3.6.3 Retinoblastoma
- •3.6.3.1 Clinical Presentation
- •3.6.3.2 Imaging
- •3.6.3.3 Histopathology
- •3.6.3.4 Treatment
- •3.6.3.5 Prognosis
- •3.6.4 Granulocytic Sarcoma
- •3.6.4.1 Clinical Presentation
- •3.6.4.2 Imaging
- •3.6.4.3 Histopathology
- •3.6.4.4 Treatment
- •3.6.4.5 Prognosis
- •3.6.5 Rhabdomyosarcoma
- •References
- •4.1 Introduction
- •4.2 Clinical and Radiological Presentation
- •4.3 Staging
- •4.4 Surgery
- •4.5 Chemotherapy
- •4.6 Radiation Therapy
- •4.7 Conclusions and Future Directions
- •References
- •5 Metastatic Orbital Tumors
- •5.1 Introduction
- •5.2 Incidence
- •5.3 Anatomical Considerations
- •5.4 Presentation and Clinical Features
- •5.5 Diagnosis
- •5.6 Treatment
- •5.7 Types of Cancer Metastatic to the Orbit
- •5.7.1 Breast Carcinoma
- •5.7.2 Lung Carcinoma
- •5.7.3 Prostate Carcinoma
- •5.7.4 Melanoma
- •5.7.5 Carcinoid Tumors
- •5.7.6 Other Cancers
- •5.8 Conclusion
- •References
- •6.1 Tumors of Intraocular and Ocular Adnexal Origin
- •6.1.1 Eyelid Tumors
- •6.1.2 Intraocular Tumors
- •6.2 Tumors of Sinus and Nasopharyngeal Origin
- •6.2.1 Squamous Cell Carcinoma
- •6.2.2 Other Tumors of Sinus and Nasopharyngeal Origin
- •6.3 Tumors of Brain Origin
- •6.3.1 Meningioma
- •6.3.2 Other Intracranial Tumors
- •References
- •7 Lacrimal Gland Tumors
- •7.1 Introduction
- •7.2 Lymphoproliferative Lesions of the Lacrimal Gland
- •7.3 Benign Epithelial Tumors of the Lacrimal Gland
- •7.3.1 Pleomorphic Adenoma
- •7.3.2 Other Benign Epithelial Tumors
- •7.4 Malignant Epithelial Tumors of the Lacrimal Gland
- •7.4.1 Adenoid Cystic Carcinoma
- •7.4.2 Other Malignant Epithelial Tumors
- •7.5 AJCC Staging for Lacrimal Gland Tumors
- •References
- •8.1 Introduction
- •8.2 Indications
- •8.3 Surgical Techniques
- •8.3.1 Medial Orbitotomy Approach
- •8.3.2 Medial Eyelid Crease Approach
- •8.3.3 Lateral Orbitotomy Approach
- •8.3.4 Lateral Canthotomy Approach
- •8.4 Possible Indications for ONSF in Cancer Patients
- •8.4.1 Metastatic Breast Cancer
- •8.4.2 Lymphomatous Optic Neuropathy Diagnosed by Optic Nerve Biopsy
- •8.4.3 Adjuvant Therapy in Optic Nerve Sheath Meningioma
- •8.4.4 Papilledema Associated with Brain Tumors
- •8.4.5 Radiation-Induced Optic Neuropathy
- •8.5 Complications of ONSF
- •8.6 Future Research
- •References
- •9 Management of Primary Eyelid Cancers
- •9.1 Introduction
- •9.2 Types of Eyelid Malignancies
- •9.2.1 Basal Cell Carcinoma
- •9.2.2 Squamous Cell Carcinoma
- •9.2.3 Melanoma
- •9.2.4 Sebaceous Gland Carcinoma
- •9.2.5 Other Primary Eyelid Malignancies
- •9.3 Management
- •9.3.1 Evaluation
- •9.3.2 Tumor Excision and Eyelid Reconstruction
- •9.3.3 Sentinel Lymph Node Biopsy
- •9.3.4 Nonsurgical Treatment
- •9.3.5 Follow-up
- •References
- •10 Management of Conjunctival Neoplasms
- •10.1 Introduction
- •10.2 Squamous Cell Neoplasms of the Conjunctiva
- •10.2.1 Conjunctival Intraepithelial Neoplasia
- •10.2.2 Invasive Squamous Cell Carcinoma
- •10.2.3 Management
- •10.2.3.1 Local Excision and Cryotherapy
- •10.2.3.2 Treatment of More Advanced Disease
- •10.2.4 Surveillance
- •10.3 Melanocytic Neoplasms
- •10.3.1 Nevus
- •10.3.2 Primary Acquired Melanosis
- •10.3.3 Conjunctival Melanoma
- •References
- •11 Surgical Specimen Handling for Conjunctival and Eyelid Tumors
- •11.1 Introduction
- •11.2 Communication with the Pathologist
- •11.3 Conjunctival Specimens
- •11.4 Eyelid Specimens
- •11.5 Mohs Micrographic Surgery
- •11.6 Summary
- •References
- •12 Neuroradiology of Ocular and Orbital Tumors
- •12.1 Introduction: Imaging and Protocol
- •12.2 Anatomy
- •12.3 Intraocular Lesions
- •12.3.1 Retinoblastoma
- •12.3.2 Uveal Melanoma
- •12.3.3 Uveal Metastases
- •12.4 Orbital Lesions
- •12.4.1 Lymphoma
- •12.4.2 Orbital Rhabdomyosarcoma
- •12.4.3 Orbital Nerve Sheath Tumors
- •12.4.4 Mesenchymal Tumors of the Orbit
- •12.4.5 Orbital Pseudotumor
- •12.4.6 Orbital Metastases
- •12.5 Optic Nerve Tumors
- •12.5.1 Optic Nerve Glioma
- •12.5.2 Optic Nerve Sheath Meningiomas
- •12.6 Lacrimal Gland Tumors
- •12.7 Secondary Tumor Spread to the Orbit
- •12.8 Periorbital Skin Cancer and Perineural Spread
- •12.9 Conclusion
- •References
- •13 Radiation Therapy for Orbital and Adnexal Tumors
- •13.1 Indications
- •13.2 Radiation Therapy Terminology
- •13.3 Radiation Therapy Techniques
- •13.4 Radiation Therapy for Squamous Cell Carcinoma of the Eyelid
- •13.5 Adjuvant Radiation Therapy for Ocular Adnexal Tumors
- •13.6 Radiation Therapy for Optic Nerve Meningiomas and Orbital Rhabdomyosarcomas
- •13.7 Toxic Effects of Radiation Therapy
- •13.8 Summary
- •References
- •14.1 Historical Perspective
- •14.2 Presentation and Workup
- •14.4 Genetics
- •14.5 Pathologic Features
- •14.6 Treatment Options
- •14.6.1 General Considerations
- •14.6.2 Enucleation
- •14.6.3 Chemoreduction
- •14.6.4 Subtenon (Subconjunctival) Chemotherapy
- •14.6.5 Unilateral Disease
- •14.6.6 Bilateral Disease
- •14.7 Focal Therapies
- •14.7.1 Cryotherapy
- •14.7.2 Laser Photocoagulation
- •14.7.3 Brachytherapy
- •14.7.4 Thermotherapy
- •14.7.5 Radiation Therapy
- •14.8 Multi-institutional Clinical Trials
- •14.9 Animal Models of Retinoblastoma
- •14.10 Gene Transfer Technology for Treatment of Retinoblastoma
- •14.11 Future Development
- •References
- •15 Management of Uveal Melanoma
- •15.1 Epidemiology
- •15.2 Clinical Features
- •15.3 Diagnosis
- •15.4 Staging and Prognostic Factors
- •15.5 Background Studies
- •15.6 Overview of Management
- •15.7 Brachytherapy
- •15.8 Charged-Particle Radiotherapy
- •15.9 Surgical Techniques
- •15.9.1 Uveal Resection
- •15.9.2 Enucleation
- •15.9.3 Transpupillary Thermotherapy
- •15.9.4 Pathologic Assessment
- •15.9.5 Histologic Examination
- •15.10 Conclusion
- •References
- •16 Uveal Metastases from Solid Tumors
- •16.1 Introduction
- •16.2 Patient Characteristics
- •16.3 Symptoms
- •16.4 Clinical Features
- •16.5 Diagnosis
- •16.6 Treatment
- •16.6.1 Observation
- •16.6.2 External-Beam Radiation Therapy
- •16.6.3 Chemotherapy
- •16.6.4 Plaque Brachytherapy
- •16.6.5 Transpupillary Thermotherapy
- •16.6.6 Enucleation
- •16.7 Prognosis
- •16.8 Conclusions
- •References
- •17 Vascular Tumors of the Posterior Pole
- •17.1 Introduction
- •17.3 Circumscribed Choroidal Hemangioma
- •17.4 Management of Posterior Choroidal Hemangiomas
- •17.5 Acquired Vasoproliferative Tumors of the Retina
- •17.6 Conclusions
- •References
- •18 Reconstructive Surgery for Eyelid Defects
- •18.1 Introduction
- •18.2 General Principles
- •18.3 Eyelid Defects Not Involving the Eyelid Margin
- •18.4 Small Defects Involving the Lower Eyelid Margin
- •18.5 Moderate Defects Involving the Lower Eyelid Margin
- •18.6 Large Defects Involving the Lower Eyelid Margin
- •18.7 Small Defects Involving the Upper Eyelid Margin
- •18.8 Moderate Defects Involving the Upper Eyelid Margin
- •18.9 Large Defects Involving the Upper Eyelid Margin
- •18.10 Lateral Canthal Defects
- •18.11 Medial Canthal Defects
- •References
- •19.1 Introduction
- •19.2 Anatomy
- •19.3 Causes of Obstruction
- •19.4 Evaluation
- •19.5 Treatment
- •References
- •20.1 Introduction
- •20.2 Ectropion
- •20.2.1 Ectropion Due to Facial Nerve Paralysis
- •20.2.2 Cicatricial Ectropion
- •20.3 Entropion
- •20.4 Ptosis
- •20.5 Eyelid Retraction
- •20.6 Periorbital Edema Secondary to Imatinib Mesylate
- •References
- •21.1 Introduction
- •21.2 Anatomic Considerations
- •21.2.1 Orbital Margin
- •21.2.2 Nasal and Paranasal Sinuses
- •21.2.3 The Lacrimal System
- •21.2.4 Maxilla
- •21.3 Repair of Orbital Defects
- •21.3.1 Overview of Approaches
- •21.3.1.1 Maxillectomy with Orbital Exenteration
- •21.3.1.2 Maxillectomy Without Orbital Exenteration
- •21.3.2 Types of Maxillary Defects and Strategies for Their Repair
- •21.3.2.1 Type I Defect
- •21.3.2.2 Type II Defects
- •21.3.2.3 Type III Defects
- •21.3.2.4 Type IV Defects
- •21.3.3 Reconstruction After Orbital Exenteration
- •21.4 Conclusion
- •References
- •22.1 Introduction
- •22.2 Surgical Technique
- •22.2.2 Resection of Optic Nerve in Patients with Retinoblastoma
- •22.2.3 Maintenance of Globe Integrity
- •22.3 Choice of Implant
- •22.4 Management of the Anophthalmic Socket After Enucleation and Radiation Therapy
- •22.4.1 Patients with Retinoblastoma
- •22.4.2 Patients with Uveal Melanoma with Microscopic Extrascleral Extension
- •22.4.3 Patients with Head and Neck Cancer
- •22.5 Evisceration
- •References
- •23.2 Indications
- •23.3 Preoperative Evaluation
- •23.4 Surgical Techniques of Orbital Exenteration
- •23.5 Reconstructive Options
- •23.6 Surgical Complications
- •23.7 Rehabilitation After Orbital Exenteration
- •Suggested Readings
- •24.1 Introduction
- •24.2 Relevant Anatomy
- •24.3 Clinical Evaluation
- •24.3.1 Evaluation of Muscle Function
- •24.3.2 Evaluation of Lacrimal Gland and Lacrimal Drainage System Function
- •24.4 Medical Management
- •24.5 Surgical Management
- •24.5.1 Treatment of Lagophthalmos and Exposure Keratopathy
- •24.5.2 Treatment of Lower Eyelid Laxity and Ectropion
- •24.5.3 Reanimation of the Midface
- •24.5.3.1 Static Reanimation
- •24.5.3.2 Dynamic Reanimation
- •24.5.4 Options for Correction of Brow Ptosis
- •24.5.5 Additional Procedures for Management of Facial Droop
- •24.6 Special Circumstances in Cancer Patients with Facial Nerve Paralysis
- •24.7 Conclusion
- •References
- •25.1 Introduction
- •25.4 Conclusions and Recommendations
- •References
- •26 Lacrimal and Canalicular Toxicity
- •26.1 Introduction
- •26.2 5-Fluorouracil
- •26.4 Docetaxel
- •26.5 Epiphora Associated with Other Chemotherapeutic Drugs
- •26.6 Conclusions
- •References
- •27.1 Introduction
- •27.2 Orbital, Periorbital, and Orbital Teratogenic Side Effects by Individual Drug
- •27.2.1 Busulfan
- •27.2.2 Capecitabine
- •27.2.3 Carmustine
- •27.2.4 Cetuximab
- •27.2.5 Cisplatin
- •27.2.6 Cyclophosphamide
- •27.2.7 Cytarabine
- •27.2.8 Docetaxel
- •27.2.9 Doxorubicin
- •27.2.10 Erlotinib
- •27.2.11 Etoposide
- •27.2.12 Fluorouracil
- •27.2.13 Imatinib Mesylate
- •27.2.14 Interferons
- •27.2.15 Interleukin-2, Interleukin-3, and Interleukin-6
- •27.2.16 6-Mercaptopurine
- •27.2.17 Methotrexate
- •27.2.18 Mitomycin C
- •27.2.19 Mitoxantrone Dihydrochloride
- •27.2.20 Plicamycin
- •27.2.21 Thiotepa
- •27.2.22 Vincristine
- •27.3 Summary
- •References
- •28.1 Introduction
- •28.2 Epidemiology
- •28.2.1 Bacterial
- •28.2.2 Viral
- •28.2.3 Fungal
- •28.3 Pathogenesis and Host Defense
- •28.4 Ocular and Orbital Manifestations of Infection
- •28.4.1 Bacterial
- •28.4.2 Viral
- •28.4.3 Fungal
- •28.4.3.1 Candida Species
- •28.4.3.2 Aspergillus Species
- •28.4.3.3 Other Fungal Species
- •28.5 Conclusion
- •References
- •29.1 Introduction
- •29.2 Ophthalmologic Findings with CN III, IV, and VI Palsies
- •29.3 CN III, IV, and VI Palsies due to Primary Cranial Nerve Neoplasms and Direct Extension from Primary Brain, Brain Stem, or Skull base Tumors
- •29.4 CN III, IV, and VI Palsies due to Metastasis to the Brain, Brain, Stem and Skull Base from Distant Sites
- •29.5 Cranial Nerve III, IV, and VI Palsies due to Head and Neck Cancers
- •29.6 Cranial Nerve III, IV, and VI Palsies due to Leptomeningeal Disease
- •29.7 Other Causes of CN III, IV, and VI Palsies in Cancer Patients
- •29.8 Conclusion
- •References
- •30 Skull Base Tumors
- •30.1 Introduction
- •30.2 Anatomy of the Skull Base
- •30.3 Imaging and Diagnosis of Skull Base Tumors
- •30.4 Skull Base Tumors and Neuro-ophthalmic Correlations
- •30.4.1 Esthesioneuroblastoma
- •30.4.2 Chordoma
- •30.4.3 Craniopharyngioma
- •30.4.4 Meningioma
- •30.4.5 Sinonasal and Nasopharyngeal Tumors
- •30.4.6 Schwannoma
- •30.4.7 Pituitary Tumors
- •30.4.8 Myeloma
- •30.4.9 Paraganglioma
- •30.4.10 Metastases
- •References
- •31.1 Optic Pathway Gliomas
- •31.1.1 Demographics and Presentation
- •31.1.2 Histopathology
- •31.1.3 Imaging and Lesion Location
- •31.1.4 Differential Diagnosis
- •31.1.5 Management
- •31.1.6 Prognosis
- •31.2 Optic Nerve Sheath Meningiomas
- •31.2.1 Incidence
- •31.2.2 Histology and Pathophysiology
- •31.2.3 Clinical Presentation
- •31.2.4 Imaging
- •31.2.5 Treatment
- •References
- •32 Leptomeningeal Disease
- •32.1 Introduction
- •32.2 Epidemiology
- •32.3 Clinical Presentation
- •32.3.1 LMD due to Solid Tumors
- •32.3.2 LMD due to Hematogenous Tumors
- •32.3.3 LMD due to Primary Brain Tumors
- •32.4 Diagnosis
- •32.4.1 Radiographic Imaging
- •32.4.2 Optic Neuropathies in LMD
- •32.5 Treatment
- •32.6 Prognosis
- •32.7 Conclusion
- •References
- •33 Paraneoplastic Visual Syndromes
- •33.1 Introduction
- •33.2 Pathogenesis
- •33.3 Carcinoma-Associated Retinopathy
- •33.4 Carcinoma-Associated Cone Dysfunction Syndrome
- •33.5 Melanoma-Associated Retinopathy
- •33.6 Autoimmune Retinopathy
- •33.7 Paraneoplastic Optic Neuropathy
- •33.8 Diagnostic Testing
- •33.9 Differential Diagnosis
- •33.10 Treatment and Prognosis
- •33.11 Conclusion
- •References
- •34.1 Introduction
- •34.2 NF1 and the Optic Pathway
- •34.3.1 Description and Clinical Issues
- •34.3.2 Evaluation and Management
- •34.4 Intraorbital Optic Nerve Glioma
- •34.4.1 Description and Clinical Issues
- •34.4.2 Evaluation and Management
- •34.5 Chiasmal and Hypothalamic Glioma
- •34.5.1 Description and Clinical Issues
- •34.5.2 Evaluation and Management
- •34.6 Intraparenchymal Astrocytoma
- •34.6.1 Description and Clinical Issues
- •34.6.2 Evaluation and Management
- •34.7 Conclusion
- •References
- •35 Other Optic Nerve Maladies in Cancer Patients
- •35.1 Introduction
- •35.2 Optic Neuropathies Related to Elevated ICP
- •35.2.1 Causes of Elevated ICP
- •35.2.2 Treatment of Elevated ICP
- •35.4 Optic Neuropathies Caused by Drugs
- •35.4.1 Optic Disc Edema Secondary to Drug-Induced Elevated ICP
- •35.4.1.1 Retinoids
- •35.4.1.2 Imatinib Mesylate
- •35.4.1.3 Cyclosporine A
- •35.4.1.4 Cytarabine
- •35.4.2 Elevated ICP Secondary to Cerebral Venous Thrombosis
- •35.4.2.1 Cisplatin
- •35.4.2.2 L-Asparaginase
- •35.4.3 Optic Disc Edema Usually Without Elevated ICP
- •35.4.3.1 Cisplatin
- •35.4.3.2 Carboplatin
- •35.4.3.3 Carmustine
- •35.4.3.4 Vincristine
- •35.4.3.5 5-Fluorouracil
- •35.4.3.6 Cyclosporine A
- •35.4.3.7 Tacrolimus
- •35.4.4 Optic Neuropathy Without Disc Edema
- •35.4.4.1 Fludarabine
- •35.4.4.2 Tacrolimus
- •35.4.4.3 Paclitaxel
- •35.4.4.4 Methotrexate
- •35.4.4.5 Cytarabine
- •35.5 Optic Neuropathies Caused by Radiation
- •References
- •36 Management of Endogenous Endophthalmitis
- •36.1 Introduction
- •36.2 Epidemiology
- •36.3 Microbiology
- •36.4 Clinical Manifestations and Diagnosis
- •36.5 Treatment
- •36.5.1 Bacterial Endophthalmitis
- •36.5.2 Fungal Endophthalmitis
- •36.5.2.1 Yeast Endophthalmitis
- •36.5.2.2 Mold Endophthalmitis
- •36.6 Prognosis
- •36.7 Summary
- •References
- •37 Viral Retinitis in the Cancer Patient
- •37.1 Introduction
- •37.2 Epidemiology
- •37.3 Clinical Features
- •37.3.1 CMV Retinitis
- •37.3.2 Acute Retinal Necrosis
- •37.3.3 Progressive Outer Retinal Necrosis
- •37.4 Treatment
- •37.4.1 CMV Retinitis
- •37.4.1.1 Intravitreal Injections
- •37.4.1.2 Ganciclovir Implant
- •37.4.2 Acute Retinal Necrosis
- •37.4.3 Progressive Outer Retinal Necrosis
- •37.5 Role of Vitreoretinal Surgery in Viral Retinitis
- •37.5.1 Argon Laser Photocoagulation
- •37.5.2 Retinal Detachment Repair
- •37.6 Prognosis
- •37.6.1 CMV Retinitis
- •37.6.2 Acute Retinal Necrosis
- •37.6.3 Progressive Outer Retinal Necrosis
- •37.7 Conclusion
- •References
- •38.1 Introduction
- •38.2 Indications for Diagnostic Vitrectomy
- •38.2.1 Vitreous Biopsy
- •38.2.2 Uveal Biopsy
- •38.3 Preoperative Considerations
- •38.3.1 Thrombocytopenia
- •38.3.2 Anesthesia
- •38.4 Vitreous Biopsy
- •38.4.1 Technique
- •38.4.2 Effect of Vitrector Gauge on Vitreous Sample
- •38.5 Uveal Biopsy
- •38.5.1 Technique
- •38.5.2 Complications
- •38.5.3 Collaboration with Pathology
- •38.6 Pathologic Processing
- •38.6.1 Cytology
- •38.6.2 Interleukin Measurement
- •38.6.3 Polymerase Chain Reaction
- •38.6.4 Genetic Analysis
- •38.6.5 Cytogenetic Uveal Melanoma Studies
- •38.7 Results of Diagnostic Vitrectomy
- •38.7.1 Common Diagnoses
- •38.7.2 Diagnostic Utility
- •38.8 Postoperative Considerations
- •38.9 Conclusion
- •References
- •39.1 Introduction and Epidemiology
- •39.2 Presentation and Diagnosis
- •39.3 Management
- •39.4 Future Considerations
- •39.5 Conclusions
- •References
- •Index
298 |
H. Chang et al. |
Fig. 24.2 Typical findings of facial nerve palsy and surgical approaches. (a) A 50-year-old man with right facial nerve paralysis after excision of a right acoustic neuroma. Note the paralytic right brow ptosis, mechanical dermatochalasis, lower eyelid ectropion, medial canthal laxity, nasolabial fold attenuation, alar collapse, lateral oral commissure droop, lower facial droop, and midfacial droop. (b) Composite photograph of the same patient illustrating the locations of various surgical approaches for comprehensive rehabilitation, including (1) insertion of an upper eyelid weight, (2) lateral canthoplasty and/or creation of a static lower eyelid sling, (3) medial canthopexy, (4) direct brow lift, (5) endoscopic forehead lift, (6) direct alar lift, (7) oral commissure lift, (8) midface lift,
(9) temporalis muscle transfer or temporalis fascia sling, and (10) deep plane rhytidectomy and neck lift
affected, leading to nasal obstruction. Dysfunction of the orbicularis oris, risorius, or depressor anguli oris muscles contributes to asymmetry and can lead to problems with speech along with drooling and biting of the oral mucosa. Loss of function of the zygomaticus major and minor muscles leads to flattening of the nasolabial fold, increasing facial asymmetry, and potentially an increase in the patient’s emotional distress.
24.3 Clinical Evaluation
The complete assessment of a patient with facial nerve paralysis includes clinical evaluation of the resting tone and the active function of muscles as well as determination of the extent of dry eye and the function of the lacrimal gland and lacrimal drainage system.
24 Periorbital Surgical Rehabilitation After Facial Nerve Paralysis |
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24.3.1 Evaluation of Muscle Function
The evaluation begins with the patient at rest with careful observation of involuntary movements and resting facial symmetry. Asking the patient to voluntarily contract the various muscle groups can further elucidate the pattern of loss of innervation. Electrophysiology testing—electromyography, electroneurography, maximal stimulation test, and nerve excitability test—can be used to further clarify the amount of degeneration of the facial nerve. Grading scales to grade the severity of the impairment of facial nerve function have been developed and emphasize the muscles of facial expression [2, 4].
As previously mentioned, loss of orbicularis oculi function is the most significant ophthalmic consequence of facial nerve paralysis and can result in lagophthalmos and paralytic ectropion, placing the ocular surface at risk for exposure and breakdown. The strength of the orbicularis oculi can be evaluated by observing the degree of lagophthalmos and the presence of Bell’s phenomenon at rest and with gentle and then forceful blinking. Orbicularis oculi tone can be further evaluated by asking the patient to close his/her eyes while the clinician tries to manually force open the patient’s eyelids. The cornea should be evaluated for both sensation and signs of exposure. The eyelid position should be assessed for the presence of laxity and for the presence of paralytic ectropion.
Evaluating frontalis muscle function can be especially helpful in determining whether facial nerve palsy is central or peripheral. Central facial nerve palsy spares frontalis muscle function as the forehead has bilateral upper motor neuron innervation. In contrast, peripheral facial nerve palsy affects ipsilateral frontalis muscle innervation, and the patient is unable to wrinkle the ipsilateral forehead, resulting in brow ptosis.
Evaluation of midfacial muscle function is also an important part of the clinical examination. The nasolabial fold is created by the zygomaticus major and minor, levator labii superioris, and levator labii superioris alaeque nasi muscles, and this fold may be effaced or absent with facial nerve palsy. The nasal ala may appear collapsed because of loss of levator labii superioris alaeque nasi function and support of the internal nasal valve. The zygomaticus major, which draws the angle of the mouth laterally, and the zygomaticus minor, which elevates and everts the upper lip, can be assessed by asking the patient to attempt to smile. The orbicularis oris muscle narrows the orifice of the mouth, purses the lips, and plays an important role in speech and oral competence. Difficulty in speech, along with the presence of drooling, lip laxity, and biting of the oral mucosa, can indicate involvement of the facial nerve branches innervating the zygomaticus and orbicularis oris muscles.
24.3.2Evaluation of Lacrimal Gland and Lacrimal Drainage System Function
Both lacrimal gland function and the lacrimal drainage system can be compromised in patients with facial nerve palsy. The parasympathetic innervation for the