- •Chapter 1
- •Ocular Adnexal Lymphoproliferative
- •1.1 Pathogenesis
- •1.2 Chronic Antigen Stimulation
- •1.3 Immunosuppression
- •1.4 Pathology
- •1.5 Cytogenetics
- •1.6 Clinical Features
- •1.7 Imaging Findings
- •1.8 Staging
- •1.9 Positron Emission Tomography
- •1.10 Treatment
- •1.11 Follicular Lymphoma
- •1.12 Mantle Cell Lymphoma
- •1.13 Radiotherapy
- •1.14 Chemotherapy
- •1.15 Immunotherapy
- •1.16 Radioimmunotherapy
- •1.17 Outcome
- •1.18 The Future
- •References
- •Chapter 2
- •2.1 General Introduction
- •2.2 The Aging Process and Facial Analysis
- •2.3 Endoscopic Brow Lift
- •2.3.1 Introduction
- •2.3.2 Endoscopic Browlift Anesthesia Pearls
- •2.3.4 Endoscopic Browlift Postoperative Care Pearls
- •2.4 Upper Blepharoplasty
- •2.4.1 Introduction
- •2.4.2 Patient Evaluation
- •2.4.3 Upper Blepharoplasty Anesthesia Pearls
- •2.4.4 Upper Blepharoplasty Surgical Procedure Pearls
- •2.5 Lower Blepharoplasty, Fillers, and Midface Augmentation
- •2.5.1 Introduction
- •2.5.2 Patient Evaluation
- •2.5.3 Lower Blepharoplasty Anesthesia Pearls
- •2.5.4 Lower Blepharoplasty Surgical Procedure Pearls
- •References
- •Chapter 3
- •3.1 Introduction
- •3.2 What Is the Diagnosis?
- •3.2.1 Pitfalls of Diagnosis
- •3.2.2 A Diagnostic Corticosteroid Trial?
- •3.2.3 The Question of Biopsy
- •3.3 Treatment
- •3.3.1 Corticosteroids
- •3.3.2 Radiation
- •3.3.3 Other Agents
- •3.4 Special Circumstances
- •3.4.1 Pediatric IOIS
- •3.4.2 Sclerosing Pseudotumor
- •3.4.3 Tolosa–Hunt Syndrome
- •References
- •Chapter 4
- •4.1 Introduction
- •4.2 Embryology, Anatomy, Physiology, and Pathophysiology of the Canalicular System
- •4.3 Infective Causes
- •4.3.1 Periocular Herpes Simplex Infection
- •4.3.2 Bacterial Canaliculitis
- •4.4.1 Lichen Planus
- •4.4.2 Ocular Cicatricial Pemphigoid
- •4.5 Iatrogenic Causes
- •4.5.1 Systemic Drugs
- •4.5.1.2 Docetaxel (Taxotere)
- •4.5.2 Radiotherapy
- •4.5.3 Topical Ophthalmic Treatments
- •4.5.3.2 Mitomycin C (MMC) Therapy
- •4.5.4 Lacrimal Stents and Plugs
- •4.6 The Surgical Approach to Managing Canalicular Disease
- •4.6.1 Surgical Technique for Dacryocystorhinostomy with Retrograde Canaliculostomy
- •References
- •Chapter 5
- •5.1 Introduction
- •5.2 Nomenclature
- •5.3 Clinical Manifestations of NF1
- •5.4 Orbitofacial Tumors in NF1
- •5.4.2 Malignant Peripheral Nerve Sheath Tumors
- •5.4.3 Optic Pathway Gliomas
- •5.5 Genetics
- •5.5.1 The NF1 Gene
- •5.5.2 Overlapping NF1-Like Phenotype (SPRED1)
- •5.6.1 Introduction
- •5.7 Surgical Management of Orbitofacial Tumors in NF1
- •5.7.1 Introduction
- •5.7.2 Timing of Surgery
- •5.7.3 Periorbital Involvement
- •5.7.3.1 The Upper Eyelid
- •5.7.3.2 The Lower Eyelid and Midface
- •5.7.4 Orbital Involvement
- •5.7.4.1 Proptosis
- •5.7.4.3 Proptosis Due to Optic Nerve Glioma
- •5.7.4.4 Orbital Enlargement with Dystopia and Hypoglobus
- •5.8 The Natural History of NF1 Tumor Growth from Birth to Senescence
- •References
- •Chapter 6
- •6.1 Introduction
- •6.2 Surgical Anatomy of the Lacrimal Drainage System
- •6.3 Basic Diagnostics for Disorders of the Lacrimal Drainage System
- •6.4 Selective Lacrimal Sac Biopsy in External Dacryocystorhinostomy
- •6.5.1 Case A
- •6.5.2 Case B
- •6.5.3 Case C
- •6.5.4 Case D
- •6.5.5 Case E
- •6.5.6 Case F
- •6.5.7 Case G
- •References
- •Chapter 7
- •7.1 Introduction
- •7.2 Patients and Methods
- •7.2.1 Patients
- •7.2.2 Examination
- •7.3 Results
- •7.3.1 Patient Data
- •7.3.3 Family History
- •7.3.4 Pregnancy History
- •7.3.5 Birth
- •7.3.6 Associated Systemic and Ocular Diseases
- •7.3.8 Neuroradiological Findings (Brain MRI)
- •7.3.9 Nasolacrimal System Findings
- •7.4 Discussion
- •7.4.1 Patients
- •7.4.2 Obstetric and Family History
- •7.4.3 Associated Pathologies
- •7.4.3.1 Ophthalmological Findings in Unilateral Disease
- •7.4.3.2 Neuroradiological Findings
- •7.4.3.3 Systemic Diseases
- •7.4.3.4 Nasolacrimal Duct Findings
- •7.5 Conclusions
- •References
- •Chapter 8
- •8.1 Introduction
- •8.2 Evaluation of Complicated Ptosis
- •8.2.1 Compensatory Eyebrow Elevation
- •8.2.3 Innervation Patterns of the Frontalis Muscle
- •8.2.4 Checklist of Preoperative Evaluation of Complicated Ptosis
- •8.3 Surgical Technique of Levator Muscle Recession
- •8.3.1 Principle
- •8.3.2 Approach to the Levator
- •8.3.3 Partial Levator Recession
- •8.3.4 Total Levator Recession
- •8.3.6 Undercorrection and Overcorrection
- •8.4 Surgical Technique of Brow Suspension
- •8.4.1 Materials for Brow Suspension
- •8.4.1.1 Nonautogenous Materials
- •8.4.1.2 Autogenous Fascia Lata
- •8.4.2 Our Technique of Harvesting Autogenous Fascia Lata
- •8.4.3 Mechanical Principals of Brow Suspension
- •8.4.4 Upper Lid Approach
- •8.4.5 Fascia Implantation
- •References
- •Chapter 9
- •Modern Concepts in Orbital Imaging
- •9.1 Computerized Tomography
- •9.2 Three-Dimensional Imaging
- •9.3 Magnetic Resonance Imaging
- •9.3.1 The T1 Constant
- •9.3.2 The T2 Constant
- •9.3.3 Creating the MR Image
- •9.4 Imaging of Common Orbital Lesions
- •9.4.1 Adenoid Cystic Carcinoma
- •9.4.2 Cavernous Hemangioma
- •9.4.3 Dermoid Cyst
- •9.4.4 Fibrous Dysplasia
- •9.4.5 Lymphangioma
- •9.4.6 Lymphoma
- •9.4.7 Myositis
- •9.4.8 Optic Nerve Glioma
- •9.4.9 Pseudotumor
- •9.4.10 Rhabdomyosarcoma
- •9.6 Positron Emission Tomography
- •9.7 Orbital Ultrasound
- •9.7.1 Physics and Instrumentation
- •9.7.1.1 Topographic Echography
- •9.7.1.2 Quantitative Echography
- •9.7.1.3 Kinetic Echography
- •9.7.2 Extraocular Muscles
- •9.7.3 Optic Nerves
- •References
- •Chapter 10
- •10.1 Introduction
- •10.3 Etiology
- •10.4 Microbiology
- •10.5 Changing Pathogens and Resistance
- •10.5.2 Orbital MRSA
- •10.6 Evaluation of Orbital Cellulitis
- •10.7 Medical Treatment of Orbital Cellulitis
- •10.8 Surgical Treatment of Orbital Cellulitis
- •10.9 Prevention of Orbital Cellulitis After Orbital Fracture
- •References
- •Chapter 11
- •11.1 Clinical Picture
- •11.1.1 Clinical Phases
- •11.2 Ocular Complications
- •11.3 Investigation
- •11.3.1 Angiography
- •11.4 Management
- •11.4.1 Active Nonintervention
- •11.4.2 Indications for Treatment
- •11.5 Modalities of Treatment
- •11.5.1 Steroids
- •11.5.1.1 Topical Steroids
- •11.5.1.2 Intralesional Corticosteroid Injection
- •11.5.1.3 Oral Corticosteroids
- •11.5.2 Interferon-Alfa
- •11.5.3 Vincristine
- •11.5.4 Laser
- •11.5.5 Embolization
- •11.5.6 Surgery
- •References
- •Chapter 12
- •12.1 Introduction
- •12.2 Epidemiology
- •12.3 Biological Behavior and Timing of Metastasis
- •12.4 Lateralization
- •12.5 Localization
- •12.6 Clinical Features
- •12.7 Imaging and Patterns of Orbital Metastatic Disease
- •12.8 Biopsy
- •12.9 Common Types of Orbital Metastases
- •12.9.1 Breast Carcinoma
- •12.9.2 Lung Carcinoma
- •12.9.3 Prostatic Cancer
- •12.9.4 Melanoma
- •12.9.5 Carcinoid Tumor
- •12.11 Treatment
- •12.11.1 Radiotherapy
- •12.11.2 Chemotherapy
- •12.11.3 Hormonal Therapy
- •12.11.4 Surgery
- •12.12 Prognosis and Survival
- •References
- •Chapter 13
- •13.1 Introduction
- •13.2 Rituximab
- •13.3 Yttrium-90-Labeled Ibritumomab Tiuxetan
- •13.4 Imatinib Mesylate
- •13.5 Cetuximab
- •References
- •Chapter 14
- •14.1 Introduction
- •14.2 Porous Orbital Implants
- •14.3 Orbital Implant Selection in Adults
- •14.4 Orbital Implant Selection in Children
- •14.5 Volume Considerations in Orbital Implant Selection
- •14.7 Which Wrap to Use
- •14.8 To Peg or Not to Peg Porous Implants
- •14.9 Summary
- •References
- •Chapter 15
- •15.1 Introduction
- •15.2 Etiology and Presentation
- •15.2.1 Etiology of Orbital Volume Loss
- •15.2.2 Etiology of Periorbital Volume Loss
- •15.2.3 Features of Orbital Volume Loss
- •15.2.4 Features of Periorbital Volume Loss
- •15.3 Background to Injectable Soft-Tissue Fillers
- •15.3.1 Historical Perspective on Volume Replacement
- •15.4 Types of Injectable Soft-Tissue Filler
- •15.4.1 Collagen Fillers
- •15.4.2 Hyaluronic acid Fillers
- •15.5 Treatment Areas
- •15.5.1 Orbit
- •15.5.2 Upper Eyelid and Brow
- •15.5.3 Tear Trough
- •15.5.4 Temple and Brow
- •15.6 Other Periorbital Uses of Injectable Soft-Tissue Fillers
- •15.6.1 Upper Eyelid Loading
- •15.6.2 Lower Eyelid Elevation
- •15.6.3 Treatment of Cicatricial Ectropion
- •15.7 Future Developments
- •References
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9 Modern Concepts in Orbital Imaging |
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b |
9
Fig. 9.17 (a) CT and (b) T1 fat saturation contrasted MRI showing the characteristic imaging findings of myositis
irregular borders. The density is usually slightly higher than for normal muscle and is homogeneous in texture. On MRI, the involved extraocular muscles are enlarged, and the inflammatory process usually does not involve adjacent orbital fat. On T1-weighted images, the muscle produces an intermediate homogeneous signal that is isointense to normal muscle. On the T2-weighted image the signal is generally isointense to fat (Fig. 9.17a, b).
9.4.8Optic Nerve Glioma
Optic nerve gliomas are uncommon neoplasms of astrocytic glia located along the visual pathways. They represent 2–4% of all orbital tumors and 66% of primary optic nerve tumors. Gliomas are seen most commonly in
children, with a mean age of 9 years at presentation. About 29% of optic gliomas are seen in the setting of neurofibromatosis. On noncontrast CT, the orbital glioma appears as a well-outlined enlargement of the optic nerve that is usually fusiform but may be more rounded or even mulitilobulated. Increased tortuosity or kinking of the nerve is a common finding. Following contrast administration, enhancement is heterogeneous and variable from imperceptible to moderate. On the T1 MRI, gliomas are isointense or slightly hypointense with respect to cortical gray mater. A dilated subarachnoid space filled with cerebral spinal fluid (CSF) may image as a hypointense zone surrounding the tumor. Low-signal hypointense areas within the lesion represent cysts of mucinous degeneration and necrosis. On T2-WI, the signal may be more variable (Fig. 9.18a, b).
a |
b |
Fig. 9.18 (a) CT and (b) T1 MRI showing the characteristic imaging findings of optic nerve glioma
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9.4 Imaging of Common Orbital Lesions |
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9.4.9 Pseudotumor |
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9.4.10 Rhabdomyosarcoma |
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Pseudotumor is a common nonneoplastic, nongranulomatous inflammatory disease of unknown cause. It accounts for about 5% of all orbital lesions. The process ranges from acute to chronic and is not associated with systemic disease. Involvement may be diffuse within the orbital fat but can also involve specific structures such as extraocular muscle, lacrimal gland, posterior sclera, or optic nerve sheath. The CT shows a streaky, irregular, heterogeneous area of increased density with shaggy borders. This lesion typically molds around the globe and along extraocular muscles and insinuates between fascial planes. On MRI, the T1-weighted image gives a heterogeneous, poorly defined signal that is isointensetomuscleandhypointensetofat.TheT2-weighted image is hypointense or isointense to fat (Fig. 9.19a, b).
Rhabdomyosarcoma is the most common soft tissue mesenchymal tumor and malignancy of the orbit in children. It arises from pleuripotential mesenchymal precursors that normally differentiate into striated muscle. It occurs primarily in children, with a mean age of 8–9 years old, but rarely may be seen in older adults. CT scan shows an irregular, but moderately well-defined, soft tissue density mass. Most tumors occupy the extraconal space, with about half extending into the intraconal compartment. The MRI shows a heterogeneous-to-homogeneous irregular mass that is isointense to slightly hypointense with respect to muscle and hypointense to fat on T1-WI. On T2-weighted sequences, the tumor signal is higher, being hyperintense to both muscle and fat (Fig. 9.20a, b).
a |
b |
Fig. 9.19 (a) CT and (b) T1 MRI showing the characteristic imaging findings of orbital pseudotumor
a |
b |
Fig. 9.20 (a) CT showing the characteristic imaging findings of an orbital rhabdomyosarcoma. (b) T2 MRI of a small rhabdomyosarcoma of the right sphenoid sinus
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9 Modern Concepts in Orbital Imaging |
9.5Di usion MRI (Di usion-Weighted Imaging)
Diffusion imaging focuses on the random Brownian
9micromovements of water molecules inside tissues [28]. Because of these motions, water molecules collide and
thereby diffuse through tissues. As they diffuse, they encounter different obstacles, such as cell membranes, proteins, and fibers, which vary according to the specific tissue type. These structures can also be modified by certain pathological conditions, such as intracellular edema, abscess, and tumors. Water diffusion is relatively unrestricted in some tissues, such as cerebral gray matter. However, in other tissues such as white matter and muscle with a fiber structure, or in highly cellular tumors, water diffusion is more restricted. Diffusion-weighted imaging (DWI) therefore provides valuable information on the structure and geometric organization of tissues [30].
In DWI diffusion of extracellular water is the imaging object of interest. Diffusion data provide indirect information about the histological and gross anatomical tissue structure surrounding the water molecules [22, 27]. Diffusion MRI produces in vivo images of biological tissues weighted according to the local microstructural characteristics that influence diffusion. As discussed, in a typical T1-weighted MRI image water molecules in the sample are excited by a strong magnetic field. This causes the protons in these water molecules to precess simultaneously, producing signals that are used to create the image. In T2-weighted images contrast is produced by measuring the loss of coherence or synchrony between the water protons. When water is in an environment where it can move freely (diffuse), relaxation tends to take longer, and this can generate increased contrast between an area of pathology and the surrounding healthy tissue [2] and can be used to image structures that may not be appreciated by conventional MR techniques [34] (Fig. 9.21).
Various diffusion-weighted sequences are designed to obtain images with contrast that is influenced by differences in water molecule mobility [5]. This is done by adding multiple diffusion gradients during the preparatory phase of an imaging sequence. The final image will depend on the speed of diffusion and on the direction of diffusion controlled in part by structures that restrict water movement, such as nerve and muscle fibers.
The image intensity in each imaged voxel is attenuated (weakened) depending on the strength and direction of the magnetic diffusion gradient as well as on the local microstructure in which the water molecules diffuse. The greater the attenuation at a given position, the more diffusion there is in the direction of the diffusion gradient, and the darker will be the image. Where diffusion is low, as in the optic
Fig. 9.21 Diffusion-weighted MRI scan of a child with an optic nerve glioma showing focal increased water diffusion
nerve, extraocular muscles, or hypercellular tumors, the signal is brighter. To measure the diffusion profile, the MR scan is repeated many times, applying different directions and strengths of the diffusion gradient for each scan. In DWI, three gradient directions are usually applied, which approximately show the trace of the diffusion tensor. The diffusion image is normalized in a variety of ways to yield different types of images based on diffusion signals. They include ADC (apparent diffusion coefficient), Dav (average diffusion constant), and TDC (true diffusion coefficient).
Summary for the Clinician
■Diffusion MRI produces an image that is based on the microscopic movement of free water in the extracellular tissue compartment.
■Water diffusion can be isotropic in some tissues or anisotropic where barriers are present that only allow diffusion in one direction; the latter is seen in white matter due to fiber orientation and in muscles.
■Pathological processes can alter diffusion characteristics.
■Diffusion-weighted MRI measures the rate and direction of water diffusion and is used to map nerve fiber patterns and locations of impediments to diffusion, such as hypercellular tumors.
Diffusion tensor imaging enables the in vivo evaluation of tissue microstructure. It provides data that can help in the diagnosis of microscopic features, such as nerve fiber anomalies in white matter, which may not be visible with standard imaging techniques [38]. DWI has become useful for the detection of tumors, infections, inflammations, trauma, and degenerative diseases. It can distinguish a solid tumor from areas of cystic degeneration and necrosis and between benign and malignant neoplasms because of its ability to distinguish hypercellular from paucicellular tumors.
9.6Positron Emission Tomography
Positron emission tomography is an imaging technique that has become useful in medicine. Unlike the CT, which images the transparency of tissues to the passage of X-rays, PET scanning measures the emission of positrons (photons) from a radiotracer that is injected intravenously [1]. The technique makes use of the concept of positron annihilation.
In a PET scan, the patient is injected with the radioactive substance and placed on a table that moves through a circular shaped housing. This housing contains the gamma ray detector array, which has a series of scintillation crystals. Each detector is connected to a photomultiplier tube that converts the gamma rays emitted from the patient to photons of light. The photomultiplier tubes convert and amplify the photons to electrical signals. These signals are then processed by a computer to generate a clinical image. As the table and patient incremen-
a
9.6 Positron Emission Tomography |
141 |
tally move forward, the process is repeated, giving a series of thin-slice images of the body. These images are then assembled into a 3D representation [32, 37, 40]. The combined use of PET and CT is proving to be even more valuable by demonstrating metabolic activity along with anatomical detail and localization [36].
The most commonly used positron-emitting nuclides are carbon-11 and fluorine-18. These replace the normal atoms in tissue compounds, and the labeled compounds are taken up by certain tissues. Thus, fluorine-18 replaces fluorine-19 in fluorinated glucose to produce [2-18F]fluoro- 2-deoxy-D-glucose (FDG). The radioactive atom decays by positron emission. When a positron is emitted by a nucleus, it immediately collides with an electron, and the pair annihilates, converting all the mass energy of the two particles into two gamma rays. The two gamma ray photons possess momentum, and the conservation of momentum requires that they travel in opposite directions. The simultaneous detection of these gamma ray photons in two detectors situated 180° apart in the scanner allows location of the source on a line directly between those two detectors.
FDG PET scanning exploits the increased glycolytic activity associated with neoplastic diseases and has proven to be superior to other imaging modalities for some tumors, such as head and neck squamous cell carcinoma and lymphoma [24, 26, 41, 42]. PET scan imaging is of particular value for imaging of the brain (Fig. 9.22a, b). The fluorine isotope 18F-labeled glucose can pass through the blood–brain barrier, where the concentration of the tracer is a measure of the level of metabolic activity at that location in the brain. In the brain and elsewhere in the
b
Fig. 9.22 (a, b) Coronal and axial PET scans showing normal metabolic activity of the brain
