- •The Sclera
- •Preface
- •Contents
- •1.1 Introduction
- •1.2 Development of the Sclera
- •1.2.1.1 First Week
- •1.2.1.2 Second Week
- •1.2.1.3 Third Week
- •1.2.1.4 Fourth Week
- •1.2.1.5 Fifth Week
- •1.2.1.6 Sixth Week
- •1.2.1.7 Seventh Week
- •1.2.1.8 Ninth Week
- •1.2.1.9 Tenth Week
- •1.2.1.10 Thirteenth Week
- •1.2.1.11 Sixteenth Week
- •1.2.1.12 Twenty-Fourth Week
- •1.2.2.1 Collagens
- •1.2.2.2 Proteoglycans
- •1.2.2.3 Glycoproteins
- •1.3 Anatomy
- •1.3.1 Gross and Microscopic Anatomy
- •1.3.1.1 Scleral Foramina
- •Anterior Scleral Foramen
- •Posterior Scleral Foramen
- •1.3.1.2 Layers of the Sclera
- •Episclera
- •Scleral Stroma
- •Lamina Fusca
- •1.3.1.3 Blood Supply and Emissary Canals
- •Vascular Distribution
- •Circulatory Dynamics
- •1.3.1.4 Nerve Supply
- •1.3.2 Ultramicroscopic Anatomy
- •1.3.2.1 Sclera
- •1.3.2.2 Vessels
- •1.4 Biochemistry
- •1.5 Immunohistochemistry
- •1.6 Biomechanics
- •1.7 Molecular Structure
- •1.7.1 Collagen
- •1.7.2 Elastin
- •1.7.3 Proteoglycans
- •1.7.4 Glycoproteins
- •1.7.6 Fibroblast Growth Regulation
- •1.8 Summary
- •References
- •2.1 General Immune Response Considerations
- •2.1.1 Components of the Adaptive Immune Response
- •2.1.1.1 Lymphocytes
- •T Lymphocytes
- •B Lymphocytes
- •Third-Population Lymphocytes or Null Lymphocytes
- •2.1.1.2 Monocytes/Macrophages
- •Phagocytosis
- •Antigen-Presenting Cells
- •2.1.1.3 Polymorphonuclear Granulocytes
- •Neutrophils
- •Eosinophils
- •Basophils/Mast Cells
- •2.1.1.4 Platelets
- •2.1.2 Immunoregulation
- •2.1.2.1 Major Histocompatibility Complex
- •2.1.2.2 Humoral Mechanisms: Antibodies
- •2.1.2.3 Cellular Mechanisms
- •2.1.2.4 Summary
- •2.1.3 Abnormalities of the Immune Response
- •2.1.3.1 Hypersensitivity Reactions
- •Type III Hypersensitivity Reactions
- •Systemic Immune Complex Disease
- •Local Immune Complex Disease (Arthus Reaction)
- •Type IV Hypersensitivity Reactions
- •2.1.3.2 Autoimmunity
- •Mechanisms of Autoimmunity
- •2.2 Connective Tissue and the Immune Response
- •2.2.1 Fibroblast Functions and the Immune Response
- •2.3 The Sclera and the Immune Response: Scleritis
- •2.3.1 Immune Characteristics of the Sclera
- •2.3.2 The Susceptible Host: Immunogenetics
- •2.3.3 Etiology
- •2.3.3.1 Exogenous Agents
- •Viruses
- •Mycobacteria
- •2.3.3.2 Endogenous Substances
- •Glycosaminoglycans
- •Collagen
- •2.3.4 Pathogenesis
- •2.4 Summary
- •References
- •3.1 Investigation of the Illness
- •3.1.1 Major Complaint and History of Present Illness
- •3.1.2 Past History
- •3.1.3 Family History
- •3.1.4 Past and Present Therapy History
- •3.1.5 Review of Systems
- •3.1.6 Systemic Examination
- •3.1.6.1 Head
- •3.1.6.2 Extremities
- •3.1.7 Ocular Examination
- •3.1.7.1 Episcleral and Scleral Examination
- •External Examination of the Eye in Daylight
- •Slit-Lamp Examination
- •Diffuse Illumination
- •Slit-Lamp Illumination
- •Red-Free Illumination
- •3.1.7.2 General Eye Examination
- •Visual Acuity
- •Pupils and Extraocular Muscles
- •Cornea
- •Anterior Uvea
- •Lens
- •Fundus
- •Intraocular Pressure
- •3.2 Diagnostic Tests
- •3.2.1 Blood Tests
- •3.2.1.1 Rheumatoid Factor
- •3.2.1.2 Anticyclic Citrullinated Peptide Antibodies
- •3.2.1.3 Antinuclear Antibodies
- •3.2.1.4 Antineutrophil Cytoplasmic Antibodies
- •3.2.1.5 Circulating Immune Complexes
- •Fluid-Phase Binding Assays
- •C1q-Binding Assay
- •Cell-Binding Assays
- •Raji Cell-Binding Assay
- •3.2.1.6 Complement
- •Quantitation Tests
- •Functional Tests
- •3.2.1.7 HLA Typing
- •3.2.1.8 Antibody Titers Against Infectious Organisms
- •3.2.1.9 Interferon-Gamma Release Assays (IGRAs)
- •3.2.2 Anterior Chamber Polymerase Chain Reaction Testing
- •3.2.3 Smears and Cultures
- •3.2.4 Skin Testing
- •3.2.5 Radiologic Studies
- •3.2.6.1 Anterior Segment Fluorescein Angiography Techniques
- •3.2.6.2 Normal Anterior Segment Fluorescein Angiography
- •Arterial Phase
- •Capillary Phase
- •Venous Phase
- •3.2.7 Anterior Segment Indocyanine Green Angiography
- •3.2.8 Other Imaging Studies
- •3.2.8.1 Ultrasonography
- •A-Scan Ultrasonography
- •B-Scan Ultrasonography
- •High-Frequency Ultrasound Biomicroscopy
- •3.2.8.2 Optical Coherence Tomography
- •3.2.8.3 Computer Tomography Scanning
- •3.2.8.4 Magnetic Resonance Imaging
- •3.3 Biopsy
- •3.3.1 Biopsy for Suspected Systemic Vasculitic Disease
- •3.4 Data Integration: Diagnosis
- •3.5 Therapeutic Plan
- •3.6 Summary
- •References
- •4.1 Episcleritis
- •4.1.1 Introduction
- •4.1.2 Patient Characteristics
- •4.1.3 Clinical Manifestations
- •4.1.4.1 Simple Episcleritis
- •4.1.4.2 Nodular Episcleritis
- •4.1.5 Associated Diseases
- •4.1.6 Precipitating Factors
- •4.2 Scleritis
- •4.2.1 Introduction
- •4.2.2 Patient Characteristics
- •4.2.3 Clinical Manifestations
- •4.2.4.1 Diffuse Anterior Scleritis
- •4.2.4.2 Nodular Anterior Scleritis
- •Differential Diagnosis
- •Paralimbic Scleromalacia
- •Senile Scleral Hyaline Plaques
- •4.2.4.5 Posterior Scleritis
- •Symptoms and Signs
- •Fundus Findings
- •Choroidal Folds
- •Subretinal Mass
- •Disk Edema and Macular Edema
- •Annular Ciliochoroidal Detachment and Serous Retinal Detachment
- •Associated Diseases
- •Complications
- •Ancillary Tests
- •Ultrasonography
- •Computerized Tomography (CT) Scanning
- •Fluorescein Angiography
- •Differential Diagnosis
- •Proptosis, Chemosis, Lid Swelling, and Limitation of Ocular Movements
- •Subretinal Mass
- •Choroidal Folds
- •Annular Ciliochoroidal Detachment and/or Serous Retinal Detachment
- •Disk and Macular Edema
- •4.2.5 Associated Diseases
- •4.2.6 Complications of Scleritis
- •4.2.6.1 Keratopathy
- •Peripheral Corneal Thinning
- •Stromal Keratitis
- •Peripheral Ulcerative Keratitis
- •4.2.6.2 Uveitis
- •4.2.6.3 Glaucoma
- •Angle-Closure Glaucoma
- •Open-Angle Glaucoma
- •Neovascular Glaucoma
- •4.2.6.4 Cataract
- •4.3 Summary
- •References
- •5: Pathology in Scleritis
- •5.1.3 Fibrinoid Necrosis
- •5.2.1 Pathology of Episcleritis
- •5.2.2 Pathology of Scleritis
- •5.2.2.1 Noninfectious Scleritis
- •Sclera
- •Cells
- •Extracellular Matrix
- •Vessels
- •Episclera
- •Conjunctiva
- •Iris, Ciliary Body, and Choroid
- •Cornea
- •Other Ocular Structures
- •Polyarteritis Nodosa
- •Allergic Granulomatous Angiitis (Churg–Strauss Syndrome)
- •Granulomatosis with Polyangiitis (Wegener)
- •Connective Tissue Diseases
- •Clinicopathological Correlates in Infectious Scleritis
- •Systemic Infections
- •Local Infections
- •5.3 Biopsy
- •5.3.1 Noninfectious Necrotizing Scleritis
- •5.3.2 Noninfectious Recurrent Diffuse or Nodular (Nonnecrotizing) Scleritis
- •5.3.3 Infectious Scleritis (Diffuse, Nodular, or Necrotizing Scleritis)
- •5.3.4 Biopsy Technique
- •5.4 Summary
- •References
- •6: Noninfectious Scleritis
- •6.1.1 Adult Rheumatoid Arthritis
- •6.1.1.1 Epidemiology
- •Signs and Symptoms of Joint Involvement
- •Extraarticular Systemic Manifestations
- •6.1.1.2 Systemic Manifestations
- •Onset
- •Tegument
- •Vessels
- •Lung
- •Heart
- •Nervous System
- •Lymph Nodes
- •Larynx
- •Felty’s Syndrome
- •Amyloidosis
- •Miscellaneous
- •6.1.1.3 Ocular Manifestations
- •Keratoconjunctivitis Sicca
- •Scleritis
- •Keratitis
- •Anterior Uveitis
- •Glaucoma
- •Cataract
- •Retinal, Choroidal, and Optic Nerve Changes
- •Motility Disturbances
- •Episcleritis
- •6.1.1.4 Laboratory Findings
- •Rheumatoid Factor
- •Antibodies to Cyclic Citrullinated Polypeptides
- •Complete Blood Count
- •Acute-Phase Reactants
- •Synovial Fluid Analysis
- •Circulating Immune Complexes
- •Antinuclear Antibodies
- •Complement
- •Cryoglobulins
- •Radiographic Evaluation
- •Diagnosis
- •6.1.2 Systemic Lupus Erythematosus
- •6.1.2.1 Epidemiology
- •6.1.2.2 Systemic Manifestations
- •Musculoskeletal
- •Tegument
- •Vessels
- •Kidney
- •Hearth
- •Nervous System
- •Lung
- •Miscellaneous
- •6.1.2.3 Ocular Involvement
- •Scleritis
- •Episcleritis
- •Other Ocular Findings
- •6.1.2.4 Laboratory Findings
- •6.1.2.5 Diagnosis
- •6.1.3 Ankylosing Spondylitis
- •6.1.3.1 Epidemiology
- •6.1.3.2 Systemic Manifestations
- •Articular Involvement
- •Extraarticular Systemic Manifestations
- •6.1.3.3 Ocular Manifestations
- •Anterior Uveitis
- •Scleritis
- •Episcleritis
- •6.1.3.5 Diagnosis
- •6.1.4 Reactive Arthritis (Reiter)
- •6.1.4.1 Epidemiology
- •6.1.4.2 Systemic Manifestations
- •Articular Involvement
- •Extraarticular Systemic Manifestations
- •6.1.4.3 Ocular Manifestations
- •Conjunctivitis
- •Anterior Uveitis
- •Scleritis
- •Episcleritis
- •Other Ocular Findings
- •6.1.4.4 Laboratory and Radiographic Findings
- •6.1.4.5 Diagnosis
- •6.1.5 Psoriatic Arthritis
- •6.1.5.1 Epidemiology
- •6.1.5.2 Systemic Manifestations
- •Skin and Articular Involvement
- •6.1.5.3 Ocular Manifestations
- •Scleritis
- •Episcleritis
- •6.1.5.4 Laboratory and Radiographic Findings
- •6.1.5.5 Diagnosis
- •6.1.6.1 Epidemiology
- •6.1.6.2 Systemic Manifestations
- •Gastrointestinal and Articular Manifestations
- •6.1.6.3 Ocular Manifestations
- •Anterior Uveitis
- •Scleritis
- •Episcleritis
- •Keratitis
- •6.1.6.4 Laboratory and Joint Radiologic Findings
- •6.1.6.5 Diagnosis
- •6.1.7 Relapsing Polychondritis
- •6.1.7.1 Epidemiology
- •6.1.7.2 Systemic Manifestations
- •6.1.7.3 Ocular Manifestations
- •Scleritis
- •Episcleritis
- •6.1.7.4 Laboratory Findings
- •6.1.7.5 Diagnosis
- •6.1.8 Polyarteritis Nodosa
- •6.1.8.1 Epidemiology
- •6.1.8.2 Systemic Manifestations
- •6.1.8.3 Ocular Manifestations
- •Scleritis
- •Episcleritis
- •6.1.8.4 Laboratory and Angiographic Findings
- •6.1.8.5 Diagnosis
- •6.1.9.1 Epidemiology
- •6.1.9.2 Systemic Manifestations
- •6.1.9.3 Ocular Manifestations
- •6.1.9.4 Laboratory Findings
- •6.1.9.5 Diagnosis
- •6.1.10 Granulomatosis with Polyangiitis (Wegener)
- •6.1.10.1 Epidemiology
- •6.1.10.2 Clinical Manifestations
- •6.1.10.3 Ocular Manifestations
- •Scleritis
- •Episcleritis
- •6.1.10.4 Laboratory Findings
- •6.1.10.5 Diagnosis
- •6.1.11 Adamantiades–Behçet’s Disease
- •6.1.11.1 Epidemiology
- •6.1.11.2 Systemic Manifestations
- •6.1.11.3 Ocular Manifestations
- •Scleritis
- •Episcleritis
- •6.1.11.4 Laboratory Findings
- •6.1.11.5 Diagnosis
- •6.1.12 Giant-Cell Arteritis
- •6.1.12.1 Epidemiology
- •6.1.12.2 Systemic Manifestations
- •6.1.12.3 Ocular Manifestations
- •Scleritis
- •6.1.12.4 Laboratory Findings
- •6.1.12.5 Diagnosis
- •6.1.13 Cogan’s Syndrome
- •6.1.13.1 Clinical Manifestations
- •Scleritis
- •Episcleritis
- •6.1.13.2 Laboratory Findings
- •6.2.1 Rosacea
- •6.3.1 Gout
- •6.5 Chemical Injury-Associated Scleritis
- •6.6 Summary
- •References
- •7: Infectious Scleritis
- •7.1 Bacterial Scleritis
- •7.1.1.1 Pathogenesis
- •7.1.1.2 Organisms
- •7.1.1.3 Management
- •7.1.1.4 Therapy
- •7.1.1.5 Prognosis
- •7.1.1.6 Our Experience
- •7.1.2 Mycobacterial Scleritis
- •7.1.2.1 Atypical Mycobacterial Disease
- •7.1.2.2 Tuberculosis
- •7.1.2.3 Leprosy
- •7.1.3 Spirochetal Scleritis
- •7.1.3.1 Syphilis
- •Epidemiology
- •Pathogenesis and Clinical Features
- •Scleritis and Episcleritis
- •Diagnosis
- •Therapy
- •7.1.3.2 Lyme Disease
- •Epidemiology
- •Pathogenesis and Clinical Features
- •Scleritis and Episcleritis
- •Diagnosis
- •7.1.3.3 Treatment
- •7.1.4 Chlamydial Scleritis
- •7.1.5 Actinomycetic Scleritis
- •7.1.5.1 Nocardiosis
- •7.2 Fungal Scleritis
- •7.2.1 Filamentous and Dimorphic Fungal Scleritis
- •7.2.1.1 Pathogenesis
- •7.2.1.2 Organisms
- •7.2.1.3 Management
- •7.2.1.4 Therapy
- •7.2.1.5 Our Experience
- •7.3 Viral Scleritis
- •7.3.1 Herpes Scleritis
- •7.3.1.1 Herpes Zoster Scleritis
- •Epidemiology
- •Pathogenesis
- •Clinical Features
- •Scleritis
- •Episcleritis
- •Diagnosis
- •Treatment
- •7.3.1.2 Herpes Simplex Scleritis
- •Epidemiology
- •Pathogenesis
- •Clinical Features
- •Scleritis
- •Episcleritis
- •Diagnosis
- •Therapy
- •Our Experience
- •7.3.2 Mumps Scleritis
- •7.4 Parasitic Scleritis
- •7.4.1 Protozoal Scleritis
- •7.4.1.1 Acanthamoeba
- •7.4.1.2 Toxoplasmosis
- •7.4.2 Helminthic Scleritis
- •7.4.2.1 Toxocariasis
- •7.5 Summary
- •References
- •8.1 Scleral Deposits
- •8.1.1 Scleral Protein Deposition
- •8.1.1.1 Porphyria
- •8.1.1.2 Cystinosis
- •8.1.1.3 Alkaptonuria
- •8.1.1.4 Amyloidosis
- •8.1.2 Scleral Lipid Deposition
- •8.1.2.1 Familial Hypercholesterolemia and Histiocytosis X
- •8.1.2.2 Age-Related Degeneration
- •8.1.3 Scleral Carbohydrate Deposition
- •8.1.3.1 Mucopolysaccharidosis
- •8.1.4 Scleral Mineral Deposition: Calcium
- •8.1.4.1 Hyperparathyroidism
- •8.1.4.2 Other Causes of Hypercalcemia
- •8.1.4.3 Age-Related Degeneration
- •Senile Scleral Hyaline Plaques
- •8.1.5 Scleral Pigment Deposition: Bilirubin
- •8.1.5.1 Jaundice
- •8.2 Scleral Thinning (Blue Sclerae)
- •8.2.1 Scleral Thinning in Inherited or Congenital Diseases
- •8.2.1.1 Marfan’s Syndrome
- •8.2.1.2 Osteogenesis Imperfecta
- •8.2.1.3 Pseudoxanthoma Elasticum
- •8.2.1.4 Ehlers–Danlos Syndrome
- •8.2.1.5 Keratoconus
- •8.2.1.6 Buphthalmos
- •8.2.1.7 Coloboma
- •8.2.1.8 Myopia
- •8.2.2 Scleral Thinning in Acquired Diseases
- •8.2.2.2 Paralimbal Scleromalacia
- •8.3 Scleral Thickening
- •8.3.1 Nanophthalmos
- •8.3.2 Scleropachynsis
- •8.3.3 Phthisis Bulbi
- •8.4 Scleral Tumors
- •8.4.1 Dermoid Choristomas
- •8.4.2 Epithelial Tumors
- •8.4.2.1 Papillomas or Intraepithelial Epitheliomas
- •8.4.2.2 Squamous Cell Carcinoma
- •8.4.3 Dense Connective Tissue Tumors
- •8.4.3.1 Nodular Fasciitis
- •8.4.3.2 Fibroma
- •8.4.3.3 Fibrous Histiocytoma
- •8.4.3.4 Sarcomas
- •8.4.4 Vascular Tumors
- •8.4.4.1 Hemangiomas
- •8.4.4.2 Lymphangiomas
- •8.4.5 Blood Cell Tumors
- •8.4.5.1 Leukemia
- •8.4.5.2 Lymphoma and Lymphosarcoma
- •8.4.6 Nervous Tumors
- •8.4.6.2 Neurilemmoma (Schwannoma)
- •8.4.7 Pigmented Tumors
- •8.4.7.1 Nevus
- •8.4.7.2 Melanocytoma
- •8.4.8 Secondary Tumors
- •8.5 Summary
- •References
- •9.1 Treatment of Episcleritis
- •9.2 Treatment of Scleritis
- •9.2.1 Medical Treatment
- •9.2.1.1 Rheumatoid Arthritis
- •9.2.1.2 Systemic Lupus Erythematosus
- •9.2.1.3 Polyarteritis Nodosa
- •9.2.1.4 Granulomatosis with Polyangiitis (Wegener)
- •9.2.1.5 Relapsing Polychondritis
- •9.2.1.7 Posterior Scleritis
- •9.2.1.8 Infectious Scleritis
- •9.2.2 Ancillary Therapy
- •9.2.3 Drug Management Responsibility
- •9.2.4 Surgical Treatment
- •9.3 Summary
- •References
- •Index
86 |
3 Diagnostic Approach of Episcleritis and Scleritis |
|
|
and retrobulbar edema are the main Þndings in posterior scleritis (Fig. 3.27) [118Ð121]. Occasionally, retinal or choroidal detachment also may be detected (Fig. 3.28). The combination of both A scan and B scan techniques simultaneously produces the most useful results in distinguishing posterior scleritis from orbital, choroidal, and retinal diseases, which clinically may mimic posterior scleritis [119].
A-Scan Ultrasonography
The A scan technique shows one-dimensional timeÐamplitude representations of echoes received along the beam path. The echoes appear as vertical deßections rising from a horizontal zero line. In the axial A echogram of the normal eye, high echoes are produced by the two corneal surfaces, two lens surfaces, and vitreoretinal interface. The vitreoretinal interface echo is followed by a complex of echoes representing retina, choroid, sclera, and retrobulbar fat. Posterior scleral thickening due to inßammation can be detected by high-amplitude continuous spikes.
Fig. 3.29 Computrized tomogram demonstrating opaciÞcation of the left maxillary sinus in this patient with WegenerÕs granulomatosis
B-Scan Ultrasonography
The B scan technique combines transducer scanning and electronic processing to produce two-dimensional cross-section images of the eye along any desired scan plane. The echoes are presented as dots instead of spikes. In the axial B echogram of the normal eye, echoes are produced by the anterior and posterior surface of the cornea separated by a sonolucent interval representing the corneal stroma, by the anterior surface of the iris, by the posterior surface of the iris merging with the anterior lens surface, and by the vitreoretinal interface. In the normal eye, echoes from the retina cannot be separated from echoes from the choroid and the sclera. Posterior scleral thickening due to inßammation can be detected by multiple reßections of the sound beam. The echoes remain after sound beam attenuation, indicating high internal reßectivity caused by multiple, relatively ßat interfaces. If retrobulbar edema surrounds the optic nerve, the ÒTÓ sign, which consists of squaring off of the normally rounded optic
nerve shadow with extension of the edema along the adjacent sclera, is seen.
High-Frequency Ultrasound Biomicroscopy
High-frequency (50Ð100 MHz) ultrasound biomicroscopy (UBM) produces high-resolution subsurface images of the eye at microscopic resolution which are four to six times greater than that of conventional ultrasound. UBM provides information on structural changes in the anterior episclera and sclera, as well as the underlying choroid, retina, and vitreous in the anterior part of the posterior segment.
3.2.8.2 Optical Coherence Tomography
Polarization-sensitive optical coherence tomography (central wavelength: 1,310 nm; A-line rate: 20 kHz) evaluates the three-dimensional structure of the anterior eye segment with the phase retardation associated with the anterior segment birefringence of the eyes. In normal sclera, a striking polarization change is observed
3.2 Diagnostic Tests |
87 |
|
|
Fig. 3.30 Magnetic resonance imaging (MRI) scan demonstrating retrobulbar Òbright zonesÓ characteristic of inßammatory pseudotumor
in the cumulative-phase retardation images, whereas in necrotizing scleritis phase retardation is low, implying diffuse destruction of the collagen tissue.
3.2.8.3 Computer Tomography Scanning
Routine ocular computerized tomography scans consist of multiple axial ÒcutsÓ at different levels of the orbit. Eye, orbital walls, extraocular muscles, and paranasal sinuses are, therefore, sectioned longitudinally in the horizontal plane [122]. The ability of the X-ray CT to delineate small, soft tissues of different densities makes it a useful diagnostic tool to detect extraocular muscle or lacrimal gland enlargement, sinus tissue involvement (Fig. 3.29), or posterior scleral thickening [119, 123], which are important features for the differential diagnosis of posterior scleritis from orbital inßammatory diseases and orbital neoplasms [123Ð125]. Radiopaque medium may be injected during the scan to enhance the detection of scleral thickening. The primary disadvantages of CT scanning are poor contrast between some soft tissues,
Fig. 3.31 Magnetic resonance imaging scan in a patient ultimately shown to have systemic lupus erythematosus. Note the T2 bright spots indicative of microinfarcts compatible with a microangiitis
radiation hazard (orbital CT scan: 2Ð3 rads, depending on the slice thickness and the number of cuts made; this is similar to an orbital series of skull X-rays), and lack of scanning in the sagittal plane.
3.2.8.4 Magnetic Resonance Imaging
The most frequent atomic nucleus in living tissue is the hydrogen nucleus. The hydrogen nucleus is composed of a single proton, which has a positive electrical charge and spins on its axis. A magnetic Þeld is generated around this rotating electrical charge. The magnetic resonance imaging (MRI) technique is based on two different tissue properties: the density of hydrogen nuclei present in the tissue and the spin-relaxation rates [122]. MRI provides superior soft tissue contrast compared to CT scanning.
Differentiation of localized inßammatory pseudotumor from posterior scleritis in patients with proptosis (Fig. 3.30) or choroidal tumors from posterior scleritis in patients with a subreti-
