- •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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Three-dimensional images combine a series of CT slices into a surface-rendered volume. The most widely used technique is shaded surface display (SSD). Here, threedimensional (3D) volume data are represented in a two-dimensional plane, displaying spatial relationships with visual depth cues. The computer algorithm determines which pixels within the volume data are displayed and how they are spatially related to other pixels in the volume set. In SSD, surfaces are modeled as a number of overlapping polygons, with surface shading added, and a virtual light source is computed for each. More sophisticated programs allow the surface models to be repositioned and manipulated. With surface rendering algorithms, interior structures are not visible (Fig. 9.4).
Volume rendering is a technique by which selected surfaces can be defined by a threshold density and overlying tissues can be made semitransparent. Transparency and colors are used to represent specific volumes. This technique allows 3D reconstructions that allow exceptional evaluation of skull anomalies, fractures, and other bony lesions.
Fig. 9.4 T hree-dimensional reconstructed CT image of a patient with fibrous dysplasia of the left face and orbit
Magnetic resonance imaging offers several advantages over CT for orbital disease [6]. Because of the low resonance signal generated from bone, soft tissue visualization in the region of the orbital apex, optic canal, and cavernous sinus is not degraded by dense surrounding bone as in CT scans [4, 11, 12]. However, because of the low signal generated by bone and foreign bodies, these structures are not well imaged on MRI. Manipulation of resonance signals from various tissues provides contrast variability and a level of tissue differentiation unobtainable with any CT technique. This is particularly useful for neural tissues such as the optic nerve and brain. Surface coil technology, improvements in signal-to-noise ratios, and techniques for suppressing the high-fat signal on T1-weighted (T1-WI) images have greatly improved visualization of many orbital lesions [14–17].
The major component of the MRI system is the magnet that provides the primary polarizing field. Located within the bore of the magnet are gradient coils that provide the spatial localization information during the imaging process. Within the gradient coils are the radio-frequency (RF) antennae (“coils”), which transmit the RF energy to the tissues and receive the returning resonance signals. The use of smaller surface coils placed immediately over the area of interest increases the signal strength and increases the sig- nal-to-noise ratio. These permit acquisition of the highresolution images of modern scanners. However, such coils are limited in the depth of penetration they can image, and they are associated with some artifact.
The generation of a magnetic resonance signal depends on the presence of magnetic isotopes of common elements in biological tissues. The atom most frequently imaged is the ubiquitous hydrogen nucleus, or proton [13]. All protons are normally in a state of axial spin. This spinning charged particle generates a magnetic field, with north and south poles. Under normal conditions, all the nuclei in a given volume of tissue are randomly oriented, but when placed within a strong external magnetic field the individual protons align with the external magnetic direction (Fig. 9.5a). Most of the axes of individual protons lie at various small angles to the external magnetic moment, and they are equally distributed 360° around it. Like spinning tops, these inclined axes wobble, or precess, around the mean magnetic direction (Fig. 9.5a). The rotating axes therefore describe a conical surface with angular momentum determined by the strength of the external magnetic field and by an intrinsic property of the particular type of atomic nucleus. The resultant angular velocity of precession is called the Larmor frequency.
When this system is exposed to an external RF pulse at the Larmor frequency, energy is absorbed by the atomic
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nuclei, and the spinning nuclei move into higher energy levels. The angular orientation of their axes with respect to the external magnetic direction increases, and in so doing they tilt away from the magnetic axis and into a plane perpendicular to it (Fig. 9.5b). In addition, the individual atomic axes group to one side of the external magnetic direction. When the RF signal is turned off, the precessing nuclei return to equilibrium by giving up energy to the environment at the specific Larmor frequency. Return to equilibrium occurs by two simultaneous decay, or relaxation, processes, which are detected as resonance signals.
9.3.1 The T1 Constant
During the T1 relaxation, the nuclear axes realign into an orientation parallel to the external magnetic direction as the spinning protons gradually give up their absorbed energy to the environment [18] (Fig. 9.5c, d). The time
Mz
T1 relaxation time
Time
Fig. 9.6 T he T1 relaxation or decay is represented as a timedependent asymptotic curve as energy is given up to the environment
required for completion of this process is an exponential rate called the T1 time (Fig. 9.6). It is influenced by the interaction of the proton with other atoms bound to the
9.3 Magnetic Resonance Imaging |
131 |
Table 9.3. Characteristic signal intensities of normal orbital and periorbital structures on magnetic resonance imaging
Tissue |
T1-WI |
T2-WI |
Air |
Very dark |
Very dark |
Blood, acute |
Dark to intermediate |
Dark |
Blood, chronic |
Dark rim with variable center |
Dark rim with variable center |
Blood, hyperacute |
Intermediate |
Intermediate |
Blood, subacute |
Bright rim |
Bright |
Bone, cortical |
Very dark |
Very dark |
Bone, marrow |
Bright |
Intermediate |
Cortical gray matter |
Dark |
Bright |
CSF |
Very dark |
Very bright |
Fat |
Very bright |
Intermediate to dark |
Muscle |
Dark |
Dark |
Optic nerve |
Dark to intermediate |
Intermediate |
Proteinaceous fluid |
Intermediate to bright |
Very bright |
Sclera |
Dark to intermediate |
Intermediate |
Vitreous |
Dark |
Bright |
Water |
Very dark |
Very bright |
White matter |
Bright |
Dark |
T1-WI T1 weighted image, T2-WI T2 weighted image
molecular lattice, by temperature, and by viscosity of the tissue. At any specific time following the RF pulse, the total amount of energy given up by the spinning protons depends on the rate at which the T1 relaxation occurs. Tissues with a short T1 constant, such as fat, give up more resonant energy per unit time and therefore appear brighter on the final MR (magnetic resonance) image than tissues with longer T1 constants, such as muscle. This is the basis for contrast intensity, and specific orbital tissues will demonstrate characteristic T1 signal intensities (see Table 9.3).
time, and is influenced by the tiny magnetic fields generated around adjacent spinning nuclei (Fig. 9.8). As with T1 constants, biochemical differences between tissues confer slightly different T2 relaxation times to their protons. At any specific time following the RF pulse, tissues with long T2 constants, such as vitreous, maintain a greater transverse vector component than tissues with short T2 constants, such as muscle. This greater transverse vector produces a higher signal and is therefore brighter on the final MR image.
9.3.2 The T2 Constant
Immediately following the RF pulse, the atomic nuclei are grouped on one side of the mean magnetic axis (Fig. 9.7a). As they rotate, they generate an RF signal as they cut across the external magnetic field and thus generate a small alternating current voltage. During the T2 relaxation, the atomic nuclei redistribute themselves evenly 360° around the external magnetic field direction (Fig. 9.7b). As they do so, the strength of this induced signal decreases because of the increasing canceling vectors. The time for complete decay of this signal (i.e., even distribution of magnetic moments) is the T2, or spin–spin relaxation
9.3.3Creating the MR Image
The signals generated by the T1 relaxation and the T2 decay are measured by RF detectors. They will detect in mass fashion all similar signals at the Larmor frequency, regardless of their specific location within the tissue. Spatial encoding of resonant signals from particular small volumes of tissue is necessary for the creation of a meaningful two-dimensional image. This is achieved by deformation of the external magnetic field using gradient coils, such that the protons in every small volume of examined tissue (voxel) has a unique magnetic field strength and therefore a unique Larmor frequency. The detected Larmor frequency therefore will identify the precise
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Fig. 9.7 (a, b) When exposed to the RF pulse, the proton magnetic moments group to one side of the external magnetic field direction. When the RF signal is removed, the moments redistribute themselves 360° around the external field by T2 relaxation
T2relaxation time
Signal
Time
Fig. 9.8 T he T2 relaxation is represented as a time-dependent asymptotic curve as energy is given up and the signal decays to zero
location of the signal, and a topographic image can be created.
The final MR image is determined by the proton density and by the variations in the T1 and T2 decay constants of specific tissue components. The T1 and T2 resonance signals can be manipulated by application of various pulsed sequences, thus altering the way the signals are collected. The MR image can therefore be weighted in favor of the T1 or the T2 information (Fig. 9.9a, b). In a T1 image, the vitreous is imaged as a dark hypointense signal compared to fat, which shows a bright hyperintense signal. On a T2 scan, the vitreous is typically bright, and the fat is dark (Fig. 9.10a, b). Pathologic lesions in the orbit often show distinctive T1 and T2 imaging characteristics that can help distinguish them from other lesions (Table 9.4) [31].
Gadolinium is a rare earth element with paramagnetic properties. In the presence of an external magnetic
a
b
Fig. 9.9 (a) Coronal T1 MRI image of a patient with a lymphoma of the medial right orbit; the lesion is isointense to normal muscle. (b) Axial T2 MRI scan of a different patient showing a lateral orbital lymphoma that is homogeneous and slightly hyperintense to muscle
9.3 Magnetic Resonance Imaging |
133 |
a |
b |
Fig. 9.10 (a) Axial T1-weighted image of a schwannoma in the right orbit that is mildly heterogeneous and hypointense. (b) T2 image of the same patient showing the lesion to be moderately hyperintense
Table 9.4. Characteristics of common orbital diseases on magnetic resonance imaging |
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Disease |
Compared to fat |
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Compared to muscle |
Gadolinium |
Texture |
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enhancement |
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T2-WI |
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T2-WI |
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Abscess |
Hypo |
Hyper |
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Hyper |
Hyper |
− |
Hetero |
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Adenoid cystic carcinoma |
Hypo |
Iso |
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Hyper |
Hyper |
++ |
Hetero |
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Alveolar soft part sarcoma |
Hypo |
Hyper |
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Iso |
Hyper |
+++ |
Hetero |
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Amyloidosis |
Hypo |
Hypo |
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Hypo |
Hypo |
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Hetero |
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Capillary hemangioma |
Hypo |
Hyper |
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Hyper |
Variable |
++ |
Homo/hetero |
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Cavernous hemangioma |
Hypo |
Hyper |
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Iso/hyper |
Hyper |
+ |
Homo/hetero |
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Cellulitis |
Hypo |
Hypo |
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Iso |
Hypo |
− |
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Dermoid cyst |
Hypo/iso |
Iso/hyper |
|
Hypo |
Iso |
− |
Home/hetero |
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Epithelial cyst |
Hypo |
Hypo |
|
Iso |
Iso |
− |
Homo |
||
Fibrous histiocytoma |
Hypo |
Iso/hyper |
|
Iso |
Hypo |
++ |
Hetero |
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Hemangiopericytoma |
Hypo |
Hyper |
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Iso |
Hypo |
++ |
Homo |
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Hematic cyst |
Hypo/iso |
Variable |
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Hypo |
Iso |
− |
Homo/hetero |
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Lymphangioma |
Hypo |
Hyper |
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Hyper |
Iso |
Variable |
Homo |
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Lymphoid neoplasm |
Hypo |
Iso/hyper |
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Iso |
Iso |
+++ |
Homo |
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Lymphoma |
Hypo |
Iso/hyper |
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Hyper |
Iso |
++ |
Homo |
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Metastases |
Hypo |
Hyper |
|
Iso |
Hyper |
Variable |
Homo/hetero |
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Mucocele |
Hypo/iso |
Hyper |
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Hypo/hyper |
Hyper |
− |
Homo/hetero |
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Neurofibroma |
Hypo |
Hyper |
|
Iso |
Hyper |
Variable |
Hetero/homo |
||
Optic nerve glioma |
Iso |
Hyper |
|
Iso |
Hyper |
++ |
Hetero |
||
Optic sheath meningioma |
Iso |
Hypo |
|
Iso |
Iso |
+++ |
Hetero |
||
Plexiform neurofibroma |
Hypo |
Hyper |
|
Hypo |
Hyper |
++ |
Hetero/homo |
||
Pseudotumor |
Hypo |
Hyper |
|
Iso |
Hyper |
++ |
Homo/hetero |
||
Rhabdomyosarcoma |
Hypo |
Hyper |
|
Iso |
Hyper |
+++ |
Homo/hetero |
||
Schwannoma |
Hypo |
Hyper |
|
Iso/hyper |
Hypo |
− |
Hetero |
||
Thyroid orbitopathy |
Hypo |
Hypo |
|
Iso/hyper |
Hyper |
+++ |
Homo |
||
Varix |
Hypo |
Hyper |
|
Iso |
Hypo |
+++ |
Homo |
||
hypo hypointense, hyper hyperintense, iso isointense, homo homogeneous, hetero heterogeneous, + mild, ++ moderate, +++ marked T1-WI T1 weighted image, T2-WI T2 weighted image
