- •Contents
- •Contributors
- •1 Introduction
- •2.1 Posterior Compartment
- •2.2 Anterior Compartment
- •2.3 Middle Compartment
- •2.4 Perineal Body
- •3 Compartments
- •3.1 Posterior Compartment
- •3.1.1 Connective Tissue Structures
- •3.1.2 Muscles
- •3.1.3 Reinterpreted Anatomy and Clinical Relevance
- •3.2 Anterior Compartment
- •3.2.1 Connective Tissue Structures
- •3.2.2 Muscles
- •3.2.3 Reinterpreted Anatomy and Clinical Relevance
- •3.2.4 Important Vessels, Nerves, and Lymphatics of the Anterior Compartment
- •3.3 Middle Compartment
- •3.3.1 Connective Tissue Structures
- •3.3.2 Muscles
- •3.3.3 Reinterpreted Anatomy and Clinical Relevance
- •3.3.4 Important Vessels, Nerves, and Lymphatics of the Middle Compartment
- •4 Perineal Body
- •References
- •MR and CT Techniques
- •1 Introduction
- •2.1 Introduction
- •2.2.1 Spasmolytic Medication
- •2.3.2 Diffusion-Weighted Imaging
- •2.3.3 Dynamic Contrast Enhancement
- •3 CT Technique
- •3.1 Introduction
- •3.2 Technical Disadvantages
- •3.4 Oral and Rectal Contrast
- •References
- •Uterus: Normal Findings
- •1 Introduction
- •References
- •1 Clinical Background
- •1.1 Epidemiology
- •1.2 Clinical Presentation
- •1.3 Embryology
- •1.4 Pathology
- •2 Imaging
- •2.1 Technique
- •2.2.1 Class I Anomalies: Dysgenesis
- •2.2.2 Class II Anomalies: Unicornuate Uterus
- •2.2.3 Class III Anomalies: Uterus Didelphys
- •2.2.4 Class IV Anomalies: Bicornuate Uterus
- •2.2.5 Class V Anomalies: Septate Uterus
- •2.2.6 Class VI Anomalies: Arcuate Uterus
- •2.2.7 Class VII Anomalies
- •References
- •Benign Uterine Lesions
- •1 Background
- •1.1 Uterine Leiomyomas
- •1.1.1 Epidemiology
- •1.1.2 Pathogenesis
- •1.1.3 Histopathology
- •1.1.4 Clinical Presentation
- •1.1.5 Therapy
- •1.1.5.1 Indications
- •1.1.5.2 Medical Therapy and Ablation
- •1.1.5.3 Surgical Therapy
- •1.1.5.4 Uterine Artery Embolization (UAE)
- •1.1.5.5 Magnetic Resonance-Guided Focused Ultrasound
- •2 Adenomyosis of the Uterus
- •2.1 Epidemiology
- •2.2 Pathogenesis
- •2.3 Histopathology
- •2.4 Clinical Presentation
- •2.5 Therapy
- •3 Imaging
- •3.2 Magnetic Resonance Imaging
- •3.2.1 Magnetic Resonance Imaging: Technique
- •3.2.2 MR Appearance of Uterine Leiomyomas
- •3.2.3 Locations, Growth Patterns, and Imaging Characteristics
- •3.2.4 Histologic Subtypes and Forms of Degeneration
- •3.2.5 Differential Diagnosis
- •3.2.6 MR Appearance of Uterine Adenomyosis
- •3.2.7 Locations, Growth Patterns, and Imaging Characteristics
- •3.2.8 Differential Diagnosis
- •3.3 Computed Tomography
- •3.3.1 CT Technique
- •3.3.2 CT Appearance of Uterine Leiomyoma and Adenomyosis
- •3.3.3 Atypical Appearances on CT and Differential Diagnosis
- •4.1 Indications
- •4.2 Technique
- •Bibliography
- •Cervical Cancer
- •1 Background
- •1.1 Epidemiology
- •1.2 Pathogenesis
- •1.3 Screening
- •1.4 HPV Vaccination
- •1.5 Clinical Presentation
- •1.6 Histopathology
- •1.7 Staging
- •1.8 Growth Patterns
- •1.9 Treatment
- •1.9.1 Treatment of Microinvasive Cervical Cancer
- •1.9.2 Treatment of Grossly Invasive Cervical Carcinoma (FIGO IB-IVA)
- •1.9.3 Treatment of Recurrent Disease
- •1.9.4 Treatment of Cervical Cancer During Pregnancy
- •1.10 Prognosis
- •2 Imaging
- •2.1 Indications
- •2.1.1 Role of CT and MRI
- •2.2 Imaging Technique
- •2.2.2 Dynamic MRI
- •2.2.3 Coil Technique
- •2.2.4 Vaginal Opacification
- •2.3 Staging
- •2.3.1 General MR Appearance
- •2.3.2 Rare Histologic Types
- •2.3.3 Tumor Size
- •2.3.4 Local Staging
- •2.3.4.1 Stage IA
- •2.3.4.2 Stage IB
- •2.3.4.3 Stage IIA
- •2.3.4.4 Stage IIB
- •2.3.4.5 Stage IIIA
- •2.3.4.6 Stage IIIB
- •2.3.4.7 Stage IVA
- •2.3.4.8 Stage IVB
- •2.3.5 Lymph Node Staging
- •2.3.6 Distant Metastases
- •2.4 Specific Diagnostic Queries
- •2.4.1 Preoperative Imaging
- •2.4.2 Imaging Before Radiotherapy
- •2.5 Follow-Up
- •2.5.1 Findings After Surgery
- •2.5.2 Findings After Chemotherapy
- •2.5.3 Findings After Radiotherapy
- •2.5.4 Recurrent Cervical Cancer
- •2.6.1 Ultrasound
- •2.7.1 Metastasis
- •2.7.2 Malignant Melanoma
- •2.7.3 Lymphoma
- •2.8 Benign Lesions of the Cervix
- •2.8.1 Nabothian Cyst
- •2.8.2 Leiomyoma
- •2.8.3 Polyps
- •2.8.4 Rare Benign Tumors
- •2.8.5 Cervicitis
- •2.8.6 Endometriosis
- •2.8.7 Ectopic Cervical Pregnancy
- •References
- •Endometrial Cancer
- •1.1 Epidemiology
- •1.2 Pathology and Risk Factors
- •1.3 Symptoms and Diagnosis
- •2 Endometrial Cancer Staging
- •2.1 MR Protocol for Staging Endometrial Carcinoma
- •2.2.1 Stage I Disease
- •2.2.2 Stage II Disease
- •2.2.3 Stage III Disease
- •2.2.4 Stage IV Disease
- •4 Therapeutic Approaches
- •4.1 Surgery
- •4.2 Adjuvant Treatment
- •4.3 Fertility-Sparing Treatment
- •5.1 Treatment of Recurrence
- •6 Prognosis
- •References
- •Uterine Sarcomas
- •1 Epidemiology
- •2 Pathology
- •2.1 Smooth Muscle Tumours
- •2.2 Endometrial Stromal Tumours
- •3 Clinical Background
- •4 Staging
- •5 Imaging
- •5.1 Leiomyosarcoma
- •5.2.3 Undifferentiated Uterine Sarcoma
- •5.3 Adenosarcoma
- •6 Prognosis and Treatment
- •References
- •1.1 Anatomical Relationships
- •1.4 Pelvic Fluid
- •2 Developmental Anomalies
- •2.1 Congenital Abnormalities
- •2.2 Ovarian Maldescent
- •3 Ovarian Transposition
- •References
- •1 Introduction
- •4 Benign Adnexal Lesions
- •4.1.1 Physiological Ovarian Cysts: Follicular and Corpus Luteum Cysts
- •4.1.1.1 Imaging Findings in Physiological Ovarian Cysts
- •4.1.1.2 Differential Diagnosis
- •4.1.2 Paraovarian Cysts
- •4.1.2.1 Imaging Findings
- •4.1.2.2 Differential Diagnosis
- •4.1.3 Peritoneal Inclusion Cysts
- •4.1.3.1 Imaging Findings
- •4.1.3.2 Differential Diagnosis
- •4.1.4 Theca Lutein Cysts
- •4.1.4.1 Imaging Findings
- •4.1.4.2 Differential Diagnosis
- •4.1.5 Polycystic Ovary Syndrome
- •4.1.5.1 Imaging Findings
- •4.1.5.2 Differential Diagnosis
- •4.2.1 Cystadenoma
- •4.2.1.1 Imaging Findings
- •4.2.1.2 Differential Diagnosis
- •4.2.2 Cystadenofibroma
- •4.2.2.1 Imaging Features
- •4.2.3 Mature Teratoma
- •4.2.3.1 Mature Cystic Teratoma
- •Imaging Findings
- •Differential Diagnosis
- •4.2.3.2 Monodermal Teratoma
- •Imaging Findings
- •4.2.4 Benign Sex Cord-Stromal Tumors
- •4.2.4.1 Fibroma and Thecoma
- •Imaging Findings
- •4.2.4.2 Sclerosing Stromal Tumor
- •Imaging Findings
- •4.2.5 Brenner Tumors
- •4.2.5.1 Imaging Findings
- •4.2.5.2 Differential Diagnosis
- •5 Functioning Ovarian Tumors
- •References
- •1 Introduction
- •2.1 Context
- •2.2.2 Indications According to Simple Rules
- •References
- •CT and MRI in Ovarian Carcinoma
- •1 Introduction
- •2.1 Familial or Hereditary Ovarian Cancers
- •3 Screening for Ovarian Cancer
- •5 Tumor Markers
- •6 Clinical Presentation
- •7 Imaging of Ovarian Cancer
- •7.1.2 Peritoneal Carcinomatosis
- •7.1.3 Ascites
- •7.3 Staging of Ovarian Cancer
- •7.3.1 Staging by CT and MRI
- •Imaging Findings According to Tumor Stages
- •Value of Imaging
- •7.3.2 Prediction of Resectability
- •7.4 Tumor Types
- •7.4.1 Epithelial Ovarian Cancer
- •High-Grade Serous Ovarian Cancer
- •Low-Grade Serous Ovarian Cancer
- •Mucinous Epithelial Ovarian Cancer
- •Endometrioid Ovarian Carcinomas
- •Clear Cell Carcinomas
- •Imaging Findings of Epithelial Ovarian Cancers
- •Differential Diagnosis
- •Borderline Tumors
- •Imaging Findings
- •Differential Diagnosis
- •Recurrent Ovarian Cancer
- •Imaging Findings
- •Differential Diagnosis
- •Value of Imaging
- •Malignant Germ Cell Tumors
- •Dysgerminomas
- •Imaging Findings
- •Differential Diagnosis
- •Immature Teratomas
- •Imaging Findings
- •Malignant Transformation in Benign Teratoma
- •Imaging Findings
- •Differential Diagnosis
- •Sex-Cord Stromal Tumors
- •Granulosa Cell Tumors
- •Imaging Findings
- •Sertoli-Leydig Cell Tumor
- •Imaging Findings
- •Ovarian Lymphoma
- •Imaging Findings
- •Differential Diagnosis
- •7.4.3 Ovarian Metastases
- •Imaging Findings
- •Differential Diagnosis
- •7.5 Fallopian Tube Cancer
- •7.5.1 Imaging Findings
- •Differential Diagnosis
- •References
- •Endometriosis
- •1 Introduction
- •2.1 Sonography
- •3 MR Imaging Findings
- •References
- •Vagina and Vulva
- •1 Introduction
- •3.1 CT Appearance
- •3.2 MRI Protocol
- •3.3 MRI Appearance
- •4.1 Imperforate Hymen
- •4.2 Congenital Vaginal Septa
- •4.3 Vaginal Agenesis
- •5.1 Vaginal Cysts
- •5.1.1 Gardner Duct Cyst (Mesonephric Cyst)
- •5.1.2 Bartholin Gland Cyst
- •5.2.1 Vaginal Infections
- •5.2.1.1 Vulvar Infections
- •5.2.1.2 Vulvar Thrombophlebitis
- •5.3 Vulvar Trauma
- •5.4 Vaginal Fistula
- •5.5 Post-Radiation Changes
- •5.6 Benign Tumors
- •6.1 Vaginal Malignancies
- •6.1.1 Primary Vaginal Carcinoma
- •6.1.1.1 MRI Findings
- •6.1.1.2 Lymph Node Drainage
- •6.1.1.3 Recurrence and Complications
- •6.1.2 Non-squamous Cell Carcinomas of the Vagina
- •6.1.2.1 Adenocarcinoma
- •6.1.2.2 Melanoma
- •6.1.2.3 Sarcomas
- •6.1.2.4 Lymphoma
- •6.2 Vulvar Malignancies
- •6.2.1 Vulvar Carcinoma
- •6.2.2 Melanoma
- •6.2.3 Lymphoma
- •6.2.4 Aggressive Angiomyxoma of the Vulva
- •7 Vaginal Cuff Disease
- •7.1 MRI Findings
- •8 Foreign Bodies
- •References
- •Imaging of Lymph Nodes
- •1 Background
- •3 Technique
- •3.1.1 Intravenous Unspecific Contrast Agents
- •3.1.2 Intravenous Tissue-Specific Contrast Agents
- •References
- •1 Introduction
- •2.1.1 Imaging Findings
- •2.1.2 Differential Diagnosis
- •2.1.3 Value of Imaging
- •2.2 Pelvic Inflammatory
- •2.2.1 Imaging Findings
- •2.3 Hydropyosalpinx
- •2.3.1 Imaging Findings
- •2.3.2 Differential Diagnosis
- •2.4 Tubo-ovarian Abscess
- •2.4.1 Imaging Findings
- •2.4.2 Differential Diagnosis
- •2.4.3 Value of Imaging
- •2.5 Ovarian Torsion
- •2.5.1 Imaging Findings
- •2.5.2 Differential Diagnosis
- •2.5.3 Diagnostic Value
- •2.6 Ectopic Pregnancy
- •2.6.1 Imaging Findings
- •2.6.2 Differential Diagnosis
- •2.6.3 Value of Imaging
- •3.1 Pelvic Congestion Syndrome
- •3.1.1 Imaging Findings
- •3.1.2 Differential Diagnosis
- •3.1.3 Value of Imaging
- •3.2 Ovarian Vein Thrombosis
- •3.2.1 Imaging Findings
- •3.2.2 Differential Diagnosis
- •3.2.3 Value of Imaging
- •3.3 Appendicitis
- •3.3.1 Imaging Findings
- •3.3.2 Value of Imaging
- •3.4 Diverticulitis
- •3.4.1 Imaging Findings
- •3.4.2 Differential Diagnosis
- •3.4.3 Value of Imaging
- •3.5 Epiploic Appendagitis
- •3.5.1 Imaging Findings
- •3.5.2 Differential Diagnosis
- •3.5.3 Value of Imaging
- •3.6 Crohn’s Disease
- •3.6.1 Imaging Findings
- •3.6.2 Differential Diagnosis
- •3.6.3 Value of Imaging
- •3.7 Rectus Sheath Hematoma
- •3.7.1 Imaging Findings
- •3.7.2 Differential Diagnosis
- •3.7.3 Value of Imaging
- •References
- •MRI of the Pelvic Floor
- •1 Introduction
- •2 Imaging Techniques
- •3.1 Indications
- •3.2 Patient Preparation
- •3.3 Patient Instruction
- •3.4 Patient Positioning
- •3.5 Organ Opacification
- •3.6 Sequence Protocols
- •4 MR Image Analysis
- •4.1 Bony Pelvis
- •5 Typical Findings
- •5.1 Anterior Compartment
- •5.2 Middle Compartment
- •5.3 Posterior Compartment
- •5.4 Levator Ani Muscle
- •References
- •Evaluation of Infertility
- •1 Introduction
- •2 Imaging Techniques
- •2.1 Hysterosalpingography
- •2.1.1 Cycle Considerations
- •2.1.2 Technical Considerations
- •2.1.3 Side Effects and Complications
- •2.1.5 Pathological Findings
- •2.1.6 Limitations of HSG
- •2.2.1 Cycle Considerations
- •2.2.2 Technical Considerations
- •2.2.2.1 Normal and Abnormal Anatomy
- •2.2.3 Accuracy
- •2.2.4 Side Effects and Complications
- •2.2.5 Limitations of Sono-HSG
- •2.3 Magnetic Resonance Imaging
- •2.3.1 Indications
- •2.3.2 Technical Considerations
- •2.3.3 Limitations
- •3 Ovulatory Dysfunction
- •4 Pituitary Adenoma
- •5 Polycystic Ovarian Syndrome
- •7 Uterine Disorders
- •7.1 Müllerian Duct Anomalies
- •7.1.1 Class I: Hypoplasia or Agenesis
- •7.1.2 Class II: Unicornuate
- •7.1.3 Class III: Didelphys
- •7.1.4 Class IV: Bicornuate
- •7.1.5 Class V: Septate
- •7.1.6 Class VI: Arcuate
- •7.1.7 Class VII: Diethylstilbestrol Related
- •7.2 Adenomyosis
- •7.3 Leiomyoma
- •7.4 Endometriosis
- •References
- •MR Pelvimetry
- •1 Clinical Background
- •1.3.1 Diagnosis
- •1.3.2.1 Cephalopelvic Disproportion
- •1.3.4 Inadequate Progression of Labor due to Inefficient Contraction (“the Powers”)
- •2.2 Palpation of the Pelvis
- •3 MR Pelvimetry
- •3.2 MR Imaging Protocol
- •3.3 Image Analysis
- •3.4 Reference Values for MR Pelvimetry
- •5 Indications for Pelvimetry
- •References
- •MR Imaging of the Placenta
- •2 Imaging of the Placenta
- •3 MRI Protocol
- •4 Normal Appearance
- •4.1 Placenta Variants
- •5 Placenta Adhesive Disorders
- •6 Placenta Abruption
- •7 Solid Placental Masses
- •9 Future Directions
- •References
- •Erratum to: Endometrial Cancer
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3.2.4\ Histologic Subtypes and Forms of Degeneration
Different histologic subtypes of leiomyomas exist, some of them showing characteristic features on MRI. Cellular leiomyomas, a subgroup of leiomyomas characterized by compact smooth muscle cells with little intervening collagen, exhibit a homogenously high signal intensity on T2-weighted images (Fig. 16). They are isointense to surrounding myometrium on T1-weighted images and tend to enhance fairly homogenously after gadolinium administration (Yamashita et al. 1993). Lipoleiomyoma is a rare type of leiomyoma which displays a signal intensity similar to subcutaneous fat on all pulse sequences due to the presence of various amounts of fat cells. Chemical shift imaging or spectral fat suppression may be useful to determine the fatty nature of these leiomyomas
a
(Tsushima et al. 1997). While MRI can distinguish among the different subtypes in only 69% of all cases, the method is highly sensitive and specific in identifying simple leiomyomas without any major degenerative changes, leiomyomas having undergone hemorrhagic infarction, and leiomyomas with cystic degenerative changes (Schwartz et al. 1998). Degeneration of uterine leiomyomas is common and is attributed to an inadequate blood supply. It is a sudden event in case of hemorrhagic degeneration while degenerative changes may develop gradually when a tumor outgrows its blood supply.
The typical MRI appearance of a smoothly marginated tumor with a nearly homogeneous low signal intensity relative to surrounding myometrium on T2-weighted images and intermediate signal on T1-weighted images (Fig. 17) is attributable to hyalinization (Oguchi et al. 1995).
b
Fig. 16 MRI of cellular leiomyoma. (a) T2-weighted sagittal image of the uterus demonstrating a large intramural cellular leiomyoma with homogenous high signal intensity compared to surrounding myometrium. Two small intramural leiomyomas show the typical low-intensity signal
(arrows). (b) T1-weighted contrast-enhanced fat-sup- pressed sagittal image showing marked enhancement of the intramural cellular leiomyoma which appears hyperintense compared to surrounding myometrium
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Fig. 17 Signal intensity characteristics of leiomyoma. (a) T2-weighted transaxial image of the uterus (secretory phase of menstrual cycle) showing a subserosal leiomyoma with typical low signal intensity compared to adjacent myometrium. Note the bright signal of the endometrium
and intermediate signal intensity of the junctional zone. (b) Corresponding T1-weighted transaxial image of the uterus showing intermediate signal intensity of the leiomyoma which can hardly be differentiated from the adjacent myometrium
Hyaline degeneration is the predominant form of degeneration and is present in about 60% of all leiomyomas. It is characterized by the accumulation of high-protein eosinophilic substrate in the extracellular spaces between strands of muscle cells. Other types of degeneration that can be differentiated are cystic, myxoid, and hemorrhagic (red) degeneration. Cystic degeneration is characterized by the presence of clearly delineated cystic lesions with a signal intensity isointense to fluid on T1and T2-weighted images. Myxoid degeneration is seen as intralesional areas of very high signal intensity on T2-weighted images. These portions are of intermediate to low signal on T1-weighted images and typically do not show enhancement after contrast medium administration (Fig. 18).
Histology demonstrates gelatinous portions containing hyaluronic mucopolysaccharides.
Haemorrhagic or red degeneration is more common during pregnancy or in women on
gestagen therapy. It is attributed to sudden infarction of leiomyoma tissue with secondary intralesional hemorrhage (Hasan et al. 1991). MRI shows a lesion with an increased internal signal and a low-signal-intensity margin on T2-weighted images while T1-weighted images depict a lesion with a heterogeneous high signal that varies with the amount of blood degradation products present and is often confined to the margin (Fig. 19) (Kawakami et al. 1994). Hemorrhagic leiomyomas typically show no enhancement after contrast medium administration. MRI confirms the diagnosis of acute hemorrhagic degeneration in conjunction with the clinical symptoms comprising acute pain, subfebrile temperature, and leukocytosis (Kawakami et al. 1994; Hamlin et al. 1985). Hydropic degeneration of a leiomyoma has been described as a rare form of degeneration and usually presents as a large and lobulated complex mass on US that displays heterogeneous mainly high T2 signal with strands of low
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Fig. 18 MRI of myxoid leiomyoma. (a) T2-weighted transaxial image of the uterus showing also heterogeneous signal intensity of the leiomyoma and a C-shaped area at the left border of the leiomyoma (arrow) of high signal intensity corresponding to myxoid degeneration. Note that high-signal-intensity stripe of the endometrium is displaced laterally. (b) On the corresponding T1-weighted fat-suppressed transaxial image the whole leiomyoma has
a heterogeneous intermediate signal intensity and the C-shaped area shows no low signal as expected if liquefaction had occurred. (c) Contrast-enhanced T1-weighted fat-suppressed transaxial image shows heterogeneous enhancement of the leiomyoma including septations of myxoid tissue, Note enhancement of endometrial stripe (arrow)
signal on MRI. A solid component as well as prominent intralesional blood vessels may be present. This appearance can be a diagnostic challenge since these imaging features overlap with malignant tumors. “PseudoMeigs’ syndrome” has been associated with hydropic leiomyomas associated with ascites and elevated serum levels of CA-125 (Horta et al. 2015).
MRI is methodologically limited in that it does not reliably show intralesional calcifications, which are frequently identified on conventional radiographs or CT scans by their popcorn-like appearance (Schwartz et al. 1998). Occasionally, calcifications take the form of a peripheral rim after hemorrhagic infraction and can be identified on T1-weighted MR images (Fig. 20).
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Fig. 19 MRI of spontaneously infarcted leiomyoma. (a) T1-weighted fat-suppressed transaxial image of a spontaneously infarcted submucosal leiomyoma. The central portion shows a slightly hyperintense signal intensity compared to the surrounding myometrium. (b) T2-weighted transaxial image of a spontaneous infarcted submucosal leiomyoma. The central portion shows a signal intensity isointense to the myometrium while a marked hypointense rim is seen which corresponds to blood degradation products (hemo-
siderin) after hemorrhagic infarction. (c) Contrast-enhanced T1-weighted fat-suppressed transaxial image confirms infarction of the leiomyoma while the surrounding myometrium is well perfused (reproduced with permission from reference 840, Kröncke TJ, Hamm B (2003) Role of magnetic resonance imaging (MRI) in establishing the indication for planning and following up uterine artery embolization (UAE) for treating symptomatic leiomyomas of the uterus [article in German]. Radiologe 43:624–633)
Fig. 20 MRI of rim calcification of a leiomyoma. T1-weighted fat-suppressed transaxial image showing a leiomyoma with a discontinuous, markedly hypointense rim corresponding to asymmetrical calcification
3.2.5\ Differential Diagnosis
In evaluating lesions in close topographic relationship to the uterus, the examiner must consider ovarian masses in the differential diagnosis. If it is not possible to definitely assign the lesion to the uterus, an intraligamentous or ovarian leiomyoma may be present if the lesion shows homogeneous low signal intensity on T2-weighted images and an intermediate signal on T1-weighted images relative to the signal intensity of the myometrium of the uterus. However, an inhomogeneous intermediate or high signal relative to the myometrium may indicate both a leiomyoma with degenerative changes or an extrauterine benign or malignant tumor.
Myometrial contractions can mimic submucosal leiomyomas or focal adenomyosis (Togashi et al. 1993a). Uterine contractions involve the
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Fig. 21 Transient uterine contraction. (a) T2-weighted sagittal image of the uterus depicting a broadening of the inner myometrium of the anterior uterine wall with bulging into the uterine cavity (arrow). (b) T2-weighted sagit-
tal image of the uterus obtained 5 min before (a) shows absence of any structural abnormality, a finding consistent with myometrial contraction
endoand myometrium but spare the outer uterine contour (Fig. 21). They are characterized by bandor stick-like low-signal-intensity areas on T2-weighted images (Masui et al. 2003). These signal changes are transient and changing appearances can be noted on sequential images obtained with a delay of 30–45 min (Togashi et al. 1993a, b).
Endometrial polyps are seen most frequently in perimenopausal and postmenopausal women, and are usually asymptomatic but may cause uterine bleeding especially in postmenopausal women (DeWaay et al. 2002). In 20% of the cases polyps are multiple. They can be broad based or pedunculated and may occur in conjunction with endometrial hyperplasia. On T2-weighted images a central fibrous core or intratumoral cysts may be visible (Grasel et al. 2000). On T1-weighted images endometrial polyps show an intermediate signal while they exhibit a slightly hypointense or isointense signal intensity relative to the endometrium on T2-weighted images and present as localized endometrial thickening (Fig. 22). Small polyps enhance and become more conspicuous after gadolinium administration, especially on
Fig. 22 Leiomyoma, diffuse adenomyosis and endometrial polyp on MRI. T2-weighted sagittal image of a patient depicts diffuse adenomyosis (arrowheads) with symmetrical broadening of the junctional zone. An endometrial polyp exhibiting similar high signal intensity as the endometrium can be clearly identified within the uterine cavity (short arrow). A fibroid is present in the fundus (long arrow)