Учебники / Head_and_Neck_Cancer_Imaging

12.8.1

Minor Salivary Glands Tumors

x Adenoid cystic carcinoma and mucoepidermoid carcinoma are the most frequent malignancies. A tumor of the palate is suspicious of a minor salivary gland tumor. Perineural spread toward the maxillary branch of the trigeminal nerve (V2) is suggestive of adenoid cystic carcinoma. Cervical lymphadenopathy may be present. Treatment consists of wide surgical resection, often associated with radiotherapy. Mucoepidermoid carcinoma often mimics a benign tumor (a well-defined, non infiltrative tumor) and has a better prognosis than adenoid cystic carcinoma (Fig. 12.29).

x Pleomorphic adenoma of minor salivary gland origin in the anterior parapharyngeal space is rare (see Chap. 9). These are usually slow-grow- ing, large tumors without much clinical symptoms, presenting with the MR characteristics of a pleomorphic adenoma: a well-defined, lobulated mass with low T1-weighted, high T2-weighted signal intensities and important enhancement. These lesions often appear heterogeneous (Fig. 12.8). The differential diagnosis is a pleomorphic adenoma arising in the deep lobe of the parotid gland (Fig. 12.9).

12.8.2

Submandibular Gland Tumors

x The role of imaging is to determine whether a submandibular lesion is either a salivary gland tumor or an adenopathy. In case of a salivary localization, the lesion appears to be malignant in 55% of patients (Kaneda et al. 1996).

x Adenoid cystic carcinoma and mucoepidermoid carcinoma are the most frequent submandibular gland tumors. On MR imaging, these tumors are usually poorly defined, with low T1-weighted, intermediate T2-weighted signal intensities and heterogeneous enhancement. The surrounding

structures, such as the adjacent cervical deep spaces, muscles, mandible and cervical lymph nodes, have to be analyzed in order to rule out tumoral involvement. Treatment consists of a wide resection with neck dissection, and frequently adjuvant radiotherapy. Imaging follow-up must last a very long time because of the possibility of late recurrence.

x Benign mixed tumor is the most frequent benign tumor arising in the submandibular gland. MR imaging characteristics are similar to those of intraparotid pleomorphic adenoma. Typical appearance on CT is a hypodense, lobulated mass with heterogeneous enhancement related to cystic

and hemorrhagic changes. Fine needle aspiration of submandibular gland tumors has poor sensitivity and specificity. Surgical resection of the submandibular gland may be proposed if the lesion is small, homogeneous, well-defined, showing MR characteristics of a benign mixed tumor. Wide surgical resection associated with neck dissection has to be performed if the lesion is larger, heterogeneous, ill-defined, suggestive of a malignant tumor.

x Chronic sialadenitis due to obstruction of the ductal system can clinically simulate a tumoral lesion of the submandibular space. Imaging is very useful to look for the obstructive calculus in Wharton’s duct and the inflammatory modifications of the submandibular gland. On imaging, the involved gland is usually enlarged, diffusely and densely enhancing, associated with dilatation of the main salivary duct, often containing a calculus at its distal part. Lithiasis is well depicted on CT (Fig. 12.30).

12.8.3

Sublingual Gland Tumors

Fig. 12.30. Chronic sialadenitis: multiple calcified lithiasis (arrows) within the left submandibular gland and Wharton’s duct

x About 80% of the sublingual gland tumors are malignant. Again, the two main etiologies are adenoid cystic carcinoma and mucoepidermoid carcinoma (Sumi et al. 1999). On MR imaging, these tumors are more or less well-circumscribed and have a low T1-weighted, an intermediate T2-weighted signal intensity and a heterogeneous enhancement (Fig. 12.31). Extension outside the sublingual space has to be looked for, such as extension to the mandible or to the cervical lymph nodes. These lesions are usually well-cir- cumscribed in case of mucoepidermoid tumor (Fig. 12.32). Treatment consists of a wide resection with neck dissection, most often associated with radiation therapy. Because of the risk of recurrence, a long term follow-up is recommended.

x A ranula is a mucous retention cyst that originates from the sublingual gland. It most commonly results from trauma or inflammation (Macdonald et al. 2003). A ranula occurs in two forms. The first one, the simple ranula, is a retention cyst that remains located in the sublingual space (Fig. 12.33). The second type is the plunging ranula, which is a mucocele extending through the mylohyoid muscle, to the submandibular space. On MR imaging, the simple ranula is a cystic formation with a low T1-weighted, a high T2-weighted

signal intensity and a thin enhancement ring on contrast-enhanced images. The plunging ranula appears as a multi-lobulated cystic formation; it sometimes shows a spontaneous high T1-weighted signal intensity because of its protein concentration, a high T2-weighted signal intensity with much more important enhancement of the cyst wall. On CT, a ranula usually has a low attenuation because of its high water content; the cyst wall may enhance after contrast administration. The differential diagnosis includes epidermoid cysts and cystic hygromas of the sublingual space.

12.9 Conclusion

Most of parotid gland lesions are benign tumors. The best imaging approach to analyze parotid gland tumors is MR imaging. In many cases, the MRI findings are indicative of a benign or malignant nature. In case of benign tumors, an etiologic diagnosis can sometimes be suggested on MRI. MR diffu- sion-weighted sequence appears to be helpful in improving the diagnostic yield in case of atypical or difficult cases.

Fig. 12.31a–c. Adenoid cystic carcinoma of the left sublingual gland: huge mass appearing hyperintense on a T2-weighted image (arrow, a), hypointense on a T1-weighted image (arrow, b), showing a moderate and heterogeneous enhancement on a contrast-enhanced T1-weighted image (arrow, c)

Fig. 12.32a–c. Small mucoepidermoid tumor of the left sublingual gland showing a high T2-weighted signal intensity (arrow, a) and an important enhancement on contrast-enhanced T1-weighted images (arrow, b), associated with two small adjacent submandibular adenopathies (arrow, c)

Parotid Gland and Other Salivary Gland Tumors

Fig. 12.33. Cystic formation in the anterior part of the right sublingual space, compressing the genioglossal muscles and extending over the midline. Confirmed simple ranula. (Courtesy of Robert Hermans, MD, PhD, Leuven, Belgium)

References

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CONTENTS

13.1Introduction 243

13.2Anatomy 243

13.2.1 Central Skull Base 244

13.2.2 Posterior Skull Base 245

13.3Clinical Presentation 247

13.5Pathology 249

13.5.3Non-region Specific, Localized Malignant Skull Base Lesions 250

13.5.4Mimics of Non-region Specific, Localized Malignant

13.5.7Mimics of Malignant Central Skull Base Lesions 259

13.6Imaging Protocol 266

13.7Radiologist’s Role 267 References 267

main reasons for the intimidation of the radiologists: The anatomical complexity of the skull base, the ability of normal anatomical structures to mimic pathology and the rarity of skull base lesions preventing dedicated training throughout residency and even during fellowship. In addition, inappropriate choice of an imaging study, imaging parameters and or sequences may amplify the insecurity of the radiologist.

Recognition of anatomical mimics and of medically treatable conditions is essential as the majority of skull base lesions are inaccessible for biopsy. The biopsy route may extend through normal pertinent anatomical structures such as inner ear in case of a petrous apex lesion, or may need to be performed via an intracranial route. Differentiation of malignant from benign lesions is critical as different surgical intervention may apply, the lesion might be vascular in nature preventing a biopsy, or occasionally treatment might be conducted without a tissue diagnosis, e.g. radiation therapy in case of paragangliomas. In addition, determination of the exact origin and extent of a lesion is crucial for radiation therapy and even more for surgical planning purposes. All these points will be addressed in this chapter.

Evaluation of skull base lesions is challenging. On the one hand, the skull base is not directly accessible for clinical evaluation, and an underlying lesion is suspected or can be only roughly outlined based on neurological deficits. On the other, cross-sectional radiological studies are excellent in demonstrating a skull base lesion and its extent, but their evaluation is intimidating to the majority of the radiologists. There are three

I. M. Schmalfuss, MD

Department of Radiology, Malcolm Randall VA Medical Center and University of Florida College of Medicine, 1601 SW Archer Road, Gainesville, Florida 32608, USA

The anatomy of the skull base is very complex; not only the bony structures play an important role but also the cranial nerves and vasculature coursing through it. Knowledge of the location of the different neural and vascular foramina and channels, as well as of the different neuronal connections, can therefore explain the wide range of clinical symptoms and facilitate the detection of extracranial tumor spread.

The skull base is formed by the ethmoid, sphenoid, and paired occipital, frontal and temporal bones. It is divided into three regions: anterior, central and posterior skull base. Only the central and the posterior skull base will be discussed in this chapter as the an-

terior skull base is included in Chap. 11. The distinction of the central to posterior skull base is ambiguous as the roof of the petrous apex represents part of the central skull base while the posterior margin borders the posterior skull base. Since the majority of the malignant petrous apex lesions are surgically approached from the posterior fossa, the petrous apex will be included in the posterior skull base in the subsequent discussion.

13.2.1

Central Skull Base

The sphenoid bone forms the middle portion of the central skull base. It is subdivided into the central sphenoid body housing the sella and the sphenoid sinuses, the greater sphenoid wings forming the boundary to the anterior skull base, the lesser sphenoid wings and the pterygoid processes that are protruding below the skull base and serve as attachments for the medial and lateral pterygoid muscles. Parts of the temporal bones compose the lateral portions of the central skull base and are formed by the mastoid, tympanic, petrous and squamous bones. The greater sphenoid wing is connected via the sphenosquamous suture and the petrosphenoidal fissure with the squamous and petrous portion of the temporal bone, respectively. The anterior portion of the squamous bone creates the lateral border of the central skull base while the petrous bone together with the clivus form the boundary towards the posterior skull base. The petrous bone and the clivus are separated by the petrooccipital fissure.

The central skull base represents the floor of the middle cranial fossa which is primarily filled with the temporal lobes laterally and the cavernous sinuses medially. The cavernous sinuses are located between the dura and the periosteum of the body of the sphenoid bone, and between the superior orbital fissure anteriorly and the petrous apex posteriorly. Each cavernous sinus contains a complex venous plexus that surrounds the internal carotid artery and the cranial nerve VI. The cranial nerve VI enters the cavernous sinus through a small bony channel within the medial petrous apex called Dorello’s canal. The cranial nerves III through V are actually located within the dural flap that forms the lateral boundary of the cavernous sinus rather than within the cavernous sinus itself. These cranial nerves and the internal carotid artery exit the intracranium through different foramina located within the central skull base.

The superior orbital fissure and the optic canal are the most anterior openings of the central skull base. The optic nerve, optic nerve sheath and the ophthalmic artery course through the optic canal while the cranial nerves III, IV and VI as well as the lacrimal, frontal and nasociliary branches of the first division of the trigeminal nerve (V1) exit the cavernous sinus into the orbital apex through the superior orbital fissure. The foramen rotundum is located just posterior to the superior orbital fissure and houses the second division of the trigeminal nerve (V2) (Fig. 13.1). The foramen rotundum communicates anteriorly with the pterygopalatine fossa where a few ganglionic branches leave V2 to travel to the pterygopalatine ganglion (Fig. 13.2) (Moore et al. 1999). V2 gives off the zygomatic and the posterior superior alveolar nerves and then continues anteriorly as the infraorbital nerve within the infraorbital canal. The third division of the trigeminal nerve (V3) courses through the central skull base within the foramen ovale that is situated posteromedially to the foramen rotundum (Fig. 13.3). V3 courses inferiorly to enter the masticator space. Just medial and posterior to the foramen ovale is a groove within the central skull base, located immediately posterior to the cavernous sinus, containing the Meckel’s cave. The Meckel’s cave houses the trigeminal ganglion anteroinferiorly where the three divisions of the trigeminal nerve are merging together (Kaufman and Bellon 1973; Williams et al. 2003). The trigeminal ganglion gives rise to multiple individual rootlets that course superiorly into

Fig. 13.1. Coronal CT image displayed in bone window demonstrating the relationship of the foramen rotundum (arrows) and vidian canal (arrowheads) to each other and the sphenoid sinus (s) within the central skull base

Malignant Lesions of the Central and Posterior Skull Base

Fig. 13.2. Axial CT image displayed in bone window illustrates the communication of the foramen rotundum (arrow) with the pterygopalatine fossa (arrowhead) that is located immediately posterior to the maxillary sinus (m). s, Sphenoid sinus

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Fig. 13.3. Axial CT image of the central skull base displayed in bone window shows the larger foramen ovale (black arrows) on each side and the smaller foramen spinosum (black arrowheads) posterior lateral to it. Both assume an oval shape. The white arrowheads demarcate the vidian canal that extends from the inferior portion of the pterygopalatine fossa (white arrows) to the foramen lacerum within the petrous apex (not demonstrated at this level). s, Sphenoid sinus

and laterally from the internal occipital protuberance housing the superior sagittal sinus and the transverse sinuses, respectively. The horizontal grooves extend anteroinferiorly to continue as the sigmoid sulci that contain the sigmoid sinus on each side. The sigmoid sinus subsequently enters the jugular foramen and continues through the skull base into the neck as the internal jugular vein.

The jugular foramen and the foramen magnum are the largest openings of the posterior skull base. The jugular foramen lies at the posterior end of the petrooccipital fissure and is bordered by the petrous bone of the temporal bone anteriorly and the occipital bone posteriorly. It is partially subdivided by the jugular spine into two compartments: the pars venosa and the pars nervosa (Fig. 13.5) (Inserra et al. 2004; Sen et al. 2001). Only occasionally the bony jugular spine continues as a fibrous or osseous septum posteriorly to completely separate these two compartments. The pars venosa lies posterolateral and contains the internal jugular bulb laterally and the cranial nerves X and XI medially (Fig. 13.5). The pars nervosa is located anterior medially and contains the cranial nerve IX medially and often the inferior petrosal sinus laterally (Fig. 13.5). The internal carotid artery enters the skull base anterior to the jugular foramen (Fig. 13.5). Therefore, all three of these cranial nerves lie between the internal jugular vein and the internal carotid artery below the skull base, with the cranial nerve IX being the most anterior lateral and the cranial nerve XI the most posterior medial in position.

The cranial nerve XI is very unique as it extends through the posterior skull base twice: Once to exit the skull base through the jugular foramen as mentioned above and once to enter the posterior cranial fossa through the foramen magnum as parts of its fibers originate from the cervical spinal cord. The re-

maining spinal accessory nerve fibers originate from the medulla oblongata that merges with the cervical spinal cord fibers at the foramen of magnum. The cranial nerves XI lie posterior to the vertebral arteries that ascend from cervical to intracranial through the foramen of magnum. The vertebral arteries give rise to the posterior cerebellar arteries that course posteroinferiorly to supply the inferior cerebellar hemispheres. In turn, the paired posterior spinal arteries arise either from the intracranial portion of the vertebral arteries or occasionally from the posterior cerebellar arteries and continue inferiorly to descend through the foramen of magnum to supply the spinal cord.

The posterior skull base has few additional,smaller openings. The porus acusticus is the medial opening of the internal auditory canal along the posterior surface of the petrous bone. It contains the cranial nerve VII and VIII as well as branches of the anterior inferior cerebellar artery that supply the inner ear. Inferior and posterior to it are the openings of the cochlear and vestibular aqueducts, respectively. The vestibular aqueduct courses almost parallel to the posterior margin of the petrous bone between the vestibule and the intracranium and contains the endolymphatic duct. In contrast, the cochlear aqueduct runs almost parallel to the internal auditory canal between the basal turn of the cochlea and the intracranium within the inferior aspect of the petrous portion of the temporal bone and transmits the perilymphatic duct (Mukherji et al. 1998). Even more inferiorly within the petrous bone is the hypoglossal foramen located just inferomedial to the jugular foramen (Fig. 13.6). It contains the cranial nerve XII, the hypoglossal venous plexus and a meningeal branch of the ascending pharyngeal artery. Below the skull base, the cranial nerve XII continues inferiorly

Malignant Lesions of the Central and Posterior Skull Base

Fig. 13.5. Axial CT image of the right jugular fossa displayed in bone window shows the jugular spine (arrow) dividing the jugular foramen into the pars venosa (pv) laterally and pars nervosa (pn) medially. The internal carotid artery (c) lies anterior to the pars venosa (pv)

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Fig. 13.6. Axial T2-weighted image through the lower clivus demonstrates the oblique course of the hypoglossal canal (arrows) along the lateral edge of the clivus on each side. The exit of the hypoglossal canal (arrows) is in close proximity to the internal carotid artery (c)

between the internal carotid artery and the internal jugular vein.

compromise or direct compression of the brain or orbital structures. The clinical symptoms of cranial nerve palsies are summarized in Table 13.1.

13.3

Clinical Presentation

Only few skull base lesions present with specific, disease related symptoms that significantly help to narrow the differential diagnosis. The Gradenigo’s triad represents one of them and is characterized by ipsilateral cranial nerve VI paralysis, severe facial pain in V1 distribution and inflammatory disease of the inner ear and/or mastoid air cells (Gradenigo 1904). As the triad indicates, this symptom complex has been associated with acute inflammatory disease of the ear. However, less than 50% of the patients present with all three of these symptoms. In particular, cranial nerve VI palsy has been described as the least reliable clinical sign of the triad making distinction to other skull base entities more difficult (Price and Fayad 2002). Hence, the majority of patients with skull base pathology present with non-specific neurological symptoms related to the mass effect caused by the lesion. These symptoms can be related to cranial nerve dysfunction, vascular

13.4

Normal Anatomical Variations

Normal anatomical variations are asymptomatic and typically discovered incidentally in patients that seek medical attention for an unrelated reason. Asymmetric aeration of the petrous apex is most likely the most common entity that is mistaken for a petrous apex mass, in particular on MR imaging (Fig. 13.7). CT certainly is easier to interpret in this regard; however, close attention to the imaging characteristics can facilitate the correct diagnosis on MR images as well. In particular, lack of mass effect and increased T1 signal intensity of the fatty bone marrow within the unaerated petrous apex is characteristic (Fig. 13.7a). Asymmetric accumulation of fluid within the petrous apex air cells will show intermediate T1 and high T2 signal intensity and may be mistaken for a chondrosarcoma; however, the lack of mass effect and of contrast enhancement as well as often accompanied fluid within the middle ear cavity