Oral cavity and oropharynx

Foreword Defining the anatomyof the oral cavity andoropharynxby conventionalradiology was always a difficult problem. The adventof cross-sectionalimaging has made radiologic examinationfar more effective and, in fact, an essentialpart of proper evaluation.It then behoovesthe radiologist to have an adequategraspof the normal anatomy and the reflections of diseasein theseanatomic areas.Drs. YatesandPhillips haveprovidedus with a splendidmonographthat providesthis important information. Theodore

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E. Keats, MD Editor-in-Chief

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Clarence B. Yates, MD, received a BS degree in biology at The Florida State University, Tallahassee, Florida. He received his medical degree at the University of South Florida, Tampa, Florida. He then completed a residency in Diagnostic Radiology at David Grant Medical Center, Travis Air Force Base, California. He is currently a fellow in neuroradiology at the University of Virginia Health Sciences Center in Charlottesville, Viiginia.

C. Douglas Phillips, MD, received Regents BA and MD degrees from Marshall University in Huntington, c West Vrrginia. He then completed a residency in diagnostic radiology and a fellowship in neuroradiology at the University of Virginia Health Sciences Center in Charlottesville, Virginia. He is an associate professor of radiology with joint appointments in the departments of neurosurgery and otolaryngology-head and neck surgery. Dr Phillips is currently the director of the Division of Neuroradiology at the University of Virginia,

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Oral Cavity and Oropharynx Cross-sectional imaging has become an essential element in the evaluation of disease processes involving the oral cavity and oropharynx. This article is an overview of the anatomy and typical pathology of the these areas. The radiologist, working in conjunction with the physical examination and the clinical evaluation of a careful head and neck surgeon, can provide information that is critical to the treatment of patients with oral cavity and oropharyngeal disease.

The oral cavity and oropharynx are areas that are easily visible and readily palpable by physical examination by referring physicians. Therefore physical examination and endoscopy are performed primarily for diagnostic evaluation. A working knowledge of imaging anatomy and pathology can be beneficial by helping referring physicians identify the extent of lesions, locate pathology in difficult examinations, and offer differential diagnoses for unknown diseases. The purpose of this article is to familiarize the reader with anatomy, imaging techniques, and disease processes. Discussion will include important anatomic relationships, imaging techniques with magnetic resonance imaging (MRI) and computed tomography (CT), and common lesions based on specific anatomic locations.

Normal Anatomy Oral Cavity The oral portion of the aerodigestive tract is divided into two major components: the oral cavity and the oropharynx.1 Distinguishing the oral cavity from the oropharynx is important because the pathologic presentations of these two areas can be very different.2,3 The oral cavity contains the anterior two thirds of the tongue, the soft palate, the buccal mucosa, the lips, the floor of the mouth, and the mandible and maxillae. The oral cavity is anterior to the oropharynx and separated from it by a ring of structures to include the soft palate, the anterior tonsillar pillars, and the circumvallate papillae. The boundaries of the oral cavity include the hard palate (maxillae) above, the buccal and gingival mucosa laterally, the anterior tonsillar pillars and circumvillate papillae posteriorly, and the mylohyoid inferiorly. The oral tongue is the central structure of the doi:10.1067/mdr.2001.113657

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oral cavity. The oral cavity is lined with squamous mucosa and subepithelial collections of minor salivary glands. Arterial supply is via external carotid artery branches including lingual, facial, and internal maxillary. Venous drainage is to the pterygoid and tonsillar plexuses. Lymphatic drainage is primarily via submental and submandibular lymph nodes (level 1), then to high internal jugular nodes (level 2). The oral cavity can be divided into four compartments: the sublingual and submandibular spaces, the mucosal surface, and the oral tongue. The mylohyoid muscle (the floor of the mouth) is a muscular sling between the medial aspects of the mandible. It divides the sublingual space from the submandibular space except along its posterior margin, where the spaces freely communicate.4,5 The tongue is a muscular organ divided into right and left halves by a fibrous and fatty septum. It lies partly in the mouth and partly in the oropharynx. Each half contains both intrinsic and extrinsic musculature; the former has attachments within the tongue, the latter outside of it. The circumvallate papillae divide the intrinsic musculature into an anterior two thirds (the oral tongue) and posterior one third (the tongue base). The oral tongue is in the oral cavity, and the tongue base is in the oropharynx. The extrinsic musculature is referred to as the tongue root. These muscles attach the tongue to the hyoid bone, the mandible, the styloid process, and the pharynx. The main extrinsic muscles are the genioglossus, geniohyoid, hyoglossus, and styloglossus. The intrinsic muscles consist of four interdigitating muscles: the superior and inferior longitudinal, the transverse, and the oblique.1,4,6 The sublingual space is superior and medial to the mylohyoid muscle. The contents include the lingual artery, vein, and nerve; the sublingual glands and ducts; the submandibular duct; and deep portions of the subCurr Probl Diagn Radiol, March/April 2001

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D FIG 1. Normal anatomy of the oral cavity. A, Axial CT after contrast (CCT). Black arrows, Mylohyoid muscle; M, body of mandible; g, genioglossus/geniohyoid complex; t, tonsil (lower pole); L, lingual tonsil; m, masseter; lc, longus coli. B, Axial T1W MRI. White arrows, Mylohyoid; g, genioglossus/geniohyoid complex; ma, masseter; sm, submandibular gland; T, tongue base; lt, lingual tonsil; P, palatine tonsil; b, buccinator; d, posterior belly digastric; lc, longus coli; sl, sublingual gland. C, Coronal CT. White arrows, Mylohyoid; g, genioglossus; h, geniohyoid; m, masseter; T, tongue base; P, medial pterygoid; b, buccinator; d, anterior belly digastric; s, sublingual gland. D, Coronal T1W MRI. White arrow, Platysma; m, mylohyoid; T, tongue; SLS, sublingual space; SMS, submandibular space; gg, genioglossus; gh, geniohyoid; Ma, masseter; M, mandible.

mandibular gland. The hyoglossus muscle is an important surgical landmark because it divides the submandibular duct, hypoglossal, and lingual nerves (lateral to the muscle) from the lingual artery and vein (medial to the muscle). An important distinction in imaging Curr Probl Diagn Radiol, March/April 2001

patients with carcinoma of the floor of the mouth is invasion of this neurovascular pedicle.4 The boundaries of the sublingual space include the mandible anteriorly, the genioglossus/geniohyoid medially, and the mylohyoid inferior and laterally. Posteriorly, no true fascial 39

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D FIG 2. Normal anatomy of the oropharynx. A, Axial contrast-enhanced computed tomography (CCT). b, Buccinator; OT, oral tongue; p, medial pterygoid; PPS, parapharyngeal space; sp, soft palate; tp, palatine tonsil; m, masseter; P, parotid gland; lc, longus coli; Ma, maxilla. B, Axial T1W MRI. T, Maxillary teeth; b, buccinator; rm, retromolar trigone; OT, oral tongue; pt, medial pterygoid; p, posterior belly digastric; PPS, parapharyngeal space; sp, soft palate; *palatine tonsil. C, Coronal CT. l, Lateral pterygoid; p, medial pterygoid; e, torus tubarius; t, palatine tonsil; L, lingual tonsil; B, base of tongue; mh, mylohyoid; m, masseter. D, Coronal T1W MRI. lp, Lateral pterygoid; p, medial pterygoid; t, palatine tonsil; L, lingual tonsil; B, base of tongue; mh, mylohyoid; m, masseter; T, tongue base; P, parapharyngeal space.

margins are present. Therefore lesions can spread freely to involve the adjacent submandibular space.5 The submandibular space is located inferior and lateral to the mylohyoid. The contents include submental and submandibular lymph nodes, the sub40

mandibular glands, the facial vessels, and the hypoglossal nerve. The structures most commonly associated with pathology are the lymph nodes and the submandibular gland.4 The boundaries of the submandibular space include the hyoid bone inferiorly, the Curr Probl Diagn Radiol, March/April 2001

mylohyoid superomedially, and the deep cervical fascia laterally (Fig 1).5

Orophayrnx The oropharynx is the central structure of the upper aerodigestive tract. It communicates with the nasopharynx, hypopharynx, oral cavity, and larynx.7 It extends from the soft palate to the level of the hyoid. The oropharyngeal boundaries are the soft palate superiorly, the tonsillar pillars laterally, the pharyngeal constrictors posteriorly, and the hypopharynx inferiorly (the level of the hyoid bone or third cervical vertebrae). Its contents include the posterior one third of the tongue (primarily made up of the lingual tonsil), the palatine tonsils, the soft palate, the upper pharyngeal constrictor muscles, and the oropharyngeal mucosa. The major blood vessels include the facial, lingual, ascending pharyngeal, and internal maxillary branches of the external carotid artery. Venous drainage is into the facial vein and the palatine plexus. The primary lymphatic drainage is to the jugulodigastric, lateral pharyngeal, and posterior cervical lymph nodes. The visceral fascia about the mucosa and musculature of the pharynx often acts as an initial barrier to contain disease processes (Fig 2).5,8,9

Imaging Techniques Computed Tomography The advantages of CT over MRI include shorter imaging time, lower cost, more availability, and less patient motion artifact. The disadvantages include the necessity of iodinated contrast administration, radiation exposure, and dental artifact obscuring tissues. Dynamic scanning is performed with contiguous axial 3- to 4mm sections. Supplemental coronal images are helpful if tolerated, particularly with pathology of the hard or soft palate, tongue, and floor of the mouth. Adjusting the gantry angle can diminish dental amalgam artifact. Helical scanning decreases scanning time and acquires a data set that can be reconstructed at any level for additional analysis. High-resolution images and multiplanar reconstructions can be performed with 1-mm collimation.10 At our institution, our neck protocols are all performed with spiral technique during contrast infusion. Spiral 3-mm scans are obtained parallel to the body of the mandible (3-mm collimation) from the coronoid process to the hyoid bone with a pitch of 1.0 to 1.5. This is often followed by 3-mm coronal scans Curr Probl Diagn Radiol, March/April 2001

from the tongue base to the anterior body of the mandible. We maintain a small (120-mm) field of view and print soft tissue windows (40W, 350L). Bone algorithm images at an extended window and level are obtained on request. When staging examinations are performed, our axial sections are extended to the thoracic inlet.

Magnetic Resonance Imaging The advantages of MRI over CT imaging include easy multi-planar capacity, no radiation exposure, and superior soft tissue contrast. The disadvantages include cost, occasional patient intolerance, longer examination time, and availability. MRI is more demanding on patients, requiring immobility in a supine position for a long period of time. Patients with head and neck cancer often have difficulty managing secretions. Claustrophobic patients or patients with severe dyspnea cannot tolerate MRI. Before the examination, patient instruction that motion (talking or swallowing) degrades the images is essential. Utilizing a dedicated surface coil, multi-planar T1-weighted (T1W), T2-weighted (T2W), and post-gadolinium T1W images are performed. Preferably, one of the post-contrast planes is obtained with fat saturation.11,12 Imaging parameters include slice thickness of 3 to 4 mm with a 0- to 1-mm gap, field of view of 20 cm × 20 cm or less, and at least two averages. The imaging matrix should be 256 × 192 or better.10 At our institution, we use a circularly polarized head coil for scans of the oropharynx and oral cavity, and we use a neck coil when performing staging examinations. Localization is performed with a sagittal T1W spin echo sequence. Axial T2W and axial T1W images are obtained from the hard palate to the hyoid bone. Axial and coronal post-gadolinium images are obtained. The axial post-gadolinium images are obtained with fat saturation. Pre-saturation pulses are useful to saturate entry slice signal and reduce phase encoding artifact. Image parameters include 4-mm slices with 1-mm gap, a field of view of 18 to 20 cm, and a matrix of 226 × 512. We routinely use a rectangular 512 matrix. Debate persists about the efficacy of CT versus MRI in imaging the oral cavity and oropharynx.13 Some authors advocate using CT for imaging infection and MRI for imaging neoplasm.5 At our institution, we have primarily relied on CT. In our practice, we image a large population of patients with head and neck cancer who have limited tolerance for being supine and stationary for the time required for MRI. MRI is pri41

FIG 3. Lingual thyroid. Sagittal T1W (left) and coronal T1W postgadolinium (right) MRI images reveal a midline, slightly angular lesion of the tongue base in the region of the foramen cecum that is hyperintense on T1W images (straight and curved arrows).

marily used for evaluation of perineural tumor spread and problem solving.14

Pathology

FIG 4. T hyroglossal duct cyst. Axial CCT image demonstrates a circumscribed cystic mass with septations (long white arrow) at the level of the hyoid. The mass is growing through the hyoid bone (arrowhead) and ipsilateral strap muscle (*contralateral strap muscle).

Oral Cavity Congenital Lingual Thyroid. The thyroid gland begins to develop in the third week of life as a median outgrowth from the primitive pharynx. This primitive thyroid originates at the foramen cecum, which lies at the junction of the anterior two thirds and posterior one third of the tongue. The thyroid descends in the neck, through the tongue and floor of the mouth, and eventually through and anterior to the developing hyoid bone into the inferior neck, then moving laterally and deep to the strap muscles by gestational week 7. During its migration, the thyroid is connected to the tongue by an epithelium-lined tubular structure, the thyroglossal duct. This normally involutes by gestational week 10. The site of origin persists as the foramen cecum; the distal portion persists as the pyramidal lobe of the thyroid. If any portion of the duct persists, epithelial secretions give rise to cystic lesions.15 Failure of the thyroid gland to descend from the foramen cecum to the lower neck results in residual thyroid tissue anywhere along the thyroglossal duct tract. The base of the tongue is the most common location, usually presenting as a midline mass. This tissue is usually asymptomatic. However, dysphagia, stridor, and dyspnea can occur as well as hypothyroidism (cretinism). No other functioning thyroid tissue is present a majority of the time, and surgical removal would ren42

der the patient hypothyroid. Ectopic thyroid malignancy is rare.16 Nuclear medicine scans with iodone 123 determine functioning thyroid tissue, both ectopic and in the neck.4 Non-contrast CT images reveal a hyperdense midline mass within the intrinsic tongue musculature. Enhancement after contrast is normal. This enhancement can be heterogeneous if goitrous or thyroiditis changes are present. At MRI, lingual thyroid tissue is isointense to hyperintense to intrinsic tongue musculature on T1W and T2W images with homogeneous contrast enhancement (Fig 3).17,18 Thyroglossal Duct Cyst. Thyroglossal duct cysts are the most common congenital neck abnormality. They often present at a young age, with 50% presenting before age 10. These lesions represent incomplete involution of the thyroglossal duct tract. Therefore they can occur anywhere along the path of the thyroglossal duct, from the foramen cecum to the thyroid gland.19 Approximately 65% are infrahyoid in location—in the region of the thyrohyoid membrane—15% are at the level of the hyoid, and 20% are suprahyoid. Infrahyoid thyroglossal duct cysts are paramedian (within 2 cm of midline), and suprahyoid thyroglossal duct cysts are typically midline between the bellies of anterior digastric muscles. Hyoid thyroglossal duct cysts grow through the hyoid Curr Probl Diagn Radiol, March/April 2001

FIG 5. Infected second branchial cleft cyst. Axial CCT images depict a cystic mass with septations, mural thickening, and adjacent soft tissue thickening (small white arrow). The mass is located just below the angle of the mandible, anterior to the sternocleidomastoid (black arrow) and posterolateral to the submandibular gland (large white arrow).

bone. Infrahyoid cysts are intimately associated with the strap muscles, with the muscles encapsulating the surface of the cyst. They typically are 2 to 4 cm in size.4 The clinical presentation is usually an enlarging, painless mass in a pediatric or young adult patient. Many clinically present as a consequence of infection.20 Rarely, thyroglossal duct abnormalities are associated with carcinoma.21 Surgical resection is via the Sistrunk procedure. This removes a portion of the hyoid bone and a core of tissue along the expected thyroglossal duct course.22 On CT, these lesions are well-circumscribed fluid density masses with thin walls and thin capsular enhancement (Fig 4). Septations can be present. Increased density within the cyst is suggestive of prior infection or hemorrhage. The adjacent soft tissues are normal unless superimposed infection is present. On MRI, the cysts are hypointense on T1W images and hyperintense on T2W images. Cyst complexity increases and signal characteristics vary after inflammation.19,23 Branchial Cleft Cysts. Embryologic development of the head and neck begins with the development of the branchial apparatus, which begins at 4 weeks of gestaCurr Probl Diagn Radiol, March/April 2001

tional age. Six branchial arches form, but only the first four proliferate, with each being responsible for the development of specific arteries, nerves, and condensations of mesoderm. The apparatus consists of six arches separated by five ectodermal clefts and five endodermal pouches. The first branchial cleft gives rise to the eustachian tube, tympanic cavity, mastoid antrum, tympanic membrane, and external auditory canal. The second through fifth clefts obliterate. The second branchial pouch gives rise to the palatine tonsils and tonsillar fossa. The third branchial pouch forms the inferior thyroid and parathyroid glands, thymus, and pyriform sinus. The fourth branchial pouch leads to the formation of the superior thyroid and parathyroid glands and the pyriform sinus apex.15 Failure of branchial apparatus development results in any combination of cyst, sinus, or fistula in predictable locations. Most present as cysts (75%), fistulas (25%), and skin tags and cartilages (1%).24 Cysts typically present in children or young adults, whereas patients with fistulas are younger, presenting in infancy or early childhood. First branchial cleft cysts are epithelium-lined cysts that typically present in young females with a history of multiple parotid infections unresponsive to treatment. The residual embryonic tract begins near the submandibular triangle, ascends through the parotid gland, and terminates near the junction of the cartilaginous and bony external auditory canal. Imaging reveals a cystic mass of the parotid. The cyst can have a fistulous component that may connect to the external auditory canal at the junction of the bony and cartilaginous portions. There may also be a cutaneous opening near the angle of the mandible. Inflammation or prior surgery will increase the complexity of lesions. Second branchial cleft cysts are the most common branchial cleft anomaly, accounting for greater than 90% of branchial cleft anomalies. Most are cysts, but any combination of cyst and fistula can occur. There may be a cutaneous opening anterior, above the clavicle. The tract ascends lateral to the carotid space to the level of the bifurcation. Then the tract passes between the external and internal carotid arteries to the pharyngeal mucosa at the level of the tonsillar fossa. The age at presentation is between 10 and 40 years of age for cysts, with fistulas presenting in the first decade. The cyst classically presents as a painless, fluctuant mass at the angle of the mandible. It can slowly enlarge and become painful if infected. Recurrent infection in this region is highly suggestive.5 43

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FIG 6. Masseter hemangioma. A, Coronal T1W MRI image reveals a mass of the right masseter that is isointense to skeletal muscle (white arrow). Coronal (B) and axial (C) T1W post-gadolinium MRI images demonstrate homogeneous enhancement of this mass (black arrow). D, Axial T2W MRI image demonstrates homogeneous hyperintense T2 signal of the hemangioma without dilated vasculature.

At CT, these cysts are typically circumscribed with thin walls. The classic location is at the angle of the mandible, along the anteromedial border of the sternocleidomastoid muscle, lateral to the carotid sheath and posterior to the submandibular gland (Fig 5). On MRI, the cysts are hypointense to intermediate intensity on T1W images and hyperintense on T2W images. 44

Mural thickness and enhancement vary, depending on the presence of inflammation.19,25 Occasionally a “beak” of tissue may be seen pointing medially between the internal and external carotid arteries. This “beak sign” is considered a pathognomonic imaging feature of a second branchial cleft cyst.5 Cysts arising from the third and fourth branchial Curr Probl Diagn Radiol, March/April 2001

FIG 7. Oropharyngeal hemangioma. Axial T1W MRI image (left) reveals a circumscribed mass in the region of the inferior palatine tonsil (white arrow) that is isointense to adjacent muscle. Axial T2W MRI image (right) demonstrates homogeneous, hyperintense T2 signal (black arrow) of the lesion without dilated vessels.

clefts are extremely rare. Despite their rarity, third branchial cleft cysts are the second most common congenital lesions of the posterior triangle after cystic hygroma. The most common imaging feature is a unilocular cystic mass in the posterior triangle. Fourth branchial cleft anomalies most commonly are fistulas. Third and fourth branchial cleft fistulas are generally intimately associated with the pyriform sinus. Sinus tracts may be present in the lower neck.5,19 Vascular Lesions. Two major types of vascular lesions are described, hemangiomas and vascular malformations. Hemangioma. Hemangiomas are the most common benign tumors of infancy. These are true neoplastic lesions, exhibiting endothelial cell proliferation and increased turnover. Hemangiomas most commonly affect the trunk and extremities; however, the head and neck are involved approximately 20% of the time.26 They can be superficial or deep. Superficial lesions are diagnosed clinically by their purplish hue. Intramuscular hemangiomas of the head and neck commonly involve the masseter and trapezius muscles (Fig 6).27 The most common oropharyngeal site is submucosal, near the base of the tongue (Fig 7).8 Hemangiomas generally present shortly after birth and undergo proliferation lasting 6 to 12 months. This is followed by an involutional phase, which is variable in length, with 50% resolution at 5 years and 70% at 7 years.28 Histologic findings during involution consist of endothelial cell reduction in size and number, vascular channel ectasia, and progressive deposition of fibrous and fatty tissue. Curr Probl Diagn Radiol, March/April 2001

On CT, hemangiomas are transspatial or welldefined homogeneous masses with intense, persistent enhancement. In the proliferative phase, a lobulated enhancing mass is seen with dilated feeding and draining vessels. On MRI, they demonstrate T1W signal isointense to skeletal muscle, hyperintense T2 signal, and enhanced post-gadolinium signal. Gradient echo images demonstrate an extensive network of vessels. During involution, hemangiomas have decreased contrast enhancement, diminished vascularity, and fibrofatty tissue deposition. Reflective of their histologic transition, involuting hemangiomas have heterogeneous imaging features.29,30 Vascular Malformations. Vascular malformations are not tumors but are congenital vascular anomalies. They are classified based on the predominant type of anomalous vessel. These include capillary, venous, arteriovenous, and mixed malformations.31 Vascular malformations are typically present at birth but manifest clinically in late infancy or early childhood. They are frequently associated with regional skeletal hypertrophy and slow growth. They do not involute. Rapid proliferation can occur with infection or puberty.4 In addition to histologic and vascular classification, it is clinically important to distinguish vascular lesions as high- or low-flow lesions.28 Capillary malformations, venous malformations, and involuting hemangiomas are characteristically low-flow lesions. Arteriovenous malformations and proliferating hemangiomas are high-flow lesions. High-flow lesions have dilated tortuous vascular structures, rapid shunting, 45

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FIG 8. Facial arteriovenous malformation. A, Axial T1W after gadolinium. Axial T2W (B) and coronal (C) T2W MRI images reveal massive dilatation of vascular structures (white arrows) in the left temporalis region without a discrete soft tissue mass

and enhancement (Fig 8). Low-flow lesions are typically soft tissue masses that are infiltrative without dilated vessels and mild enhancement. Capillary malformations are low-flow lesions and are observed most frequently as a component of a syndrome such as Sturge-Weber. Venous malformations are the most common vascular malformations to involve the oral cavity. The presence of phleboliths is diagnostic.32 Arteriovenous malformations can be distinguished 46

from proliferating hemangiomas by lack of any discrete soft tissue mass.33 Oral and facial arteriovenous malformations and proliferating hemangiomas are difficult lesions to treat. A variety of therapies have been used with varying degrees of success. These include steroid administration, laser photocoagulation, sclerotherapy, embolization, and surgical resection.34 Cystic Hygroma. A cystic hygroma is a congenital Curr Probl Diagn Radiol, March/April 2001

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FIG 9. Congenital cystic hygroma. Coronal T1W (A) and coronal T2W (B) MRI images reveal a transspatial cystic mass with septations (hypointense on T1W image and hyperintense on T2W image). The mass originates in the posterior triangle of the neck and descends into the axilla and lateral chest wall.

malformation of the lymphatics. Lymphatic malformations are classified into three types based on the size of the anomalous lymphatic spaces. These include capillary hemangioma or lymphangioma simplex (small cysts), cavernous lymphangiomas (medium cysts), and cystic hygroma (large cysts).5 These malformations result from a defect of the lymphatic channels draining into the venous system. The majority of these lesions are present at birth, with 90% presenting by age 2 years, the age of greatest lymphatic growth.19 The remainder present as neck masses in young adults or can be post-traumatic, post-surgical, or sequelae of infection. The most common location is the posterior triangle (posterior to the sternocleidomastoid). Submandibular, parotid, and sublingual spaces are less common locations. Although rare in adults, they are more commonly found in the submandibular space.4 The most common presentation is a painless soft compressible mass. The mass may rapidly enlarge if there is evidence of infection, inflammation, or hemorrhage. The lesions are characteristically infiltrative in nature and do not respect fascial planes. Consequently, they can extend from the posterior cervical triangle into the axilla or mediastinum (Fig 9). A number of conditions are associated with lymphatic malformation, including Turner’s syndrome, Down’s syndrome (trisomy 21), trisomies 18 and 13, and others.35 Curr Probl Diagn Radiol, March/April 2001

FIG 10. Bilateral lymphangiomas. Coronal T2W image (top) and axial T2W MRI image (bottom) reveal multi-loculated cystic lesions of the masseteric and submandibular regions (white arrows) that infiltrate the normal structures.

The appearance on CT is that of a transspatial multilocular cystic mass that insinuates in and around normal neurovascular structures. The relationship to adjacent structures is best depicted with MRI. On MRI, 47

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B FIG 11. “Diving” ranula. A, Axial T2W MRI image demonstrates a linear hyperintense lesion in the sublingual space (large white arrow) between the genioglossus muscle (small white arrow) and the mylohyoid muscle (open white arrow). Note the “tail” of fluid dissecting posteriorly around the free edge of the mylohyoid (long white arrow). B, Coronal T1W image confirms the sublingual space location of this hypointense (cystic) lesion superior and medial to the mylohyoid (white arrow). The lesion conforms to the sublingual space.

FIG 12. Cystic hygroma versus epidermoid. Axial CCT images reveal a unilocular cystic mass in the right submandibular space displacing the mylohyoid medially (black arrow). Epidermoid versus cystic hygroma cannot be distinguished by imaging. The lack of sublingual space involvement excludes a ranula. The ventral location of the lesion to the submandibular gland makes a second branchial cleft cyst an unlikely diagnosis.

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lymphatic malformations are hyperintense on T2W images and hypointense on T1W images (Fig 10). Most have signal intensity greater than that of cerebrospinal fluid on both T1W and T2W images, suggesting proteinaceous fluid. They may enhance, and the margins may undulate.26,33 Treatment is surgical and often difficult because of the close proximity and adherence of normal adjacent structures. Dermoid/Epidermoid. Dermoid cysts, epidermoid cysts, and teratoid cysts compose the spectrum of teratomas, which are defined as neoplasms whose tissue is foreign to that part of the body from which the tumor arises. Epidermoid cysts are simple cysts with epithelial lining surrounded by a fibrous capsule. Dermoid cysts are like epidermoids, with the additional presence of skin appendages (hair follicles and sebaceous glands). Teratoid cysts contain skin appendages as well as mesenchymal connective tissue derivatives.19 Dermoid cysts usually present during the second and third decades of life. Epidermoids and dermoids usually present as slow-growing submandibular and sublingual masses, respectively. Imaging reveals unilocular masses in their respective locations. Epidermoids display fluid characteristics and may enhance peripherally. Dermoids exhibit imaging appearances that reflect their fat content. This manifests as low attenuation on CT and hyperintensity on T1W images, with a heterogeneous internal appearance.32 Curr Probl Diagn Radiol, March/April 2001

FIG 13. Sublingual space abscess. Axial CCT images depict a peripherally enhancing fluid collection in the sublingual space (arrowhead) with surrounding soft tissue edema. An absent tooth root of the second molar identifies the infection source (long white arrow). The delayed post-contrast coronal image (bottom right) confirms the sublingual location of the abscess (arrowhead) above the mylohyoid (long white arrow).

Ranula. Ranulas are post-inflammation retention cysts of the sublingual gland. They are epitheliumlined cystic masses found in the floor of the mouth that usually present with painless swelling of the sublingual space. If the simple cyst ruptures, fluid may dissect posteriorly into the submandibular space around the free edge of the mylohyoid. This is caused by the incomplete fascial boundary.5 This is then termed a “diving” or “plunging” ranula. “Diving” ranulas lack an epithelial lining and are actually psuedocysts.36 On CT, ranulas are unilocular, non-enhancing masses of low density that conform to the fascial boundaries of the sublingual space. On MRI, these lesions are homogeneously hypointense on T1W images and hyperintense on T2W images (Fig 11). “Diving” ranulas have a characteristic “tail” within the sublingual space between the mylohyoid and genioglossus muscles. Simple ranulas cannot be distinguished by imaging from epidermoids and cystic hygromas (Fig 12).5 Infection. The clinical presentation depends on the location of the infection. Peritonsillar abscesses are usually preceded by pharyngitis. Dental manipulation usually precedes odontogenic infections. This can be Curr Probl Diagn Radiol, March/April 2001

FIG 14. Submandibular stone with abscess. Axial CCT images reveal an amorphous calcific density in the left submandibular duct region (small white arrow) with an adjacent peripherally enhancing fluid collection. The ipsilateral submandibular gland is enlarged with surrounding soft tissue edema (curved white arrow) indicative of inflammation.

associated with osteomyelitis and parapharyngeal space spread. The relationships of the apices of the mandibular teeth to the mylohyoid sling may determine which region of the floor of the mouth is involved by dental infections. The roots of the second and third molar lie below the mylohyoid, such that infection of these teeth tends to involve the submandibular space. Infections of the first or premolars, located above the mylohyoid, involve the sublingual space (Fig 13).4 Submandibular and parotid calculi can be sources of inflammation and infection.37 Infection in the oropharynx and the oral cavity can involve the draining lymph nodes, which can lead to lymphadenitis, nodal abscess, and extra-capsular infection spread. Because of the proximity of neurovascular structures, psuedoaneurysm, thrombophlebitis, and nerve paralysis are all potential complications.5 Enhanced CT is the preferred method of imaging. CT has the ability to identify the infection source (dental lesion, calculi, etc) and is moderately sensitive for osteomyelitis (Fig 14). Delayed post-contrast images in the area of interest are helpful in evaluating for delayed peripheral enhancement of abscesses. Abscesses are 49

FIG 15. Transspatial infection. Axial CCT images demonstrate heterogeneous enhancement, diffuse edema, and enlargement of the soft tissues of the mid face (curved arrows) with contiguous inflammatory change in the masticator, carotid, and parapharyngeal spaces (black arrows). Central low density is not evident to suggest an abscess.

single or multi-loculated collections that have fluid density centers surrounded by peripheral enhancement. Cellulitis is enhancing soft tissue with cutaneous and subcutaneous stranding without central low density (Fig 15). Lymphadenitis is enlargement of lymph nodes with stranding of the surrounding capsular and extracapsular tissues (Fig 16). Supporative adenitis is defined as lymph nodes with fluid-filled centers. Mixed density lymph nodes with associated calcification are suggestive of granulomatous infection.5 Ludwig’s angina is a severe form of cellulitis, usually caused by staphylococcal or streptococcal bacteria. Before the development of antibiotics, the infection would spread inferiorly along fascial planes into the mediastinum, thus producing chest pain. The cellulitis of Ludwig’s angina always involves the sublingual and submandibular spaces. It is commonly bilateral and produces gangrene or serosanguinous phlegmon with little or no frank pus. The fascia, connective tissue, and muscle are involved, but glandular structures are not. Spread is by contiguity, not lymphatics.38 The infection is typically encountered after mandibular extrac50

FIG 16. Lymphadenitis. Axial CCT images reveal multiple enlarged enhancing bilateral lymph nodes (white arrows) with ill-defined margins and low density in the adjacent soft tissues indicative of extracapsular disease. Central necrosis is not evident.

FIG 17. Pleomorphic adenoma. Axial T1W (left) and axial T2W (right) MRI images depict a circumscribed mass in the right parapharyngeal space (white arrows) that is isointense to muscle on the T1W image and hyperintense signal on the T2W image.

tion. Imaging is used to determine airway patency, document gas-forming organisms, detect underlying dental infection or osteomyelitis, and identify drainable abscesses. Diffuse cellulitis is the typical imaging appearance.32 Tumors Benign Tumors. Benign tumors are rare in the oral cavity. Curr Probl Diagn Radiol, March/April 2001

FIG 18. Fibrolipoma. Axial CCT images demonstrate a septated mass at the junction of the oropharynx/hypopharynx that contains both fat and soft tissue elements (white arrows).

PLEOMORPHIC ADENOMA. Pleomorphic adenomas arise from minor salivary gland tissue and are the most common benign tumors that occur in submandibular and sublingual spaces. Although the majority of pleomorphic adenomas occur in the parotid gland, 8% originate in the submandibular gland, 0.5% arise in the sublingual gland, and 6.5% occur in minor salivary gland rests throughout the upper aerodigestive tract. On CT, they are usually circumscribed masses that can have heterogeneous internal composition. On MRI, they are usually isointense to skeletal muscle on T1W images and homogeneously hyperintense on T2W images (Fig 17).4 LIPOMA. Lipomas are benign encapsulations of mature adipose tissue. Thirteen percent of lipomas occur in the head and neck. Most commonly, they occur in the posterior triangle. The remaining locations are rare, occurring in the pharynx, oral cavity, parotid gland, and larynx. Lipomas represent 1% to 4% of benign oral cavity tumors. Some variants have been classified histologically, according to the kind and amount of tissue, other than fat, that may be present. The most common variant is the fibrolipoma, which contains an increased amount of fibrous connective tissue (Fig 18).39 At CT and MRI, lipomas exhibit the same imaging characteristics of subcutaneous fat. They typically are well demarcated, although rarely they can be infiltrative. AGGRESSIVE FIBROMATOSIS. Aggressive fibromatosis is an infiltrative fibrous tumor that grows rapidly. These tumors are benign in histology but are locally aggressive, with high recurrence rates. They most commonly occur in children less than 5 years of age. The neck and supraclavicular regions are common sites

Curr Probl Diagn Radiol, March/April 2001

FIG 19. Vagal schwannoma. Axial T2W (top left), axial T1W (top right), coronal T1W (bottom left), and axial T1W post-gadolinium with fat saturation (bottom right) MRI images demonstrate a complex mass of the left carotid space (white arrows). This mass is isointense to muscle on the T1W images, has multi-loculated hyperintense signal on the T2W images, and has heterogeneous enhancement with central areas of low intensity, indicating cystic areas.

of involvement; involvment of the oral cavity occurs much less frequently.32 Desmoid is a term for a subtype of these lesions. Aggressive fibromatosis infiltrates fatty planes and may be inseparable from adjacent muscle, nerves, and vessels.4 CT reveals a homogeneous soft tissue mass that may enhance. On MRI, these tumors exhibit variable signal characteristics, typically isointense or hypointense to skeletal muscle on T1W images and hypo- to hyperintense on T2W sequences. NEUROGENIC NEOPLASMS. Schwannomas and neurofibromas may occur in the oral cavity. The tongue is a common oral cavity location. On CT, these lesions are well-circumscribed homogeneous masses. On MRI, they are hyperintense on T2W images and isointense to muscle on T1W images. Schwannomas enhance after contrast or after gadolinium. Cystic areas are common with larger schwannomas (Fig 19).4 Malignant Tumors SQUAMOUS CELL CARCINOMA. Squamous cell carcinoma (SCCA) is the most common malignant tumor 51

encountered in the oral cavity and oropharynx, representing greater than 90% of all neoplasms. Tumors occur mostly in men more than 45 years of age and are associated with tobacco and alcohol use.40 The radiologist’s role is to define the stage of lesions. It is important to discuss the physical examination or endoscopic evaluation performed by the referring physician before interpretation. Important issues when imaging the oral cavity and oropharynx are the extent of the lesion identified, depth of invasion, and nodal involvement. The American Joint Commission on Cancer staging system for SCCA of the oral cavity is as follows: T0, no evidence of primary tumor; T1, greatest diameter of primary tumor is 2 cm or less; T2, greatest diameter of primary tumor is more than 2 cm but less than 4 cm; T3, greatest diameter of primary tumor is more than 4 cm; T4, greatest diameter of primary tumor is more than 4 cm, with deep invasion involving the maxillary antrum, pterygoid muscles, base of the tongue, or skin of the neck.41 With oral cavity cancers, the issues of depth of invasion (tongue and base of tongue), pterygomandibular raphe invasion, mandible and maxillary invasion, and pterygopalatine fossa invasion are all important in assessing the primary disease.42 Nodal spread significantly affects patient outcome (reducing 5-year survival by 50%), emphasizing the importance of identifying pathologic lymph nodes in all patients with cancer.43 Because of the rich lymphatics of the oral cavity, approximately one third of patients with SCCA of the oral cavity have clinical evidence of lymph node invasion at initial presentation. The primary drainage sites are level 1 (submandibular and submental) nodes for anterior oral cavity and lip carcinomas. Posterior oral cavity and oropharyngeal carcinomas primarily drain to level 2 (high internal jugular chain) nodes.44 Bilateral lymphadenopathy is common. Early distant metastasis is rare.2 At CT, most SCCAs will enhance to some degree after contrast. Contrast uptake may be difficult to identify when the lesion originates contiguous with bone, such as in the anterior floor of the mouth, because of beam hardening artifacts. On MRI, tumors commonly exhibit low signal intensity comparable to that of skeletal muscle on T1W images and have intermediate or high signal intensity on T2W images, making them very conspicuous against dark muscle on fat-suppressed T2W images. As with CT, most tumors enhance after gadolinium administration on T1W images, and fat suppression increases tumor conspicuity.11,12 CT is preferred for evaluating bone invasion. MR imaging with 52

fat saturation is superior for detecting perineural tumor spread.45 Squamous cell carcinoma of the lip is the most common malignant lesion of the oral cavity. On CT and MRI, the primary tumor may appear as a mass with or without ulceration. Lip carcinomas can invade adjacent bone along the buccal surface of the alveolar ridge and are best detected with CT. Tumors can extend into the mental and inferior alveolar canals via perineural extension, without bone destruction.10 The floor of the mouth is the second most common site of SCCA in the oral cavity.2 Most tumors originate in the anterior portion of the floor of the mouth within 2 cm of midline. Penetration beneath the mucosa into the sublingual space can obstruct the submandibular duct, resulting in chronic inflammation, and predispose the patient to infection of the submandibular gland. Inferior extension to the genioglossus and geniohyoid muscles can ultimately lead to tongue invasion. Denervation atrophy can result from invasion of hypoglossal and lingual nerves. Mylohyoid invasion signifies spread into the submandibular space. Medial tumor spread across the midline (invading the contralateral lingual neurovascular pedicle) precludes local resection with hemiglossectomy as a surgical treatment option. Extension into the oral vestibule is recognized clinically, since the tumor extends over the mandibular occlusal ridge. Mandibular invasion is difficult to detect clinically. The mandibular periosteum acts as an effective tumor barrier. Mandibular invasion is typically a late manifestation, although extension toward the gingiva and periosteum of the mandible occurs early and frequently. Large tumors may destroy the inner cortex of the mandible (Fig 20).10 Tumors arising in the lateral floor of the mouth are less common but have similar dissemination patterns. Advanced lesions may extend beyond the oral cavity and infiltrate other contiguous spaces of the suprahyoid neck. Particularly at risk are the fatty parapharyngeal and masticator spaces. The medial pterygoid (of the masticator space) inserts into the inner cortex of the angle of the mandible and may be invaded relatively early by tumors of the lateral floor of the mouth.46 Nearly all SCCAs of the oral tongue originate on the lateral and undersurface of the tongue. SCCAs tend to remain confined to the tongue until quite large, and in general, the prognosis of oral tongue cancer is more favorable than carcinoma of the tongue base. Oral tongue carcinomas typically first invade the lateral musculature. Then they invade the lingual vascular Curr Probl Diagn Radiol, March/April 2001

A

FIG 20. Floor of mouth SCCA. Axial CCT images demonstrate a large ill-defined enhancing mass of the floor of mouth with mandibular invasion (small black arrow, top left), ipsilateral lingual vascular pedicle invasion (large white arrow), submandibular duct obstruction (large black arrow, top left), and bilateral pathologic level 1 and level 2 lymph nodes (small white arrows).

pedicle, lingual septum, and the contralateral tongue. Tumor extension across midline and invasion of the contralateral lingual neurovascular pedicle preclude surgical resection for cure at most institutions because of the morbidity associated with total glossectomy. Because of the anatomic position of the genioglossus muscle, it constitutes a natural path for tumor extension toward the anterior floor of the mouth and mandible. Posterior lesions grow into the floor of the mouth, the glossotonsillar sulcus, the oropharyngeal tonsil, and underlying deep structures. Superior extension occurs into the soft palate via the palatoglossus muscle. Further extension to the nasopharynx can occur via the veli palatini muscles (Fig 21).42 The retromolar trigone is a small triangle-shaped area posterior to the last molars. Because of this critical anatomic location, SCCAs originating may have complex patterns of spread. The pterygomandibular raphe attaches superiorly to the medial pterygoid and inferiorly to the posterior mandible. This forms a junction between the oral cavity, oropharynx, and nasoCurr Probl Diagn Radiol, March/April 2001

B FIG 21. Oral tongue SCCA. Axial CCT image (A) and coronal delayed CCT image (B) demonstrate a focal enhancing mass (white and black arrows) of the lateral oral tongue that medially displaces the ipsilateral lingual vascular pedicle.

pharynx. It also serves as a common insertion site for the orbicularis oris, the buccinator, and the superior constrictor muscles. Therefore, tumors arising in the retromolar trigone may grow anteriorly into the buccal region, posteriorly into the palatine tonsils, superiorly into the skull base, and inferiorly into the floor of the mouth. Because of the close proximity of the maxilla 53

A

FIG 22. Retromolar trigone SCCA. Axial CCT image reveals an illdefined enhancing mass of the right retromolar trigone with erosion of the adjacent cortex of the maxilla (black arrow).

and ramus of the mandible, tumors can invade bone early (Fig 22).47 The treatment of malignant neoplasms of the tongue and floor of the mouth is beyond the scope of this discussion and is based on a compromise between oncotherapeutic imperatives and functional as well as aesthetic requirements. There is no general consensus, and treatment protocols vary among institutions. Current treatment options for the primary tumor include surgery (with or without postoperative radiation), brachytherapy, external-beam radiation with hyperfractionation, and induction chemotherapy.46 MINOR SALIVARY GLAND MALIGNANCIES. Carcinomas other than SCCA in the oral cavity are rare. The majority of cases are carcinomas that arise from minor salivary glands and are identical to those that occur in the major salivary glands. These include adenoid cystic carcinoma, mucoepidermoid carcinoma, adenocarcinoma, and mixed cell types. Approximately 50% of minor salivary gland tumors are malignant, with adenoid cystic being the most common histologic type (Fig 23). Adenoid cystic carcinoma tends to infiltrate neurovascular bundles early and often, accounting for a high incidence of local recurrence. Mucoepidermoid carcinomas arise from ductal epithelium, recur locally, and metastasize to regional lymph nodes (Fig 24). Adenocarcinomas are rare in the oral cavity, but they 54

B FIG 23. Retromolar trigone adenoid cystic carcinoma. A, Axial T1W post-gadolinium MRI image depicts an enhancing mass of the left retromolar trigone (black arrow). B, Axial T2W image demonstrates corresponding hyperintense T2 signal of the lesion (black arrow).

have the worst prognosis of the minor salivary gland neoplasms. The imaging findings are non-specific and cannot distinguish minor salivary tumors from SCCA.8 LYMPHOMA. Lymphoma represents the second most common malignancy to affect the extra-cranial head and neck after squamous cell carcinoma. The nonHodgkin’s form accounts for approximately 75% of lymphoma, and Hodgkin’s disease accounts for the remaining 25%.8 Hodgkin’s and non-Hodgkin’s lymphomas occur commonly in the head and neck and rarely isolated to the oral cavity. Large and often bilatCurr Probl Diagn Radiol, March/April 2001

FIG 24. Mucoepidermoid carcinoma. Axial CCT reveals a poorly defined mass of the right submandibular space with dystrophic calcification, invasion of the ipsilateral mylohyoid, and mandibular cortical erosion (black arrow). This lesion originated from the mandible.

eral, homogeneously enhancing lymph nodes are the predominant imaging finding in head and neck lymphoma (Fig 25). However, the imaging appearance of lymphoma, particularly non-Hodgkin’s, can vary considerably.44 Although central necrosis may be seen in non-Hodgkin’s lymphoma, it is rare in Hodgkin’s unless treatment has been rendered. This may help distinguish lymphoma from metastatic lymphadenopathy.8 NonHodgkin’s lymphoma more frequently involves extranodal sites. Waldeyer’s ring (nasopharyngeal adenoids, palatine, and lingual tonsils) is a common extra-nodal site. Extra-nodal primary sites are unusual in Hodgkin’s lymphoma. Contiguous disease and a dominant nodal mass are common manifestations.44 Miscellaneous Lesions DENERVATION ATROPHY. Cranial nerves supply motor innervation to various muscles and muscle groups in the head and neck. When the innervation is interrupted by neural involvement with tumor or infection, there is loss of motor function ipsilateral to the lesion. This results in fatty infiltration and hemiatrophy of the involved muscles. On imaging studies, the fatty atrophy is easily appreciated. However, the asymmetry can be mistaken for tumor due to the relative enlargement of the normal side. The hypoglossal nerve provides innervation to the intrinsic and extrinsic muscles of the tongue. Lesions affecting the nerve can result in muscle atrophy in 2 to 3 weeks. When present, a search for pathology along Curr Probl Diagn Radiol, March/April 2001

FIG 25. Non-Hodgkin’s lymphoma. Axial CCT image demonstrates a large soft tissue mass in the right jugulodigastric region with marked mass effect on the adjacent carotid and parapharyngeal spaces (long white arrow).

FIG 26. Hypoglossal nerve denervation atrophy. Axial CCT image depicts volume loss and fatty infiltration of the ipsilateral oral tongue (long white arrow). This patient has an inferior tonsil SCCA with vascular space invasion (note thickening around the ipsilateral internal carotid artery).

the entire course of the hypoglossal nerve to include the brainstem is indicated (Fig 26). The mandibular nerve provides motor innervation to the muscles of mastication, tensor tympani, and tensor 55

FIG 28. Palatine tonsil SCCA. Axial T1W post-gadolinium MRI images depict an ill-defined mass of the left palatine tonsil with mild enhancement (white arrows, bottom left images) that extends superiorly through the foramen ovale into the left cavernous sinus (top images, white arrows).

FIG 27. Mandibular nerve (V3) denervation atrophy. Axial T1W MRI images (top) reveal volume loss and fatty infiltration of the right masseter and pterygoid muscles (white and black arrows). Coronal and axial T1W MRI images after gadolinium with fat saturation (bottom) demonstrate an ill-defined enhancing mass in the right foramen ovale (large white and curved arrows)

veli palatini. Via the mylohyoid nerve, motor innervation is also supplied to the anterior belly of the digastric and the mylohyoid muscles. Injury to the mandibular nerve results in fatty atrophy of all the above muscles (Fig 27). Isolated injury to the mylohyoid nerve results in injury only to the anterior belly of the digastric and the mylohyoid muscles. Search for neural pathology along the entire course of the mandibular nerve to include the brainstem is required when V3 atrophy is present.14,32

Oropharynx Malignant Tumors. Malignant lesions from the oral mucosa are the predominant diseases. Among these, 95% are SCCA. Other lesions are rare: lymphoma, minor salivary gland tumors, adenocarcinoma, sarcoma, and melanoma. Imaging has little specificity, and histologic diagnosis is always needed. Squamous Cell Carcinoma. Oropharyngeal SCCAs are usually poorly differentiated and locally advanced at the time of clinical presentation. The overall inci56

dence of cervical lymph node metastasis is 50% to 70%. Therefore prognosis is often poor.3 Staging of oropharyngeal carcinoma uses the same T1 through T3 criteria as used for staging in the oral cavity. Advanced disease may involve the mandible, maxilla, soft tissues of the neck, or extrinsic muscles of the tongue, pterygoid muscles, or hard palate.41 A handful of critical areas determine the extent of surgery for oropharyngeal carcinoma, which include pre-epiglottic fat, mandible, maxillae, prevertebral musculature, pterygopalatine fossa, pterygomandibular raphe, and midline or deep invasion into the base of the tongue.42 Carcinoma of the tonsil is prone to spread posterolaterally to the lateral pharyngeal wall; inferiorly to the glossotonsillar sulcus, parapharyngeal space, pterygoid muscles, base of tongue, and floor of mouth; and superiorly to the soft palate and pharynx. Invasion into the parapharyngeal and masticator spaces may be associated with carotid artery encasement or extension superiorly along the fascia to the skull base. If tumor encasement is greater than 270 degrees of the circumference of the carotid artery on axial images, it is less likely that the tumor can be resected without carotid resection.48 Lymph node metastasis occurs primarily in the upper internal jugular (level 2) or retropharyngeal lymph nodes (Fig 28). Curr Probl Diagn Radiol, March/April 2001

FIG 29. SCCA of the tongue base. Axial CCT images demonstrate an enhancing mass of the right tongue base that extends superiorly to involve the right lateral oropharynx (top black arrows). Ipsilateral pathologic level 2 adenopathy (bottom white arrows) is present with poorly defined margins and surrounding low density suggestive of extra-capsular nodal disease in the carotid space.

SCCA of the base of the tongue is an aggressive, deeply infiltrative tumor with a 75% incidence of nodal metastasis at presentation. It may extend laterally to involve the mandible and medial pterygoid muscles; superiorly to involve the tonsillar fossae and soft palate; anteriorly to the oral tongue and floor of the mouth; and inferiorly to the vallecula, pre-epiglottic space, and epiglottis or hypopharynx (Fig 29). Normal lymphoid tissue at the base of the tongue may have imaging characteristics and enhancement similar to neoplasms. Histologic evaluation is the only way to differentiate the two.47 Carcinomas of the posterior oropharyngeal wall have the worst prognosis of all squamous cell carcinoma of the oral cavity and oropharyngeal carcinomas. These tumors spread in both a caudal direction into the hypopharynx and a cephalad direction onto the nasopharynx. They commonly spread submucosally, invading the retropharyngeal fat. The prevertebral fascia acts as a barrier to tumor spread, and invasion of the prevertebral muscles is uncommon at initial presentation.10 Curr Probl Diagn Radiol, March/April 2001

FIG 30. Peritonsillar abscess. Axial CCT images and delayed axial post-contrast image (bottom right) demonstrate a peripherally enhancing fluid collection with surrounding soft tissue edema of the right peritonsillar region (small black arrows) that extends into the right parapharyngeal and carotid spaces. Enlarged level 2 and posterior triangle lymph nodes are also present (large black arrows).

Treatment of oropharyngeal carcinoma is comparable to that of carcinoma of the oral cavity. Many disciplines are used with no general consensus and variable treatment protocols.47 Minor Salivary Gland Tumors. The soft palate is the most common site of origin of minor salivary gland tumors. In the soft palate, the incidence of minor salivary gland tumors is almost equal to that of SCCA. These tumors are usually off midline in the posterolateral portion of the soft palate, and they are not typically found anterior to a line drawn between the upper third molars. Spread may occur anteriorly to involve the hard palate. The radiographic findings are nonspecific, and the diagnosis is made by histologic analysis.8 Infection Peritonsillar Abscesses. Acute tonsillitis is usually a self-limited febrile illness in adolescents or young adults. Oral florae (Staphylococcus, Streptococcus, and Haemophilus) are the most common offending bacterial organisms. Supportive infection of the tonsils can result in peritonsillar or tonsillar abscesses. A severe sore throat and pharyngeal edema despite anti57

biotic therapy are the usual clinical presentations. Tonsillar abscesses are clinically evident, and imaging is usually not required. A peritonsillar abscess is accumulation of pus around the palatine tonsils.8 They typically are confined to the tonsillar fossa by the superior constrictor muscle. If the superior constrictor is penetrated, abscesses can extend outside the tonsillar fossa to involve the lateral retropharyngeal, parapharyngeal, submandibular, or prevertebral spaces (Fig 30). Trismus develops if the medial pterygoid muscle is involved. Septic thromboses of the adjacent jugular vein and erosion into the carotid artery are rare complications.10 REFERENCES 1. Mukherji SK, Castillo M. Normal cross-sectional anatomy of the nasopharynx, oropharnyx, and oral cavity. Neuroimaging Clin N Am 1998; 8:211-8. 2. Million RR, Cassisi NJ, Mancuso AA. Oral Cavity. In: Million RR, Cassisi NJ, editors. Management of head and neck cancer. A multidisciplinary approach. 2nd ed. Philadelphia: JB Lippincott; 1994. 3. Million RR, Cassisi NJ, Mancuso AA. Oropharynx. In: Million RR, Cassisi NJ, editors. Management of head and neck cancer. A multidisciplinary approach. 2nd ed. Philadelphia: JB Lippincott; 1994. 4. Smoker WRK. Oral cavity. In: Som PM, Curtin HD, editors. Head and neck imaging. 3rd ed. St Louis: Mosby; 1996. 5. Harnsberger HR. Handbook of head and neck imaging. 2nd ed. St Louis: Mosby; 1995. 6. Hiatt JL, Gartner LP. Textbook of head and neck anatomy. 2nd ed. Baltimore: Williams & Wilkins; 1987. 7. Sigal R. Oral cavity, oropharynx, and salivary glands. Neuroimaging Clin N Am 1996;6:379-400. 8. Suresh KM, Weissmann JL, Holliday RA. Pharynx. In: Som PM, Curtin HD, editors. Head and neck imaging. 3rd ed. St. Louis: Mosby; 1996. 9. Gray H. Anatomy. 38th ed. New York: Pearson Professional Limited; 1995. 10. Becker M. Oral cavity, oropharynx, and hypopharynx. Semin Roentgenol 2000;35:21-30. 11. Dubin MD, Teresi LM, Bradley WG, et al. Conspicuity of tumors of the head and neck on fat suppressed MR images: T2W fast spin echo versus contrast enhanced T1W conventional spin echo sequences. Am J Roentgenol 1995;164:1212. 12. Ross MR, Schomer DF, Chappell P, et al. MR imaging of head and neck tumors: Comparison of T1W contrast enhanced fat suppressed images with conventional T2W and fast spin echo T2W images. Am J Roentgenol 1994;163:173. 13. Leslie A, Fyfe E, Guest P, et al. Staging of squamous cell carcinoma of the oral cavity and oropharynx: a comparison of MRI and CT in T- and N- staging. J Comput Assist Tomogr 1999;23:43-9. 14. Laine FJ, Braun IF, Jensen ME, Nadel L, Som PM. Perineural extension through the foramen ovale: evaluation with MRI. Radiology 1990;174:65-71. 15. Moore K. The developing human. 3rd ed. Philadelphia: Saunders; 1988. 16. Okstad S, Mair IW, Sundsford JA, et al. Ectopic thyroid tissue in the head and neck. J Otolaryngol 1986;15:52-5.

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17. Willinsky RA, Kassell EE, Cooper PW, et al. Computed tomography of lingual thyroid. J Comput Assist Tomogr 1987;11:182-3. 18. Johnson JC, Coleman LL. Magnetic resonance imaging of lingual thyroid gland. Pediatr Radiol 1989;19:461-2. 19. Koeller KK, Alamo L, Adair CF, Smirniotopoulos JG. Congenital cystic masses of the neck: radiologic pathologic correlation. Radiographics 1999;19:121-46. 20. Sturgis EM, Miller RH. Thyroglossal duct cysts. J La State Med Soc 1993;145:459-61. 21. Boswell WC, Zoller M, Williams JS, et al. Thyroglossal duct carcinoma. Am Surg 1994;60:650-5. 22. Allard R. The thyroglossal duct cyst. Head Neck Surg 1982;5:134-46. 23. Reede DL, Bergeron RT, Som PM. CT of thyroglossal duct cysts. Radiology 1985;157:121-5. 24. Telander R, Deane S. Thyroglossal and branchial cleft cysts and sinuses. Surg Clin North Am 1977;57:779-91. 25. Harnsberger H, Mancuso A, Muraki A, et al. Branchial cleft anomalies and their mimics: computed tomographic evaluation. Radiology 1984;152:739-48. 26. Woodruff WW, Kennedy TL. Non-nodal neck masses. Semin Ultrasound CT MR 1997;18:182-204. 27. Rossier JL, Hendrix RA, Tom LWC, et al. Intramuscular hemangioma of the head and neck. Head Neck Surg 1993;108:18-26. 28. Fishman SJ, Mulliken JB. Hemangiomas and vascular malformations of infancy and childhood. Pediatr Clin North Am 1993;40:1177-200. 29. Baker LL, Dillon WP, Heishima GB, et al. Hemangiomas and vascular malformations of the head and neck: MR characterization. AJNR Am J Neuroradiol 1993;14:307-14. 30. Dubois J, Garel L, Grignon A, et al. Imaging of hemangiomas and vascular malformations in children. Acad Radiol 1998;5:390-400. 31. Mulliken JB, Glowacki J. Hemangiomas and vascular malformations in infants and children: a classification based on endothelial characteristics. Plast Reconstr Surg 1982;69:41220. 32. Laine FJ, Wendy WRK. Oral cavity: anatomy and pathology. Semin Ultrasound CT MR 1995;16:527-45. 33. Fordham LA, Chung CJ, Donnelly LF. Imaging of congenital vascular and lymphatic anomalies of the head and neck. Neuroimaging Clin N Am 2000;10:1. 34. Dubois J, Garel L. Imaging and therapeutic approach of hemangiomas and vascular malformations in the pediatric age group. Pediatr Radiol 1999;29:879-83. 35. Descamps P, Jourdain O, Paillet C, et al. Etiology, prognosis, and management of nuchal cystic hygroma: 25 new cases and literature review. Eur J Obstet Gynecol Reprod Biol 1997;71:3-10. 36. Charnoff SK, Carter BL. Plunging ranula: CT diagnosis. Radiology 1987;158:467-8. 37. Ginsberg LE. Inflammatory and infectious lesions of the neck. Semin Ultrasound CT MRI 1997;18:205-19. 38. Grodinsky MD. Ludwig angina: an anatomical and clinical study with review of the literature. Surgery 1939;5:678-96. 39. Som PM, Scherl MP, Rao VM, et al. Rare presentations of ordinary lipomas of the head and neck: a review. AJNR Am J Neuroradiol 1986;7:657-64. 40. Close LG, Lee NK. Cancer of the oral cavity and oropharynx. In: Meyerhoff WL, Rice DH, editors. Otolaryngology. Philadelphia (PA): Saunders; 1992. p. 611-29. 41. Beahrs OH, Henson DE, Hutter RVP, Kennedy BJ, editors. Manual for staging of cancer: American Joint Committee on Cancer. 5th ed. Philadelphia: JB Lippincott Company; 1997.

Curr Probl Diagn Radiol, March/April 2001

42. Yousem DM, Chalian AA. Oral cavity and pharynx. Radiol Clin North Am 1998;36:967-81. 43. Som PM. Lymph nodes of the neck. Radiology 1987;165:593. 44. Kaji VK, Mohuchy T, Swartz JD. Imaging of cervical lymphadenopathy. Semin Ultrasound CT MR 1997;18:220-49. 45. Caldemeyer KS, Mathews VP, Righi PD, Smith RR. Imaging features and clinical significance of perineural spread or extension of head and neck tumors. Radiographics 1998;18: 97-110.

Curr Probl Diagn Radiol, March/April 2001

46. Sigal R, Zagdanski A-M, Schwaab G, et al. CT and MR imaging of squamous cell carcinoma of the tongue and floor of the mouth. Radiographics 1996;16:787-810. 47. Mukherji SK, Pillsbury HR, Castillo M. Imaging squamous carcinomas or the upper aerodigestive tract: what clinicians need to know. Radiology 1997;205:629-46. 48. Yousem DM, Hatabu H, Hurst MD, et al. Carotid artery invasion by head and neck masses: prediction with MR imaging. Radiology 1995;195:715-20.

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