Parotid Gland Tumour Mri Radiology

Figure 2.30. Axial CT scan (a) and corresponding PET scan (b) at the level of the parotid gland. Note the asymmetric slightly higher uptake on the right corresponding to partially resected parotid gland on the left, confirmed by CT.

into the substance of the gland. The parotid duct emanates from the superficial anterior part of the gland and is positioned along the superficial surface of the masseter muscle. Along the anterior aspect of the masseter muscle the duct turns medially, posterior to the zygomaticus major and minor muscle, to penetrate the buccinator muscle and


The submandibular gland is located in the upper neck in the submandibular space (SMS) and the posterior oral cavity in the sublingual space (SLS). The SMG is more difficult to measure, but the average adult superficial SMG measures 3.5 cm in oblique AP, 1.4 cm in oblique LR, and 3.3 cm in SI dimensions. The gland "wraps" around the posterior border of the mylohyoid muscle and traverses the two spaces. The superficial portion is in the SMS adjacent to level one lymph nodes (level 1b). The deep portion of the submandibular gland is located in the SLS. The SMS is bordered inferiorly by the hyoid bone and platysma and superiorly by the mylohyoid muscle. It is bordered laterally by the mandible and it is surrounded by the superficial layer of deep cervical fascia. Its medial border is a combination of the mylohyoid sling and anterior belly of the digastric muscle (Beale and Madani 2006) (Figures 2.31 through 2.37).

The submandibular duct emanates from the anterior-superior aspect of the gland and turns anteriorly and lies along the superior surface of the mylohyoid muscle between the genioglossus muscle medially and the sublingual gland laterally. The

Figure 2.31. Axial CT at the level of the submandibular gland demonstrating density higher than skeletal muscle.
Figure 2.32. Reformatted coronal CT at the level of the submandibular gland demonstrating its relationship to the mylohyoid muscle and floor of the mouth.
Figure 2.33. Reformatted sagittal CT at the level of the submandibular gland demonstrating its relationship to the floor of the mouth. Note the slight notch at the hilum of the gland. Majority of the gland "hangs" below the mylohyoid muscle.
Sublingual Gland Axial
Figure 2.34. Axial T1 MRI of the submandibular gland demonstrating slight hyperintensity to muscle. Note the bright subcutaneous fat.

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Figure 2.35. Coronal fat saturated T2 MRI of the submandibular gland. Note the slightly incomplete fat suppression and the engorged and edematous mucosa of the nasal cavity and turbinates.

Figure 2.36. Sagittal T1 fat saturated MRI of the submandibular gland demonstrating the well-defined appearance on a fat suppressed background. Note the slight notch at the hilum. Also note the entire internal jugular vein is visualized.

Parotid Gland Tumor Right Mri Images
Figure 2.37. Axial CT (a) and corresponding PET (b) of the submandibular gland demonstrating slight normal uptake. Note the strong asymmetry of uptake on the PET corresponds to the absent submandibular gland on the right confirmed by the CT.

a ducts open into the anterior medial (paramidline) floor of the mouth at the sublingual papillae.

On CT scans the submandibular gland has a density that is isodense to slightly hyperdense relative to skeletal muscle. The gland does not become as fatty replaced as the parotid gland. The SMG demonstrates a signal characteristic similar to that of skeletal muscle on T1 and T2 weighted images and is less intense when compared to the parotid gland secondary to less fatty replacement. The FDG uptake is moderate but higher than that of the parotid gland. The SMG undergoes contrast enhancement by CT and MRI (Kaneda 1996).


The sublingual gland is the smallest of the major salivary glands and is the least likely to be involved with pathology. The SLG measures approximately 3.5 cm in oblique AP, 1.0 cm in oblique LR, and 1.5 cm in SI dimensions. Anatomically, the SLGs are located in the floor of the mouth and lie on the superior surface of the mylohyoid muscle, bordered anteriorly and laterally by the mandible, and medially by the submandibular duct, genioglossus muscle, and geniohyoid muscle. The submandibu-lar gland serves as its posterior border (Figures 2.38 through 2.40). The sublingual gland commu-

Sublingual Gland Axial

Figure 2.38. Axial CT of the neck at the level of the sublingual gland demonstrating mild normal enhancement along the lateral floor of the mouth.

Sublingual Gland Axial

Figure 2.39. Axial contrast enhanced T1 MRI of the sublingual gland demonstrating enhancement (a). Note the deep lobe of the submandibular glands seen at the posterior margin of the sublingual glands. Coronal T2 weighted image demonstrating the sublingual gland "cradled" between the mandible laterally, the genioglossus muscle medially, the geniohyoid muscle inferomedially, and the combined mylohyoid and digastric muscles inferiorly (b).

Figure 2.39. Axial contrast enhanced T1 MRI of the sublingual gland demonstrating enhancement (a). Note the deep lobe of the submandibular glands seen at the posterior margin of the sublingual glands. Coronal T2 weighted image demonstrating the sublingual gland "cradled" between the mandible laterally, the genioglossus muscle medially, the geniohyoid muscle inferomedially, and the combined mylohyoid and digastric muscles inferiorly (b).

Figure 2.38. Axial CT of the neck at the level of the sublingual gland demonstrating mild normal enhancement along the lateral floor of the mouth.

Sublingual Gland Axial
Figure 2.40. Axial PET of the sublingual gland demonstrating the intense uptake seen in the sublingual glands bilaterally medial to the mandible (photopenic linear regions).

nicates with the oral cavity via multiple small ducts (ducts of Rivinus) that open into the floor of the mouth adjacent to the sublingual papilla. These small ducts may be fused and form a larger single duct (duct of Bartholin) and empty into the submandibular duct (Beale and Madani 2006).

The SLG can be seen by CT and MRI and is similar in appearance to the SMG, although smaller (Sumi et al. 1999a). FDG uptake is less well defined since it is small and closely approximated to adjacent skeletal muscle, but the uptake is moderate.

Occasionally accessory salivary tissue is found in the SMS along the anterior aspect (anterior to the normal submandibular gland). This is caused by herniation of SLG through defects in the mylohyoid muscle, called a mylohyoid boutonniere, which typically occurs between the anterior and posterior parts of the mylohyoid muscle. The accessory gland may be accompanied by sublingual branches of the facial artery and vein. Although the accessory tissue may mimic a tumor, this should be readily identified as normal since the accessory tissue has the same characteristics on CT and MRI as normal sublingual or subman-dibular gland (Hopp, Mortensen, and Kolbenstvedt

2004; White, Davidson, and Harnsberger et al. 2001).


The minor salivary glands are unevenly distributed throughout the upper aerodigestive tract and are submucosal in location. They are more concentrated in the oral mucosa, where they inhabit the mucosa of the hard and soft palate, buccal mucosa, and floor of the mouth, as well as the mucosa of the lips, gingiva, and tongue. They are also found in the pharynx (nasal and oral), sinonasal spaces, larynx, trachea, and bronchi. Functionally they are either mucinous (predominantly in the palatal mucosa) or mixed seromucinous glands. The serous minor salivary glands are found only on the tongue at the circumvallate papilla. The minor salivary glands do not have large defined ducts but do contain multiple small excretory ducts. MRI of minor salivary glands has been achieved with high-resolution surface coils of the upper and lower lips. Patients with Sjogren's disease had a smaller gland area relative to normal, best demonstrated in the upper lip (Sumi et al. 2007).

Pathology of the Salivary Glands

Pathologic states of the salivary glands include tumors (epithelial and non-epithelial), infections and inflammation, autoimmune diseases, vascular lesion, and non-salivary tumors.

Of all salivary gland tumors, the vast majority (80%) are found in the parotid gland. The submandibular gland contains approximately 10%, with the remainder in the sublingual and minor salivary glands. Of all parotid gland tumors, 80% are benign and 20% malignant. About 50% of submandibular gland tumors are benign and the vast majority of sublingual gland tumors are malignant. About 50% of minor salivary gland tumors are benign. The smaller the gland, the more likely that a mass within it is malignant. The pleomor-phic adenoma and papillary cystadenoma lympho-matosum (Warthin's) account for the vast majority of benign salivary tumors, with the former being the more common at about 80% of benign and the latter less common at about 15% of benign masses. Most of the malignant salivary gland tumors are represented by mucoepidermoid and adenoid cystic carcinomas.

Malignancies of the parotid gland may result in metastatic involvement of intraparotid and adjacent level II and III jugular chain lymph nodes. The SMG drains primarily into adjacent level Ib lymph nodes and then into the jugular chain and deep cervical nodes. The SLG drains into both level IA and IB nodes and then subsequently into the jugular chain and deep cervical nodes.


Lymphangioma (Cystic Hygroma)

The cystic hygroma is included in this discussion because of its transpatial location and the fact that it may mimic other cystic masses. It is typically multilocular and has an epicenter in the posterior triangle, but it may be found in the submandibular space and less commonly in the sublingual space. The imaging characteristics are those of cysts and follow fluid density on CT and signal intensity on MRI, although they do typically demonstrate internal architecture from septation with varying thickness. CT typically demonstrates isodensity to simple fluid or slight hyperdensity if infected or if it contains products of hemorrhage (Koeller et al. 1999; Makariou, Pikis, and Harley 2003) (Figure 2.41). US demonstrates anechoic spaces consistent with simple fluid with septa of variable thickness. Like cystic lesions (and a few solid lesions), there is increased through-transmission. Infection and hemorrhage cause variable degrees of echogenicity and thicker septations (Koeller et al. 1999; Makariou, Pikis, and Harley 2003). MRI, however, can be variable on both T1 and T2 sequences based on the fluid characteristics. With simple fluid, T1 and T2 are isointense to simple fluid (CSF), but with infection or hemorrhage products, the increased protein concentration as well as cellular debris and iron from hemoglobin can result in varying degrees of T1 hyperintensity and variable hypo- or hyperintensity on T2 (Figure 2.42). Any of these modalities may demonstrate fluid-fluid or fluid-debris layers. Both CT and MRI will demonstrate enhancement in the setting of infection (Macdonald, Salzman, and Hansberger 2003). These lesions are more common in the pediatric age group, although small lesions may persist into adulthood. When found in the submandibular or sublingual space, they may be mistaken for a ranula (especially giant or plunging ranulae) and less likely hemangioma or thyroglossal duct cyst if midline (Kurabayashi, Ida, and Yasumoto et al.

Hypo Thyroglossal Duct Cyst

Figure 2.41. Axial contrast enhanced CT of the neck at the level of the submandibular glands demonstrating a low-density structure on the right of approximately fluid density (compare to the CSF in the spinal canal), which is intermediate in density relative to the muscles and subcutaneous fat. A large lymphangioma associated with the right submandibular gland was diagnosed.

Figure 2.41. Axial contrast enhanced CT of the neck at the level of the submandibular glands demonstrating a low-density structure on the right of approximately fluid density (compare to the CSF in the spinal canal), which is intermediate in density relative to the muscles and subcutaneous fat. A large lymphangioma associated with the right submandibular gland was diagnosed.

Subcutaneous Lymphangioma Mri
Figure 2.42. Coronal STIR MRI of the face of a different patient with a very large lymphangioma with large septations. Note the lymphangioma fluid is brighter than the CSF and there is fat suppression of the subcutaneous fat.

2000; Macdonald, Salzman, and Hansberger 2003). Although dermoids are in the differential diagnosis, they are usually identified by their imaging characteristics secondary to their contents of fat and dermal elements. Epidermoid cysts may be more difficult to differentiate from cystic hygromas and ranulae because of similar imaging characteristics (Koeller et al. 1999). Because the lymphangiomas have a vasculolymphatic origin, they may be associated with venous anomalies and rarely saccular venous aneurysms (Makariou, Pikis, and Harley 2003). Vascular flow signals may be seen with Doppler US. The venous anomalies or aneu-rysms may be difficult to differentiate from other vascular malformations; however, their association with typical findings of lymphangiomas may assist in diagnosis.


Hemangiomas are typically found in the pediatric age group. The majority are of the cavernous type and less likely the capillary type. They are best demonstrated by MRI and show marked enhancement. They are also very bright on T2 MRI. Foci of signal void may be vascular channels or phlebo-liths (Figures 2.43 through 2.45). They are typically slow flow lesions and may not be angiographically evident. US can vary from hypoechoic to heteroge-nous (Wong, Ahuja, and King et al. 2004).

Other rare vascular lesions within salivary glands, most commonly the parotid gland, include aneurysms, pseudoaneurysms, and arteriovenous fistulae (AVFs). The aneurysms or pseudoaneu-rysms are most commonly associated with trauma or infection (mycotic). MRI in high flow lesions demonstrates "flow voids" or an absence of signal, but slow flow lesions or turbulent flow can demonstrate a heterogenous signal mimicking a mass. Contrast enhancement and magnetic resonance angiography (MRA) can help delineate vascular lesions from masses. CT without contrast, however, demonstrates a mass or masses isodense to skeletal muscle or normal blood vessels. With contrast the often large vascular channels become more obvious, although smaller lesions may still mimic a mass. US (especially Doppler US) can reveal characteristic flow patterns of arterial waveforms in the venous channels for AVFs. US can also delineate aneurysms with their turbulent flow patterns. Angiography is typically reserved for endo-vascular treatment. CTA or MRA is useful for non-invasive assessment of arterial feeders and

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Figure 2.43. Direct coronal CT displayed in bone window demonstrating smooth erosion of the hard palate on the right lateral aspect, along with a dense calcification consistent with a phlebolith (arrow). A hemangioma is presumed based on this CT scan.

Hard Palate Pathologies
Figure 2.44. Coronal fat suppressed contrast enhanced T1 MRI image corresponding to the same level as Figure 2.43, demonstrating a sharply marginated homogenously enhancing mass (arrow).
Viral Sialadenitis
Figure 2.45. Coronal fat saturated T2 MRI image demonstrating a well-demarcated hyperintense mass with a focal signal void centrally. A hemangioma containing a phlebolith (arrow) was presumed based on this MRI.

venous anatomy in AVFs and in defining aneurysms (Wong, Ahuja, and King et al. 2004).


Acute sialadenitis may be bacterial or viral in nature and may be a result of obstruction from a calculus, stricture, or mass (see chapters 3 and 5). Viral parotitis or mumps may be caused by a variety of viruses but most commonly the paramyxovirus is the culprit. The patient presents with an enlarged, tender, and painful gland. Acute sup-purative parotitis (sialadenitis) presents in a similar manner as viral parotitis with the additional sign of purulent exudate. Oral bacterial pathogens are the causative agents, with staphylococcal and streptococcal species being the most common. CT scan demonstrates an enlarged gland with ill-defined margins and infiltration of the surrounding fat by edema fluid. The gland, especially the parotid, is increased in density because of the edema fluid, which is of higher density than fat. CT contrast demonstrates heterogenous enhancement and may show an abscess. On T1 MRI scan the overall gland signal may be decreased slightly from the edema but does enhance heterogenously with contrast. T2 MRI scan shows increased signal

Dirty Fat Sign
Figure 2.46. Axial CT with contrast at the level of the mas-seter muscles demonstrating a left accessory parotid gland abscess.

secondary to edema. Both CT and MRI may demonstrate enhancement and enlargement of the parotid (or sublingual) duct. US shows slight decrease in echogenicity relative to normal. These patterns are not unique to bacterial or viral infection or inflammation and may be seen with autoimmune diseases such as Sjogren's syndrome or a diffusely infiltrating mass. The surrounding subcutaneous fat also demonstrates heterogenous increased density from edema resulting in a "dirty fat" appearance. There is also thickening of fascia and the platysma muscle (Bialek, Jakubowski, and Zajkowski et al. 2006; Madani and Beale 2006a; Shah 2002).

With acute submandibular sialadenitis the gland becomes enlarged and may be associated with a dilated duct if a sialolith is present. By CT the calculus may be readily identified but not as easily seen by MRI. There may be varying degrees of cellulitis or frank abscess formation. The inflamed gland undergoes greater contrast enhancement. MRI demonstrates an enlarged heterogenous gland with a dilated fluid-filled duct and gland, which on T2 images is of high signal. On ultrasound the acutely inflamed gland demonstrates enlargement with focal hypoechoic foci (Bialek, Jakubowski, and Zajkowski et al. 2006; Madani and Beale 2006a; Shah 2002) (Figures 2.46 through 2.48).

Coronal View Parotid Tail

Figure 2.47. Axial contrast enhanced fat saturated T1 MRI demonstrating heterogenous enhancement consistent with abscess of the left accessory parotid gland.


Figure 2.47. Axial contrast enhanced fat saturated T1 MRI demonstrating heterogenous enhancement consistent with abscess of the left accessory parotid gland.

Scan Abscess Tooth
Figure 2.48. Reformatted coronal CT demonstrating enlargement and enhancement of the submandibular glands consistent with viral sialadenitis.

The etiology of chronic inflammatory states of the salivary glands varies by the particular gland in question. Chronic inflammatory changes in the parotid gland tend to be related to autoimmune disease (Sjogren's syndrome), recurrent suppurative parotitis, or radiation injury. Other etiologies include granulomatous infections such as tuberculosis or sarcoidosis. Chronic inflammation of the submandibular gland and to a lesser degree the sublingual gland is more commonly due to obstructive disease, particularly sialolithiasis. In the chronically inflamed state the glands are enlarged but over longer periods of time progressively reduced in size, and heterogenous density may be seen on CT with extensive fibrosis and small focal (punctate) calcification. The density on CT is often increased due to cellular infiltration and edema during acute phases of exacerbation. The surrounding subcutaneous fat may not show signs of edema as is seen with acute sialadenitis. MRI demonstrates similar changes with heterogenous signal on both T1 and T2. The duct or ducts may be dilated, strictured, or both. Both may be visible by contrast CT and MRI (Bialek, Jakubowski, and Zajkowski et al. 2006; Madani and Beale 2006a; Shah 2002; Sumi et al. 1999b). Chronic sclerosing sialadenitis (aka Kuttner tumor) can mimic a mass of the salivary (most commonly submandibular) glands (Huang et al. 2002). It presents with a firm, enlarged gland mimicking a tumor. The most common etiology is sialolithiasis (50-83%), but other etiologies include chronic inflammation from autoimmune disease (Sjogren's syndrome), congenital ductal dilatation and stasis, and disorders of secretion (Huang et al. 2002). It is best diagnosed by gland removal and pathologic examination as fine needle aspiration biopsy may be misleading (Huang et al. 2002). Chronic sialadeni-tis can also be caused by chronic radiation injury. US studies have demonstrated a difference in imaging characteristics between submandibular sialadenitis caused by acalculus versus calculus disease. The acalculus sialadenitis submandibular gland US demonstrates multiple hypoechoic lesions, mimicking cysts, with diffuse distribution throughout a heterogenous hypoechoic gland. They do not, however, demonstrate increased through-transmission, which is typically seen with cysts and some soft tissue tumors. Sialadenitis caused by calculus disease demonstrates hypere-

choic glands relative to the adjacent digastric muscle, but some are iso- or hypoechoic relative to the contralateral gland (Ching, Ahuja, and King et al. 2001).


These lesions are comprised of mixed cystic and solid masses within the parotid (much less in the SMG and SLG). CT shows multiple cystic and solid masses with associated parotid enlargement. IV contrast shows mild peripheral enhancement in the cysts and more heterogenous enhancement in the solid lesions (Figure 2.49). MRI of the cysts is typical with low signal on T1 and high on T2. The more solid lesions are of heterogenous soft tissue signal on T1 and increase on T2. Contrast MRI images follow the same pattern as CT (Holliday 1998). The US images show heterogenous cystic lesions with internal architecture of septation and vascularity and a slightly hypoechoic signal of the solid masses. Mural nodules may be seen in a predominantly cystic lesion. Associated cervical lymphadenopathy is commonly seen, as well as hypertrophy of tonsillar tissues. Differential diagnosis of these findings includes Sjogren's

Glandula Submandibular Tomografia
Figure 2.49. Axial CT demonstrating a large cystic lesion in the right parotid gland and multiple small lesions in the left parotid diagnosed as lymphoepithelial cysts.

syndrome, lymphoma, sarcoidosis, other granulomatous diseases, metastases, and Warthin's tumor (Kirshenbaum and Nadimpalli et al. 1991; Madani and Beale 2006a; Martinoli, Pretolesi, and Del Bono et al. 1995; Shah 2002; Som, Brandwein, and Silver 1995).


The mucous escape phenomenon most commonly results from obstruction in the sublingual gland resulting in a back-up of salivary secretions (see chapter 4). Ductal obstruction may be caused by calculi, stricture from prior infection, or trauma. The chronic dilatation of the duct and accumulation of fluid produces a cystic mass by CT, MRI, and US. The simple ranula remains in the sublingual space and typically presents with a unilocular, well-demarcated, and homogenous structure unless complicated by hemorrhage or infection. The walls may enhance slightly if a ranula remains contained above the mylohyoid muscle. However, it may rupture into the surrounding tissues and extravasate along a path of least resistance and extend inferiorly into the submandibular space or posteriorly into the parapharyngeal space, under which circumstances it is termed a "plunging ranula" (see chapter 4). The non-plunging ranula has a dilated ovoid configuration on axial images, but when it herniates into the submandibular space the dilated space shrinks into a tail-like configuration in the sublingual space. The tail sign is pathognomonic for ranulae and may be seen in both simple and plunging types. The ranula can usually be differentiated from a hemangioma and lymphangioma by its lack of internal architecture (unless complicated). The ranulae are typically homogenous internally with well-defined margins, unless infected or hemorrhagic, and follow fluid density on CT (isodense to simple fluid) and intensity on MRI (low on T1 and high on T2). Both simple and plunging ranulae have these characteristics. The plunging component may be in the parapha-ryngeal space if the lesion plunges posterior to the mylohyoid muscle or in the anterior submandibu-lar space if it plunges through the anterior and posterior portions of the mylohyoid muscle or through a defect in the muscle. Involvement of the parapharyngeal space and the submandibular space results in a large cystic mass termed "giant ranula" and may mimic a cystic hygroma

(Kurabayashi, Ida, and Yasumoto et al. 2000; Macdonald, Salzman, and Hansberger 2003; Makariou, Pikis, and Harley 2003; Cholankeril and Scioscia 1993).


Sialadenosis, also known as sialosis, is a painless bilateral enlargement of the parotid glands and less commonly the submandibular and sublingual glands (see chapter 6). It is typically bilateral and without inflammatory changes. No underlying mass is present. It has been associated with malnutrition, alcoholism, medications, and a variety of endocrine abnormalities, the most common of which is diabetes mellitus. In the early stages there is gland enlargement, but it may progress to fatty replacement and reduction in size by late stages. By CT there is a slight increase in density of the entire gland in the early setting, but the density decreases in the late stage when the gland is predominantly fatty. On T1 weighted MRI images in the early stage, the gland demonstrates a slight decrease in signal corresponding to the lower fat content and increased cellular component. T2 images show a slight increase in signal (Bialek, Jakubowski, and Zajkowski et al. 2006; Madani and Beale 2006a; Som and Curtin 1996).


Approximately 80-90% of salivary calculi form in the submandibular gland due to the chemistry of the secretions as well as the orientation and size of the duct in the floor of the mouth. Eighty percent of submandibular calculi are radio-opaque, while approximately 40% of parotid sialoliths are radio-opaque (see chapter 5). CT without contrast is the imaging modality of choice as it easily depicts the dense calculi (Figures 2.50 through 2.52). MRI is less sensitive and may miss calculi. Vascular flow voids can be false positives on MRI. MR sialogra-phy as previously discussed may become more important in the assessment of calculi not readily visible by CT or for evaluation of strictures, and it is more important as part of therapeutic maneuvers. US can demonstrate stones over 2 mm with distal shadowing (Bialek, Jakubowski, and Zajkowski et al. 2006; Madani and Beale 2006a; Shah 2002).

Figure 2.50. Reformatted coronal contrast enhanced CT of the submandibular gland demonstrating a sialolith in the hilum of the right submandibular gland.
Scan Mono Lymph Nodes
Figure 2.51. Axial contrast enhanced CT of the parotid gland demonstrating a small left parotid sialolith (arrow).
Submandibular Gland Axial
Figure 2.52. Axial contrast enhanced CT at the level of the submandibular glands with a very large left hilum sialolith (arrow).


This autoimmune disease affects the salivary glands and lacrimal glands and is called "primary Sjogren's" if no systemic connective tissue disease is present, but it is considered secondary Sjogren's if the salivary disease is associated with systemic connective tissue disease (Madani and Beale 2006a). The presentations vary radiographically according to stage. Typically early in the disease the gland may appear normal on CT and MRI. Early in the course of the disease there may be premature fat deposition, which may be demonstrated radiographically and may be correlated with abnormal salivary flow (Izumi, Eguchi, and Hideki et al. 1997). Also in the early course of the disease tiny cysts may form consistent with dilated acinar ducts and either enlarge or coalesce as the disease progresses. These can give a mixed density appearance of the gland with focal areas of increased and decreased density by CT and areas of increased and decreased signal on T1 and T2 MRI giving a "salt and pepper" appearance (Takashima, Takeuchi, and Morimoto et al. 1991; Takashima, Tomofumi, and Noguchi et al. 1992). There may be diffuse glandular swelling from the inflammatory reaction, or this may present as a focal area of swelling. The diffuse swelling may mimic viral or bacterial sialadenitis. The focal swelling may mimic a tumor, benign or malignant, including lymphoma. Pseudotumors may be cystic lesions from coalescence or formation of cysts or dilatation of ducts, or they may be solid from lym-phocytic infiltrates (Takashima, Takeuchi, and Morimoto et al. 1991; Takashima, Tomofumi, and Noguchi et al. 1992). As glandular enlargement and cellular infiltration replace the fatty elements, the gland appears denser on CT and lower in signal on T1 and T2 MRI. But when chronic inflammatory changes have progressed, tiny or coarse calcifications may develop. The cysts are variable in size, and the larger cysts may represent confluent small cysts or abscesses. The CT and MRI appearance can be similar to that of lymphoepithial lesions seen with HIV but does include calcifications. Typically there is no diffuse cervical lymphadenopathy. The development of cervical adenopathy may indicate development of lymphoma (Takashima, Tomofumi, and Noguchi et al. 1992). Solid nodules or masses can also represent underlying lymphoma (non-Hodgkin's type) to which these patients are prone. The latter stages of the disease produce a smaller and more fibrotic gland (Bialek, Jakubowski, and Zajkowski et al. 2006; Madani and Beale 2006a; Shah 2002).


Sarcoidosis is a granulomatous disease of unknown etiology (see chapter 6). It typically presents with bilateral parotid enlargement. It may be an asymptomatic enlargement or may mimic a neoplasm with facial nerve palsy. The parotid gland usually demonstrates multiple masses bilaterally, which is a nonspecific finding and can also be seen with lymphoma, tuberculosis (TB), or other granuloma-tous infections, including cat-scratch disease. There is usually associated cervical lymphadenop-athy. The CT characteristics of the masses are slightly hypodense to muscle but hyperdense to the more fatty parotid gland. MRI also demonstrates nonspecific findings. Doppler US demonstrates hypervascularity, which may be seen with any inflammatory process. The classically described "panda sign" seen with uptake of 67Ga-citrate in sarcoidosis is also not pathognomonic for this disease and may be seen with Sjogren's syndrome, mycobacterial diseases, and lymphoma.

Abscess Near The Parotid Gland

Figure 2.54. Axial contrast enhanced CT of the maxillofa-cial soft tissues with a cystic mass interposed between the left submandibular gland and sternocleidomastoid muscle, consistent with a type II branchial cleft cyst.


First Branchial Cleft Cyst

This congenital lesion is in the differential diagnosis of cystic masses in and around the parotid gland along with lymphoepithelial lesions, abscesses, infected or necrotic lymph nodes, cystic hygromas, and Sjogren's syndrome. Pathologically the first branchial cleft cyst is a remnant of the first branchial apparatus. Radiographically it has typical characteristics of a benign cyst if uncomplicated by infection or hemorrhage, with water density by CT and signal intensity by MRI. It may demonstrate slightly increased signal on T1 and T2 images if the protein concentration is elevated and may be heterogenous if infected or hemorrhagic. Contrast enhancement by either modality is seen if infection is present. Ultrasound demonstrates hypoechoic or anechoic signal if uncomplicated and hyperechoic if infected or hemorrhagic. There is no increase in FDG uptake unless complicated. Anatomically it may be intimately associated with the facial nerve or branches. They are classified as type I (Figure 2.53) if found in the external auditory canal (the less common of the two types) and type II if found in the parotid gland or adjacent to the angle of the mandible (Figure 2.54) and may extend into the

Figure 2.54. Axial contrast enhanced CT of the maxillofa-cial soft tissues with a cystic mass interposed between the left submandibular gland and sternocleidomastoid muscle, consistent with a type II branchial cleft cyst.

Branchial Cleft Cyst Adults Type
Figure 2.53. Axial contrast enhanced CT (a) of the head with a cystic mass at the level of the left external auditory canal and sagittal T2 MRI of a different patient (b) consistent with a type I branchial cleft cyst.

parapharyngeal space. It may have a fistulous connection to the external auditory canal or the skin surface. Infected or previously infected cysts may mimic a malignant tumor. Although not typically associated with either the parotid or submandibular glands, the second branchial cleft cyst, which is found associated with the sternocleidomastoid muscle and carotid sheath, may extend superiorly to the tail of the parotid or antero-inferiorly to the posterior border of the submandibular gland. It has imaging characteristics similar to the first branchial cleft cyst. Therefore this must be differentiated from cervical chain lymphadenopathy or exophytic salivary masses. The third and fourth branchial cleft cysts are rare, are not associated with the salivary glands, and are found in the posterior triangle and adjacent to the thyroid gland, respectively (Koeller et al. 1999).


Pleomorphic Adenoma

Pleomorphic adenoma (PA) is the most common tumor of the salivary glands and is comprised of epithelial, myoepithelial, and stromal components. It is also the most common benign tumor of the minor salivary glands (Jansisyanont, Blanchaert, and Ord 2002). Typically unilateral, lobulated, and most commonly sharply marginated, the PA can vary in size, be up to 8 cm in long dimension, and involve superficial and deep parotid lobes. The lobulated regions are sometimes referred to as a "cluster of grapes" (Shah 2002). The majority (80%) are located in the superficial lobe of the parotid gland. Small lesions are better circumscribed, have homogenous enhancement, and are of uniform soft tissue density (skeletal muscle). There can be mild to moderate enhancement and the lesion is relatively homogenous. The larger lesions have a heterogenous density, enhancement pattern, and low attenuation foci from necrosis and cyst formation as well as calcification. The T1 signal can be as variable as the density on CT but tends to follow muscle or soft tissue signal against a background of fat of the normal parotid gland (Figure 2.55). The masses may be hypointense when small, and then become heterogenous with the cystic and calcific changes, and can be hyper-intense secondary to areas of hemorrhage and calcifications. The T2 imaging characteristic is that of

Scan Mono Lymph Nodes
Figure 2.55. Axial contrast enhanced CT of the parotid gland with a heterogenous mass with cystic changes. A pleomorphic adenoma (arrow) was diagnosed at surgery.

high signal intensity, with a thin low signal rim, except when hemorrhage may cause the signal to be heterogenous. The cystic or necrotic regions will tend to be low to intermediate signal on T1 and high on T2. There is mild homogenous enhancement when small and heterogenous when large. US usually demonstrates a homogenous hypoechoic mass but may also have heterogenous hypoechoic features with slight increase in through-transmission (Madani and Beale 2006b). These features may be shared with other benign and malignant lesions, but only tumors that have both lobulation of the contour and a well-defined pseudocapsule are benign (Ikeda, Tsutomu, and Ha-Kawa et al. 1996). The tumor's components, cellular or myxoid, determine the MRI signal. The hypercellular regions have lower signal on T2 and STIR sequences as well as reduced ADC values on DWI and earlier time vs. signal intensity curves (TIC) peak on dynamic MRI (Motoori, Yamamoto, and Ueda et al. 2004). The high cellular components may be seen with other tumor types including malignant types. The myxoid components, which are more diagnostic of PAs, result in high T2 and STIR signal, high ADC values on DWI, and progressive enhancement on dynamic MRI (Motoori, Yamamoto, and Ueda et al. 2004). In fact, of the three types of PAs, myxoid, cellular, and classic, the myxoid is the most common and the most common to recur (Moonis, Patel, and Koshkareva et al. 2007). MRI with T2 and STIR sequences has been shown to be quite sensitive in detecting recurrent PA of the myxoid type by demonstrating the focal, diffuse, or multifocal high signal of the myxoid material (Kinoshita and Okitsu 2004; Moonis, Patel, and Koshkareva et al. 2007). While most PAs demonstrate the benign and nonaggressive features of smooth margins and homogenous enhancement, the more aggressive and invasive features may be seen with carcinoma-ex pleomorphic adenoma, which is seen in areas of previously or concurrently benign PAs. Carcinoma-ex pleomorphic adenomas can result in distance metastatic foci, including the brain (Sheedy et al. 2006). Heterogenous signal within PAs can indicate a concurrent high-grade malignancy, which can be low on T1 and T2 (Kinoshita and Okitsu 2004). FDG PET can be variable but tends to have increased uptake (Figure 2.56). Benignancy cannot be determined by imaging and therefore the differential includes primary parotid malignancy, metastases, and lymphoma as well as benign Warthin's tumors (Madani and Beale 2006b; Shah 2002; Thoeny 2007).

Warthin's Tumor

Papillary cystadenoma lymphomatosum, or War-thin's tumor, is the second most common benign lesion of the salivary glands. These tumors are typically well marginated but inhomogenous and found in the parotid tail of the superficial lobe. Fifteen percent present as bilateral or multicentric disease (Madani and Beale 2006b). There is by CT a heterogenous density and very mild enhancement (Figure 2.57). They typically have small cysts but do not demonstrate calcifications; therefore differential includes lymphoepithelial cysts, primary neoplasms, metastatic disease, and lymphoma. MRI signal on T1 is generally low but may be heterogenous, and T2 is either high signal based on its more cystic features or heterogenous. If the tumor is primarily solid, the imaging characteristics may mimic a PA with relatively homogenous hypoechoic architecture. Contrast with Gd follows CT characteristics. FDG uptake can be high on PET imaging. Warthin's tumors contain oncocytes and

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