诊断

Review

Imaging of Nasopharyngeal Carcinoma

Michael Chan1, Arjun Sahgal2, Girish Fatterpekar3, Eugene Yu4

 

1Radiology Resident, University of Toronto, 263 McCaul Street, 4th Floor, Toronto, Ontario, Canada M5T 1W7

2Associate Professor of Radiation Oncology and Surgery, University of Toronto Deputy Chief of Radiation Oncology, Sunnybrook Odette Cancer Centre 2075 Bayview Avenue Toronto, Ontario, Canada M4N 3M5

3Associate Professor of Radiology, New York University Langone Medical Center 660 First Avenue Floor 2 Room 224 New York, New York 10016

4Associate Professor of Medical Imaging and Otolaryngology, Head and Neck Surgery, University of Toronto Princess Margaret Cancer Centre 610 University Avenue Room 3-959 Toronto, Ontario, Canada M5G 2M9

Corresponding author: Eugene Yu; Email: Eugene.Yu@uhn.ca.

 

 

Citation: Chan M, Sahgal A, Fatterpekar G, Yu E. Imaging of Nasopharyngeal Carcinoma. J Nasopharyng Carcinoma, 2014, 1(11): e11. doi:10.15383/jnpc.11.

Competing interests: The authors have declared that no competing interests exist.

Conflict of interest: None.

Copyright: image001.gif2014 By the Editorial Department of Journal of Nasopharyngeal Carcinoma. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

 

Abstract: Nasopharyngeal carcinoma (NPC) is the most common primary neoplasm to arise in the nasopharynx. It is an aggressive tumor with a propensity for local tumour invasion and a high incidence of metastases to cervical lymph nodes. Due to its central location in the nasopharynx, primary tumours have many potential routes of local spread, including into important spaces such as the orbital and intracranial spread. This article discusses the current imaging techniques used in the diagnosis and staging of nasopharyngeal carcinoma, and reviews the 7th edition of the International Union Against Cancer (UICC) and American Joint Committee on Cancer (AJCC) TMN staging system for nasopharyngeal carcinoma.

Keywords: Nasopharyngeal Carcinoma; Imaging

 

 

Introduction

Nasopharyngeal carcinoma (NPC), the most common neoplasm to arise in the nasopharynx, is a locally aggressive tumor with a high incidence of cervical nodal metastases. It typically arises from the epithelial lining of the lateral nasopharyngeal wall, particularly inthe lateral pharyngeal recesses. Histologically, the World Health Organization classifies NPC into threesubtypes: keratinizing squamous cell carcinoma (type 1), non-keratinized carcinoma (type 2), and undifferentiated carcinoma (type 3). The tumor has a propensity towards extensive invasion into adjacent tissues, particularly laterally into the parapharyngeal space and superiorly into the skull base. However spread to the palate, nasal cavity, and oropharynx have also commonly reported. Distant metastases can arise within bone, lung, the mediastinum and, more rarely, the liver [1]. Although NPC is rare in North America and Europe with an incidence of 0.5-2 per 100,000, intermediate incidence rates are seen in Southeast Asia, the Mediterranean Basin, and the Arctic ranging from 0.5 to 31.5 per 100,000 person-years in males and 0.1 to 11.8 person-years in females [2, 3]. In southern China, NPC is endemic with overall NPC incidence rates reaching 20-30 per 100,000 person-years and 15-20 per 100,000 person-years amongst males and females, respectively, in the province of Guangdong [4, 5]. NPC has a male to-female ratio of2-3:1 [6], and is most common among patients 40–60 years old with bimodal age peaks in the second and sixth decades of life [7].

The etiology of NPC is multifactorial, involving both environmental and genetic risk factors. Diets high in salt-preserved foods – such as the salted fish, meat, eggs, fruits, and vegetables in a Southern Asian diet – have been identified as possible causative agents acting through the carcinogen, N-nitrosodimethylamine [2]. Studies have also indicated a causal role for the Epstein-Barr virus (EBV) with EBV DNA, RNA, and gene products detected in tumor cells [2].

 

Role of Imaging

Imaging plays an important role in all stages of NPC management, from diagnosis and staging to treatment and follow-up. Since up to 10% of primary NPC tumors are missed on endoscopy [8, 9], cross-sectional imaging studies, such as magnetic resonance imaging (MRI) or computed tomography (CT), are required for diagnosis. Imaging also allows forassessment of the exact boundaries of pharyngeal wall involvement and tumor invasion into surrounding structures. One study demonstrated diagnostic sensitivity and specificity of 100% and 93% for MR imaging, 90% and 93% for endoscopy, and 95% and 100% for endoscopic biopsy, respectively [8]. Currently, MRI and CT are not routinely used for screening purposes; however, the radiologist should consider NPC in high-risk patients, such as those of Asian descent being evaluated for otitis media or with incidental findings of middle ear opacification.

Cross sectional imaging contributes to both prognosis and treatment planning [10, 11].MRI is currently the imaging modality of choice for tumor staging and nodal assessment due to its superior soft tissue resolution and excellent ability to assess primary tumor invasion into surrounding soft tissue and bony structures, such as the pharyngobasilar fascia, sinus of Morgagni, skull base, cavernous sinus, and nerves [11-13]. MRI is also more reliable for differentiating between the primary tumor and retropharyngeal adenopathy [14-17].

The staging MRI protocol for NPC will vary from center to center. In general, the images should cover the area from above the frontal sinuses to the thoracic inlet on axial studies, and from the tip of the nose to the fourth ventricle on coronal sequences. At our institution, axial and coronal T1- and T2-weighted images, as well as a sagittal T1 or T2 fat saturation series covering these regions are obtained. A head and neck imaging coil is routinely used for both the 1.5T and 3.0T MRI scanners. The axial, coronal and sagittal T1 series are performed using a T1-FLAIR technique. Post gadolinium-enhanced axial images with fat saturation and coronal images without fat saturation are also acquired using a conventional spin echo T1 technique. A study by Lau et al. found that the axial pre-contrast and post-contrast series were the most informative MRI sequences for evaluating primary tumor extension and achieved approximately 100% diagnostic accuracy in T-staging of NPC [18]. We find that a combination of axial and coronal T2 and non-contrast T1-weighted images are the best for providing detailed views of the local NP anatomy and surrounding structures.Post-contrast images also allow for accurate assessment of perineural disease along major nerves, as well as the cavernous sinus [11].

Early findings of NPC on imaging include asymmetry of the nasopharynx and an obstructed Eustachian tube (ET)  [19]. Most NPC masses originate in the fossa of Rosenmüller, otherwise known as the lateral pharyngeal recess. NPC has been shown to spread in a step-wise pattern via paths of least resistance, such as via the neuroforamina [20]. Critical structures located near the nasopharynx including the cavernous sinus, pituitary gland, orbit, and brainstem must be accurately evaluated for disease involvement so that they can be appropriately treated, or more importantly, spared from unnecessary radiation dose if they are deemed to be clear of disease. On T2-weighted images, NPC usually exhibits an intermediate signal that is mildly hyperintense to muscle, while on T1-weighted images, NPC has a signal intensity that is hypo- to isointense to muscle. With contrast administration, the tumor tends to enhance less than normal mucosa, but more than muscle.

CT has a role in the assessment of bony skull base involvement [21]. However, CT is inferior to MRI for delineating soft tissue involvement, and it is often difficult to differentiate NPC from hypertrophied lymphoid tissue. For patients with advanced N3 nodal stage and/or clinical evidence of distant metastases, positron emission tomography–computed tomography (PET-CT) may be performed [7, 22].PET has been shown to be superior to CT and MRI for the detection of nodal disease, as well as for the diagnosis of local residual or recurrent NPC [23, 24]. A study by Comoretto et al. demonstrated that the combined use of MRI and FDG PET-CT had a greater diagnostic accuracy for detecting residual or recurrent disease compared to either modality individually [25]. In addition, PET is reportedly useful for differentiating recurrent NPC tumors from post-radiation changes, such as tissue necrosis, fibrosis and edema [23, 26-29]. However, in the early post-radiation period, FDG uptake can be elevated secondary to inflammation following radiotherapy. Higher sensitivity and specificity is achieved when PETimaging is performed at least 3 to 4 months after treatment.

Follow-up evaluation involves a baseline imaging study that is typically performed 2 to 3 months after completion of radiation treatment, followed by imaging every 3 to 6 months for the first 2 post treatment years [19].Any soft tissue signal abnormalities on MRI in the nasopharynx, deep face or skull base, should remain stable over this period or show further reduction in volume.Recurrent disease is seen as any increase in the volume of abnormal signal from baseline imaging.Most recurrences, localor systemic, occur within the first 2 years after treatment [19]. Of the patients with recurrence, 10% to 20% may be curable with additional treatment [19]. After 2 years without evidence of recurrence, the imaging interval is typically extended to every 6 to 12 months.Although not yet the mainstay of patient follow up, one meta-analysis demonstrated that FDG-PET/CT is more sensitive and specific than CT and MRI for the diagnosis of local residual

or recurrent NPC [22].

 

Anatomy of the Nasopharynx

The nasopharynx is the superior-most aspect of the aerodigestive tract. The space opens anteriorly to the nasal cavity through the nasal choanae and inferiorly to the oropharynx at the level of the hard palate or the C1/2 junction. The roof of the nasopharynx abuts the sphenoid sinus floor, and slopes posteroinferiorly along the clivus to the upper cervical vertebrae. Laterally, it is limited by the margins of the superior constrictor muscle, the pharyngobasilar fascia (PBF), and the parapharyngeal space (PPS). Involvement of the PPS, a fibrofatty space separating the nasopharynx from the masticator space, serves as an important marker for tumor staging. The posterolateral limits of the nasopharynx consist of the carotid space, which is essentially synonymous with the post-styloid parapharyngeal space. The walls of the nasopharynx are lined with mucosa comprised of squamous epithelium, a muscular layer, and a fibrous layer consisting predominantly of the PBF. Remains of adenoid tissue may persist into adulthood and exist as tags in the roof of the nasopharynx. The buccopharyngeal fascia, which is derived from the middle layer of the deep cervical fascia, forms a fascial sling around the lateral and posterior portions of the nasopharynx and provides a fascial limit to neighbouring tissues.

The pharyngobasilar fascia is a tough aponeurosis connecting the superior constrictor muscles to the skull base. This important structure extends from the posterior margin of the medial pterygoid plate anteriorly and the occipital pharyngeal tuber and prevertebral muscles posteriorly to the superior pharyngeal constrictor inferiorly. The PBF is continuous with the foramen lacerum, which is a fibrocartilaginous structure that forms part of the floor of the horizontal carotid canal and roof of the nasopharynx. It is a route for the extension of naspharyngeal tumors into the cavernous sinus and intracranial cavity

The torus tubarius is a prominent anatomical landmark corresponding to the mucosal-lined projection of the distal cartilaginous ends of the paired Eustachian tubes into the lumen of the nasopharynx. It can be visualized at the superior aspect of the posterolateral walls. The ostia of the Eustachian tubes are located anterior and inferior to the torus tubarius(Figure 1). The Eustachian tubes and the medial fibers of the levator veli palatine muscle penetrate into the nasopharynx through the sinus of Morgagni, which is a posterolateral defect in the pharyngobasilar fascia where muscular fibers are absent. Given this anatomical characteristic, the sinus of Morgagni is an important route for malignant dissemination into adjacent spaces, including the parapharyngeal space. Located posterior and superior to the torus tubarius, the lateral pharyngeal recess originates in a mucosal herniation through the sinus of Morgagni. It is the most common site of origin of NPC. The salpingopharyngeal fold, which forms the anterior limit of the lateral pharyngeal recess, is a mucosal protrusion overlying the salpingopharyngeus muscle. Asymmetry

of these mucosal landmarks is a common incidental finding, especially the lateral pharyngeal recesses, and should not be mistaken for tumors.

The retropharyngeal space, a potential space containing the medial and lateral retropharyngeal lymph nodes (RPN), is located posterior to the nasopharynx. The lateral retropharyngeal lymph nodes, also known as the nodes of Röuviere, are the first nodes of lymphatic drainage along with Level II cervical nodes, and thus, are reported to be the most common site of nodal metastases [30]. These nodes can be visualized on MRI from the skull base to the level of C3. The medial retropharyngeal nodes do not form a discrete chain and are not visible on imaging.

Other important structures include the foramen rotundum and pterygoid (or Vidian) canal, which communicate with the pterygopalatine fossa and are thus potential routes of perineural tumor spread.

 

 

 

Figure 1. Axial T2 weighted image showing the anatomic features of the nasopharynx. Torus tubarius TT, Eustachian tube opening (*), tensor veli palatini (short arrow), levator veli palatini (long arrow), longus musculature (LM).

 

 

Staging of NPC

Currently, the 7th edition of the International Union Against Cancer (UICC) and American Joint Committee on Cancer (AJCC) TMN staging system is used, which was revised and released in January 2010. As previously described, most cases of NPC originate in the lateral pharyngeal recess and spread submucosally

with early infiltration into deeper neck spaces. NPC tends to have well-defined patterns of spread.

 

Primary Tumor (T) Stage T1

Stage T1 refers to disease that is confined to the nasopharynx (Figure 2), as well as disease with extension inferiorly to involve the oropharynx or anteriorly to involve the nasal cavity.  This stage includes all tumors that are superficial to the pharyngobasilar fascia, with no evidence of PBF invasion.

The nasal cavity is commonly involved in NPC. Stage T1 disease also includes tumors with anterior extension beyond the plane of the posterior choanae into the nasal cavity (Figure 3). The nasal cavity represents the most common route for direct tumor invasion into the pterygopalatine fossa via the sphenopalatine foramen. Oropharyngeal extension is readily noted on coronal or sagittal MR imaging as tumor that has extended inferiorly past the plane of palate.On axial sections, the oropharynx is considered involved when tumor is seen inferior to the C1/C2 junction.

 

 

Figure 2. Axial T1 weighted image shows a left sided tumor mass (*) localized to the nasopharynx (T1 disease).

 

Figure 3. Axial T2 weighted image shows anterior extension of a nasopharyngeal carcinoma into the right posterior nasal cavity (arrow). This is still T1 disease.

 

Stage T2

Stage T2 refers to disease that has invaded beyond the PBF and infiltrated posterolaterally into the parapharyngeal space. This stage is associated with an increased risk of tumor recurrence and distant metastases [31-34]. It is recognized on imaging as a breach of tumor beyond the intrapharyngeal portion of the levator veli palatini muscle, or infiltration of the tensor veli palatini (which is a thin strip of muscle located lateral to the levator veli palatini).Advanced PPS disease is demonstrated on imaging as the presence of tumor mass invading into the hyperintense fat of the PPS (Figure 4). From here, further progression can see involvement of the poststyloid PPS structures, such as the carotid sheath.

Posterior or retropharyngeal tumorspread is common in NPC. This refers to disease that has invaded posteriorly to involve the longus musculature and prevertebral space. This region contains lymphatics and a venous plexus, which increases the risk of distant metastases. At present, the current UICC/AJCC system does not specifically make note of the presence of prevertebral disease extension in the staging scheme.

 

Figure 4. Parapharyngeal tumor extension (T2). Note that the left sided mass has extended laterally to infiltrate across the levator and tensor veli palatini musculature. Tumor is also present within the prestyloid parapharyngeal fat (short arrow) ad has extended to become intimate with the left internal carotid artery (long arrow).

 

 

Stage T3

Stage T3 refers to disease that is characterized by involvement of the bony structures of the skull base and/or the paranasal sinuses. Superior extension of NPC is the most frequent route of direct extension, with the most common sites of involvement being the clivus, pterygoid bones, body of the sphenoid bone, and apices of the petrous temporal bones [35]. Skull base invasion is seen in up to 60% of NPC patients at diagnosis [36, 37]. Assessment for skull base involvement can be achieved with T1-weighted MRI sequences or CT, and should focus on five key regions: clivus, right pterygoid base, left pterygoid base, right petrous apex, and left petrous apex [35]. On T1-weighted images, bony involvement is demonstrated as replacement of the normal hyperintense MR signal of fatty yellow bone marrow with an intermediate or low signal, which can is indicative of reactive change and/or actualtumorinvasion (Figure 5). CT will show the presence of bony cortical loss and medullary soft tissue lytic change.

Involvement of the paranasal sinuses can result from direct tumor extension. Maxillary sinus involvement is rare and is usually a late finding occurring after nasal or infratemporal maxillary wall erosion in the setting of extensive disease. Involvement of the ethmoid sinus usually occurs via direct spread from the sphenoid sinus or nasal cavity. With ethmoid sinus involvement, the optic nerves become more vulnerable to the radiation dose during radiation therapy. Sphenoid sinus involvement is common in NPC as tumor will extend superiorly through the sphenoid sinus floor (Figure 6). Infiltration of a sinus can be visualized as opacification with fluid or tumor, and loss of contiguity of the sinus walls.

 

     A   B          C

Figure 5A, B, C: 5A is a sagittal T1 weighted image showing a lobulated NPC (*). Note the replacement of the normal hyperintense fatty marrow signal within the adjacent overlying clivus (arrow). 5B and 5C are coronal T1 images from another patient showing the presence of abnormal intermediate T1 signal within the right body of the sphenoid (arrow in 5B) and the right petrous temporal bone apex (PA) and clivus (arrow in 5C).

 

Figure 6. Coronal T1 image following gadolinium contrast administration shows superior extension of a large NPC (*) into the right sphenoid sinus (arrow).

 

 

Stage T4

refers to instances with intracranial extension and/or involvement of the cranial nerves, hypopharynx, orbit, or masticator space. NPC has a propensity for invasion of the skull base foramina and their corresponding nerves or vessels  – such as the foramen rotundum (containing the maxillary nerve), foramen ovale (containing the mandibular nerve), foramen lacerum (containing the internal carotid artery), and the vidian canal (containing the vidian artery and nerve). The foramen ovale and lacerum are the most common routes for tumor extension into the intracranial cavity (Figure 7). Such nerve involvement will signify stage T4 disease. Assessment of the skull base foramina is best achieved on coronal imaging. Less common findings include invasion of the hypoglossal nerve canal (containing the hypoglossal nerve) and jugular foramen (containing cranial nerves IX-XI). Disease involving the pterygopalatine fossa is important as it is an important crossroads that connects with a number of other anatomic regions. Disease reaching the pterygopalatine fossa can spread: (1) in a perineural fashion along the maxillary nerve through the foramen rotundum into the middle cranial fossa, (2) posteriorly through the vidian canal to the petrous carotid canal, (3) laterally through the pterygomaxillary fissure into the masticator space, (4) superiorly through the inferior orbital fissure into the orbital apex, with subsequent intracranial extension via the superior orbital fissure, and (5) inferiorly through the pterygopalatine canal into the oral cavity.

Features that constitute intracranial extension include the presence of meningeal involvement (appearing as nodular enhancement), soft tissue masses within the middle and/or posterior cranial fossa, as well as evidence of perineural spread. Direct invasion of the brain is rare at diagnosis [35].  There are multiple routes into the cavernous sinus, including perivascular extension along the horizontal portion of the internal carotid artery through the foramen lacerum (Figure 7A, B), perineural extension along the V3 through the foramen ovale(Figure 7C), as well as direct extension from the orbital fissures or through the skull base [35]. With cavernous sinus involvement, cranial nerves III, IV, V1, V2, and VI are vulnerable to tumor invasion, often resulting in multiple cranial nerve palsies. True perineural spread; however, is uncommon in the pre-treatment setting [35]. Cranial nerve invasion is associated with a higher rate of distant metastases and decreased survival [11]. Post-contrast T1-weighted images with fat saturation are used to assess for cranial nerve involvement, especially for the maxillary nerve (V2) along the foramen rotundum and the mandibular nerve (V3) in the foramen ovale (Figure 8). Nerve involvement is suspected when abnormal enlargement or enhancement of the nerves or obliteration of fat pads adjacent to neurovascular foramina is observed. Contrast-enhanced images show perineural disease extension and cavernous sinus involvement as asymmetric nodular thickening and abnormal enhancement. A late sign is expansion of the bony canals in which these nerves travel.

Disease spread via the inferior orbital fissure represents the most common route of orbital invasion. NPC can also extend into masticator space, where the medial and lateral pterygoid muscles, temporalis muscle, infratemporal fat, as well as the mandibular nerve will all be vulnerable to tumor infiltration. From the masticator space, NPC can also gain access to the intracranial cavity and cavernous sinus via direct extension through the floor of the middle cranial fossa or via the foramen ovale (Figure 9).The hypopharynx, which is the most inferior site included in the TMN staging system, is rarely involved at diagnosis. NPC has a tendency to spread superiorly rather than inferiorly [35].

 

  A B   C

Figure 7A, B, C: Two coronal T1 images (7A, B) shows a left sided NPC with extension superiorly into the left foramen lacerum (arrows in 7A). Also note the abnormal signal within the adjacent left aspect of the clivus. Image 7B shows that the tumor is also involving the left cavernous sinus (*). Coronal T2 image in another patient (7C) shows a left NPC that has extended into the ipsilateral masticator space (MS) with subsequent perineural tumor spread along an enlarged V3 , through foramen ovale and into the cavernous sinus (arrows 7C).

 

 

Figure 8. Axial contrast enhanced T1 image shows enhancing tumor within the left orbit (arrows). The patient has an NPC which involved the cavernous sinus with subsequent tracking along foramen rotundum into the pterygopalatine fossa and the inferior orbital fissure.

 

 

Figure 9. Coronal contrast enhanced T1 weighted shows a large right NPC that has infiltrated the right masticator space (MS) with contiguous extension superiorly onto the cavernous sinus, right sphenoid sinus (Sph) and along the floor of the middle cranial fossa.

 

 

Regional Lymph Nodes (N)

Up to 90% of NPC cases will present with lymph node metastases at presentation. Thus, only 10% to 40% of patients will present without nodal disease (N0)  [19, 38]. Positive nodal disease is associated with increased risk of local recurrent and distant metastases [38]. NPC generally follows a sequential pattern of nodal spread, beginning with involvement of retropharyngeal lymph nodes (RPN) occurring before other nodal groups along the internal jugular chain (chain II to IV), spinal accessory chain (Va and Vb), as well as supraclavicular nodes. Although the RPN are generally considered the first echelons of metastatic spread, studies have shown that this is not true in all cases [30, 39-41]. The RPN may be bypassed in up to 19% of cases [41]. In addition, Ng et al. also reported skip metastases in the lower neck lymph nodes and the supraclavicular fossa in 7.9% of cases, and distant metastases to thoracic and abdominal nodes in 3-5% of cases [41]. Level IIa and b nodes are the most common site of non-retropharyngeal nodal involvement [40]. Unlike other head and neck squamous cell carcinomas, nodal disease in NPC is more frequently bilateral.

Stage N1 refers to the presence of unilateral metastasis in cervical lymph node(s) and/or unilateral or bilateral retropharyngeal lymph nodes. In both cases, the diameter is less than 6 cm in the greater dimension. Nodes greater than 3 cm in size are generally considered “nodal masses” and are indicative of confluent nodes. Stage N2 refers to bilateral nodal disease involving cervical lymph node(s) that are also less than 6 cm in the greatest dimension. Unlike other carcinomas in the neck, N2 is not further divided into substages. In both N1 and N2, disease is restricted to above the supraclavicular fossa, which is defined by three points: (1) the superior margin of the sternal end of the clavicle, (2) the superior margin of the lateral end of the clavicle, and (3) the point where the neck meets the shoulder. Supraclavicular nodes refer to all lymph nodes seen on the same axial images as a portion of the clavicle, and include caudal portions of levels IV and Vb nodes. Nodal disease greater than 6 cm in diameter signifies stage N3a disease, while involvement of supraclavicular fossa lymph nodes denotes stage 3b disease.

While distinguishing between the primary tumor mass and adjacent RPN is best assessed with MRI, cervical lymph nodes can be evaluated accurately with both MRI and CT [42]. T2-weighted imaging with fat saturation shows nodes as bright structures in the pos­terior cervical fat. The higher resolution of CT facilitates the visualization of neck adenopathy, as well as nodal necrosis and extracapsular extension, with the latter manifesting as loss or irregularity of the nodal margins, and/or haziness of the adjacent fat [11].There are several imaging features suggestive of positive nodal disease, including large size (generally, >1.5 cm for levels I and II, >1 cm for levels IV-VII, and >5 mm for retropharyngeal lymph nodes in the shortest transaxial dimension), 3 or more lymph nodes borderline in size, rounded nodes with loss of the normal fatty hilum, and necrosis [35, 38]. If identified, necrosis is considered 100% specific. Necrosis is visualized as a hypointense area on T1-weighted images with rim enhancement on contrast administration, and a hyperintense area on T2-weighted images. On CT, necrosis is seen as a focal area of hypoattenuation with or without rim enhancement. Patients with nodes showing necrosis and extranodal spread have a very poor prognosis with a 50% decreased 5-year survival rate [43].

 

Distant Metastasis (M)

The M stage of NPC is similar to that of other malignancies, whereby M0 signi­fies the absence of distant metastasis and M1 refers to the presence of such disease. NPC has the highest incidence of distant metastasis among head and neck cancers, with a rate as high as 11% at diagnosis [34, 44]. Distant metastases most commonly affect bone, lung and liver [45].Thus, bones and lung apices should be evaluated for tumor involvement in head and neck MRI studies, especially in patients with risk factors such as metastatic cervical nodes extending to the supraclavicular fossa (stage N3).

The exact method for the evaluation of distant metastasis will vary from institution to institution.  Imaging options include bone scintigraphy, chest x-ray, CT of the thorax, abdomen and pelvis, and PET/CT. Studies have shown fluorodeoxyglucose PET/CT imaging to have a higher sensitivity and specificity in detecting

distant metastases [11, 22, 24, 25, 46-50].

 

Summary

Nasopharyngeal carcinoma is a relatively rare neoplasm that most commonly arises in the lateral pharyngeal recess and has a tendency toward local invasion and spread to surrounding structures. Cervical lymphadenopathy is also very common at presentation. Diagnosis of NPC can be made on endoscopically-guided biopsy; however, cross-sectional imaging, particularly MRI, plays a key role for accurate assessment of tumor volume and extent. A thorough understanding of the anatomy of the nasopharynx and surrounding structures, as well as the natural history of the disease is essential, as NPC has a propensity towards early infiltration into deeper neck spaces and has well-defined patterns of spread. Staging of NPC is based on the most up-to-date 2010 AJCC guidelines. MRI is currently the best tool for assessing tumor extent under the current staging system, while PET/CT is emerging as the most accurate modality for assessing distant metastases andtumor recurrence.

 

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