Учебники / Head_and_Neck_Cancer_Imaging

7.3.4

Posterior Oropharyngeal Wall Cancer

Isolated cancer in the posterior oropharyngeal wall is rare (Fig. 7.11); more commonly, this wall is invaded by cancers originating from the lateral oropharyngeal wall.Along the posterior wall, mucosal or submucosal spread to the hypopharynx and/or nasopharynx is possible.

Fixation to or direct invasion of the prevertebral fascia precludes the possibility of surgical resection of pharyngeal cancer, and is associated with a poor prognosis. The absence of prevertebral space involvement is reliably predicted on CT and MR images by demonstrating the preservation of the retropharyngeal fat plane. The negative predictive value of this sign varies between 82% and 97.5% (Righi et al. 1996; Hsu et al. 2005). However, cross-sectional imaging is poor in predicting involvement of the prevertebral space. Obliteration of the retropharyngeal fat plane, asym-

metric enlargement of the prevertebral muscles (on CT studies), and thickening and signal abnormalities (on MR studies) are all unreliable signs to diagnose extension into this space (Righi et al. 1996; Loevner et al. 1998; Hsu et al. 2005) (Fig. 7.11). Open neck exploration with direct evaluation of the prevertebral muscles is superior to CT and MRI and should be considered in these patients. However, the decision to surgical resection is influenced in these patients by a number of factors in addition to involvement of the prevertebral space, including carotid artery encasement, perineural spread,retropharyngeal adenopathy and overall patient performance status.Also, the majority of lesions on the posterior pharyngeal wall are treated by radiotherapy or combined chemotherapy and radiotherapy, as the reported cure rates are similar to those of surgery alone or combined surgery and radiotherapy (Million et al. 1994). Nevertheless, as surgical reconstruction methods improve,resection with postoperative radiotherapy can be considered in selected cases (Julieron et al. 2001).

7.3.5

Lymphatic Spread

Lymphatic spread usually occurs in a predictable way, from superior to inferior, the upper parajugular lymph nodes (level II) being the first echelon at risk. Retropharyngeal adenopathy is relatively common and usually associated with lymphadenopathy in other neck levels; isolated retropharyngeal adenopathy without involvement of other lymph nodes also occurs, particularly in posterior oropharyngeal wall cancer.

Bilateral adenopathies are commonly seen in soft palate cancer, as well in base of the tongue cancer.

The imaging criteria for diagnosing metastatic neck adenopathy are described in Chap. 15.

7.4 Treatment

Oropharyngeal cancer is treated with curative intent by radiotherapy, surgery or a combination of both modalities. Depending on anatomical localisation, small lesions (T1 or T2) are treated by either radiotherapy or surgery; cancer of the soft palate or uvula is treated by irradiation, as surgery of these structures interferes with palatal function. Larger lesions (T3 or T4) are, if possible, surgically treated, with postopera-

tive radiotherapy. Inoperable oropharyngeal cancer is treated by concomitant chemoradiotherapy.

Several studies indicated, in glottic, supraglottic, hypopharyngeal and nasopharyngeal squamous cell carcinoma, the value of CT-determined primary tumour volume as prognostic parameter for local outcome after radiation treatment; increasing volume of the primary tumour indicates an increased likelihood of local failure (Mukherji et al. 2004). Such imagingderived information allows better stratification of patients in a lowor high-risk group for local failure than clinical examination alone. This opens perspectives for more optimized treatment modulation in patients with head and neck squamous cell carcinoma. It also allows the identification of a patient group potentially benefiting from frequent post-therapy imaging surveillance, in order to identify tumour persistence or recurrence at an early stage.

However, studies on oropharyngeal cancer in general (Nathu et al. 2000), and tonsillar cancer in particular (Hermans et al. 2001), revealed an only marginal impact of CT-determined primary tumour volume on local outcome, while T category was very significantly correlated with local outcome. Despite the pronounced variability within each T category, tumour volume could not be used to separate patients within the same T category in groups with different local outcome (Hermans et al. 2001). Why the relation between tumour volume and local outcome is less pronounced in oropharyngeal cancer compared

to other head and neck sites, is not clear. Clinically, a relation between the growth pattern of a cancer and its response to radiotherapy has been noted, with exophytically growing cancers generally being more radiosensitive than infiltrating cancers. This may be related to a larger anoxic compartment in deeply growing cancers, as was suggested by Fletcher and Hamberger (1974) in a study on supraglottic cancer. In this context, the variable degree of deep tissue infiltration by oropharyngeal cancer may dilute the volume effect.

7.5

Post-treatment Imaging

The expected neck tissue changes after radiotherapy are described in Chap. 4. Within the oropharyngeal region, mainly thickening of the muscular pharyngeal walls, reduced volume of the tonsillar lymphoid tissue, some degree of retropharyngeal edema, and increased attenuation of the fatty tissue planes is expected. After successful irradiation, the tumor bed is expected to show similar characteristics as the surrounding normal tissues (Fig. 7.12).

Although currently no hard data are available on the value of surveillance imaging for oropharyngeal cancer after radiotherapy, obtaining a baseline fol-

low-up CT or MR study 3–6 months after the end of therapy can be considered. In a number of cases, local failure can be detected at an earlier stage than by clinical examination alone. Persisting or recurring tissue asymmetry and/or increased tissue enhancement after therapy, are suspect for persisting or recurring tumor (Fig. 7.13). Such findings need further exploration; when no clinical correlate is apparent, it is safe to perform an additional nuclear imaging study or to obtain a follow-up CT/MR study about 4 months later. In case of persisting or progressive tissue changes, tissue sampling is required.

When an oropharyngeal cancer is treated primarily by surgery, often extensive removal of soft tissues, and possibly also mandibular bone is needed to obtain oncologically safe resection margins. To reconstruct the created tissue defects, and to obtain a better functional and/or cosmetic result, tissue transfer from a body donor site to the oropharyngeal region may be required. These flaps are vascularized by local vessels, anastomosed to the flap by microvascular techniques. Different kinds of free flaps are in use, for example cutaneous flaps to reconstruct defects in the oropharyngeal cavity, or osseous flaps (e.g. fibula) to reconstruct mandibular defects (Fig. 7.14). A CT or MR study, obtained about 4 months after the end of such a complex procedure, may be helpful as a baseline study allowing earlier diagnosis of subsequent tumor recurrence.

7.6.

Other Neoplastic Disease

7.6.1

Non-Hodgkin Lymphoma

Due to the abundant lymphoid tissue in the oropharynx (lingual and palatine tonsils), non-Hodgkin lymphoma occurs in this region as extranodal lymphatic disease. The diagnosis of lymphoma can

often be suggested based on the imaging findings, as these tumours frequently appear large and homogenous on imaging studies. Also, adenopathies may be present at sites unusual for an untreated carcinoma (Fig. 7.15), or the oropharyngeal lesion may be associated with another extranodal neck lymphoma localisation (Hermans et al. 1994). Such findings, occurring in patients without risk factors for head and neck carcinoma, are suggestive for lymphoma.

Neck lymphoma is described in more detail in Chap. 16.

7.6.2

Salivary Gland Tumors

These oropharyngeal neoplasms originate from minor salivary glands. In the soft palate, these are often benign pleiomorphic adenomas, but in other oropharyngeal sites malignant tumors, such as mucoepidermoid and adenoid cystic carcinoma, predominate (Watkinson et al. 2000) (Fig. 7.16).

7.6.3 Other

The thyroid gland is formed during embryologic life as an epithelial proliferation from the ventral pharyngeal wall; this proliferation is known as the medial thyroid anlage and the place where it arises corresponds later to the foramen caecum, at the border between the oral tongue and the tongue base. This medial thyroid anlage migrates downwards along the neck midline to its final position. Ectopic thyroid tissue can be found anywhere along this tract, but most commonly in the tongue. Patients with a lingual thyroid gland have no thyroid tissue in the neck in 70%–80% of the cases (Fig. 7.17). Ectopic thyroid

is subject to the same diseases as the anatomically correct positioned thyroid, such as nodular hyperplasia and rarely neoplastic degeneration (Fig. 7.18). Development of a mass lesion is often the reason why this ectopic thyroid tissue becomes symptomatic.

Other benign tumoral lesions, such as hemangioma or schwannoma, may be encountered in the oropharynx. As these masses occur submucosally,

Fig. 7.16. Axial T2-weighted spin echo image. Well demarcated hyperintense soft tissue mass (arrowhead) posterolaterally in the tongue base. Biopsy revealed mucoepidermoid carcinoma

References

Chong VFH, Mukherji SK, Ng SHH, et al. (1999) Nasopharyngeal carcinoma: review of how imaging affects staging. JCAT 23:984–993

Dubin MG, Ebert CS, Mukherji SK, Pollock HW, Amjadi D, Shockley WW (2002) Computed tomography’s ability to predict sacrifice of hypoglossal nerve at resection. Laryngoscope 112:2181–2185

Farina D, Hermans R, Lemmerling M, et al. (1999) Imaging of the parapharyngeal space. J Belge Radiol 82:234–239

Ginsberg LE, DeMonte F (1998) Imaging of perineural tumor spread from palatal carcinoma. AJNR Am J Neuroradiol 19:1417–1422

Hermans R, Lenz M (1996) Imaging of the oropharynx and oral cavity. Part I: normal anatomy. Eur Radiol 6:362–368

Hermans R, Horvath M, De Schrijver T, et al. (1994) Extranodal non-Hodgkin lymphoma of the head and neck. J Belge Radiol 77:72–77

Hermans R, Op de beeck K, Van den Bogaert W, et al. (2001) The relation of CT-determined tumor parameters and local and regional outcome of tonsillar cancer after definitive radiation treatment. Int J Radiat Oncol Biol Phys 50:37–45 Hsu WC, Loevner LA, Karpati R, et al. (2005) Accuracy of magnetic resonance imaging in predicting absence of fixation of head and neck cancer to the prevertebral space. Head

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Julieron M, Kolb F, Schwaab G, et al. (2001) Surgical management of posterior pharyngeal wall carcinomas: functional and oncologic results. Head Neck 23:80–86

Loevner LA, Ott IL, Yousem DM, et al. (1998) Neoplastic fixation to the prevertebral compartment by squamous cell carcinoma of the head and neck. AJR Am J Roentgenol 170:1389–1394

Million RR, Cassisi NJ, Mancuso AA (1994) Hypopharynx: pharyngeal walls, pyriform sinus, postcricoid pharynx. In: Million RR, Cassisi NJ (eds) Management of head and neck cancer: a multidisciplinary approach. J.B. Lippincott Co, Philadelphia, p 516

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Mukherji SK, Schmalfuss IM, Castelijns J, Mancuso AA (2004) Clinical applications of tumor volume measurements for predicting outcome in patients with squamous cell carcinoma of the upper aerodigestive tract. AJNR Am J Neuroradiol 25:1425–1432

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UICC, International Union Against Cancer (2002) TNM classification of malignant tumours, 6th edn. Wiley-Liss, New York, p 27, 29

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Vincent F. H. Chong

CONTENTS

8.1Introduction 143

8.2Normal Anatomy 144

8.3Pathologic Anatomy 145

8.3.1Anterior Spread 145

8.3.2Lateral Spread 145

8.3.3Posterior Spread 149

8.3.4Inferior Spread 149

8.3.5Superior Spread 149

8.4Metastasis 150

8.4.1Nodal Metastasis 150

8.4.2Distant Metastasis 150

8.5 TNM Staging System 151

8.5.1T Staging 152

8.5.1.1T1 Tumors 152

8.5.1.2T2 Tumors 152

8.5.1.3T3 Tumors 153

8.5.1.4T4 Tumors 153

8.5.2N Staging 153

8.6Imaging Technique 153

8.7Imaging Modalities 154

8.8Imaging Strategies 155

8.8.1Occult Malignancy 155

8.8.2Staging 155

8.8.3 Follow-up Issues and Problems 155

8.8.3.1Tumor Recurrence 155

8.8.3.2Treatment Complications 156

8.8.3.3Neurological Complications 157

8.8.3.4Non-neurological Complications 158

V. F. H. Chong, MD, MBA

Department of Diagnostic Radiology, National University Hospital,Yong Loo Lin School of Medicine, National University of Singapore, 5 Lower Kent Ridge Road, Singapore 119074, Singapore

8.1 Introduction

The nasopharyngeal mucosa consists of epithelium that is largely squamous in adult life,with foci of pseudostratified respiratory type surface epithelium, lymphoid submucosal stroma and seromucinous glands. A wide variety of malignant neoplasms can theoretically originate from the nasopharyngeal mucosa but regardless of geographic distribution, undifferentiated carcinoma is the most common form of malignancy, accounting for up to 98% of all nasopharyngeal malignancies in the Orient (Shanmugaratnam et al. 1979). Nasopharyngeal carcinoma (NPC) is a unique malignancy, representing the outcome of interactions of genetic factors, environmental factors and the Epstein-Barr virus (EBV). Patients with NPC show consistently high levels of antibodies to EBV antigens and these antibodies are very useful diagnostic markers.

NPC also shows a unique geographical distribution. The highest incidence rates (up to 50 per 100,000 population) are found in Southern China and Hong Kong followed by Singapore and US Chinese (Parkin et al. 1997). Intermediate incidence rates are seen in Eskimos, Polynesians and North Africans (Nielson et al. 1977). The incidence rates in Whites are very low (less than 1 per 100,000 population). NPC may affect children and adolescents but is much more frequently seen in the middle-aged (Seow et al. 2004). This malignancy is more common in males with a male to female ratio of 2.5:1.

NPC is distinct from the other squamous cell tumors of the head and neck. It shows aggressive local infiltration and a high frequency of cervical nodal metastasis despite apparently early primary lesions. Systemic failure is also common in patients with locally advanced disease (Ahmad and Stefani 1986). Radiation therapy is the mainstay of treatment. Chemotherapy is usually used for recurrent or metastatic disease but in recent years, a combination of radiation and chemotherapy has been tried for treatment of locally advanced disease. Surgery plays only

a minor role and is limited to resection of residual or recurrent disease in the nasopharynx and neck nodes.

8.2

Normal Anatomy

The nasopharynx is a fibromuscular sling suspended from the skull base. The boundaries of the nasopharynx are as follows: superiorly, the floor of the sphenoid sinus and the clivus; anteriorly, the nasal choanae; inferiorly, the oropharynx; posteriorly, the prevertebral musculature; and, laterally the parapharyngeal space (PPS) (Fig. 8.1).

The lateral pharyngeal recess (fossa of Rosenmüller) is located superior and posterior to the torus tubarius. The inverted J-configuration of the

torus tubarius explains why the fossa of Rosenmüller appears posterior (on axial images) and superior (on coronal images) to the eustachian tube orifice. The eustachian tube enters the nasopharynx through the sinus of Morgagni, a defect in the pharyngobasilar fascia. The pharyngobasilar fascia (a tough aponeurosis), is the cranial extension of the superior constrictor muscle. It begins at the level of the soft palate and superiorly it is attached to the skull base.

The PPS separates the wall of the nasopharyngeal visceral space from the masticator space (MS). NPC frequently extends across the PPS resulting in the infiltration of the muscles of mastication and potential perineural spread along the mandibular nerve into the intracranial cavity (Chong et al. 1996a). Anatomically, the retrostyloid PPS, containing the carotid space (CS), is at risk for invasion by NPC (see also Chap. 9).

Most tumors originate in the fossa of Rosenmüller (Fig. 8.2). Tumors tend to spread submucosally with early infiltration of the palatal muscles, in particular, the levator veli palatine (Sham et al. 1990a). This muscle is responsible for opening the eustachian tube orifice during swallowing.Muscular dysfunction leads to disequilibrium in the air pressure in the middle ear and the nasopharynx. The tumor may also obstruct the orifice of the eustachian tube, or spread along the this tube into the middle ear (Fig. 8.3). These factors commonly result in serous otitis media.

NPC spreads along well-defined routes and these routes are well reflected in the TNM staging system (Sobin and Wittekind 2002).

8.3.1

Anterior Spread

Tumors often spread anteriorly into the nasal fossa and this may be associated with erosion into the maxillary sinus (Chong et al. 1995b). From the nasal fossa, the tumor may infiltrate the pterygopalatine fossa (PPF) through the sphenopalatine foramen. The earliest sign of involvement of the PPF is obliteration of the normal fat content. Once the tumor gains access into the PPF, it can extend along the maxillary nerve and through the foramen rotundum into the cranium (Chong and Fan 1996a). Tumor in the PPF may spread further superiorly into the inferior orbital

b

Fig. 8.2a,b. Early NPC. a Axial contrast-enhanced MR image shows enhancing tumor in right fossa of Rosenmüller (opposing arrows). Note inflammatory changes in right mastoid secondary to eustachian tube obstruction. b Axial contrastenhanced MR image shows associated right retropharyngeal lymphadenopathy (arrow)

fissure and the orbital apex (Fig. 8.4). From the orbital apex, tumor can readily extend intracranially through the superior orbital fissure (Chong et al. 1998).

8.3.2

Lateral Spread

This is the most common direction of spread and can be recognized by infiltration of the fat-filled PPS (Fig. 8.5). Further lateral spread involves the MS and infiltration of the muscles of mastication (Fig. 8.6) (Chong 1997). Once the tumor is within the MS, the mandibular nerve is vulnerable to perineural