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management policies. Persistent or residual disease may be due to firstly, a “geographic miss” on the irradiation plan; secondly, the relative radio-insensitivity of the tumor; thirdly, an insufficiently high radiation dose, and fourthly, the time taken to deliver the dose was too long.

Patients are often followed-up clinically at 1- to 2-monthly intervals in the first year, 2- to 3-monthly intervals in the second year and 3- to 4-monthly intervals in the third year. These patients can be seen at 6-monthly intervals subsequently. Tumor recurrence is usually detected by endoscopy and imaging is requested for the assessment of tumor extent (Sham et al. 1992). Imaging is also used to confirm deep recurrences not apparent on endoscopy but suspected on the basis of history and symptomology (Fig. 8.13).

Differentiating fibrosis from tumor recurrence is difficult on CT since the attenuation values of these tissues are similar. Separating tumor recurrence from fibrosis on MRI is only easier if the scar is mature. Early fibrous tissue is hypercellular and produces high signals on T2-weighted images. Both immature scar and tumor show contrast-enhancement on MRI and high signals on T2-weighted images. Mature scar, which is hypocellular, does not show contrastenhancement and is characterized by low signal intensity on T2-weighted images.

The simultaneous dynamic processes of fibrosis and tissue reaction to irradiation often produce a confusing picture.Residual disease or recurrent tumor may be hypointense relative to granulation tissue in the early

stage. Scar tissue may also show high signal intensity in T2-weighted images. Furthermore, areas of high signals on T2-weighted images may be seen in corresponding areas showing no contrast enhancement. Differentiating tumor recurrence from fibrosis, therefore, can be a formidable task (Chong and Fan 1997).

To overcome the above mentioned problems, regular follow-up should be performed. It is important to obtain a baseline study around 6 months after radiation therapy and another scan 6 months later. These studies can be used for comparison with future yearly follow up studies over the next 3 years (and longer if required). A stable appearance can provide reassurance that the abnormality seen is most likely to be due to the effects of radiation.

Positron emission tomography (PET) using 2-[F- 18] fluoro-2-deoxy-D-glucose (FDG) has demonstrated value in detecting NPC recurrence following radiotherapy (Kao et al. 1998; Tsai et al. 2002). The advent of PET CT has provided even more information by co-registering tracer uptake with anatomic information.

8.8.3.2

Treatment Complications

The complications of radiation therapy can be divided into neurological and non-neurological sequelae. Neurological complications include temporal lobe necrosis, encephalomyelopathy and cranial nerve palsies. Non-neurological complications include at-

rophy of salivary glands, muscles of mastication, and radiation associated tumors.

8.8.3.3

Neurological Complications

8.8.3.3.1

Temporal Lobe Necrosis (TLN)

NPC shows high frequencies of skull base erosion and intracranial extension and is frequently associated with perineural infiltration. The natural history of tumor spread requires adequate radiation treatment coverage of the skull base and the middle cranial fossa. Radiation doses below 6000 cGy at conventional 200 cGy daily are inadequate for tumor control. Hence, the effective radiation dose for the treatment

of NPC exceeds the quoted tolerance limit for the neural tissues resulting in a substantial risk of radia- tion-induced brain damage. Lee et al. (1992) reported a 3% cumulative incidence of TLN in her series of 4527 patients. TLN is probably under diagnosed as 39% of patients had only vague symptoms while 16% had none at all. The latent interval ranged from 1.5 to 13 years (median, 5 years).

The inferior and medial portions of both temporal lobes are at risk as they are included in the target volume. Cerebral edema is the earliest radiologic sign. This is followed by foci of necrosis that may be located in the gray matter, white matter or both (Fig. 8.14). White matter lesions are characteristically associated with florid edema while gray matter lesions may show minimal or no edema (Chong et al. 2000). Early lesions may heal completely but ex-

tensive involvement frequently results in temporal lobe atrophy or macrocystic encephalomalacia. With the introduction of conformal and intensity modulated radiation therapy (IMRT), the frequency of TLN should gradually decrease.

The differential diagnosis of TLN includes intracranial tumor recurrence and cerebral metastasis. An important point of distinction is whereas recurrent tumor is almost always an extra-axial lesion, TLN is an intra-axial pathologic process. In addition, NPC with intracranial extension, unlike TLN, is usually not associated with cerebral edema. Cerebral metastases are exceedingly rare in NPC (Leung et al. 1991). In clinical practice, cerebral metastasis is seldom placed high on the list of differential diagnosis. If, there are difficulties in differentiating these entities, other modalities based on functional imaging may provided the additional information required for accurate diagnosis. These techniques include MR spectroscopy and PET imaging.

In recent years, MR spectroscopy is increasingly used to study the metabolic changes in the brain following radiation injury. MR spectroscopy in patients with radiation-induced changes in the temporal lobes showed reduced N-acetyl-aspartate levels and relatively stable creatine levels. However, the choline levels may be increased, normal or reduced. The increase choline levels may mimic the presence of primary brain tumor. However, given the known clinical setting, it is unlikely to confuse TLN with the presence of a primary brain neoplasm (Chong et al. 1999, 2001). In addition to MR spectroscopy, PET CT can be used to separate TLN from tumor recurrence. Brain necrosis typically shows no uptake of tracers while tumor recurrence will demonstrate increased metabolic activity.

8.8.3.3.2

Brainstem Encephalopathy

In the past it was widely known that radiation therapy could damage the brainstem and cervical spinal cord in up to 3% of patients (Mesic et al. 1981). The frequency is now considerably less with improved radiation techniques and shielding. Patients with radiation induced cord injury usually present with clinically unmistakable symptoms and signs of corticospinal tract damage. This major complication has a median

latent interval of 3 years (range 0.4–9 years). There is no effective way of reverting or arresting this pathologic process. The majority of patients will develop severe motor disability (Lee and Yau 1997).

8.8.3.3.3 Cranial Nerves

Cranial nerves are relatively radioresistant. The reported frequencies of radiation-induced palsies range from 0.3% to 6% (Flores et al. 1986; Hoppe et al. 1976). This entity is diagnosed by exclusion, as the involved cranial nerves usually appear radiologically unremarkable. The XIIth cranial nerve is the most commonly affected nerve. The optic nerve is the second most commonly damaged nerve followed by the VIth cranial nerve. The IVth, Vth and VIIth nerves are usually involved as part of the brainstem damage syndrome.

8.8.3.4

Non-neurological Complications

8.8.3.4.1 Salivary Glands

Almost all patients have varying degrees of xerostomia and thickening of saliva. Subsequent development of dental caries is common. Radiologically, almost all salivary glands show atrophy. Imaging not infrequently reveals intense salivary gland enhancement. Rarely, patients show acute parotitis, which may develop rapidly over a few days. With the advent of IMRT, the frequency and severity of radiation induced parotitis has decreased.

8.8.3.4.2

Soft Tissue Fibrosis

Marked soft-tissue fibrosis in the neck is common following irradiation with large fractional doses. Although neck fibrosis per se rarely causes serious functional limitation, it may mask nodal recurrence. When the neck is woody hard, palpation is unreliable and the recommended strategy is to use CT to detect lymphadenopathy.

Trismus due to fibrosis around the temporomandibular joints and adjacent muscles of mastication

can result in feeding difficulties. This may be aggravated by pharyngeal mucositis and stricture.

8.8.3.4.3

Radiation Associated Tumors

The tumor induction potential of ionizing radiation is a well-recognized phenomenon. The term radia- tion-induced tumor is frequently used to describe second tumors appearing within previously irradiated fields. However, ascribing the second tumor as a direct consequence of irradiation is often difficult. This entity is better called radiation-associated tumors (RATs).

The criteria for diagnosing RATs include a history of irradiation; the second neoplasm occurring within irradiation field; a difference in the histology of the second neoplasm from the primary tumor; and finally, an arbitrary latency period of at least 5 years (Cahan et al. 1948).

The frequency of head and neck RATs is unknown although it has been estimated to occur between 0.4% to 0.7% (Steeves and Bataini 1981). The reported types of RATs include sarcomas (Fig. 8.15), meningiomas, schwannomas, gliomas, thyroid tumors and squamous cell carcinomas (Fig. 8.16) (Mark et al. 1993; Rubinstein et al. 1989; Bernstein and Laperriere 1991). The improvement of radiation therapy techniques has contributed to increased survival rates of patients with NPC. We can, therefore, expect to see more long-term complications like RATs (Goh et al. 1999) (Fig. 8.16).

8.9

Other Neoplasms of the Nasopharynx

In comparison with undifferentiated carcinoma, nasopharyngeal adenoid cystic carcinoma is rare (Mukherji and Chong 2004). The vast majority of adenoid cystic carcinomas are found in the salivary glands, the mucosa of the oral cavity, nasal fossa and the paranasal sinuses. This tumor affects patients in the middle age and there is no reported sex predilection. Unlike NPC, patients with adenoid cystic carcinomas rarely present with cervical lymphadenopathy.

Fig. 8.15. Radiation associated tumor (RAT) – parosteal sarcoma. Patient had a history of irradiation for NPC (undifferentiated carcinoma) 11 years previously. Axial CT shows a large dense (asterisk) bone tumor arising from the right pterygoid process

Although lymphoid tissues are normally found in the nasopharynx, primary lymphomas in the nasopharynx are uncommon. These tumors are more commonly seen in conjunction with system disease. Nasopharyngeal lymphomas affect all age groups but are more commonly encountered in middle and old age. The majority of these tumors belong to the non-Hodgkin group. Nasopharyngeal involvement is usually detected during the staging process of known disease elsewhere.

Plasma cell neoplasms can be grouped into three categories: multiple myeloma,plasmacytoma of bone, and extramedullary plasmacytoma. Extramedullary plasmacytomas account for approximately 20% of all plasma cell neoplasms and 80% of these lesions are found in the head and neck. Plasmacytomas are most commonly seen in the sixth and seventh decades and have an 80% male preponderance. Plasmacytomas are most frequently seen in the upper airways such as the epiglottis, larynx and nasopharynx (Ching et al. 2002). Approximately 30% of patients with extramedullary plasmacytoma will have systemic disease after 20 years.

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CONTENTS

9.1Introduction 163

9.2Anatomy 163

9.2.1 Fascial Layers and Compartments 163

9.2.2Radiological Anatomy 165

9.3.2.1Prestyloid Lesions 166

9.3.2.2Retrostyloid Lesions 169

9.1 Introduction

The parapharyngeal space (PPS) is a deep space of the neck shaped as a tilted up pyramid with its base attaching to the skull base and the apex reaching the level of the hyoid bone, and almost exclusively containing fat. Primary neoplasms arising in this space are quite rare, accounting for only 0.5% of all head and neck tumors (Olsen 1994; Miller et al. 1996; Pang et al. 2002), whereas the PPS is more commonly displaced or infiltrated by lesions arising in the adjacent spaces, including the pharyngeal mucosal, masticator, parotid, and retropharyngeal spaces. Approximately 70%–80% of the tumors originating from the PPS itself are benign (Luna-Ortiz et al. 2005).

Small tumors of the PPS, with a size of less than 2.5 cm, are often incidental findings. Larger tumors produce aspecific signs and symptoms, including sore throat, ear fullness, dysphagia and, less frequently, jaw pain combined with cranial nerves palsy. These last two symptoms may be caused by a ma-

R. Hermans, MD, PhD

Professor, Department of Radiology, University Hospitals Leuven, Herestraat 49, 3000 Leuven, Belgium

D. Farina, MD

Department of Radiology, University of Brescia, Piazzale Spedali Civili 1, 25123 Brescia, BS, Italy

lignant lesion. Clinical assessment of tumors in this region is often difficult, commonly causing a delay between the onset of clinical manifestations and the diagnosis. Bulging of the lateral nasopharyngeal wall may be appreciated, associated with displacement of the soft palate and palatine tonsil. When a PPS lesion grows laterally, facial swelling may result at the level of the parotid or submandibular region. Rarely, the mandible will be displaced by a slowly growing tumor (Farina et al. 1999).

Physical examination may not allow differentiation between a PPS neoplasm and a parotid gland lesion originating in the deep lobe.Before the advent of crosssectional imaging techniques, such as CT and MR, treatment was performed via a transparotid approach. Nowadays, when a CT or MR study demonstrates the lesion to be in the PPS, most patients are operated via a transcervical approach, with or without resection of the deep lobe of the parotid gland. In large tumors, mandibulotomy may be required to remove the tumor. In selected small tumors, a transoral approach may be sufficient. The use of imaging studies has resulted in a significant decrease of transient or permanent damage to the facial nerve (Stell et al. 1985; Olsen 1994; Miller et al. 1996; Luna-Ortiz et al. 2005).

Lesions arising from the adjacent spaces displace the PPS in a particular way, allowing the radiologist to identify precisely the space of origin. Combining the imaging characteristics of the lesion with a limited space-specific differential diagnosis often allows a precise diagnosis. Knowledge of the anatomy is, therefore, the key to unlock the PPS and its related spaces.

9.2 Anatomy

9.2.1

Fascial Layers and Compartments

Medially, the PPS is in close contact with the pharyngeal mucosal space, bordered by the middle layer of

the deep cervical fascia (also known as buccopharyngeal fascia), which curves around the posterior and lateral side of the pharyngeal mucosal space, surrounding the constrictor muscles (Figs. 9.1 and 9.2). Superiorly, the pharyngeal constrictor muscle does not reach the skull base; at that level, the lumen of the nasopharynx is held open by the thick pharyngobasilar fascia. This fascia lies within the middle layer of the deep cervical fascia. The pharyngobasilar fascia is interrupted at the level of the sinus of Morgagni, an opening through which the cartilaginous part of the Eustachian tube and the levator veli palatini muscle enter the nasopharynx. This area should be carefully inspected on imaging studies of the nasopharynx, as it is a common route of spread for nasopharyngeal carcinomas from the mucosal space to the skull base (see Chap. 8). Just posterior to the Eustachian tube is the fossa of Rosenmüller, a mucosal recess where most of the nasopharyngeal carcinomas arise.

The superficial layer of the deep cervical fascia is lateral to the PPS, separating this space from the masticator space. This fascia curves around the medial surface of the pterygoid muscles and extends from the mandible to the skull base, where it attaches just medial to the foramen ovale. As a consequence, the mandibular nerve (V3), as it courses through this foramen, directly enters the masticator space.

In its posterolateral portion, the PPS is in contact with the deep lobe of the parotid gland. The existence of a fascial layer at this level is controversial.

The anterior border of the PPS is the pterygomandibular raphe. Inferiorly, the PPS gradually becomes narrower and ends at the level of the hyoid bone and superior margin of the submandibular salivary gland.

The posterior border of the PPS is the most complex and controversial; different descriptions are found in the literature. Some authors consider the PPS completely separate from the more posterior carotid space: the anterior surface of the carotid sheath (made up of the three layers of deep cervical fascia) draws the borderline between the two spaces. From a radiological point of view such a separation allows a precise and reliable space-specific differential diagnosis (Som and Curtin 1995). Others, in contrast, consider the carotid sheath and, consequently, the carotid space to be part of the PPS (Mukherji and

Castillo 1998).

Three more fascial structures are described, acting as anatomical landmarks subdividing the PPS. The tensor-vascular-styloid fascia (TVS) is a layer that extends from the inferior border of the tensor veli palatini muscle, posterolaterally and inferiorly to the styloid process and muscles (Fig. 9.2). Anteriorly, it reaches the pterygomandibular raphe and there-

fore it closes the gap between the skull base, the tensor veli palatini muscle and the styloid process (Som and Curtin 1995). The stylopharyngeal fascia splits on a coronal plane connecting the styloid process to the pharyngobasilar fascia, at the level of the fossa of Rosenmüller. In this same site a third layer, Charpy’s fascia, also known as the ‘cloison sagittale’, arises, oriented on a sagittal plane and posteriorly reaching the prevertebral fascia where it attaches to the lateral cervical processes.

The TVS fascia allows further subdivision of the parapharyngeal space into two compartments: the prestyloid compartment, lying between the pterygoid muscles and the TVS fascia, and the retrostyloid compartment, just medial to the TVS fascia itself and including the carotid space (Maroldi et al. 1994;

Nasser and Attia 1990).

The PPS mainly contains fat tissue and loose connective tissue. In the prestyloid compartment ectopic minor salivary glands and vascular structures (pharyngeal ascending and internal maxillary artery, pharyngeal venous plexus) are found. The retrostyloid PPS contains the internal carotid artery (ICA), the internal jugular vein (IJV), the cranial nerves IX–XII, and the sympathetic plexus. Lymph nodes of the deep cervical chain, known as the jugulodigastric lymph nodes, are present in the retrostyloid compartment, below the level of the posterior belly of the digastric muscle (Grégoire et al. 2003).

9.2.2

Radiological Anatomy

When dealing with pathology at the level of the PPS, MRI has an advantage over CT because of its higher contrast resolution. CT better demonstrates subtle bone erosion. However, MR yields unique information about the medullary bone, which normally has a hyperintense signal on the unenhanced T1-weighted images (due to its fatty content). This signal will become hypointense on the same sequence when the medullary bone is replaced by neoplastic tissue. This signal decrease is a very sensitive sign for neoplastic infiltration, but it is rather aspecific, because edema and inflammatory bone reactions also cause a signal decrease in the medullary bone on T1-weighted images.

In the axial plane the prestyloid compartment of the PPS is recognized as a triangular fat-filled space (Fig. 9.1) with maximum width at the level of the soft palate. While CT is unable to display the pharyngobasilar fascia, this fascia is visible on MRI as a hypointense line (Fig. 9.3).

The sinus of Morgagni is not visible with MR, but the Eustachian tube, particularly at the torus tubarius, where it opens in the nasopharyngeal lumen, can be used as an anatomical landmark.

The TVS, stylopharyngeal and Charpy’s fascia can not be routinely identified on MR. Their course can be