Учебники / Head_and_Neck_Cancer_Imaging

skin. The histological nature of the lesion is the second major determinant for the therapeutic strategy.

Other factors determining the therapeutic options are the general and psycho-social status of the patient. Figure 10.13 summarizes the available therapeutic options in HN cancers, also applying to those of the MS. Key points are the curability and the complete surgical resectability of the neoplasm.

Basic principles of therapeutics in HN malignancies (including those of the MS) are:

•Avoidance of ‘partial’ surgery, except for the purpose of palliative care.

•Avoidance of systematic multiple therapies if unnecessary, e.g. if surgery alone is curative, chemotherapy and radiation therapy are ‘reserved’ therapeutic options for salvaging possible recurrence.

•Imaging guidance for both surgery and radiation therapy volume delineation.

Regarding MS structures:

•Tumoral spread along the V3 course requires complete excision and/or irradiation of the nerve.

•Muscle infiltration requires the resection and/or irradiation of all involved muscles.

•Mandibular invasion requires the resection of diseased bone segments.

•Skull base invasion almost precludes any surgical curative option.

10.5.3.2

Potential Roles for Imaging Monitoring During and After Treatment

Three main goals are potentially achieved by posttreatment imaging follow-up examinations: the assessment of the response to the treatment, the visualisation of treatment complications, and the early detection of tumoral recurrence. Frequency and interval of imag-

ing follow-up examinations are usually defined by local institutional guidelines (ours at http://www.md.ucl. ac.be/ccmf/guidelines). The response to the treatment is primarily assessed by clinical examination. In our institution, a follow-up examination is routinely performed within 1–3 months after treatment completion in patients treated by radiation therapy and/or chemotherapy. In operated cases, early imaging follow-up has lower interest and is usually not performed. Neither treatment complications nor tumoral recurrence are systematically investigated using imaging modalities in asymptomatic patients. Basic principles of posttherapeutic imaging are the clinical guidance for triggering follow-up imaging and the clinical relevance of imaging findings. Only patients in whom clinical signs

like reappearance of pain, abnormal swelling, newly appeared mucosal changes, or reappearance of masticator spasm (trismus) or V3 dysaesthesias, suggest a treatment complication or tumor recurrence have follow-up imaging in an “à la carte” mode.

The second basic principle is to perform followup imaging only when imaging findings may subsequently alter the therapeutic strategy. If no more curative option exists then follow-up imaging loses clinical relevance and has only scientific relevance in the peculiar frame of prospective therapeutic trials.

Clinical triggering and relevance aside, a limitation of post-treatment imaging is that CT and/or MR images may be inconclusive because of the difficulty to distinguish post-therapeutic benign changes from

not resectable RT ± CT

INCURABLE best supportive care (palliative treatments)

Fig. 10.13. Algorithm of therapeutic options for HN malignancies. CT, chemotherapy; RT, radiation therapy

active disease. In such cases PET or PET-CT studies may be helpful.

10.5.3.3

Imaging of Treatment Complications

Main complications of surgical treatment are functional impairment of mastication function and VIIth/Vth cranial nerve dysfunction. Reconstructive surgery efficiently corrects the unsightly effects of radical surgery on physical appearance. However, the compensation for functional impairment may be less satisfactory.

The main complications of radiation therapy include damage to normal tissues such as spinal cord or brainstem injury and optic neuritis leading to chronic neurological impairment. Xerostomia due to radia- tion-induced involution of major salivary glands is reduced by sparing unaffected glands in anatomical irradiation planning. Finally, mucosal and bone necrosis may occur within a variable delay after irradiation. Mandibular osteoradionecrosis (ORN) is an uncommon ‘collateral’ tissue damage after radiation therapy due to radiation-induced vasculitis reducing the arterial blood supply to bone which results in decreased capabilities for repairing micro-/mac- roscopic bone injuries. CT shows variable degrees of loss of trabeculae within spongious bone, permeative disruptions in cortical bone margins, bone fragmentation and sequestrations, and even gas within damaged bone tissues. Fracture, osteomyelitis, and fistulas are seen (Hermans 2003). Prominent but benign soft tissue swelling may mimick tumor recurrence in this condition (Chong et al. 2000).

References

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CONTENTS

11.1Introduction 191

11.4Imaging Appearance and Extension Patterns

of Sinonasal Neoplasms 194

11.4.1Appearance of the Tumor Mass on CT

11.5Tumor Types 198

11.5.2Non-epithelial Tumors 205

11.5.2.1Neuro-ectodermal and Nervous System Tumors 205

11.5.2.2Mesenchymal Neoplasms 207

11.5.2.3Lymphoreticular Tumors 212

11.5.2.4Fibro-osseous Disease 213

11.1 Introduction

Many different types of malignant tumors arise within the sinonasal cavities. These tumors constitute less than 1% of all malignant neoplasms. The incidence of these tumors shows geographical dif-

R. Hermans, MD, PhD

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

ferences, being clearly higher in parts of Africa and Japan than in the US. Sinonasal carcinoma is a disease mainly occurring in the age range of 50–70 years, although some tumor types (such as lymphoma, minor salivary gland tumors or esthesioneuroblastoma) also occur in younger patients.

The risk for developing certain types of sinonasal carcinoma is associated with exposure to certain exogenous factors: woodworkers have a much higher risk for developing an adenocarcinoma; exposure to nickel correlates with a higher risk for squamous cell carcinoma.

Tumors arising in the paranasal sinuses have abundant place to grow without causing many symptoms. The symptoms themselves are usually aspecific; sometimes associated inflammatory disease overshadows the tumor. For these reasons, sinonasal neoplasms are usually diagnosed in an advanced stage, except for occasional nasal cavity lesions presenting early because of nasal obstruction (Parsons et al. 1994). Deformation of or extension into the hard palate or maxillary alveolar process may cause pain or mal fitting of a denture. Extension through the ventral maxillary wall causes swelling of the face; trismus may develop with extension through the posterior maxillary wall and infiltration of the masticatory muscles. Orbital symptoms occur by interference with the lacrimal apparatus or neoplastic infiltration of the orbit. Different neurologic symptoms, mainly pain and cranial nerve paralysis, may be encountered when the skull base is invaded; especially the pterygopalatine fossa and neighbouring fissures and foramina, as well the floor of the anterior cranial fossa are at risk for tumor invasion.

The nasal vestibule is covered with skin, and malignant tumors arising at this site are often squamous cell carcinomas, with a natural history resembling skin cancer. Early lesions present as a small ill-healing ulcer or crust. Tumors at this site may already show a more extensive spread as thought after initial clinical evaluation; they grow toward the upper lip and nasal septum, and in a later stage also towards the maxilla, nasal and oral cavity.

11.2

Normal Radiological Anatomy

Anatomical structures, relevant to the radiological description of sinonasal tumor extent, are shown in Figs. 11.1 and 11.2.

11.3

Indications for Imaging Studies

Imaging is necessary for evaluating paranasal extension and possible intracranial spread, orbital involve-

ment, infratemporal extension, spread to the nasopharynx, oropharynx or oral cavity and spread along neurovascular bundles (Table 11.1).

The neck and facial lymph nodes (Tart et al. 1993) are not routinely studied in cases of sinonasal cancer. When there is extension into the skin, oral cavity or pharynx, or when a recurrent tumor is present, the facial lymph nodes and the upper neck nodes are at risk, and should be included in the imaging study. The presence of metastatic lymph nodes is a sign of poor prognosis.

Often CT will adequately show the tumor extension. Involvement of the delicate bony structures in this region is better seen with CT than with MRI. CT

194

Table 11.1. Issues to be addressed during imaging of nasosinusal cancer. CT and MRI are often complementary methods in the evaluation of sinonasal cancer; imaging method best suited for a particular issue is between parentheses

Tumor Mass

Tissue characteristics, such as vascularity (MR) Presence of intratumoral calcifications (CT)

Subtle bone expansion or erosion at tumor border (CT) Differentiation from surrounding inflammation (MR)

Tumor Extension in neighboring structures Skull base (CT/MRI)

Intracranial compartment (MRI) Orbit (MRI)

Perineural spread (MRI)

Neck (when extension into skin, oral cavity or pharynx, or in case of recurrent tumor)

Lymph nodes (CT)

demonstrates the presence of intratumoral calcifications, which is helpful in the differential diagnosis. MRI is indicated as complementary study when the tumor is growing closely to the intracranial compartment (usually at the roof of the nose and ethmoidal sinuses, sometimes along the posterior wall of the frontal sinus or posterolateral walls of the sphenoid sinus), to evaluate possible dural involvement or transdural extension. MRI is also best to evaluate subtle orbital involvement. The precise borders of a cancer growing into the extrasinusal soft tissues can be more precisely determined with MRI. Subtle perineural spread may also be detected more easily with MRI. A major advantage of MRI over CT is the better differentiation of tumor tissue from accompanying inflammatory changes in the paranasal sinuses (Som et al. 1988).

In patients who had only a limited CT study of the paranasal sinuses (usually unenhanced coronal sections), because the symptoms of the patient were initially attributed to inflammatory disease, a complementary MRI study is indicated to evaluate more comprehensively the tumor extent.

11.4

Imaging Appearance and Extension Patterns of Sinonasal Neoplasms

11.4.1

Appearance of the Tumor Mass on CT and MRI

Most lesions appear as a solid, moderately enhancing mass lesion on CT studies. Local bone destruction is characteristic of malignant tumors, as opposed to

R. Hermans

the expansion of the sinus cavity seen with benign tumors and mucocoeles (Lloyd 1988).

Such imaging findings are highly suggestive for a malignant tumor, but no specific histological diagnosis can be made based on these findings. Punctate intralesional calcifications are occasionally seen in squamous cell carcinoma (Lloyd 1988); intratumoral calcifications may be seen in some other epithelial tumors, such as inverted papilloma or adenocarcinoma; calcifications may also be present in esthesioneuroblastoma, a tumor from neurogenic origin (see below). A calcified or ossified matrix is often present in the rare chondroand osteosarcomas, but these lesions rather affect the bone structures and invade secondarily the nose and/or sinuses (see below).

On MRI sinonasal neoplasms usually show an intermediate signal intensity, both on T2and T1weighted sequences. The intermediate T2 signal intensity allows separation of the tumor mass from high intensity inflammatory changes (Fig. 11.3). Only some sinonasal tumors show a high T2 signal intensity: this is mainly seen with tumors from salivary gland origin or neuromas, and in these cases differentiation from surrounding inflammatory changes may be more difficult on T2-weighted images (Som et al. 1988). Also some carcinomas may show hyperintense areas on T2-weighed images, presumably due to necrosis (Fig. 11.4). In such cases the gadoliniumenhanced T1-weighted images will help to differentiate the enhancing mass lesion from non-enhanced edema or fluid within the sinonasal cavities.

Tissue characterisation is not possible using MRI: the observed signal intensities in different tumors show substantial overlap (Yousem et al. 1992). Sinonasal melanoma may show spontaneous hyperintensity on T1-weighted images and low signal intensity on T2-weighted images, attributed to the presence of melanin, which is a paramagnetic substance (Loevner and Sonners 2002). However, not all melanomas contain melanin.

11.4.2

Extension Towards Neighbouring Structures

11.4.2.1

Anterior Cranial Fossa

When the tumor extends to the nasoethmoidal roof, intracranial spread through the floor of the anterior cranial fossa may occur. Coronal and sagittal sections are best suited for demonstration of such spread.

Neoplasms of the Sinonasal Cavities

a

b

c

195

The first sign of anterior cranial fossa involvement is erosion of the delicate bone interface between the sinonasal cavity and the anterior cranial fossa; such early bone invasion is best detected on coronal CT images.

Tumor spread beyond the bony nasoethmoidal roof is best seen using MRI. Linear dural enhancement as seen on coronal or sagittal T1-weighted images is not specific for dural invasion; it often represents reactive (inflammatory) changes. Dural enhancement with focal nodularity, dural thickening of more than 5 mm, and pial enhancement are highly suggestive for neoplastic dural invasion (Eisen et al. 1996) (Fig. 11.5).

Brain invasion is seen as enhancement of the brain parenchyma; this is better visualized on MR studies than on CT studies, as is the often associated localized brain edema surrounding the area of brain parenchyma invasion (Kraus et al. 1992) (Fig. 11.6).

11.4.2.2 Orbit

Involvement of the orbit usually occurs through the medial or inferior wall; coronal sections are therefore best suited to detect such spread. Just as with the floor of the anterior cranial fossa, the earliest sign of orbital involvement is erosion of the delicate bony orbital borders (lamina papyracea and/or floor of the orbit). With further tumor growth, the extraconal fat will get displaced without direct invasion. This occurs because the strong periorbita (the orbital ‘periost’) acts as a barrier to tumor spread, walling off the tumor from the orbital fat (Fig. 11.4).

CT can quite accurately show erosion of the bony orbital walls, a condition which occurs frequently in

Fig. 11.3a–c. Coronal T2-weighted spin echo image (a), plain (b) and gadolinium-enhanced (c) T1-weighed spin echo images. Soft tissue mass in the right nasal cavity, adherent to the nasal septum, focally growing through this structure (arrowhead). The lesion reaches the lamina cribrosa, but the anterior cranial fossa structures (including the olfactory bulb) appear normal (arrow). Retro-obstructive inflammatory changes are seen in the ipsilateral maxillary sinus; compared to the peripheral part, the central part of the maxillary sinus shows lower intensity on the T2-weighted image and higher intensity on the plain T1-weighted image due to thickening of intraluminal secretions. Also in the posterior ethmoid cells (curved arrow) inflammatory changes are seen, separating the tumor from the lamina papyracea. The tumor mass shows moderate enhancement. In the anterior cranial fossa, no dural enhancement is seen. The tumor was successfully removed by endoscopic surgery; postoperative radiotherapy was administered. The lesion corresponded to an intestinal-type adenocarcinoma

196

a

b

c

R. Hermans

ethmoidal cancer. However, erosion of the lamina papyracea is not a crucial finding, as this bone is partially or completely resected at surgery (Maroldi et al. 1997). More important is the assessment of the periorbita, as the degree of involvement of this structure determines largely the surgical management of the orbital structures.

At present, there are no absolutely reliable imaging findings for invasion of the periorbita. Both on CT and MRI, displacement of the periorbita can not be distinguished from neoplastic invasion of the periorbita (Graamans and Slootweg 1989). A nodular interface with the orbit is a slightly more specific, but less sensitive sign of orbital invasion (Eisen et al. 2000).

When the tumor has crossed the periorbit, direct tumoral invasion of the different intra-orbital structures becomes possible. Enlargement, abnormal signal and/or enhancement of the extra-ocular muscles, when present, are very specific signs of orbital invasion (Fig. 11.7). Also infiltration of the orbital fat is a sign with high specificity for orbital invasion (Eisen et al. 2000).

Tumor extension may occur by invasion and tracking of the nasolacrimal canal. Invasion of the nasolacrimal duct and sac can be diagnosed by CT or MRI with high accuracy (Eisen et al. 2000).

11.4.2.3

Infratemporal Fossa and Middle Cranial Fossa

Extension towards the infratemporal fossa occurs through the posterolateral wall of the maxillary sinus, and is therefore best detected on axial slices. The earliest sign is cortical erosion of the maxillary wall, best seen on CT images (Fig. 11.8). After infiltration of the retromaxillary fat, the tumor will reach the masticatory muscles, causing mass effect and eventually infiltration of these structures.

Fig. 11.4a–c. Coronal T2-weighted spin echo image (a), coronal plain (b) and gadolinium-enhanced (c) T1-weighted spin echo images. Large nasoethmoidal soft tissue mass on the right side, displacing (possibly invading) the nasal septum. The lesion largely appears very intense on the T2-weighted image, isointense to the retro-obstructive inflammation in the right maxillary sinus. Better differentiation between the tumor mass and retro-obstructive secretions is possible by integrating the information from the T1-weighted images. Slight lateral displacement of the medial orbital wall is seen, without infiltration of the orbital fat. During surgery, the lesion was contained by the (non-involved) periorbita. Pathologic examination revealed an intestinal-type adenocarcinoma, showing a very myxoid stroma