Imaging of neoplasms of the paranasal sinuses

Magn Reson Imaging Clin N Am 10 (2002) 467–493

Imaging of neoplasms of the paranasal sinuses Laurie A. Loevner, MDa,*, Adina I. Sonners, BSb a

Department of Radiology, University of Pennsylvania Medical Center, 3400 Spruce Street, Philadelphia, PA 19104, USA b University of Pennsylvania School of Medicine, University of Pennsylvania Medical Center, 3400 Spruce Street, Philadelphia, PA 19104, USA

Carcinomas of the sinonasal cavity constitute 3% to 4% of all head and neck neoplasms [1–4]. Squamous cell carcinoma accounts for approximately 80% of these cancers, whereas adenoid cystic and adenocarcinomas account for 10% [2,5]. In general, these carcinomas have a relatively poor prognosis because many present at advanced stages of disease. Reasons for delayed diagnosis and presentation include a relative paucity of pain associated with these neoplasms. Because there is frequently coexistent inflammatory disease in the paranasal sinuses that may elicit pain, a carcinoma may initially be overlooked because the patient is treated for presumed infection. Whereas pain in the early stages of sinonasal malignancies is uncommon, the presence of pain indicates advanced disease. Pain may indicate perineural tumor spread, skull base extension, or spread to the infratemporal fossa. Other clinical presentations include nasal congestion and epistaxis. The assessment of sinonasal malignancies requires a multidisciplinary team approach that includes radiologists, head and neck surgeons, neurosurgeons, oral prosthetics specialists, radiation oncologists, and medical oncologists. Advances in pretherapeutic imaging have contributed significantly to the management of sinonasal tumors. CT and MR imaging play complementary roles in the assessment and staging of these malignancies [6–8]. The treatment of choice for sinonasal carcinoma usually includes combined surgery and irra-

* Corresponding author. E-mail address: [email protected] (L.A. Loevner).

diation [9–13]. Overall survival rates for radiation therapy prior to or following surgery are similar. Orbital exenteration is performed for tumors involving the periorbita, usually confirmed during surgery by frozen section [14,15]. In the setting of extension into the central skull base or the nasopharynx, curative surgery is usually not attempted. The main cause of treatment failure is local recurrence [1,16].

Normal anatomy To understand the clinical and radiologic appearance of neoplasms originating from the paranasal sinuses, and the coexistant inflammatory changes that usually occur with such tumors, knowledge of the normal anatomy and the patterns of pneumatization and drainage of sinus secretions is necessary. An understanding of the natural history of sinus carcinomas is also paramount in assessing patterns of tumor spread, in determining surgical management, and in determining radiation portals. There are paired maxillary, ethmoid, sphenoid, and frontal sinuses, each named after the bones of the skull in which they are localized. As each sinus develops, pneumatization may extend into the adjacent bones (ie, the frontal and maxillary sinuses may extend into the zygomatic bones). The maxillary sinuses are the first of the paranasal sinuses to develop. The ethmoid air cells arise from numerous evaginations from the nasal cavity, beginning with the anterior air cells and progressing to the posterior air cells. The ethmoid air cells attain their adult proportions by puberty. The sphenoid sinus usually develops by age 10. The frontal sinuses are the only sinuses consistently

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absent at birth. Their development is variable, beginning during the first few years of life, and completed in early adolescence. The sinonasal cavity is lined by ciliated, pseudostratified columnar epithelium, which contains mucinous and serous glands. The common drainage pathway for the frontal sinuses, maxillary sinuses, and anterior ethmoid air cells is through the ostiomeatal complex, made up of the maxillary sinus ostium, the infundibulum, the hiatus semilunaris, and the middle meatus (Fig. 1) [17]. Secretions in the maxillary sinuses circulate to the maxillary sinus ostium, propelled by cilia [18,19]. From the ostium, secretions circulate through the infundibulum located lateral to the uncinate process (an osseous extension of the lateral nasal wall); through the hiatus semilunaris (an air-filled channel anterior and inferior to the ethmoidal bulla); and then pass into the middle meatus, the nasal cavity, and the nasopharynx where they are swallowed [18,19].

The frontal sinuses drain inferiorly via the frontal recess/nasofrontal duct into the middle meatus, also the common drainage site for the anterior ethmoid air cells, which have ostia in contact with the infundibulum of the ostiomeatal complex [17]. The nasofrontal duct is between the inferomedial frontal sinus and the anterior part of the middle meatus [17]. The anterior-most ethmoid air cells are located in front of the middle turbinates, which are in turn located anterior, lateral, and inferior to the frontal ethmoidal recess. The posterior ethmoid air cells are located behind the middle turbinate, and secretions drain through the superior and supreme meati and other tiny ostia under the superior turbinate into the sphenoethmoidal recess, the nasal cavity, and finally into the nasopharynx. Cilia are necessary for the drainage of the spenoid sinus because the ostia are located above the sinus floor. There are paired superior, middle, and inferior turbinates in the nasal cavity. Occasionally, there

Fig. 1. Anatomy of important landmarks in the sinonasal cavity shown on coronal CT imaging photographed for bone detail. (A) Image obtained at the ventral sinonasal cavity. Frontal sinuses (F), cartilaginous nasal septum (C). (B) Image at the level of the ostiomeatal unit. Medial orbital wall/laminae papyrecia (black arrows), uncinate process of the ostiomeatal unit (short white arrow), cribriform plate (long white arrow), circulatory pathway of secretions (small white squares), osseous nasal septum (N). (C) Coronal CT image at the level of the pterygoid bone shows the paired vidian canals (arrows) and the foramen rotundum (r).

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Fig. 1 (continued )

may be a supreme turbinate located above the superior turbinate. An aerated middle turbinate (concha bullosa) is present in up to 50% of imaged patients. Large, opacified concha bullosa may obstruct the ostiomeatal complex. The nasal septum separates the right and left nasal turbinates, dividing the nasal cavity in half. The anterior and inferior nasal septum is made up of cartilage, whereas the posterior portion is osseous. The superoposterior osseous portion is the perpendicular plate of the ethmoid bone, whereas the inferoposterior osseous portion is the vomer. The septum within the nasal cavity is lined by squamous epithelium.

There is normal cyclic passive congestion and decongestion of each side of the nasal cavity and ethmoid air cells that includes temporary unilateral mucosal thickening of these structures. The nasolacrimal duct courses from the lacrimal sac at the medial canthus, runs along the anterior and lateral nasal wall, and drains into the inferior meatus. Blood supply to the sinonasal structures comes from the internal and external carotid arteries. The arterial supply to the frontal sinuses is from supraorbital and supratrochlear branches of the ophthalmic artery, whereas venous drainage is through the superior ophthalmic vein. The

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ethmoid air cells and sphenoid sinus also receive their blood supply from branches of the sphenopalatine artery (arising from the external carotid) and ethmoidal branches of the ophthalmic artery (arising from the internal carotid). Venous drainage is via nasal veins into the nasal cavity, and/or ethmoidal veins that drain into the opthalmic veins, which then drain into the cavernous sinus. The maxillary sinuses are predominantly supplied by branches of the external carotid artery, most notably the maxillary artery. These sinuses drain through facial and maxillary veins, the latter communicating with the pterygoid venous plexus.

Neoplasms Squamous cell carcinoma Squamous cell carcinoma accounts for 80% of sinonasal malignancies [4]. Approximately 25% to 60% of these carcinomas involve the maxillary anthrum; however, the maxillary sinus is secondarily involved by direct extension in 80% of patients (Fig. 2). The nasal cavity is the site of origin in approximately 30% of cases, and the ethmoid air cells in 10% of cases. The sphenoid and frontal sinuses account for less than 2% of all sinonasal carcinomas [1]. These are typically seen in patients who range in age from 60 to 70 years, more commonly in men [20]. Occupation exposures include nickel, chromium pigment, Bantu snuff, Thorotrast, mustard gas, polycyclic hydrocarbons, and cigarettes [4,21]. People involved in the production of wood furniture, isopropyl alcohol, and radium also are at increased risk. The average 5-year survival rate for squamous carcinoma of the sinonasal cavity is approximately 25% to 30% [22]. More aggressive surgical management and improvements in administering irradiation over the last decade may improve survival rates. Local recurrences occur in approximately 25% to 35% of cases [1], and the most cases present in the first year following diagnosis. Ten percent of cases have distant metastases. Definitive treatment for early lesions (T1 and T2) includes surgery (maxillectomy) and/or radiation therapy. Although the mainstay of therapy is surgery, some small-scale studies have shown successful management with irradiation alone. For advanced tumors (T3 and T4), treatment requires surgery and irradiation [10–13]. Adjuvant chemotherapy has recently been added to the treatment regimen; however, its impact remains to be determined.

Minor salivary gland malignancies Approximately 10% of sinonasal tumors originate in the glands [1]. There is a spectrum of histologic types, including adenoid cystic, mucoepidermoid, undifferentiated, and adenocarcinoma. The adenocarcinomas may represent minor salivary gland tumors or intestinal-type adenocarcinomas, and have a predilection for the ethmoid sinuses [23,24]. These may be more common in wood and leather workers [23]. They are frequently advanced at presentation, with cribriform plate erosion present in up to 50% of cases. Dural invasion is not uncommon [24]. Treatment frequently consists of craniofacial resection followed by irradiation when tumors are close to or eroding the cribriform plate, invading the dura, or in the setting of positive surgical margins [24]. Most minor salivary gland tumors arise from the palate and secondarily extend into the nasal cavity and paranasal sinuses. Adenoid cystic carcinomas are most common, accounting for one third of minor salivary gland neoplasms [25]. Up to one half of these tumors arise in the maxillary sinus, and one third arise in the nasal cavity. Less than 5% of tumors originate in the sphenoid and frontal sinuses. Adenoid cystic carcinomas have variable histologic patterns (cribriform or tubular). They have a relatively high incidence of perineural spread (including skip lesions along nerves; Fig. 3), with secondary extension into the orbit and intracranial compartment. When feasible, surgical resection is the treatment of choice. Adjuvant radiation therapy allows for better local control. Local recurrence is seen in more than one half of patients at 1-year follow-up, and 75% of patients at 5 years [1]. Tumors may progress from being well differentiated (tubular), to moderately differentiated (cribriform), to poorly differentiated [26]. Approximately one half of patients with adenoid cystic carcinoma have distant metastases, most commonly to the lungs, brain, and bones [1]; therefore, CT imaging of the chest, abdomen, and pelvis should be included in the routine evaluation of these patients. Melanoma Sinonasal melanomas may arise from melanocytes that have migrated during embryologic development from the neural crest to the mucosa of the sinonasal cavity [27]. Less than 4% of melanomas arise in the sinonasal cavity, with most of these originating in the nose [27,28]. Within the

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Fig. 2. A 58-year-old man with squamous cell carcinoma of the maxillary sinus. (A) Axial fast-spin echo T2-weighted MR image shows a large, poorly demarcated, hypointense mass (m) emanating from the right maxillary sinus, with frank extension through the anterior sinus wall into the facial soft tissues/cheek. (B) Corresponding enhanced axial fast multiplanar spoiled gradient echo MR image utilizing fat suppression shows extension outside the confines of the maxillary sinus.

nasal cavity, the most common sites of melanomas are the anterior nasal septum, lateral nasal wall, and the inferior turbinates (Fig. 4) [29]. In the paranasal sinuses, the maxillary anthrum is the site of

origin in 80% of cases. Sinonasal melanomas may be associated with melanosis, in which there is field deposition of melanin along the mucosa in the sinonasal cavity. This is best assessed on physical

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Fig. 3. Perineural spread of adenoid cystic sinonasal carcinoma. Coronal CT image photographed for soft tissue detail shows enlargement of the left vidian canal (v) and foramen rotundum (r), with soft tissue consistent with tumor in these foramina.

examination. These tumors may also be multifocal [29]. Most sinonasal melanomas are melanotic; 10% to 30% are amelanotic [30]. Wide local surgical resection with or without postoperative radiation therapy is the standard

treatment. In general, sinonasal melanomas have a poor prognosis, with a mean survival of approximately 2 years [31]. As many as 40% of patients present with cervical nodal metastases. Up to two thirds of patients have local recurrence or

Fig. 4. Nasal cavity melanoma. Axial T2-weighted MR image shows a hypointense mass (arrows) in the right nasal cavity consistent with melanotic melanoma.

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metastases within the first year after treatment. Hematogenous metastases affect the lungs, brain, liver, and skin. Neurotrophic spread is not uncommon (Fig. 5). Nasal melanomas have a better prognosis than those originating in the paranasal sinuses. Olfactory neuroblastoma (esthesioneuroblastoma) Esthesioneuroblastomas occur in the upper nasal cavity/ethmoid vault, arising from the olfactory nerves. They have a bimodal age distribution, presenting in boys and middle-aged adults. They have a marked propensity for crossing the cribriform plate and extending intracranially (Fig. 6) [32,33]. When intracranial extension is present, a craniofacial surgical approach and adjuvant radiation therapy are necessary. Though uncommon, subarachnoid seeding may occur. This spread may be because of direct tumor extension or may be a consequence of surgery.

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are more readily resected en bloc and are less problematic. Important landmarks of the ethmoid air cells include the fovea ethmoidalis and the cribriform plate superiorly, which provide only a moderately resilent barrier to intracranial spread [15]. Intracranial spread usually necessitates a craniofacial resection with the combined efforts of the head and neck surgeons and neurosurgeons [9]. The lateral wall of the ethmoid air cells—the lamina papyracea—when violated, may result in intraorbital spread that usually requires orbital exenteration (see Fig. 9) [14,35–37]. Though rare, cancer arising in the sphenoid sinus is difficult to resect because of its central location in the skull base where it is surrounded by numerous vital structures. The sphenoid sinus is bounded superiorly by the pituitary sella and visual tracts; laterally by the carotid arteries and cavernous sinuses; anteriorly by the posterior ethmoid air cells; and inferiorly by the vidian canal, the PPF, and the nasopharynx.

Other neoplams Other aggressive neoplasms involving the sinonasal cavity include ameloblastomas, sarcomas (osteogenic sarcoma, chondosarcoma, fibroma/ fibrosarcoma), hemangiopericytomas (Fig. 7), and lymphomas (Fig. 8); however, these constitute a small fraction of all sinonasal malignancies.

Patterns of tumor spread Sinonasal malignancies usually spread by direct (see Figs. 6, 9) or perineural extension (see Figs. 3, 5) [6,8,34]; therefore, an understanding of the anatomic boundaries of the individual paranasal sinuses and their contiguous structures is important in mapping the extent of disease and in determining the extent of surgical resection. The superior and posterior boundaries of the maxillary sinuses are important prognostically and in designing the surgical management [15]. The maxillary sinuses are bounded superiorly by the orbit and ethmoid air cells, and posteriorly by the pterygoid plates and the pterygopalatine fossa (PPF). Direct extension into the orbit, or spread to the intracranial compartment via the ethmoid air cells, makes obtaining tumor-free surgical margins difficult. Extension posteriorly by direct extension or perineural spread may result in neoplastic invasion of the masticator space, the orbit, and/or the intracranial compartment. The other margins of the maxillary sinuses (medially the nasal cavity and inferiorly the alveolus)

Metastases Lymphatic drainage and nodal metastases The lymph node drainage for sinonasal neoplasms is dependent on the origin of the neoplasm, the stage of the neoplasm, and the histology. Whereas the primary nodal drainage site for the paranasal sinuses is the lateral retropharyngeal nodes, these lymphatic channels may be inconstant. Therefore, the upper internal jugular and submandibular nodes are the most common sites for nodal metastases. Regional lymph node metastases from sinonasal malignancies are relatively uncommon, but when present are a poor prognostic sign and usually indicate tumor extension outside of the sinonasal cavity [38]. Cervical nodal metastases are most common with tumors originating from the maxillary anthrum, seen at presentation in up to 15% of cases. Nodal metastases are uncommon with ethmoid cancers, and rare with sphenoid and frontal sinus neoplasms. Distant metastases Less than 10% of all sinonasal carcinomas have systemic metastases. Hematogenous spread to the lungs is most common, with occasional bone metastases. The presence of cervical nodal disease places the patient at increased risk for distant metastases [38]. Approximately one half of patients with adenoid cystic carcinomas have distant

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Fig. 5. A 54-year-old woman with sinonasal melanoma. (A) Unenhanced axial T1-weighted MR image shows abnormal soft tissue in the right pterygopalatine fossa (arrows) and extending into the skull base at the level of the vidian canal (small white squares) and the clivus (c). (B) Corresponding enhanced fat-suppressed axial T1-weighted MR image shows diffuse enhancement of the tissue consistent with tumor.

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Fig. 6. Esthesioneuroblastoma with intracranial extension. (A) Axial fast-spin echo T2-weighted MR image shows a hypointense mass (M) in the upper nasal vault. (B) Enhanced coronal T1-weighted MR image shows an enhancing mass (M) within the nasal cavity and adjacent ethmoid air cells. There is extension to the cribriform plate/skull base (arrows). Opacification of the right maxillary sinus and nasal cavity with rim-enhancing fluid (F) is noted. (C) Enhanced coronal T1-weighted MR image posterior to Fig. 6B shows the mass (M) extending through the cribriform plate/planum sphenoidale (arrow) along the floor of the left anterior cranial fossa.

metastases, most commonly to the lungs, brain, and bone. Hematogenous metastases are not uncommon with melanoma and affect the brain, liver, and skin. Although the incidence of meta-

static disease is relatively high with adenoid cystic carcinoma and melanoma, it is important to recognize that these tumors together account for less than 8% of all sinonasal malignancies.

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Fig. 6 (continued )

Classification and staging Staging systems are used to define the extent of neoplastic disease, and to provide some basis to determine prognosis. In the paranasal sinuses, staging is usually discussed primarily in the context of epithelial neoplasms because these represent the vast majority of sinonasal tumors. Carcinoma of the maxillary sinus is most common, followed by ethmoid cancers. Malignancies of the frontal and sphenoid sinsues are rare, and hence are generally not included in staging.

T staging Evaluation and staging of maxillary and ethmoid sinus carcinomas is achieved through a combination of clinical assessment and pretreatment CT and MR imaging with close scrutiny of the sinonasal cavity, orbits, nasopharynx, oral cavity, and cranial nerves. Imaging is especially important in assessing the skull base, intracranial compartment, and in distinguishing tumor from coexistent inflammatory changes. The tumor, nodes, and metastases (TNM) system of classification of maxillary sinus cancers is based on Ohngren’s imaginary line drawn on a lateral view extending from the medial canthus of the eye to the angle of the mandible, separating the

maxillary anthrum into anteroinferior and superoposterior compartments. On a coronal view, the maxillary anthrum may be divided into an infrastructure, mesostructure, and suprastructure, with the lines of division drawn through the anthral floor of the maxillary sinus, and the anthral roof. Tumors are usually resected by partial or total maxillectomy; however, tumors extending into the suprastructure also often require an orbital exenteration. T1 tumors are confined to the mucosa, T2 lesions are associated with osseous erosion or destruction, and T3 and T4 tumors extend outside the sinonasal cavity into the masticator space, cheek (see Fig. 2), adjacent paranasal sinuses, orbital apex, base of skull, nasopharynx, or intracranially (Table 1) [39,40]. Ethmoid sinus carcinomas may be confined to the ethmoid air cells (T1), or they may extend into the nasal cavity (T2), the maxillary sinus and/or anterior orbit (T3), the orbital apex, intracranial compartment, skin, or frontal/sphenoid sinuses (T4) (Table 2) [31]. N staging In evaluating regional metastases, nodal size is the major criterion by which N1 to N3 disease is categorized (Table 3) [40]. To distinguish N1 from N2 disease, 3 cm is used, whereas 6 cm distinguishes N2 from N3 disease [40].

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Fig. 7. Hemangiopericytoma of the left maxillary sinus that grew during pregnancy in a 33-year-old woman who presented with pain and numbness in the right cheek. (A) Enhanced axial CT shows an avidly enhancing mass (M) in the right maxillary sinus. (B) CT image obtained at the level of the orbital floor shows extension of the tumor into the infraorbital foramen (small squares), confirmed at biopsy.

Imaging sinonasal neoplasms It is often difficult for the radiologist to hone down on a particular histologic diagnosis because of the marked overlap of the imaging appearance of different tumors on CT and MR images [41]. The major contribution by the radiologist is accurate mapping of tumor extent and an understanding of the anatomic sites that will influence or alter surgical resection, treatment planning, and prognosis. In the setting of sinonasal malignancies, a combination of CT and MR imaging are usually acquired [8,34,42]. When possible, these should be completed prior to surgical intervention, includ-

ing biopsy. Preoperative imaging may allow optimal localization for biopsy, and may be useful in preparing and minimizing complications of surgery, including blood loss in the setting of vascular neoplasms. Tumors extending into the nasal cavity may be amenable to transnasal biopsy. CT and MR imaging play complementary roles in the assessment of sinus neoplasms (see Fig. 9) [2,4,8,34,43–45]. CT is more sensitive and accurate in assessing the osseous margins of the sinonasal cavity, the osseous floor of the anterior cranial fossa, and the walls of the orbit [34,46,47]. CT may detect early cortical skull base erosion [42,48].

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Fig. 8. Sinonasal non-Hodgkin lymphoma in a 53-year-old patient following a lung transplant. (A) Unenhanced axial CT image obtained at the skull base shows opacification of the pterygoid extension of the left sphenoid sinus with osseous erosion (black arrows). There is also erosion of the posterior aspect of the ethmoid (white arrow). Note soft tissue opacification of the left pterygopalatine fossa ( pf ). (B) Coronal T2-weighted MR image shows tumor (T) in the sphenoid sinus, and replacing the pterygoid bone (P). Tumor is seen in the masticator space (curved arrows), with edema in the temporalis muscle (t). (C) Unenhanced coronal T1-weighted MR image shows tumor in the sphenoid sinus with cortical erosion of the roof of the sinus (thin arrows) and extension into the posterior aspect of the cavernous sinus (c). There is tumor in foramen ovale on the left (thick arrows), with spread of disease into the left masticator space (M). (D) Enhanced axial T1-weighted image shows extension of tumor through the lateral wall of the sphenoid sinus, and direct extension along the dural margin (arrows) of the left middle cranial fossa. Note tumor (T) along the left temporalis muscle.

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Fig. 8 (continued )

MR imaging offers soft tissue resolution, contrast, and multiplanar capabilities. In most instances, excellent resolution may be acquired using a standard head coil. On occasion, imaging of the sinonasal cavity may be performed with a surface coil positioned over the face [49]. MR imaging of sinonasal tumors must include high-resolution unenhanced and enhanced thin-section (3 mm) images not only of the sinonasal cavity but also of the orbit, skull base, and the adjacent intracra-

nial compartment [43,48,50,51]. Tumor extension into these structures is frequently not evident on clinical assessment and/or endoscopy. Images should be acquired in both axial and coronal planes. Contrast-enhanced imaging is essential to assess the extent of local disease, and the presence of perineural spread and intracranial extension. Extension of neoplasm outside of the sinonasal cavity into adjacent anatomic locations significantly impacts on the following: the patient’s

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Fig. 9. Sinonasal squamous cell carcinoma with orbital extension. (A) Coronal CT image photographed for bone detail shows a mass in the right nasal cavity. There is destruction of the superolateral nasal wall and floor of the right frontal sinus (black arrows) and marked thinning and bowing of the right medial orbital wall (white arrows). (B) Unenhanced coronal T1-weighted MR image shows the mass in the right nasal cavity and adjacent ethmoid air cells (M). There is extension through the floor of the right frontal sinus (white arrow), with hyperintense proteinaceous secretions (s) filling the remainder of the right frontal sinus. There is nodularity at the interface between the tumor and the periorbita (black arrows). At surgery, orbital invasion was confirmed. (C) Coronal T2-weighted MR image with fat suppression acquired at the same level as Fig. 9B shows hypointense tumor, extension into the frontal sinus, and invasion of the right periorbita. Inspissated secretions in the right frontal sinus are intermediate in signal intensity because of protein.

operability, the type of resection that will occur, the surgical approach, the necessity for radiation therapy, the placement of radiation portals, and the prognosis. Potential areas of tumor extension that must be assessed in all patients with sinonasal malignancies include intracranial spread (the anterior and middle cranial fossa), the palate, the orbits, the PPF, and the skull base [41,43,50,51]. The hallmark of malignancies involving the sinonasal cavity is the presence of osseous destruction (see Figs. 2, 9) [41]. Bone involvement is seen in approximately 80% of CT scans assessing sinonasal squamous cell carcinomas. Squamous and adenocarcinomas, and the much less common esthesioneuroblastoma, are usually intermediate to hypointense on T2-weighted images compared with gray matter (see Figs. 2, 6, 9), and most enhance in a solid fashion [32]. Adenoid cystic car-

cinomas have variable signal intensity on MR imaging, possibly reflecting the histologic pattern (cribriform or tubular) and the presence of cystic changes, tumor cellularity, and necrosis. Tissue specificity is not possible with MR or CT techniques except perhaps in some cases of melanoma. In most melanomas, which contain melanin, the neoplasms may be hyperintense to gray matter on unenhanced T1-weighted images, with more variable signal characteristics on corresponding T2-weighted MR images [30,52]. Whereas the T1 hyperintensity of melanomas has been attributed to the presence of blood products [53], T1 shortening in nonhemorrhagic, melanin-containing melanomas is common because of the paramagnetic effects of melanin [30,31,54]. Some investigators believe that the T1 shortening is related to the presence of free radicals [54], whereas others speculate

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Fig. 9 (continued )

that the shortening effect is caused by paramagnetic metal ions that may be bound to melanin [55]. Differentiating secretions and inflammatory changes from tumor One of the advantages of MR imaging versus CT is its ability to help discern complex sinonasal secretions and inflammatory disease from malignancy [32,47,56–58]. Secretions and mucosal disease frequently have a high water content, yielding high-signal intensity on T2-weighted images with peripheral enhancement (Fig. 10). In contrast, most histologic types of sinonasal tumors are highly cellular, resulting in intermediate- to low-signal intensity of these tumors on T2weighted images with a more solid pattern of enhancement (see Figs. 2, 6) [57,59]. Benign masses such as polyps, however, may also demonstrate only peripheral enhancement (see Fig. 10). A combination of T1- and T2-weighted images is extremely useful in distinguishing secretions and

mucosal inflammation from neoplasm [58]. Both pulse sequences are important because of the marked variability in the signal intensity of sinonasal secretions, which is the result of variable protein concentrations, the presence and extent of mobile water protons, and the viscosity that may occur with inspissated secretions. The changes in signal intensity associated with increasing protein concentrations are likely caused by extensive cross-linking of the glycoproteins present within hyperproteinaceous secretions. As a result, the relative amount of mobile water protons decreases. With low protein concentrations (\10%) and high free-water content, secretions in the paranasal sinuses are typically hypointense on T1-weighted images and hyperintense on T2-weighted images [60]. As the protein concentration increases, secretions on T1-weighted images become more hyperintense. When concentrations approach 20% to 25%, secretions typically are hyperintense on both T1-weighted and T2-weighted sequences. When protein concentrations exceed 25%, they are

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Fig. 9 (continued )

hyperintense on T1-weighted and hypointense on T2-weighted images (see Figs. 9, 10). Finally, when protein concentrations are extremely high (exceeding 28%), they are hypointense on both T1- and T2-weighted sequences and can mimic an aerated sinus. Bone destruction Osseous erosion or destruction is most commonly seen with carcinomas (see Fig. 9) [41]. Though much less common, it may also be seen with lymphomas, metastases, and sarcomas. Sclerosis secondary to tumor is rare. The presence of sclerosis is normally related to coexistent chronic inflammatory changes. Though uncommon, osteomyelitis in the sinonasal cavities may occur and is usually associated with rarefaction and sclerosis of bone. Calcification of sinonasal tumors is uncommon. Though prior literature has suggested that the presence of calcification with certain tumors is typical, it is more likely that,

in many cases, the findings interpreted as calcifications actually corresponded to fragmented bone. Skull base invasion Sinonasal masses that frequently erode the skull base and spread intracranially include carcinomas (poorly or undifferentiated squamous cell), esthesioneuroblastoma (see Fig. 6), lymphoma (see Fig. 8), and sarcomas [42]. Benign lesions that may erode the skull base include inverted papilloma, polyps, and mucoceles. The pattern of osseous destruction for benign and malignant lesions is similar at the skull base, because osseous remodeling in this location is unusual. Whereas CT may detect cortical erosion of the skull base [34], MR imaging is probably more sensitive in assessing skull base invasion [61]. It is particularly well suited to study bone marrow because it can differentiate fat from other tissues. The signal intensity is directly related to the relative amounts of fat, water, and cells in the marrow.

L.A. Loevner, A.I. Sonners / Magn Reson Imaging Clin N Am 10 (2002) 467–493 Table 1 American Joint Committee on Cancer T system for staging sinonasal malignancies: maxillary sinus TX T0 Tis T1 T2

T3

T4

Primary tumor cannot be assessed No evidence of primary tumor Carcinoma in situ Tumor limited to the antral mucosa with no erosion or destruction of bone Tumor causing bone erosion or destruction, except for the posterior antra wall, including extension into the hard palate and/or the middle nasal meatus Tumor invades any of the following: bone of the posterior wall of maxillary sinus, subcutaneous tissues, skin of cheek, floor or medical wall of orbit, infratemporal fossa, pterygoid plates, ethmoid sinuses Tumor invades orbital contents beyond the floor or medial wall including any of the following: the orbital apex, cribriform plate, base of skull, nasopharynx, sphenoid, frontal sinuses

Data from American Joint Committee on Cancer. Cancer staging handbook. 5th edition. Philadelphia: Lippincott-Raven Publishers; 1998; with permission of the American Joint Committee on Cancer (AJCCÒ), Chicago, IL.

In adults, the marrow in the normal skull base and cranium is hyperintense on unenhanced T1weighted images because it contains predominantly fat [62–64]; therefore, skull base involvement by tumor may be detected when the normal hyperintense appearance caused by fat is replaced with hypointense tissue (see Fig. 5) [65]. The presence of normal-appearing marrow at the skull base is usually a good indicator of absence of skull base

invasion; however, fixation to the periosteum cannot be excluded. The presence of hypointense tissue, however, does not always mean the presence of tumor. Hypointense tissue on unenhanced T1weighted images may also correspond to edema or hematopoietic marrow [62,66,67]. In the presence of abnormal hypointense T1 signal, it is important to assess the corresponding T2-weighted and enhanced images, which may help in differentiating tumor from nonmalignant changes. Perineural spread An especially important anatomic location for detection of tumor spread is the pterygopalatine fossa (PPF; see Figs. 5, 8) [6,68]. When tumor from the sinonasal cavity spreads to this location, extension into the adjacent orbit, infratemporal fossa, skull base, and intracranial compartment may subsequently occur [6,41,43]. Specifically, tumor may spread from the PPF to the pterygomaxillary fissure, allowing subsequent extension into the masticator space. From the PPF, tumor may extend to the inferior orbital fissure and the orbital apex. Neoplasm may spread to the vidian canal, and from there to the foramen lacerum and the Table 3 American Joint Committee on Cancer T system for staging sinonasal malignancies: regional lymph nodes NX N0 N1 N2

Table 2 American joint Committee on Cancer T system for staging sinonasal malignancies: ethmoid sinus T1 T2 T3 T4

Tumor confined to the ethmoid with or without bone erosion Tumor extends into the nasal cavity Tumor extends to the anterior orbit, and/or maxillary sinus Tumor with intracranial extension, orbital extension including apex, involving sphenoid, and/or frontal sinus and/or skin of external nose

Data from American Joint Committee on Cancer. Cancer staging handbook. 5th edition. Philadelphia: Lippincott-Raven Publishers; 1998; with permission of the American Joint Committee on Cancer (AJCCÒ), Chicago, IL.

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N3

Regional lymph nodes cannot be assessed No regional lymph node metastasis Metastasis in a single ipsilateral lymph node, 3 cm or less in greatest dimension Metastasis in a single ipsilateral lymph node, more than 3 cm but not more than 6 cm in greatest dimension, or in multiple ipsilateral lymph nodes, none more than 6 cm in or in bilateral or contralateral lymph nodes, none more than 6 cm in greatest dimension N2a Metastasis in a single ipsilateral lymph node more than 3 cm but not more than 6 cm in greatest dimension N2b Metastasis in multiple ipsilateral lymph nodes, none more than 6 cm in greatest dimension N2c Metastasis in bilateral or contralateral lymph nodes, none more than 6 cm in greatest dimension Metastasis in a lymph node more than 6 cm in greatest dimension

Data from American Joint Committee on Cancer. Cancer staging handbook. 5th edition. Philadelphia: Lippincott-Raven Publishers; 1998; with permission of the American Joint Committee on Cancer (AJCCÒ), Chicago, IL.

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Fig. 10. An 18-year-old man with a nasal choanal mass (M) protruding into the nasopharynx, and mucosal disease and retained secretions in the left maxillary sinus. (A) Axial fast-spin echo T2-weighted MR image shows the mass (m) in the right nasal cavity/nasopharynx. In the left maxillary sinus there is peripheral high signal intensity (small squares), consistent with mucosal disease. The material in the central portion of the sinus is hypointense, consistent with proteinaceous secretions (s). (B) Corresponding unenhanced axial T1-weighted MR image shows the peripheral mucosal disease is hypointense and the central secretions (s) hyperintense, consistent with the presence of protein. (C) Enhanced fat-suppressed axial T1-weighted MR image shows only minimal peripheral enhancement of the mucosal changes.

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Fig. 10 (continued )

intracranial compartment. In addition, tumor may spread from the PPF to foramen rotundum, and in such cases, patients may present with a fifth cranial neuropathy (see Fig. 3). From the foramen rotundum, perineural spread of tumor to the inferior orbital fissure, the orbital apex, the superior orbital fissure, and subsequently the intracranial compartment may occur. Orbital invasion Tumor involvement of the orbit and nasolacrimal system impacts negatively on prognosis, and significantly alters surgical planning [15]. The absence of orbital symptoms is not a reliable indicator of the absence of orbital invasion. The orbit is a coned-shaped space contained within the frontal bone, the greater and lesser wings of the sphenoid bone, the ethmoid bone, the lacrimal bone, the zygoma, and the maxilla [69]. The periorbita comprises the periosteum of these bones. It is continuous with the dura mater at the superior orbital fissure and the optic foramen [69]. When tumor penetrates through the periorbita (see Fig. 9), exenteration is usually required if the patient is a surgical candidate in order to obtain tumor-free margins [14]. If the periorbita is intact, the eye can be preserved and there is also a lower risk of local recurrence [12,13,36,37,70]. Erosion of sinonasal malignancies through orbital bone without invasion of the periorbita frequently may be man-

aged with orbital preservation [14,70]. In addition, some investigators have suggested that when tumor involves a limited amount of periorbita, the eye might be preserved without increasing the chance of local recurrence [14]. The preoperative imaging assessment of orbital invasion has not been extensively studied. CT and MR imaging are both important, each offering their own advantages and pitfalls. Osseous destruction with involvement of the orbital fat, which manifests as soft tissue stranding in the fat, has been one of the hallmarks used to suggest orbital invasion (see Fig. 9); however, some investigators have found a significant number of false negatives (low sensitivity: 40%, MR imaging; 60%, CT) for orbital fat involvement [50]. Therefore, although the presence of orbital fat invasion strongly indicates orbital invasion, the absence of abnormality in the orbital fat cannot exclude invasion. Other criteria evaluated include the following: the relationship between the tumor and the periorbita (abutting, displacing, or bowing the periorbita), the presence of nodularity at the interface between the tumor and the periorbita, assessment of the extraocular muscles (enlargement, displacement, and signal abnormalities), and evaluation of the integrity of the osseous structures comprising the orbital walls adjacent to tumor [50]. None of these criteria is very accurate (each 65%). Whereas tumor adjacent to the periorbita was the most sensitive criterion, it suffered from

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low specificity (29–44%). In this study, a comparison between the results of MR and CT findings for orbital invasion showed CT to be more accurate than MR imaging for most criteria [50]. The strength of CT is its ability to evaluate both bone and fat; however, it is difficult to distinguish tumor that compresses versus invades the periorbita [35]. MR imaging tends to underestimate orbital invasion, in part because it cannot distinguish periorbita from bone, because both are hypointense on T1- and T2-weighted imaging. In cases in which the imaging is ambiguous, intraoperative assessment with histology on frozen section remains the preferred method for determining invasion of the periorbita. Intracranial and dural invasion Contrast-enhanced MR imaging allows better identification of tumor extension intracranially,

including the optic canal, cavernous sinus, and perineural spread at the skull base (see Figs. 5, 6, 8). MR imaging also provides more detailed and accurate information than CT in assessing for the presence of dural, pial, and parenchymal brain invasion (Fig. 11) [43,51,71]. Smooth, continuous linear enhancement of the dura may be present in the setting of malignant infiltration; however, this appearance may also be seen in benign reactive and/or fibrovascular changes and therefore does not necessarily indicate dural tumor [71]. MR imaging findings that favor the presence of malignant involvement of the dura include the presence of discontinuous dural enhancement (multiple regions of enhancement with skip areas), regions of thickening and/or nodularity greater than 5 mm (see Fig. 8D), and the presence of T2 hyperintensity within the adjacent brain parenchyma [71]. Therefore, in addition to enhanced fat-suppressed T1-weighted images, it is also

Fig. 11. A 21-year-old man with subarachnoid seeding of a poorly differentiated carcinoma of the ethmoid air cells. (A) Enhanced axial T1-weighted MR image of the brain shows multiple areas of pathologic enhancement along the piaarachnoid/subarachnoid space (arrows) over the cerebral convexities. (B) Enhanced coronal T1-weighted MR image shows tumor seeding the meninges of the cerebrum and cerebellum.

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Fig. 11 (continued )

important to acquire T2-weighted images to assess for associated parenchymal abnormality. In the setting of pial invasion (subarachnoid seeding), multifocal areas of peripheral enhancement in the subarachnoid spaces are present (see Fig. 11). This spread may occur from direct extension of the lesion or as a consequence of surgery. Features of nodal metastases In addition to size and location, other features of pathologic nodes that should be assessed on imaging include the presence of extracapsular spread, carotid encasement, and nodal fixation, all of which impact negatively on patient prognosis. Imaging findings that should be viewed as suspicious for the presence of extracapsular spread, in addition to nodal size, are the presence of poorly defined nodal margins and soft tissue stranding of the fat and soft tissues in the adjacent neck. The presence of carotid encasement is a relative contraindication to surgery [72,73]. This complication of nodal metastases is relatively uncommon in sinonasal malignancies; it is most prevalent in patients with pharyngeal or laryngeal cancer [74–76].

Functional imaging in the treated patient New imaging techniques in addition to crosssectional imaging have focused on the physiologic properties of tumors and tissue characterization, rather than anatomic detail. Positron emission tomography (PET) using 2-[F-18]fluoro-2-deoxyD-glucose (FDG) relies on the metabolic activity of neoplasms relative to adjacent tissues (normal neck soft tissues, scar, fibrosis, or inflammatory changes) in positively identifying the presence of tumor. In the setting of sinonasal cancers, PET imaging may be useful in guiding endoscopic biopsies, in evaluating recurrent tumors [77,78], and in distinguishing recurrent neoplasm from radiation changes. One of the potential pitfalls of CT and MR imaging is their inability to distinguish treatment changes from recurrent tumor. Frequently, the radiologist is asked to help aid in distinguishing scar/fibrosis from neoplasm, and radiation necrosis from tumor. In general, recurrent neoplasms show significant uptake of FDG compared with fibrotic tissue and radiation-induced changes [77–79]; however, occasionally, radiation necrosis may demonstrate increased metabolic activity resulting in significant uptake of FDG [80].

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Furthermore, the timing of PET following irradiation is important in the distinction of radiation changes from tumor. PET performed shortly after radiotherapy may not accurately reflect disease activity, whereas PET acquired several months afterward may more reliably identify recurrence [78,81]. Treatment decisions and planning Sinonasal carcinoma is usually treated with both surgery and irradiation [10–13,15,82,83]. Although the results in the literature differ, overall survival rates for radiation therapy preoperatively or postoperatively are similar. Furthermore, postoperative irradiation is associated with fewer complications [1]. The main cause of treatment failure is local recurrence [1]. Orbital exenteration is performed for tumor involving the orbital periosteum, often detected on imaging and documented during surgery [14,35–37]. In the setting of extension into the central skull base, the PPF, and/or the nasopharynx, curative surgery is usually not attempted. Issues to consider when treating these patients with surgery include preservation of social functions (swallowing, phonation, speech), cosmetic deformity, and limited surgical options regarding complete resection because of the complexity of the anatomy in and around the paranasal sinuses. Surgical resection is usually done with the intent to cure the patient. Tumors confined to the infrastructure of the sinonasal cavity in which adequate surgical margins may be achieved are managed with primary surgical resection. In instances where tumors extend superiorly or posteriorly, or where tumors have vascular or neurotrophic spread, surgery and radiation therapy are necessary. In patients undergoing radiation therapy, and in those with secondary sinusitis, an adequate drainage portal for the sinonasal cavity must be created. Palliative excisions may be performed in the setting of intractable pain, to debulk massive lesions prior to irradiation, to reduce cosmetic deformity, or to allow for decompression of vital structures (eg, the contents of the orbit/optic chiasm). Criteria that may make a patient unresectable include distant metastases, intracranial extension, poor underlying general medical condition, and advanced age (Table 4). Imaging following treatment The follow-up of patients focuses predominantly on the early detection of recurrent tumor, especially in the first 2 years after treatment. Clin-

Table 4 Criteria for nonresectability of sinonasal malignancies 1. 2. 3. 4.

Distance metastases Extensive cerebral involvement Invasion of the optic chiasm Bilateral cavernous sinus/carotid infiltration (it should be noted that depending on the institution, cavernous sinus and optic chiasm invasion are relative contraindications for surgery) 5. Poor general medical condition–relative 6. Advanced age–relative 7. Patient refusal–relative

ical assessment and cross-sectional imaging play complementary roles. Issues include distinguishing treatment changes from tumor recurrence, and managing treatment-related complications, such as cerebral radiation necrosis (Fig. 12) [84–86], xerostomia related to changes in the salivary glands included in the radiation field (associated with prominent enhancement followed by atrophy), and cranial nerve palsies [87–95]. Tumor recurrence versus treatment changes Tumor recurrence implies that the patient has had a documented time interval following treatment that was disease free, clinically and radiologically. Incomplete resolution of disease after surgery and/or radiation therapy is completed represents residual (not recurrent) neoplasm. One of the most significant challenges facing the radiologist is distinguishing neoplasm from scar. CT in this regard has limited utility because these tissues frequently have overlapping densities, making their distinction difficult. MR imaging can be more sensitive in aiding in this distinction. Postoperative granulation tissue, scar, and fibrosis are dynamic tissues that may have a wide range of intensity and enhancement characteristics. In the paranasal sinuses, scar material may also have overlapping imaging characteristics with mucosal and inflammatory changes [49]. Early scar and granulation tissue tend to be hyperintense on T2weighted images and enhance following the administration of contrast material, which may make distinction from tumor difficult. A baseline post-treatment scan is useful, allowing the radiologist to assess on subsequent examinations for increased mass effect in the surgical bed, suggesting recurrent tumor and not contraction of tissue, which favors scar but does not entirely exclude tumor. A stable appearance or retraction of tissue on serial examinations provides reassurance that

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the changes are related to treatment and not recurrent disease. Mature scar can usually be distinguished from tumor because it typically has little or no mass effect, is hypointense on T2-weighted images because of the presence of fibrosis, and does not avidly contrast-enhance. In some instances, however, one is not able to exclude residual or recurrent neoplasm, and in these cases, biopsy or FDG-PET is necessary [77–79].

Complications of treatment Radiation necrosis

Fig. 12. A 55-year-old man previously treated with irradiation for left ethmoid adenocarcinoma. The patient was asymptomatic and presented for routine follow-up at which time he was found to have cerebral radiation necrosis. (A) Axial fluid attenuated inversion recovery MR image obtained at the level of the cavernous sinus shows abnormal signal intensity in the white matter of the bilateral anteroinferior temporal lobes. (B) Corresponding enhanced axial T1-weighted MR image shows solid enhancement in the left temporal lobe (arrow).

Radiation necrosis is not an infrequent complication of nasopharyngeal, sinonasal, and skull base neoplasms treated with irradiation [84– 86,96]. Because of the radiation portals and the field covered, the temporal lobes are most commonly affected (see Fig. 12), followed by the frontal lobes. The total dose, duration, and fractionation of radiation play an important role in the development of radiation necrosis [86,96]. The incidence of radiation necrosis following the treatment of head and neck cancer and skull base neoplasms ranges from 3% to 10% [86,96,97]. Radiation necrosis is probably more common than reported because many patients are asymptomatic and therefore are not imaged, leading to underdetection. Irradiation can also result in radiation vasculitis, which affects the deep perforating arteries leading to ischemic sequela in the basal ganglia, thalami, brainstem, and the deep white matter (Fig. 13). Symptoms of radiation arteritis are dependent on the regions of the brain affected and may include change in mental status, focal neurologic deficits, and occasionally seizures. Changes in the brain caused by radiation necrosis may occur early (during therapy) or be delayed. Delayed radiation changes can be further divided into early (within 3 to 4 months of therapy) and late (months to years following therapy). In early and early-delayed injury, MRI typically shows T2 hyperintensity representing edema and demyelination, which is frequently reversible [97,98]. Late-delayed injury is usually related to vascular injury, demyelination, and inflammatory infiltrates. This is characterized on MR imaging by T2 hyperintensity, mass effect, and enhancement that may be solid or ringlike (peripheral enhancement around a necrotic cavity) [97,98]. In burnt-out radiation necrosis, there is frequently temporal lobe encephalomalacia. Whereas the differential diagnosis of radiation necrosis includes

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metastatic disease, in the setting of primary head and neck or skull base malignancies, cerebral metastases are relatively uncommon. Intracranial extension of these neoplasms usually presents with extra-axial (extracerebral) masses, whereas the changes of radiation necrosis are intracerebral. Cranial neuropathies The cranial nerves are relatively radioresistant. The optic and hypoglossal nerves are most commonly affected [89,91,92,94]. Clinically, cranial nerve XII nerve palsies may present with fasciculations, weakness, and deviation of the tongue, and problems with deglutitution [88,91]. On imaging, ipsilateral edema in the early stages, followed later by fatty replacement and atrophy, may be present [91]. Optic neuritis caused by irradiation may present with visual loss, enlargement and enhancement of the involved optic tracts, or chiasm on MR imaging [89,94]. Cranial nerves IV through VII are less commonly affected and their involvement may be related to primary changes in the nerves themselves, or sequela of brainstem injury from radiation vasculitis. Radiation-induced neoplasms Radiation-associated or radiation-induced neoplasms typically occur in the radiated field. Criteria in diagnosing a tumor induced by irradiation include a histology different from the primary tumor treated, and a latency period of at least 5 years. A wide spectrum of radiation-induced neoplasms have been reported, including meningiomas, sarcomas, schwannomas, squamous cell carcinoma, and thyroid carcinoma [99–102]. Summary

Fig. 13. Radiation vasculitis in a 54-year-old man 1 year following completion of radiation therapy for skull base lymphoma, who presented with sensory deficits and right-sided weakness. (A) Axial fluid attenuated inversion recovery (FLAIR) MR image obtained at the level of the upper pons shows multiple new foci of increased signal intensity. (B) Axial FLAIR MR image shows numerous foci of increased signal intensity in the white matter of the corpus striatum and the deep gray matter, consistent with radiation-induced vasculitis and subsequent lacunar infarction.

The assessment of sinonasal malignancies requires a multidisciplinary team approach. Advances in pretherapeutic imaging have significantly contributed to the management of sinonasal tumors. CT and MR imaging play complementary roles in the assessment and staging of these malignancies by determining the presence or absence of extension of disease into the skull base and its foramina, the orbit, and the intracranial compartment. References [1] Barnes L, Verbin RS, Gnepp DR. Diseases of the nose, paranasal sinuses, and nasopharynx. In: Barnes L, editor. Surgical pathology of the head and neck. Vol 1. New York: Marcel Dekker; 1985. p. 403–51.

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