Imaging of neoplasms of the paranasal sinuses

Imaging of neoplasms of the paranasal sinusesLaurie A. Loevner, MDa,*, Adina I. Sonners, BSb

aDepartment of Radiology, University of Pennsylvania Medical Center,

3400 Spruce Street, Philadelphia, PA 19104, USAbUniversity 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 approxi-

mately 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 ad-

vanced disease. Pain may indicate perineural

tumor spread, skull base extension, or spread to

the infratemporal fossa. Other clinical presenta-

tions 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, radia-

tion oncologists, and medical oncologists. Advan-

ces 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 malig-

nancies [6–8].

The treatment of choice for sinonasal carci-

noma usually includes combined surgery and irra-

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 naso-

pharynx, curative surgery is usually not attempted.

The main cause of treatment failure is local recur-

rence [1,16].

Normal anatomy

To understand the clinical and radiologic

appearanceofneoplasmsoriginating fromthepara-

nasal sinuses, and the coexistant inflammatory

changes that usually occur with such tumors,

knowledge of the normal anatomy and the pat-

terns of pneumatization and drainage of sinus

secretions is necessary. An understanding of the

natural history of sinus carcinomas is also para-

mount in assessing patterns of tumor spread, in

determining surgical management, and in deter-

mining 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 progres-

sing 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

* Corresponding author.

E-mail address: [email protected] (L.A.

Loevner).

1064-9689/02/$ - see front matter � 2002, Elsevier Science (USA). All rights reserved.

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Magn Reson Imaging Clin N Am

10 (2002) 467–493

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, pseu-

dostratified columnar epithelium, which contains

mucinous and serous glands. The common drain-

age 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 semilu-

naris, and the middle meatus (Fig. 1) [17]. Secre-

tions 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 pro-

cess (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 fron-

tal recess/nasofrontal duct into the middle meatus,

also the common drainage site for the anterior eth-

moid air cells, which have ostia in contact with the

infundibulum of the ostiomeatal complex [17]. The

nasofrontal duct is between the inferomedial fron-

tal 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).

468 L.A. Loevner, A.I. Sonners / Magn Reson Imaging Clin N Am 10 (2002) 467–493

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 sep-

tum 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 perpendicu-

lar plate of the ethmoid bone, whereas the infero-

posterior osseous portion is the vomer. The

septum within the nasal cavity is lined by squa-

mous epithelium.

There is normal cyclic passive congestion and

decongestion of each side of the nasal cavity and

ethmoid air cells that includes temporary unilat-

eral 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

Fig. 1 (continued )

469L.A. Loevner, A.I. Sonners / Magn Reson Imaging Clin N Am 10 (2002) 467–493

ethmoid air cells and sphenoid sinus also receive

their blood supply from branches of the spheno-

palatine artery (arising from the external carotid)

and ethmoidal branches of the ophthalmic artery

(arising from the internal carotid). Venous drain-

age 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 sup-

plied by branches of the external carotid artery,

most notably the maxillary artery. These si-

nuses 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 second-

arily 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,

Bantusnuff,Thorotrast,mustardgas,polycyclichy-

drocarbons, 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 man-

agement and improvements in administering ir-

radiation over the last decade may improve

survival rates. Local recurrences occur in approxi-

mately 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 manage-

ment with irradiation alone. For advanced tumors

(T3 and T4), treatment requires surgery and irradi-

ation [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 ori-

ginate in the glands [1]. There is a spectrum of

histologic types, including adenoid cystic, muco-

epidermoid,undifferentiated,andadenocarcinoma.

The adenocarcinomas may represent minor sali-

vary gland tumors or intestinal-type adenocarci-

nomas, and have a predilection for the ethmoid

sinuses [23,24]. These may be more common in

wood and leather workers [23]. They are fre-

quently advanced at presentation, with cribriform

plate erosion present in up to 50% of cases. Dural

invasion is not uncommon [24]. Treatment fre-

quently 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 carci-

nomas 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 histo-

logic 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 ther-

apy allows for better local control. Local recur-

rence 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 differ-

entiated (tubular), to moderately differentiated

(cribriform), to poorly differentiated [26]. Approxi-

mately one half of patients with adenoid cystic car-

cinoma 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 melano-

cytes that have migrated during embryologic

development from the neural crest to the mucosa

of the sinonasal cavity [27]. Less than 4% of mela-

nomas arise in the sinonasal cavity, with most of

these originating in the nose [27,28]. Within the


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 para-

nasal 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

Fig. 2. A 58-year-old man with squamous cell carcinoma of the maxillary sinus. (A) Axial fast-spin echo T2-weightedMR

image shows a large, poorly demarcated, hypointense mass (m) emanating from the right maxillary sinus, with frank

extension throughtheanterior sinuswall into the facial soft tissues/cheek. (B)Correspondingenhancedaxial fastmultiplanar

spoiled gradient echoMR image utilizing fat suppression shows extension outside the confines of the maxillary sinus.


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 approxi-

mately 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. 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.

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

cavity consistent with melanotic melanoma.


metastases within the first year after treatment.

Hematogenous metastases affect the lungs, brain,

liver, and skin. Neurotrophic spread is not uncom-

mon (Fig. 5). Nasal melanomas have a better prog-

nosis than those originating in the paranasal

sinuses.

Olfactory neuroblastoma (esthesioneuroblastoma)

Esthesioneuroblastomas occur in the upper

nasal cavity/ethmoid vault, arising from the olfac-

tory nerves. They have a bimodal age distribution,

presenting in boys and middle-aged adults. They

have a marked propensity for crossing the cribri-

form plate and extending intracranially (Fig. 6)

[32,33]. When intracranial extension is present, a

craniofacial surgical approach and adjuvant radia-

tion 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.

Other neoplams

Other aggressive neoplasms involving the sino-

nasal 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 ana-

tomic boundaries of the individual paranasal

sinuses and their contiguous structures is impor-

tant in mapping the extent of disease and in deter-

mining 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 sur-

gical 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 (medi-

ally the nasal cavity and inferiorly the alveolus)

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]. Intra-

cranial spread usually necessitates a craniofacial

resection with the combined efforts of the head

and neck surgeons and neurosurgeons [9]. The lat-

eral wall of the ethmoid air cells—the lamina pap-

yracea—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 sur-

rounded by numerous vital structures. The sphe-

noid 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.

Metastases

Lymphatic drainage and nodal metastases

The lymph node drainage for sinonasal neo-

plasms 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 incon-

stant. Therefore, the upper internal jugular and

submandibular nodes are the most common sites

for nodal metastases.

Regional lymph node metastases from sino-

nasal malignancies are relatively uncommon, but

when present are a poor prognostic sign and usu-

ally indicate tumor extension outside of the sino-

nasal 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 meta-

stases. The presence of cervical nodal disease pla-

ces the patient at increased risk for distant

metastases [38]. Approximately one half of pa-

tients with adenoid cystic carcinomas have distant


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.


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 recog-

nize that these tumors together account for less

than 8% of all sinonasal malignancies.

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.


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 eth-

moid sinus carcinomas is achieved through a com-

bination 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 compart-

ment, and in distinguishing tumor from coexistent

inflammatory changes.

The tumor, nodes, and metastases (TNM) sys-

tem of classification of maxillary sinus cancers is

based on Ohngren’s imaginary line drawn on a lat-

eral view extending from the medial canthus of the

eye to the angle of the mandible, separating the

maxillary anthrum into anteroinferior and supero-

posterior compartments. On a coronal view, the

maxillary anthrum may be divided into an infra-

structure, 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 ex-

enteration. 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 intra-

cranially (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 distin-

guishes N2 from N3 disease [40].

Fig. 6 (continued )


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 accu-

rate mapping of tumor extent and an understand-

ing of the anatomic sites that will influence or alter

surgical resection, treatment planning, and prog-

nosis. 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 opti-

mal localization for biopsy, and may be useful in

preparing and minimizing complications of sur-

gery, including blood loss in the setting of vascular

neoplasms. Tumors extending into the nasal cavity

may be amenable to transnasal biopsy.

CT andMR 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].

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.


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.


MR imaging offers soft tissue resolution, con-

trast, and multiplanar capabilities. In most instan-

ces, 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 signi-

ficantly impacts on the following: the patient’s

Fig. 8 (continued )


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 ante-

rior 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 destruc-

tion (see Figs. 2, 9) [41]. Bone involvement is seen

in approximately 80% of CT scans assessing sino-

nasal 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 withMR or CT

techniques except perhaps in some cases of mela-

noma. Inmostmelanomas, which containmelanin,

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 shorten-

ing in nonhemorrhagic, melanin-containing mela-

nomas is common because of the paramagnetic

effects of melanin [30,31,54]. Some investigators

believe that the T1 shortening is related to the pres-

ence of free radicals [54], whereas others speculate

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 sup-

pression 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.


that the shortening effect is caused by paramag-

netic metal ions that may be bound tomelanin [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 malig-

nancy [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 T2-

weighted 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 sino-

nasal secretions, which is the result of variable pro-

tein 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 rel-

ative 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, secre-

tions on T1-weighted images become more hyper-

intense. 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

Fig. 9 (continued )


hyperintense on T1-weighted and hypointense on

T2-weighted images (see Figs. 9, 10). Finally, when

protein concentrations are extremely high (exceed-

ing 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 com-

monly 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 pres-

ence of sclerosis is normally related to coexistent

chronic inflammatory changes. Though uncom-

mon, 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 calcifica-

tions actually corresponded to fragmented bone.

Skull base invasion

Sinonasal masses that frequently erode the

skull base and spread intracranially include carci-

nomas (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 remodel-

ing in this location is unusual.

Whereas CT may detect cortical erosion of the

skull base [34], MR imaging is probably more sen-

sitive in assessing skull base invasion [61]. It is par-

ticularly well suited to study bone marrow because

it can differentiate fat from other tissues. The sig-

nal intensity is directly related to the relative

amounts of fat, water, and cells in the marrow.

Fig. 9 (continued )


In adults, the marrow in the normal skull base and

cranium is hyperintense on unenhanced T1-

weighted images because it contains predomi-

nantly fat [62–64]; therefore, skull base involve-

ment by tumor may be detected when the normal

hyperintense appearance caused by fat is replaced

with hypointense tissue (see Fig. 5) [65]. The pres-

ence of normal-appearing marrow at the skull base

is usually a good indicator of absence of skull base

invasion; however, fixation to the periosteum can-

not be excluded. The presence of hypointense tis-

sue, however, does not always mean the presence

of tumor. Hypointense tissue on unenhanced T1-

weighted images may also correspond to edema

or hematopoietic marrow [62,66,67]. In the pres-

ence of abnormal hypointense T1 signal, it is im-

portant to assess the corresponding T2-weighted

and enhanced images, which may help in differen-

tiating 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, exten-

sion into the adjacent orbit, infratemporal fossa,

skull base, and intracranial compartment may sub-

sequently 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 1

American Joint Committee on Cancer T system for

staging sinonasal malignancies: maxillary sinus

TX Primary tumor cannot be assessed

T0 No evidence of primary tumor

Tis Carcinoma in situ

T1 Tumor limited to the antral mucosa with no

erosion or destruction of bone

T2 Tumor causing bone erosion or destruction,

except for the posterior antra wall, including

extension into the hard palate and/or the

middle nasal meatus

T3 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

T4 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 (AJCC�),

Chicago, IL.

Table 2

American joint Committee on Cancer T system for

staging sinonasal malignancies: ethmoid sinus

T1 Tumor confined to the ethmoid with or without

bone erosion

T2 Tumor extends into the nasal cavity

T3 Tumor extends to the anterior orbit, and/or

maxillary sinus

T4 Tumor with intracranial extension, orbital

extension including apex, involving sphenoid,

and/or frontal sinus and/or skin of external nose





Chicago, IL.

Table 3

American Joint Committee on Cancer T system for

staging sinonasal malignancies: regional lymph nodes

NX Regional lymph nodes cannot be assessed

N0 No regional lymph node metastasis

N1 Metastasis in a single ipsilateral lymph node,

3 cm or less in greatest dimension

N2 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

N3 Metastasis in a lymph node more than 6 cm in

greatest dimension





Chicago, IL.


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.


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 rotun-

dum, perineural spread of tumor to the inferior

orbital fissure, the orbital apex, the superior orbi-

tal fissure, and subsequently the intracranial com-

partment may occur.

Orbital invasion

Tumor involvement of the orbit and nasolacri-

mal system impacts negatively on prognosis, and

significantly alters surgical planning [15]. The

absence of orbital symptoms is not a reliable indi-

cator of the absence of orbital invasion. The orbit

is a coned-shaped space contained within the fron-

tal bone, the greater and lesser wings of the sphe-

noid bone, the ethmoid bone, the lacrimal bone,

the zygoma, and the maxilla [69]. The periorbita

comprises the periosteum of these bones. It is con-

tinuous 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 sino-

nasal 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 inves-

tigators have found a significant number of false

negatives (low sensitivity: 40%, MR imaging;

60%, CT) for orbital fat involvement [50]. There-

fore, although the presence of orbital fat invasion

strongly indicates orbital invasion, the absence of

abnormality in the orbital fat cannot exclude inva-

sion. Other criteria evaluated include the follow-

ing: the relationship between the tumor and the

periorbita (abutting, displacing, or bowing the

periorbita), the presence of nodularity at the inter-

face between the tumor and the periorbita, assess-

ment 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

Fig. 10 (continued )


low specificity (29–44%). In this study, a compari-

son 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 inva-

sion, in part because it cannot distinguish perior-

bita from bone, because both are hypointense on

T1- and T2-weighted imaging. In cases in which

the imaging is ambiguous, intraoperative assess-

ment 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, con-

tinuous 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 paren-

chyma [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 pia-

arachnoid/subarachnoid space (arrows) over the cerebral convexities. (B) Enhanced coronal T1-weighted MR image

shows tumor seeding the meninges of the cerebrum and cerebellum.


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 progno-

sis. Imaging findings that should be viewed as sus-

picious 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 complica-

tion 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 cross-

sectional 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-deoxy-

D-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 biop-

sies, 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 treat-

ment changes from recurrent tumor. Frequently,

the radiologist is asked to help aid in distinguish-

ing scar/fibrosis from neoplasm, and radiation

necrosis from tumor. In general, recurrent neo-

plasms 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].

Fig. 11 (continued )


Furthermore, the timing of PET following irradia-

tion is important in the distinction of radiation

changes from tumor. PET performed shortly after

radiotherapymaynot accurately reflectdisease acti-

vity, whereas PET acquired several months after-

ward may more reliably identify recurrence [78,81].

Treatment decisions and planning

Sinonasal carcinoma is usually treatedwithboth

surgery and irradiation [10–13,15,82,83]. Although

the results in the literature differ, overall survival

rates for radiation therapy preoperatively or post-

operativelyare similar.Furthermore,postoperative

irradiation is associated with fewer complications

[1]. The main cause of treatment failure is local re-

currence [1]. Orbital exenteration is performed

for tumor involving the orbital periosteum, often

detected on imaging and documented during sur-

gery [14,35–37]. In the setting of extension into the

central skullbase, thePPF,and/or thenasopharynx,

curative surgery is usually not attempted.

Issues to consider when treating these patients

with surgery include preservation of social func-

tions (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 infra-

structure 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, sur-

gery and radiation therapy are necessary. In

patients undergoing radiation therapy, and in those

with secondary sinusitis, an adequate drainage por-

tal 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 unre-

sectable include distant metastases, intracranial

extension, poor underlying general medical condi-

tion, and advanced age (Table 4).

Imaging following treatment

The follow-up of patients focuses predomi-

nantly on the early detection of recurrent tumor,

especially in the first 2 years after treatment. Clin-

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 atro-

phy), and cranial nerve palsies [87–95].

Tumor recurrence versus treatment changes

Tumor recurrence implies that the patient has

had a documented time interval following treat-

ment that was disease free, clinically and radiolog-

ically. Incomplete resolution of disease after

surgery and/or radiation therapy is completed rep-

resents 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. Post-

operative 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 T2-

weighted 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 radiol-

ogist 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

Table 4

Criteria for nonresectability of sinonasal malignancies

1. Distance metastases

2. Extensive cerebral involvement

3. Invasion of the optic chiasm

4. 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


the changes are related to treatment and not recur-

rent disease. Mature scar can usually be distin-

guished 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 instan-

ces, 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

Radiation necrosis is not an infrequent compli-

cation 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 frac-

tionation 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 underde-

tection. Irradiation can also result in radiation vas-

culitis, 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 enhance-

ment 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

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) Corres-

ponding enhanced axial T1-weighted MR image shows

solid enhancement in the left temporal lobe (arrow).


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 com-

monly affected [89,91,92,94]. Clinically, cranial

nerve XII nerve palsies may present with fascicula-

tions, 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 enhance-

ment of the involved optic tracts, or chiasm on

MR imaging [89,94]. Cranial nerves IV through

VII are less commonly affected and their involve-

ment 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. Cri-

teria 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 neo-

plasms have been reported, including meningio-

mas, sarcomas, schwannomas, squamous cell

carcinoma, and thyroid carcinoma [99–102].

Summary

The assessment of sinonasal malignancies

requires a multidisciplinary team approach.

Advances in pretherapeutic imaging have signifi-

cantly contributed to the management of sinonasal

tumors. CT and MR imaging play complementary

roles in the assessment and staging of these malig-

nancies by determining the presence or absence of

extension of disease into the skull base and its for-

amina, theorbit, and the intracranial compartment.

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Imaging of neoplasms of the paranasal sinuses