Paranasal sinus imaging

A

n

t

l

ta©

K

1

bbpnsfp

cIepat

bsp

0d

European Journal of Radiology 66 (2008) 372–386

Paranasal sinus imaging

Roberto Maroldi ∗, Marco Ravanelli, Andrea Borghesi, Davide FarinaDepartment of Radiology, University of Brescia, Piazzale Spedali Civili 1, Brescia 25123, Italy

Received 16 January 2008; accepted 17 January 2008

bstract

Endonasal surgery is currently extending its application beyond inflammatory sinonasal lesions to successfully treat both benign and malignanteoplasms. This progression has been possible by the detailed information provided by imaging techniques (CT, MRI and PET).

Inflammatory diseases are the “domain” of CT. CT provides excellent details about the thin bony sinonasal walls separating the ethmoid fromhe anterior skull base and the orbit.

Benign and malignant neoplasms are the “domain” of MRI because the tumor is more easily separated from adjacent structures, the periosteal
inings (periorbita, dura mater) and perineural spread can be accurately shown.
Whereas MRI precisely assess pre-treatment tumor extent, early submucosal local recurrences are difficult to demonstrate because of post-reatment changes of the anatomy and of the signal of treated tissues. Though diffusion-weighted imaging and dynamic contrast-enhanced techniquesre promising developments, PET-CT may overcome the limits of morphological MRI.

2008 Elsevier Ireland Ltd. All rights reserved.

imagi

ebsaoM

2

ie

tpl

eywords: Paranasal sinus; Computed tomography (CT); Magnetic resonance

. Introduction

Endonasal surgery is currently extending its applicationeyond inflammatory sinonasal lesions to successfully treat bothenign and malignant neoplasms [1]. This progression has beenossible by the detailed information provided by imaging tech-iques (CT, MRI and PET). On the other hand, as endonasalurgeons face new horizons – as the only-endoscopic cranio-acial resection – new questions raise to the radiologists, as arecise grading of the intracranial extent.

For each imaging technique, specific fields of clinical appli-ation emerge from the medical literature in the present decade.nflammatory diseases are the “domain” of CT. CT providesxcellent details about the thin bony sinonasal walls (laminaapyracea, cribriform plate) separating the ethmoid from thenterior skull base and the orbit. In addition, both thickening ofhe mucosa and retained mucous secretions are demonstrated.

Benign and malignant neoplasms are the “domain” of MRI
ecause the tumor is more easily separated from adjacenttructures, the periosteal linings (periorbita, dura mater) anderineural spread can be accurately shown.
∗ Corresponding author.E-mail address: [email protected] (R. Maroldi).

mn[

ooi[

720-048X/$ – see front matter © 2008 Elsevier Ireland Ltd. All rights reserved.oi:10.1016/j.ejrad.2008.01.059

ng (MRI); Perineural spread

Whereas MRI precisely assess pre-treatment tumor extent,arly submucosal local recurrences are difficult to demonstrateecause of post-treatment changes of the anatomy and of theignal of treated tissues. Though diffusion-weighted imagingnd dynamic contrast-enhanced techniques are promising devel-pments, PET-CT may overcome the limits of morphologicalRI.

. Acute rhinosinusitis

Only complicated acute rhinosinusitis requires CT for mak-ng a correct diagnosis. Otherwise, the symptoms and thendoscopic examination are sufficient [2].

If an orbital complication is suspected, generally secondaryo acute ethmoiditis, CT allows to differentiate between edema,hlegmon and abscess, and to precisely identify the site of theesion, in order to define a correct treatment planning [3]; CTay provide a correct diagnosis in up to 91% of cases, being sig-

ificantly more accurate than clinical examination alone (81%)4].

Preseptal cellulitis is confined to the anterior compartment
f the orbit (eyelid, periorbital soft tissues) without involvementf the orbital cavity. CT shows thickening of the orbital septum,ncreased density of orbital septum and periorbital soft tissues5].
mailto:[email protected]

dx.doi.org/10.1016/j.ejrad.2008.01.059

rnal of Radiology 66 (2008) 372–386 373

iu

atbtpt

aasleC

s[

sTadrsret

anteo

bp

v

3

n[ialtc

rsyl

Ft(

ea

rtc

di

3

i

epais

3

ditmaAi

R. Maroldi et al. / European Jou

Orbital cellulitis is characterized by increased density ofntraorbital fat tissue, often observed at the level of the retrob-lbar space amid muscles and optic nerve.

On both CT and MRI, subperiosteal abscess is demonstrateds a fluid collection with a peripheral enhancing rim betweenhe inner surface of the orbital walls and the periorbita. CTetter depicts subtle defects of the bony walls adjacent tohe abscess [6]. Gas bubbles within the collection herald theresence of anaerobic agents or indicate fistulization from con-iguous paranasal cavities.

Orbital abscesses secondary to ethmoid sinusitis are gener-lly located along the lamina papyracea, displacing the orbitnteriorly and laterally; fluid collections complicating frontalinusitis are observed along the superior orbital wall and dis-ocate the ocular bulb anteriorly and inferiorly. Intraconalxtension of the abscess is the main key point to be ruled out atT.

MRI better demonstrates further vascular complications,uch as superior ophthalmic vein or cavernous sinus thrombosis5,6].

Intracranial complications are generally secondary to frontalinusitis and are more frequent in the pediatric population [7].hey are observed even in the absence of sinus wall defects,s they may be secondary to thrombophlebitis of valvelessiploic veins [8]. Imaging is mandatory, in order to make a cor-ect grading of intracranial involvement. In this setting, MRIhould be considered the technique of choice, because its accu-acy is superior to CT in differentiating dural reaction frompidural/subdural or intracerebral abscess, and in demonstratinghrombosis of sagittal or cavernous sinus [3,4,9,10].

CT findings of meningitis may be unremarkable. Early signsre represented by mild enlargement of ventricles and subarach-oid spaces. In later stages, dural enhancement (especially athe level of the falx, tentorium and convexity) and inflammatoryxudate within the subarachnoid spaces may be observed at MRIn Gd-enhanced SE T1 images [4].

At CT, subdural/epidural abscess is detected as an extracere-ral fluid collection with a convex shape, separated from thearenchyma by a thick and enhancing rim.

The CT appearance of brain abscesses (Fig. 1) is widelyariable in the different phases of evolution.

. Chronic rhinosinusitis

Chronic rhinosinusitis is defined as an inflammation of theose and paranasal sinuses mucosa lasting more than 12 weeks11]. Pathogenesis is multifactorial with several predispos-ng factors: nasal allergy, ASA-syndrome, dental infections,natomic variants, immunodeficiencies, mucociliary anoma-ies and iatrogenic factors (mechanical ventilation, nasogastricubes, nasal packing, post-operative scarring in the ostiomeatalomplex).

Sinonasal polyposis is a quite common finding in chronic
hinosinusitis, ranging from 2 to 16% of cases [12,13]. Macro-copically, nasal polyps appear as edematous formations,ellow-white in appearance and soft in consistency. Histo-ogically, they consist of respiratory epithelium covering an
3

s

ig. 1. Complicated acute rhinosinusitis: brain abscess. Coronal CT after con-rast administration shows fluid inflammatory material in the maxillary sinusasterisk) and intraparenchymal abscess in the frontal lobe (arrows).

dematous stroma infiltrated by inflammatory cells. Eosinophilsre found in 80% of the cases [14].

In case of chronic rhinosinusitis, the role of CT is to accu-ately assess the pattern of mucociliary drainage impairment,o identify anatomical variants predisposing the inflammatoryhanges and/or conditioning the endoscopic approach [15].

Based on obstruction of different drainage pathways, fiveifferent patterns of chronic rhinosinusitis have been describedn the literature [16].

.1. Infundibular pattern

Infundibular pattern is the most limited model. Ethmoidnfundibulum and maxillary sinus alone are involved.

This pattern is mainly due to the presence of mucosal thick-nings or isolated polyps along the infundibulum. Anatomicredisposing factors are infraorbital cells, uncinate process vari-nts, and hypoplasia of the maxillary sinus. CT promptly detectsnfundibular obstruction and inflammatory changes of maxillaryinus mucosa.

.2. Ostiomeatal unit pattern

Ostiomeatal unit pattern reflects the obstruction of allrainage systems in the middle meatus. As a consequence, its heralded by maxillary, frontal, and anterior ethmoid sinusi-is. Aspecific mucosal thickenings as well as nasal polyps

ost commonly induce ostiomeatal unit pattern; concha bullosand marked septal deviation are anatomic predisposing factors.dditionally, lesions arising from the lateral nasal wall, such as

nverted papilloma, may cause this model.

.3. Spheno-ethmoid recess pattern

Spheno-ethmoid recess pattern is rather rare; it consists ofphenoid sinusitis and (not infrequently) posterior ethmoiditis,

3 rnal o

sod

3

batrafplsirtaAtsiap

scpc

mhaT

aoa[

cpoUh

r

acssad[

3

sdac

mir

slir

otcl

raiacsb2t

ltmadd

iifc

upoboaacm

74 R. Maroldi et al. / European Jou

econdary to spheno-ethmoid recess obstruction. Obliterationf the recess and inflammatory mucosal thickenings are betterepicted with axial CT.

.4. Pattern of nasal polyposis

This pattern is characterized by the involvement – mostlyilateral – of middle meati, ethmoid infundibula (often widened)nd nasal cavity. Most inflammatory polyps originate in rela-ion to sinus outlets, from the mucosa investing ostia, clefts andecesses in the ostiomeatal complex, the ethmoid infundibulum,nd the uncinate process. Less commonly, they may originaterom the superior meatus, the frontal recess or the anteriorart of ethmoid bulla [17,18]. At CT, they appear as lobulatedesions with soft-tissue attenuation filling ethmoid, nasal fos-ae and sinusal cavities. CT attenuation may be elevated whennspissated mucus is trapped within the mucosal folds. Boneemodelling is associated, due to mechanical pressure exerted byhe polyps but also by the local release of inflammatory medi-tors and by bacterial invasion of bone and periosteum [19].s a result, thinning and displacement of subtle bone struc-

ures (such as ethmoid labyrinth and lamina papyracea) andclerosis of thicker sinusal walls (such as posterolateral max-llary sinus wall) may be observed. Bone erosion is infrequentnd may be demonstrated in cases of long-standing, aggressiveolyposis.

Two additional signs are described as common features ofinonasal polyposis: widening of ethmoid infundibulum, espe-ially bilateral, and truncation of the more distal, bulbousart of the middle turbinate (bilateral in up to 80% of theases).

MRI signal pattern reflect the stages of polyp growth (ede-atous, cystic or fibrous). Most frequently it is composed of

yper T2 signal and a combination of hyperintensity (mucosa)nd hypointensity (edematous stroma) on contrast-enhanced1.

Even though bone changes and bilateral pattern of growthre quite typical, it must be emphasized that density patternf nasal polyps is not completely specific; therefore severaluthors recommend thorough evaluation of surgical specimens20].

A peculiar variant of sinonasal polyp is represented by antro-hoanal polyp. This lesion arises in the maxillary sinus androtrudes in the middle meatus through ethmoidal infundibulumr through an accessory ostium, reaching typically the choana.sually, the intramaxillary portion is cystic (hypodensity on CT,yper T2 signal on MRI), while the intranasal portion is solid.

Sphenochoanal and ethmoidochoanal polyps are extremelyare variants.

As a consequence of their growth through constrictive ostia,ll sino-choanal polyps are subject to strangling and vascularompromise. When this occurs, the intranasal portion of theino-choanal polyp shows dilation and stasis of feeding ves-
els, resulting in bright enhancement after contrast mediumdministration (angiomatous polyp) [21,22]. Prolonged vascularamage may induce necrosis of the polyp with autopolypectomy23].
ivPi

f Radiology 66 (2008) 372–386

.5. Sporadic pattern

In the sporadic pattern, inflammatory changes of paranasalinuses are unrelated to impairment of any of mucociliaryrainage pathways. A wide list of different conditions, suchs isolated sinusitis, retention cyst, mucocele, post-surgicalhanges are included in this group.

Mucosal thickenings are an extremely common finding inaxillary and sphenoid sinuses; within ethmoid cells, it is often

mpossible to differentiate them from inflammatory polyps oretained secretions.

CT findings consist of partial or complete obliteration of ainusal cavity by thickened mucosa with smooth – occasionallyobulated – surface and homogeneously low density, reflect-ng chronic inflammatory edema of the submucosal layer. Noelevant bone changes are generally associated.

At MRI, thickened mucosa shows a uniformly bright signaln SE T2 sequences, whereas SE T1 after contrast adminis-ration demonstrates hyperintensity of the enhancing mucosaombined with hypointense signal of the edematous submucosalayer.

CT and MRI appearance of retained secretions is strictlyelated to the composition of the entrapped fluid. Protein contentnd viscosity of chronically retained secretions progressivelyncrease, resulting in higher CT density. Raised HU values arelso observed within pus or blood collections. At MRI, an inverseorrelation is observed between protein concentration and T2ignal (at 40–45% protein concentration the T2 signal becomeslack). On plain T1 sequence, signal rises to a peak at about5–30% protein concentration and then progressively decreaseso hypointensity [24].

Retention cysts are more frequently observed in the maxil-ary sinus (in the alveolar recess or at the level of the roof closeo infraorbital canal). They are secondary to obstruction of a

ucosal or minor salivary gland. At CT, retention cysts appears hypodense fluid-like lesions with smooth and convex bor-ers, and variable size. MRI signal pattern is similar to the oneescribed for retained secretions.

Nonetheless, it must be emphasized that all mucosal thicken-ngs and retention cysts can be observed as incidental findingsn 30–50% of patients submitted to imaging studies of the heador non-sinusal pathologies, with no significant correlation withlinical symptoms [25–27].

Mucocele may be defined as an accumulation of prod-cts of secretion, desquamation, and inflammation within aaranasal sinus with expansion of its bony walls. The devel-pment of the lesion occurs as the result of sinus ostiumlockage. Imaging plays a crucial role in defining extensionf mucoceles, particularly towards orbit, anterior cranial fossand optic nerve canal [28]. Sinus expansion with bulging ofll its bony walls is the most typical presentation of muco-ele. Nonetheless, these changes are often focal in post-operativeucoceles, may be due to post-surgical sinusal compartmental-

zation [29] (Fig. 2). CT density and MRI intensity are largelyariable, according with the composition of entrapped material.eripheral rim enhancement is observed on both CT and MRI

mages.

R. Maroldi et al. / European Journal of Radiology 66 (2008) 372–386 375

Fig. 2. (a–d) Frontal sinus mucocele after endoscopic surgery. CT shows the frontal sinus mucocele (M); this is due to a synechia between the residual middlet tive c(

3

psdriDsttiC

4

po

s

-

-

capbsfp

hhcrghH[a

urbinate and lateral nasal wall which occludes the frontal recess (arrows). Reacarrowhead).

.6. Imaging after endonasal surgery for chronic sinusitis

CT after endoscopic surgery is indicated in symptomaticatients (headache, rhinoliquorrea, recurrence of pre-treatmentymptoms) and must be focused on critical areas, in order toemonstrate the post-operative outcome and detect possibleecurrences and complications. Mucosal thickening or synechiaento the fronto-nasal recess may cause frontal sinus blockage.ehiscences may occur in the lamina papyracea, in the sphenoid

inus walls and in the ethmoid roof, due to direct penetration ofhe endoscope or traction exerted on connected structures (i.e.,urbinates). Although CT is the technique of choice in detect-ng acute post-operative complications, MRI is mandatory whenSF leak or meningo-(encephalo)-cele is suspected.

. Aggressive inflammatory lesions

Fungal rhinosinusitis can be defined as an infection ofaranasal sinuses in which fungi play a role of primary pathogensr cause an inflammation due to their presence.

According to the presence or lack of sinonasal mucosa inva-
ion [30], fungal rhinosinusitis is classified into:
non-invasive forms: fungus ball and eosinophilic fungal rhi-nosinusitis [31];

naso

hanges of right frontal sinus walls is well demonstrated. Bulla frontalis type IV

invasive forms: acute fulminant rhinosinusitis, chronic inva-sive fungal rhinosinusitis and granulomatous invasive fungalrhinosinusitis.

In non-invasive fungal rhinosinusitis, the lesion is usuallyonfined by sinusal walls for a long time. Eventually, remodelingnd destruction of the walls occur, due to the mass-like growthattern of fungal debris and mucus within the sinus (fungusall, usually an isolated lesion) or to the mechanical pres-ure exerted by diffuse accumulation of mucine (eosinophilicungal rhinosinusitis, frequently associated with sinonasal poly-osis).

CT and MRI findings in non-invasive forms depend on theigh content of calcium, iron and manganese within fungalyphae. On CT, spontaneous hyperdensity and scattered cal-ifications may be observed. Both iron and manganese causeelevant shortening of T1 and T2. Therefore, on MRI, both fun-us ball and eosinophilic fungal rhinosinusitis will appear asypointense/signal-void lesions filling the naso-sinusal cavity.yperintense signal on T1 has been shown in Bipolaris infection

32]. As in the eosinophilic rhinosinusitis the mucosa is undam-ged, the sinonasal cavities appeared bordered by the thickened
on-invaded mucosa, which has high SI on T2-weighted imagesnd enhances on post-contrast T1-weighted images [33]. Expan-ion of sinusal walls and bone thinning are more commonlybserved in eosinophilic fungal rhinosinusitis [34] (Fig. 3),

376 R. Maroldi et al. / European Journal of Radiology 66 (2008) 372–386

F e (c) afi s of p( (aste

wb

oeaisf

dwiedic

ta

tmiodm

ivlo

iUsid

ct[ts

ff

-

ig. 3. (a–d) Eosinophilic fungal rhinosinusitis. Axial CT (a and b), SE T1 beforlled by spontaneously hyperdense material. Bone remodelling and focal areaarrows and arrowheads). In (c and d) fungal hyphae exhibit hypointense signal

hereas sclerosis of sinusal walls is more typical in a fungusall (Fig. 4).

Invasion of mucosa, bone and vessels is the hallmarkf invasive fungal rhinosinusitis. These forms are generallyncountered in immunocompromised patients. Acute fulminantnd chronic invasive fungal rhinosinusitis share common imag-ng features; actually, the differential diagnosis is based on theeverity and rapidity of the clinical course, which, in the acuteulminant form, is often lethal.

On MRI, due to the vascular invasion, the necrotic mucosaoes not enhance. It may show variable signal intensity on T2-eighted images, probably reflecting different stages of tissue

schemia (Fig. 5). Frequently, the infected, devascularized tissuextends beyond the sinusal walls with involvement of the dura,ural sinuses and the brain. Early extent into the orbital apex andnvasion of the skull base (with cavernous sinus involvement)an be observed, particularly in the acute fulminant form [35].

Wegener’s granulomatosis is a chronic, granulomatous necro-izing vasculitis affecting the upper and lower respiratory tractnd the kidneys.

At imaging, sinonasal mucosal changes in the early stage ofhe disease are non-specific and very similar to chronic inflam-

atory changes. Only in the late stage of the disease, signal
ntensity of mucosa and submucosa switches to hypointensityn both T2-weighted and T1-weighted sequences, with variableegrees of contrast enhancement [36]. This is mostly due to sub-ucosal granuloma formation. In advanced stages of the disease,
nd after Gd-DTPA administration (d). In (a and b) ethmoid cells are completelyressure demineralization are depicted at the level of both laminae papyraceaerisk), the mucosal lining is preserved.

nflammatory infiltrate and granulomatous lesions within smallessels walls lead to obliteration of the lumen and to avascu-ar necrobiosis. This is the pathologic basis of bone destruction,ften involving midline structures like the nasal septum.

A similar pattern of bone destruction can be observedn advanced cocaine abusers (midline destructive syndrome).nfortunately, Wegener’s granulomatosis and cocaine abuse

hare overlapping histopathologic features and ANCA test-ng may give positive results also in cocaine induced midlineestructive lesions.

Imaging may be useful for the differential diagnosis. Inocaine abusers, not only the septum but also the adjacenturbinates may be destroyed, in a sort of centrifugal pattern37]. In addition, differently from Wegener’s granulomatosis,he destruction of hard and soft palate may occur, usually in latetages.

Wegener’s granulomatosis may involve deep spaces of theace and spread to central skull base. MR is decisive in identi-ying the cause of nerve impairment:

Direct granuloma extension into fissures or foramina of theskull base, as the pterygopalatine fossa, the orbital fissureor the vidian canal. On MRI, the granulomatous lesions
show hypointense signal on both T2-weighted and plainT1-weighted sequences. Contrast enhancement is usuallyobserved. It ranges from mild inhomogeneous to hyperintense[38].


Fig. 4. (a–e) Fungus ball. Coronal CT (a and b) shows right maxillary sinus completely filled by high density material with central nodular calcification (arrowhead).In axial CT (c–e) right sphenoid sinus is filled by material with multiple punctuate calcifications. Reactive changes (thickening and sclerosis) of right sphenoid sinuswalls are clearly shown (arrows).

Fig. 5. (a and b) Invasive mycoses. (a) Acute fulminant fungal rhinosinusitis. Coronal TSE T2 image shows inhomogeneous inflammatory material within the sphenoidsinus with invasion of the mucosa and erosion of the sinus floor (arrowhead). Irregular sclerosis of right pterygoid process (asterisk). Pterygoid and maxillary nerves(arrows). (b) Chronic invasive fungal rhinosinusitis. Axial TSE T2 image shows destruction of the maxillary sinus wall (arrows) with sclerosis of the residual boneand extension of the disease into the pterygopalatine and infratemporal fossae (M).

3 rnal of Radiology 66 (2008) 372–386

-

-

il

5

mEsncttbf

cersps

5

m

soc

pgoiaal“meaprtat

d

Fig. 6. (a and b) Fibrous dysplasia. The disease involves the temporal, sphenoidand maxillary bone. Three different patterns of this bone disorder are shownbaf

aabCrwotlfiqa

jm

awcc


Perineural granulomatous spread along trigeminal/parasy-mpathetic nerve branches. MR findings include asymmetri-cal nerve thickening, enlargement and late destruction of therelated foramina and fissures [39].Central nervous system localization of the disease.

However, involvement of deep spaces of the face and/or per-neural spread is indistinguishable from malignant neoplasms,ike non-Hodgkin lymphoma.

. Sinonasal tumors

The first step in the diagnostic work-up of both benign andalignant sinus neoplasms consists of fiber-optic examination.ndoscopy allows adequate demonstration of the superficialpread of the lesion and may guide a biopsy. The discrimi-ation between benign and malignant tumors and the preciseharacterization of the lesion are, in most cases, far beyondhe capabilities of imaging. CT and MRI are better focused onhe precise mapping of deep lesion extension in all those areaslinded at fiber-optic examination, especially anterior cranialossa, orbit, and pterygopalatine fossa.

In this setting, MRI is the technique of choice because itlearly differentiates tumor from retained secretions; it allowsarly detection of perivascular/perineural spread; it may accu-ately grade orbital/dural invasion. On the other hand, thetrengths of CT consist of a superior definition of cortical bonearticularly in the case of subtle erosions; faster and easier acqui-itions; superior accessibility and inferior cost.

.1. Benign lesions

A great variety of benign neoplasms and tumor-like lesionsay involve sinonasal region.The capability of optimally display bony structures makes CT

uperior to MRI in demonstrating fibro-osseous lesions, such assteoma, fibrous dysplasia, ossifying fibroma and aneurysmalysts.

Osteoma is the most frequent benign tumor of the nose andaranasal sinuses, since it is found in 1% of patients under-oing plain sinus radiographs and in 3% of CT examinationsbtained for sinonasal symptoms About 80% of osteomas occurn the frontal sinus, while ethmoid and maxillary sinuses areffected in about 20% of cases [40]. Three histological categoriesre described, regarding the type of bone which constitutes theesion: ivory or “eburnated” osteoma; osteoma spongiosum ormature osteoma”; mixed osteoma. According to the amount ofineralized bone within the lesion, at CT scans osteomas may

xhibit very high density, resembling cortical bone, or a gradu-lly decreasing density to a “ground-glass” pattern. All differentatterns can be found at once in the same lesion. CT multiplanareconstructions allow to precisely identify the site of origin ofhe lesion, to fully depict course and patency of all sinus paths,
nd to correctly assess the integrity of thin bony walls such ashe lamina papyracea or the cribriform plate.
Fibrous dysplasia and ossifying fibroma are two distinctiseases. Fibrous dysplasia is a non-neoplastic disorder, char-

ctst

y CT in the same patient: pagetoid (sphenoid bone), sclerotic (temporal bone)nd cystic bone changes (maxillary bone). Pterygopalatine fossa (arrowheads),oramen rotundum (white arrow), pterygoid canal (black arrow).

cterized by replacement of medullary bone by fibrous tissuend immature woven bone (Fig. 6). Ossifying fibroma is a trueenign neoplasm with variable local aggressiveness (Fig. 7).T density pattern ranges from radiolucent to ground glass in

elation to the degree of mineralization of the fibrous tissueithin the lesion. This makes the differential diagnosis betweenssifying fibroma and fibrous dysplasia rather difficult. Site ofhe lesion may be of help: isolated sphenoid or temporal boneesions as well as diffuse craniofacial involvement better apply tobrous dysplasia, whereas ossifying fibroma involves more fre-uently zygomatic bone and mandible. Fronto-ethmoid lesionsre, conversely, rather unpredictable [41].

Among benign soft tissue lesions, inverted papilloma anduvenile angiofibroma exhibit distinctive MRI features that, in

ost cases allow a reliable diagnosis.Inverted papilloma (IP) is an epithelial benign neoplasm char-

cterized by the infolding of the mucosa in the underlying stromaithout crossing the basement membrane. It is one of the most

ommon benign neoplasms of the sinonasal tract [42]. Its asso-iation with sinonasal malignancies, in particular squamous cell
arcinoma, is well established (the incidence ranging from 1.5o 56%). In a recent review the prevalence of metachronous andinchronous carcinoma is reported to be 3.6 and 7.1%, respec-ively [43]. IP may be suspected whenever an isolated, unilateral


Fig. 7. (a–b) Ossifying fibroma. CT shows a right ethmoid high density lesion (asterisk) narrowing the spheno-ethmoid recess and displacing the nasal septum(arrow).

Fig. 8. (a–d) Inverted papilloma. CT (a and b) demonstrates a soft tissue mass filling the maxillary sinus and remodelling its walls. The focal sclerotic bony spur seenin the postero-lateral sinus wall (arrowhead) represents the site of origin of the lesion. Greater palatine (white arrow) and lesser palatine (black arrow) canals. MR (cand d) shows a soft tissue mass with striated inner pattern (opposite arrows) extending from the maxillary sinus into the nasal cavity. A bone spur (black arrowheads)is demonstrated in the lateral recess.

3 rnal o

pnIcithp[tlOmt

tStMiml

lm

FIt


olypoid lesion is detected by imaging studies. No pathog-omonic appearance has been shown on CT examination. At CT,P appears as a soft tissue density mass with non-homogeneousontrast enhancement, and calcifications may be seen represent-ng remnants of involved bone structures [44]. CT can predicthe site of attachment of inverted papilloma by detecting focalyperostosis on sinusal walls [45] (Fig. 8). MRI reveals theresence of a pattern described as “septate striated appearance”42] or as “convoluted cerebriform pattern” [46]. On SE T2,he epithelium shows hypointense signal (due to its high cel-
ularity), whereas the edematous stroma appears hyperintense.n the other hand, on enhanced SE T1 the epithelium showsild enhancement, inferior to the underlying stroma. The jux-
aposition of several epithelial and stromal layers accounts for

cttt

ig. 9. (a–c) Juvenile angiofibroma. Axial TSE T2 image (a) shows soft tissue mass (wntense enhancement after Gd-DTPA injection is demonstrated on axial VIBE imagehe sphenoid sinus floor (black arrows) with a small part of the tumor abutting into th

f Radiology 66 (2008) 372–386

he columnar pattern shown on both sequences (Fig. 8). ThinE T1 sections and acquisition of slices in the three planes of

he space improve the detectability of this peculiar pattern [47].RI can be useful to select cases in which endoscopic approach

s feasible, although the assessment of frontal sinus involve-ent may be difficult and overestimation may occur at this

evel.Juvenile angiofibroma (JA) is a lesion composed of vascu-

ar and fibrous elements, which typically occurs in adolescentales. It has been recently suggested that the lesion should be

onsidered a vascular malformation [48] (or hamartoma) ratherhan a tumor. Peculiar findings of JA are its tendency to grow inhe submucosa and the early invasion of the cancellous bone athe pterygoid root. From there, the lesion may further grow lat-

hite arrow) with intermediate signal and an intralesional flow-void (arrowhead).(b). Coronal-enhanced SE T1 image (c) demonstrates upward displacement ofe left sphenoid sinus.

rnal o

einMTlJrevavtc

epm

rtt

baedep

ma(gmbalsnim

5m

cfsmM[opmn

5

aros

acfd

pbestTib

pb

r

s

tbadn

wd

ks(pt

swmcsmbtn


rally into the greater wing of the sphenoid bone (Fig. 9). At CT,ntra-diploic spread may be demonstrated by differentiating theormal medullary content from the strongly enhancing JA. OnRI, this discrimination may be achieved by combining a plain

1 with a post-contrast T1 without or with fat saturation. Theatter permits to easily distinguish the hyperintense-enhancedA from the suppressed signal of the surrounding bone mar-ow. From its site of origin in the pterygopalatine fossa, the JAxtends: (a) medially into the nasal cavity (and nasopharynx),ia enlargement and erosion of the sphenopalatine foramen; (b)nteriorly with bowing of the maxillary sinus wall; (c) laterally,ia the pterygo-maxillary fissure; (d) superiorly into the apex ofhe orbit through the inferior orbital fissure, and into the middleranial fossa via the superior orbital fissure.

Enhanced CT or MRI provide a precise mapping of thextent into these spaces by detecting the enhancing “finger-likerojections” of the JA, characterized also by sharp and lobulatedargins.Intracranial extent is mainly due to “finger-like projections”

unning along canals or through foramina. Rarely does it occurhrough the destruction of the inner table of the greater wing orhe lateral sphenoid sinus walls.

Follow-up is a crucial topic in imaging the juvenile angiofi-roma. In fact, a high rate of persistence/recurrence is presentfter surgery, especially in advanced lesions [49]. Contrast-nhanced CT has been shown to be accurate in detecting residualisease in the days after the resection [50]. In our experience,arly post-operative MRI is adequate in excluding un-resectedersistent disease.

A large spectrum of unusual lesions has been reported. Theyay arise from minor salivary glands (such as pleomorphic

denoma, monomorphic adenoma) or arise from soft tissuessuch as benign fibrous histiocytoma, hemangioma, pyogenicranuloma, inflammatory myofibroblastic tumor, leiomyoma,yxoma, paraganglioma, schwannoma). Information provided

y imaging rarely suggest the histologic diagnosis, but theyre essential to discriminate the liquid vs solid content of theesion, as well as its degree of vascularization (crucial forafe biopsy planning). Moreover, imaging may detect con-ection or extent to the anterior cranial fossa, crucial topicn the planning of an endoscopic or an open surgical treat-

ent.

.2. Essential information in managing naso-sinusalalignancies

Although on overall infrequent, sinonasal neoplasms areharacterized by numerous different histotypes, a distinctiveeature which reflects the peculiar density of diverse anatomictructures being present in this area. About 80% arise from theaxillary sinus and up to 73% are squamous cell carcinoma.ost of the remaining tumors arise from the ethmoid sinus

51]: in this site adenocarcinoma, squamous cell carcinoma and
lfactory neuroblastoma are prevalent histotypes. As a result,atterns of tumor spread may be generalized into two differentodels, according to their site of origin (i.e., maxillary area vs.
aso-ethmoidal area).

Ctip

f Radiology 66 (2008) 372–386 381

.3. Mapping naso-ethmoidal malignancies

In managing naso-ethmoidal neoplasm, the most criticalreas include the orbit (particularly the roof and the poste-ior lamina papyracea, where most post-operative recurrencesccur), the floor of the anterior cranial fossa (ACF) and thephenoid sinus.

It is a widely accepted notion that orbit may be preservedt surgery, even when its bony walls are completely eroded, onondition that the periorbita is not (or minimally) invaded. Inact, it has been demonstrated that a more aggressive approachoes not improve survival [52].

Displacement and distortion of orbital walls by ethmoid neo-lasms occur frequently. The mineral content of the wall maye partially or completely eroded leading to a questionable CTvaluation. On MRI, when a thin and regular hypointensity istill detectable on T2 images between neoplasm and orbital fat,he periorbita should be considered intact [53] (Figs. 10 and 11).hough definitive assessment of the integrity of the periorbita

s obtained in most cases intraoperatively, information providedy MRI may be crucial for surgical planning.

Furthermore, if imaging suggests orbital infiltration, theatient should be informed that an exenteratio orbitae mighte required.

Assessment of anterior cranial fossa floor invasion is alsoelevant for treatment planning.

Similarly to orbital walls invasion, bone destruction of thekull base is better demonstrated by CT.

However, at the skull base level imaging findings differ fromhose observed in other bone interfaces of the paranasal sinusesecause when the skull base is invaded, the dura mater usu-lly shows abnormal thickening and enhancement that can beue either to neoplastic invasion or to an inflammatory, non-eoplastic reaction.

Since dural invasion implies both a worse prognosis and aider surgical resection, imaging should focus on precising theepth of skull base invasion [54,55].

MRI has been reported to be more accurate than CT. Theey aspect is the analysis of the MRI signal intensity of thetructures located at the interface between the ethmoid roofbelow) and brain (above): the cribriform plate and its doubleeriosteal covering (lower layer); the dura mater (middle layer);he subarachnoid space (superior layer).

On enhanced sagittal and coronal SE T1 or 3D GE fatat T1 (VIBE) sequences the three layers compose a “sand-ich” of different signals (bone–periosteum complex, duraater, CSF) [56]. When a sinonasal neoplasm abuts against the

ribriform plate interface, without interrupting its hypointenseignal, the lesion should be considered extracranial. Efface-ent of the hypointense signal lower layer by tumor implies

one–periosteum penetration. In this case, if an uninterruptedhickened and enhancing dura mater (middle layer) is seen, theeoplasm may be graded as intracranial-extradural (Fig. 12).
onversely, focal or more extensive replacement of enhanced
hickened dura mater by tumor signal indicate intracranial-ntradural invasion (Fig. 13). Brain invasion is suspected in theresence of edema.

382 R. Maroldi et al. / European Journal of Radiology 66 (2008) 372–386

Fig. 10. (a and b) Recurrent adenocarcinoma. Coronal and axial TSE T2 imagesshow a soft tissue mass abutting the right medial orbital wall. The demonstrationof a hypointense line (arrows) in between the lesion and the orbital contentsuggests that the perioribita is uninterrupted, thus the orbit is not invaded. Onthe coronal T2 image, the crista galli and fovea ethmoidalis (arrowheads) areinvaded.

Fig. 12. (a and b) Recurrent adenocarcinoma. Coronal and sagittal Gd-enhancedVIBE images show a nodular lesion in the ethmoid roof with moderate enhance-ment. A thickened enhancing dura (arrows) separates the tumor from the brain(intracranial extradural invasion).

Fig. 11. (a and b) Neuroendocrine carcinoma. Coronal Gd-enhanced T1 images show a large naso-ethmoidal mass with intracranial intradural invasion (white arrow)and bilateral orbital involvement (black arrows).

R. Maroldi et al. / European Journal o

Fig. 13. Squamous cell carcinoma. Sagittal Gd-enhanced T1 image shows amhe

rv

5

apflbrcl

FTp

orstt

sbbaoia

esc(ms

5

ttptet

ass with intracranial extension. The thickened and enhancing dura (arrow-eads) is encroached by tumor (arrows), indicating intradural spread. No braindema is seen.

Patients with limited brain invasion treated by craniofacialesection are reported to have non-significant decrease in sur-ival compared to those with dural invasion only.

.4. Mapping maxillary sinus malignancies

The critical areas of neoplasms arising from the maxillaryrea include the posterior wall of maxillary sinus, the infratem-oral and pterygopalatine fossa, the hard palate, and the orbitaloor. The main goal of imaging is to assess the integrity of the
ony–periosteal barrier. It is well known that MRI is less accu-ate than CT in the assessment of focal bone erosions, since itsalcium content cannot be adequately detected [57]. Neverthe-ess, it is also known that the most effective barrier to spread
ig. 14. (a and b) Adenoid cystic carcinoma. Coronal TSE T2 image (a) shows a sohe lesion causes lateral displacement of the maxillary sinus mucosa (white arrowterygopalatine fossa (black arrow).

p

ep

f Radiology 66 (2008) 372–386 383

f aggressive lesions beyond sinusal walls is the periosteumather than the mineralized bony walls. Therefore, neoplasticpread beyond the periosteum of the sinusal walls is, in effect,he critical information for therapeutic planning because relatedo extrasinusal infiltration.

The thin sinusal walls appear hypointense in every MRIequence because of the reduced water content of the corticalone and of the periosteum. The entire thickness of the wall cane appreciated when invested by thickened mucosa or when their on one/both side(s) has been replaced by mucous secretionsr neoplastic tissue. Of course, the proper frequency encod-ng direction has to be selected in order to avoid asymmetricppearance of cortical bone due to chemical shift artefact.

Posterior spread into the pterygopalatine fossa is a relevantlement in the treatment planning. On MRI, neoplastic inva-ion of the pterygopalatine fossa is suspected whenever its fatontent has been replaced/effaced by soft tissue intensity [58]Fig. 14). Pterygoid canal and nerve, foramen rotundum andaxillary nerve are well demonstrated on axial and coronal MRI

equences.

.5. Imaging of perineural spread

Although the term “perineural spread” should be limitedo tumor spreading along the perineurium which envelopeshe nerve bundles, the term actually encompasses either neo-lasms invading all compartments and their neural sheaths orumor involving single compartments, as the space between thepineurium and the nerve bundles, or single sheaths—mainlyhe perineurium.

Nerve enhancement and nerve enlargement are the signs more

ft tissue submucosal mass arising from the medial wall of the right maxillary.s). Enhanced VIBE image (b) demonstrates solid enhancing tissue into the

redictive of the perineural spread.The tumor growth induces an increased permeability of the

ndoneurial capillaries and, eventually, causes breakage of theerineurium. The rupture of the blood–nerve barrier allows leak-

384 R. Maroldi et al. / European Journal o

Fig. 15. (a–d) Adenoid cystic carcinoma. The tumor, located at the level ofthe right choana (T), reaches the sphenopalatine foramen. In (a and b) tumorextends into the pterygopalatine fossa (white arrows) from which it spreads bothantegradely along the infraorbital nerve (opposite arrows) and retrogradely alongthe maxillary nerve (arrowheads), reaching the Meckel cave V2 (black arrows).In(

aao

dtTVast

iwit

a“m[sn[

“c

tdmote

eeo“sbi

MRes

hwf

mtsp

5

eiagftbga

n (c and d) enhanced VIBE images show perineural spread along mandibularerve (white arrow), greater superficial petrosal nerve (black arrows), greaterGP) and lesser (LP) palatine nerves.

ge and accumulation of iodinated or paramagnetic contrastgents, therefore accounting for segmental nerve enhancementn MRI (Fig. 15).

In detecting segmental nerve enhancement MRI has beenemonstrated to be more sensitive than CT [59]. Several MRIechniques have been proposed, with or without fat-saturation.he use of high-spatial resolution post-contrast fat saturationIBE (with isotropic voxel ranging from 0.5 to 0.7 mm) permitsdetailed evaluation of skull base foramina without artifacts. Its

patial resolution enables to clearly image the normal nerve andhe surrounding vascular plexus [60].

Segmental nerve enhancement, however, is not unique to per-
neural spread. It can be present in several non-neoplastic lesionshich result in blood–nerve barrier disruption, as inflammation,
schemia, infarct, trauma, demyelination, and axonal degenera-ion. These conditions may account for false positive MRI.

cirt

f Radiology 66 (2008) 372–386

Moreover, for segments as the V2, V3, XII and inferiorlveolar nerves crossing foramina/canals one should expect thetarget” or “tram-track-like” enhancement patterns to be nor-ally present, and not to be interpreted as abnormal findings

61]. Conversely, if these enhancement patterns are demon-trated in the labyrinthine and/or mastoid segments of the facialerve, breakage of the blood–nerve barrier should be suspected62].

Abnormal enhancement of the central nerve on “target” ortram-track-like” patterns without nerve enlargement has beenorrelated to minimal burden of perineural spread [63].

Further growth of tumor cells along the nerve gives riseo increased nerve diameter (Fig. 15), which can be directlyemonstrated on MRI, with or without abnormal nerve enhance-ent. Direct detection of an enlarged nerve is possible on CT,

n condition that the nerve is mainly surrounded by fat (i.e.,he infraorbital nerve). Indirect signs at CT are widening and,ventually, erosion of bony fissures and foramina.

However, the enlarged nerve may recover its normal diam-ter while it runs along a bony canal instead of remodeling orrode its inner bone surface, skipping the tract. Once it exits thepposite side, perineural spread regains a macroscopic size. Thisresurfacing phenomenon” is a mechanism of perineural exten-ion which deserves particular attention on CT and MRI. It cane observed with hard or soft palate tumors which “resurface”nto the PPF.

Retrograde (central) spread may lead the tumor to theeckel’s cave (through V2 or V3) and to the cavernous sinus.eplacement of fluid signal in the Meckel’s cave by solidnhancing tissue and bulging and enlargement of the cavernousinus indicate neoplastic invasion (Fig. 15).

If an intravascular paramagnetic contrast agent is used andigh-definition post-contrast GE sequences (VIBE) is acquiredith a delay of about 2 min, the tumor can be better separated

rom the venous signal within the cavernous sinus.Furthermore, when perineural spread leads to the damage of a

otor branch of a cranial nerve, MRI can detect the changes intohe denervated muscles during both the acute phase (hyperinten-ity in T2 images and abnormal enhancement) and the chronichase (atrophy and fat replacement).

.6. Follow-up

During follow-up, role of MRI is to detect asymptomaticxtra-mucosal disease. The interpretation of post-treatmentmaging studies may be quite challenging because of anatomicalnd functional changes induced by treatment(s). These changesreatly reduce the differences both in morphology and signaleatures between the persistent/recurrent disease and adjacentissues. Tissue changes secondary to resection can be predictedased on the surgical report. As craniofacial resection is the sur-ical treatment of choice, a thorough knowledge of the normalppearance after open or endoscopic or combined craniofa-
ial resection is necessary. Since these surgical approaches arendicated because a portion of the skull base floor is invaded,ecurrences are more frequently expected at the boundaries ofhe resection and reconstruction. Hence, a detailed evaluation of

rnal o

tbptmiiiRbtpme

ciDa[oricidt

nr

R

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[


he meningo-galeal complex, which replaces the anterior skullase floor, has to be obtained. Both coronal and sagittal T2 andost-contrast non-fat-suppressed T1 images are indicated. Focalhickness changes and lost of the “multiple-layer aspect” of theeningo-galeal complex during the follow-up are clues suggest-

ng neoplastic recurrence. When a local or revascularized flaps used after orbital or maxillary resection, the regularity of thenterface between the flap and adjacent tissues must be assessed.eactive mucosal changes resulting from radiation-therapy orone resection and subperiosteal dissection may result difficulto separate from recurrent disease, especially during the earlyost-treatment phase [64]. In the late phase, progression towardature scar is suggested by hypointensity on T2 and absence of

nhancement [65].The difficulty to discriminate between post-treatment

hanges and residual/recurrent disease accounts for the risingnterest towards more sophisticated ways to interrogate tissues.ynamic contrast-enhanced MRI exploits the vascularization

nd permeability of the endothelium of neoplastic microvessels66]. Diffusion-weighted imaging studies the diffusion motionf water protons in the tissues. With this technique, signal iselated to the freedom of water molecules to move within thentercellular spaces, thereby permitting to distinguish highlyellular tissues (tumor), where movement of water moleculess restricted, from inflammatory changes [67]. PET/CT mayemonstrate the increased glucidic metabolism of neoplasticissues.

Though all promising, none of the above-mentioned tech-iques is still part of standardized follow-up protocols and theirole is still far to be established.

eferences

[1] Nicolai P, Castelnuovo P, Lombardi D, et al. Role of endoscopic surgeryin the management of selected malignant epithelial neoplasms of the naso-ethmoidal complex. Head Neck 2007;29(12):1075–82.

[2] Phillips CD. Current status and new developments in techniques for imag-ing the nose and sinuses. Otolaryngol Clin North Am 1997;30(3):371–87.

[3] Hahnel S, Ertl-Wagner B, Tasman AJ, Forsting M, Jansen O. Relative valueof MR imaging as compared with CT in the diagnosis of inflammatoryparanasal sinus disease. Radiology 1999;210(1):171–6.

[4] Younis RT, Anand VK, Davidson B. The role of computed tomography andmagnetic resonance imaging in patients with sinusitis with complications.Laryngoscope 2002;112(2):224–9.

[5] Oliverio PJ, Benson ML, Zinreich SJ. Update on imaging for func-tional endoscopic sinus surgery. Otolaryngol Clin North Am 1995;28(3):585–608.

[6] Yousem DM. Imaging of sinonasal inflammatory disease. Radiology1993;188(2):303–14.

[7] Hakim HE, Malik AC, Aronyk K, Ledi E, Bhargava R. The prevalenceof intracranial complications in pediatric frontal sinusitis. Int J PediatrOtorhinolaryngol 2006;70(8):1383–7.

[8] Lerner DN, Choi SS, Zalzal GH, Johnson DL. Intracranial complications ofsinusitis in childhood. Ann Otol Rhinol Laryngol 1995;104(4 Pt 1):288–93.

[9] Rao VM, Sharma D, Madan A. Imaging of frontal sinus disease: con-
cepts, interpretation, and technology. Otolaryngol Clin North Am 2001;34(1):23–39.
10] Mafee MF, Tran BH, Chapa AR. Imaging of rhinosinusitis and its com-plications: plain film, CT, and MRI. Clin Rev Allergy Immunol 2006;30(3):165–86.

[

f Radiology 66 (2008) 372–386 385

11] Brooks I, Gooch 3rd WM, Jenkins SG, et al. Medical management ofacute bacterial sinusitis. Recommendations of a clinical advisory com-mittee on pediatric and adult sinusitis. Ann Otol Rhinol Laryngol Suppl2000;182:2–20.

12] Settipane GA. Epidemiology of nasal polyps. Allergy Asthma Proc1996;17(5):231–6.

13] Holmstrom M, Holmberg K, Lundblad L, Norlander T, Stierna P. Currentperspectives on the treatment of nasal polyposis: a Swedish opinion report.Acta Otolaryngol 2002;122(7):736–44.

14] Kramer MF, Rasp G. Nasal polyposis: eosinophils and interleukin-5.Allergy 1999;54(7):669–80.

15] Aygun N, Zinreich SJ. Imaging for functional endoscopic sinus surgery.Otolaryngol Clin North Am 2006;39(3):403–16.

16] Sonkens JW, Harnsberger HR, Blanch GM, Babbel RW, Hunt S. Theimpact of screening sinus CT on the planning of functional endoscopicsinus surgery. Otolaryngol Head Neck Surg 1991;105(6):802–13.

17] Larsen PL, Tos M. Origin of nasal polyps: an endoscopic autopsy study.Laryngoscope 2004;114(4):710–9.

18] Andrews AE, Bryson JM, Rowe-Jones JM. Site of origin of nasalpolyps: relevance to pathogenesis and management. Rhinology 2005;43(3):180–4.

19] Giacchi RJ, Lebowitz RA, Yee HT, Light JP, Jacobs JB. Histopatho-logic evaluation of the ethmoid bone in chronic sinusitis. Am J Rhinol2001;15(3):193–7.

20] Busaba NY, de Oliveira LV, Kieff DL. Correlation between preoperativeclinical diagnosis and histopathological findings in patients with rhinosi-nusitis. Am J Rhinol 2005;19(2):153–7.

21] Batsakis JG, Sneige N. Choanal and angiomatous polyps of the sinonasaltract. Ann Otol Rhinol Laryngol 1992;101(7):623–5.

22] De Vuysere S, Hermans R, Marchal G. Sinochoanal polyp and its variant,the angiomatous polyp: MRI findings. Eur Radiol 2001;11(1):55–8.

23] Pruna X. Morpho-functional evaluation of osteomeatal complex in chronicsinusitis by coronal CT. Eur Radiol 2003;13(6):1461–8.

24] Som PM, Dillon WP, Fullerton GD, Zimmerman RA, Rajagopalan B,Marom Z. Chronically obstructed sinonasal secretions: observations onT1 and T2 shortening. Radiology 1989;172(2):515–20.

25] Cooke LD, Hadley DM. MRI of the paranasal sinuses: incidentalabnormalities and their relationship to symptoms. J Laryngol Otol1991;105(4):278–81.

26] Wani MK, Ruckenstein MJ, Parikh S. Magnetic resonance imaging of theparanasal sinuses: incidental abnormalities and their relationship to patientsymptoms. J Otolaryngol 2001;30(5):257–62.

27] McNeill E, O’Hara J, Carrie S. The significance of MRI findings for non-rhinological disease. Clin Otolaryngol 2006;31(4):292–6.

28] Koike Y, Tokoro K, Chiba Y, Suzuki SI, Murai M, Ito H. Intracranialextension of paranasal sinus mucocele: two case reports. Surg Neurol 1996Jan;45(1):44–8.

29] Han MH, Chang KH, Lee CH, Na DG, Yeon KM, Han MC. Cystic expan-sile masses of the maxilla: differential diagnosis with CT and MR. Am JNeuroradiol (AJNR) 1995;16(2):333–8.

30] deShazo RD, O’Brien M, Chapin K, Soto-Aguilar M, Gardner L, SwainR. A new classification and diagnostic criteria for invasive fungal sinusitis.Arch Otolaryngol Head Neck Surg 1997;123(11):1181–8.

31] Ponikau JU, Sherris DA, Kern EB, et al. The diagnosis and incidence ofallergic fungal sinusitis. Mayo Clin Proc 1999;74(9):877–84.

32] Aribandi M, Bazan 3rd C. CT and MRI features in Bipolaris fungal sinusitis.Australas Radiol 2007;51(2):127–32.

33] Rao VM, Sharma D, Madan A. Imaging of frontal sinus disease: con-cepts, interpretation, and technology. Otolaryngol Clin North Am 2001Feb;34(1):23–39.

34] Mukherji SK, Figueroa RE, Ginsberg LE, et al. Allergic fungal sinusitis:CT findings. Radiology 1998;207(2):417–22.

35] Howells RC, Ramadan HH. Usefulness of computed tomography and mag-
netic resonance in fulminant invasive fungal rhinosinusitis. Am J Rhinol2001;15(4):255–61.
36] Muhle C, Reinhold-Keller E, Richter C, et al. MRI of the nasal cavity,the paranasal sinuses and orbits in Wegener’s granulomatosis. Eur Radiol1997;7(4):566–70.

3 rnal o

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[

[


37] Trimarchi M, Gregorini G, Facchetti F, et al. Cocaine-induced midlinedestructive lesions: clinical, radiographic, histopathologic, and serologicfeatures and their differentiation from Wegener granulomatosis. Medicine(Baltimore) 2001;80(6):391–404.

38] Keni SP, Wiley EL, Dutra JC, Mellott AL, Barr WG, Altman KW. Skullbase Wegener’s granulomatosis resulting in multiple cranial neuropathies.Am J Otolaryngol 2005;26(2):146–9.

39] Marsot-Dupuch K, De Givry SC, Ouayoun M. Wegener granulomatosisinvolving the pterygopalatine fossa: an unusual case of trigeminal neu-ropathy. Am J Neuroradiol (AJNR) 2002;23(2):312–5.

40] Earwaker J. Paranasal sinus osteomas: a review of 46 cases. Skeletal Radiol1993;22(6):417–23.

41] Som PM, Lidov M. The benign fibroosseous lesion: its association withparanasal sinus mucoceles and its MR appearance. J Comput Assist Tomogr1992;16(6):871–6.

42] Yousem DM, Fellows DW, Kennedy DW, Bolger WE, Kashima H, Zin-reich SJ. Inverted papilloma: evaluation with MR imaging. Radiology1992;185(2):501–5.

43] von Buchwald C, Bradley PJ. Risks of malignancy in inverted papillomaof the nose and paranasal sinuses. Curr Opin Otolaryngol Head Neck Surg2007;15(2):95–8.

44] Som PM, Lidov M. The significance of sinonasal radiodensities: ossi-fication, calcification, or residual bone? Am J Neuroradiol (AJNR)1994;15(5):917–22.

45] Lee DK, Chung SK, Dhong HJ, Kim HY, Kim HJ, Bok KH. Focal hyperos-tosis on CT of sinonasal inverted papilloma as a predictor of tumor origin.Am J Neuroradiol (AJNR) 2007;28(4):618–21.

46] Ojiri H, Ujita M, Tada S, Fukuda K. Potentially distinctive features ofsinonasal inverted papilloma on MR imaging. Am J Roentgenol (AJR)2000;175(2):465–8.

47] Maroldi R, Farina D, Palvarini L, Lombardi D, Tomenzoli D, Nico-lai P. Magnetic resonance imaging findings of inverted papilloma:differential diagnosis with malignant sinonasal tumors. Am J Rhinol2004;18(5):305–10.

48] Schick B, Plinkert PK, Prescher A. Die vaskulare Komponente:Gedanken zur Entstehung des Angiofibroms. Laryngorhinootologie2002;81(4):280–4.

49] Marshall AH, Bradley PJ. Management dilemmas in the treatment andfollow-up of advanced juvenile nasopharyngeal angiofibroma. ORL JOtorhinolaryngol Relat Spec 2006;68(5):273–8.

50] Kania RE, Sauvaget E, Guichard JP, Chapot R, Huy PT, Herman P. Earlypostoperative CT scanning for juvenile nasopharyngeal angiofibroma:
detection of residual disease. Am J Neuroradiol (AJNR) 2005;26(1):82–8.
51] Cantu G, Solero CL, Mariani L, et al. Anterior craniofacial resectionfor malignant ethmoid tumors—a series of 91 patients. Head Neck1999;21(3):185–91.

[

[

f Radiology 66 (2008) 372–386

52] Perry C, Levine PA, Williamson BR, Cantrell RW. Preservation of theeye in paranasal sinus cancer surgery. Arch Otolaryngol Head Neck Surg1988;114(6):632–4.

53] Kim HJ, Lee TH, Lee HS, Cho KS, Roh HJ. Periorbita: computedtomography and magnetic resonance imaging findings. Am J Rhinol2006;20(4):371–4.

54] Kraus DH, Lanzieri CF, Wanamaker JR, Little JR, Lavertu P. Comple-mentary use of computed tomography and magnetic resonance imaging inassessing skull base lesions. Laryngoscope 1992;102(6):623–9.

55] Shah JP, Kraus DH, Bilsky MH, Gutin PH, Harrison LH, Strong EW. Cran-iofacial resection for malignant tumors involving the anterior skull base.Arch Otolaryngol Head Neck Surg 1997;123(12):1312–7.

56] Ishida H, Mohri M, Amatsu M. Invasion of the skull base by carcino-mas: histopathologically evidenced findings with CT and MRI. Eur ArchOtorhinolaryngol 2002;259(10):535–9.

57] Som PM, Shapiro MD, Biller HF, Sasaki C, Lawson W. Sinonasal tumorsand inflammatory tissues: differentiation with MR imaging. Radiology1988;167(3):803–8.

58] Tomura N, Hirano H, Kato K, et al. Comparison of MR imaging with CT indepiction of tumour extension into the pterygopalatine fossa. Clin Radiol1999;54(6):361–6.

59] Hanna E, Vural E, Prokopakis E, Carrau R, Snyderman C, Weissman J. Thesensitivity and specificity of high-resolution imaging in evaluating perineu-ral spread of adenoid cystic carcinoma to the skull base. Arch OtolaryngolHead Neck Surg 2007;133(6):541–5.

60] Maroldi R, Ambrosi C, Farina D. Metastatic disease of the brain: extra-axialmetastases (skull, dura, leptomeningeal) and tumour spread. Eur Radiol2005;15(3):617–26.

61] Williams LS, Schmalfuss IM, Sistrom CL, et al. MR imaging of the trigem-inal ganglion, nerve, and the perineural vascular plexus: normal appearanceand variants with correlation to cadaver specimens. Am J Neuroradiol(AJNR) 2003;24(7):1317–23.

62] Martin-Duverneuil N, Sola-Martınez MT, Miaux Y, et al. Contrast enhance-ment of the facial nerve on MRI: normal or pathological? Neuroradiology1997;39(3):207–12.

63] Williams LS. Advanced concepts in the imaging of perineural spreadof tumor to the trigeminal nerve. Top Magn Reson Imaging 1999;10(6):376–83.

64] Loevner LA, Sonners AI. Imaging of neoplasms of the paranasal sinuses.Neuroimaging Clin North Am 2004;14(4):625–46.

65] Lell M, Baum U, Greess H, et al. Head and neck tumors: imaging recur-rent tumor and post-therapeutic changes with CT and MRI. Eur J Radiol
2000;33(3):239–47.
66] Shah GV, Fischbein NJ, Gandhi D, Mukherji SK. Dynamic contrast-enhanced MR imaging. Top Magn Reson Imaging 2004;15(2):71–7.

67] Hermans R, Vandecaveye V. Diffusion-weighted MRI in head and neckcancer. Cancer Imaging 2007;7:126–7.

Documents

Paranasal sinus imaging