European Journal of Radiology 66 (2008) 372–386

Paranasal sinus imaging

Roberto Maroldi ∗ , Marco Ravanelli, Andrea Borghesi, Davide Farina
Department of Radiology, University of Brescia, Piazzale Spedali Civili 1, Brescia 25123, Italy
Received 16 January 2008; accepted 17 January 2008

Abstract
Endonasal surgery is currently extending its application beyond inflammatory sinonasal lesions to successfully treat both benign and malignant
neoplasms. 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 from
the 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
linings (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-
treatment changes of the anatomy and of the signal of treated tissues. Though diffusion-weighted imaging and dynamic contrast-enhanced techniques
are promising developments, PET-CT may overcome the limits of morphological MRI.
© 2008 Elsevier Ireland Ltd. All rights reserved.

Keywords: Paranasal sinus; Computed tomography (CT); Magnetic resonance imaging (MRI); Perineural spread

1. Introduction Whereas MRI precisely assess pre-treatment tumor extent,

Endonasal surgery is currently extending its application
beyond inflammatory sinonasal lesions to successfully treat both
benign and malignant neoplasms [1]. This progression has been
possible by the detailed information provided by imaging tech-
niques (CT, MRI and PET). On the other hand, as endonasal
surgeons face new horizons – as the only-endoscopic cranio-
facial resection – new questions raise to the radiologists, as a
precise grading of the intracranial extent.
For each imaging technique, specific fields of clinical appli-
cation emerge from the medical literature in the present decade.
Inflammatory diseases are the “domain” of CT. CT provides
excellent details about the thin bony sinonasal walls (lamina
papyracea, cribriform plate) separating the ethmoid from the
anterior skull base and the orbit. In addition, both thickening of
the mucosa and retained mucous secretions are demonstrated.
Benign and malignant neoplasms are the “domain” of MRI
because the tumor is more easily separated from adjacent
structures, the periosteal linings (periorbita, dura mater) and
perineural spread can be accurately shown.
∗ Corresponding author.
E-mail address: maroldi@med.unibs.it (R. Maroldi).
early submucosal local recurrences are difficult to demonstrate
because of post-treatment changes of the anatomy and of the
signal of treated tissues. Though diffusion-weighted imaging
and dynamic contrast-enhanced techniques are promising devel-
opments, PET-CT may overcome the limits of morphological
MRI.
2. Acute rhinosinusitis
Only complicated acute rhinosinusitis requires CT for mak-
ing a correct diagnosis. Otherwise, the symptoms and the
endoscopic examination are sufficient [2].
If an orbital complication is suspected, generally secondary
to acute ethmoiditis, CT allows to differentiate between edema,
phlegmon and abscess, and to precisely identify the site of the
lesion, in order to define a correct treatment planning [3]; CT
may provide a correct diagnosis in up to 91% of cases, being sig-
nificantly more accurate than clinical examination alone (81%)
[4].
Preseptal cellulitis is confined to the anterior compartment
of the orbit (eyelid, periorbital soft tissues) without involvement
of the orbital cavity. CT shows thickening of the orbital septum,
increased density of orbital septum and periorbital soft tissues
[5].

0720-048X/$ – see front matter © 2008 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.ejrad.2008.01.059
 R. Maroldi et al. / European Journal of Radiology 66 (2008) 372–386
Orbital cellulitis is characterized by increased density of
intraorbital fat tissue, often observed at the level of the retrob-
ulbar space amid muscles and optic nerve.
On both CT and MRI, subperiosteal abscess is demonstrated
as a fluid collection with a peripheral enhancing rim between
the inner surface of the orbital walls and the periorbita. CT
better depicts subtle defects of the bony walls adjacent to
the abscess [6]. Gas bubbles within the collection herald the
presence of anaerobic agents or indicate fistulization from con-
tiguous paranasal cavities.
Orbital abscesses secondary to ethmoid sinusitis are gener-
ally located along the lamina papyracea, displacing the orbit
anteriorly and laterally; fluid collections complicating frontal
sinusitis are observed along the superior orbital wall and dis-
locate the ocular bulb anteriorly and inferiorly. Intraconal
extension of the abscess is the main key point to be ruled out at
CT.
MRI better demonstrates further vascular complications,
such as superior ophthalmic vein or cavernous sinus thrombosis
[5,6].
Intracranial complications are generally secondary to frontal
sinusitis and are more frequent in the pediatric population [7].
They are observed even in the absence of sinus wall defects,
as they may be secondary to thrombophlebitis of valveless
diploic veins [8]. Imaging is mandatory, in order to make a cor-
rect grading of intracranial involvement. In this setting, MRI
should be considered the technique of choice, because its accu-
racy is superior to CT in differentiating dural reaction from
epidural/subdural or intracerebral abscess, and in demonstrating
thrombosis of sagittal or cavernous sinus [3,4,9,10].
CT findings of meningitis may be unremarkable. Early signs
are represented by mild enlargement of ventricles and subarach-
noid spaces. In later stages, dural enhancement (especially at
the level of the falx, tentorium and convexity) and inflammatory
exudate within the subarachnoid spaces may be observed at MRI
on Gd-enhanced SE T1 images [4].
At CT, subdural/epidural abscess is detected as an extracere-
bral fluid collection with a convex shape, separated from the
parenchyma by a thick and enhancing rim.
The CT appearance of brain abscesses (Fig. 1) is widely
variable in the different phases of evolution.
3. Chronic rhinosinusitis
Chronic rhinosinusitis is defined as an inflammation of the
nose and paranasal sinuses mucosa lasting more than 12 weeks
[11]. Pathogenesis is multifactorial with several predispos-
ing factors: nasal allergy, ASA-syndrome, dental infections,
anatomic variants, immunodeficiencies, mucociliary anoma-
lies and iatrogenic factors (mechanical ventilation, nasogastric
tubes, nasal packing, post-operative scarring in the ostiomeatal
complex).
Sinonasal polyposis is a quite common finding in chronic
rhinosinusitis, ranging from 2 to 16% of cases [12,13]. Macro-
scopically, nasal polyps appear as edematous formations,
yellow-white in appearance and soft in consistency. Histo-
logically, they consist of respiratory epithelium covering an
373
Fig. 1. Complicated acute rhinosinusitis: brain abscess. Coronal CT after con-
trast administration shows fluid inflammatory material in the maxillary sinus
(asterisk) and intraparenchymal abscess in the frontal lobe (arrows).
edematous stroma infiltrated by inflammatory cells. Eosinophils
are found in 80% of the cases [14].
In case of chronic rhinosinusitis, the role of CT is to accu-
rately assess the pattern of mucociliary drainage impairment,
to identify anatomical variants predisposing the inflammatory
changes and/or conditioning the endoscopic approach [15].
Based on obstruction of different drainage pathways, five
different patterns of chronic rhinosinusitis have been described
in the literature [16].
3.1. Infundibular pattern
Infundibular pattern is the most limited model. Ethmoid
infundibulum and maxillary sinus alone are involved.
This pattern is mainly due to the presence of mucosal thick-
enings or isolated polyps along the infundibulum. Anatomic
predisposing factors are infraorbital cells, uncinate process vari-
ants, and hypoplasia of the maxillary sinus. CT promptly detects
infundibular obstruction and inflammatory changes of maxillary
sinus mucosa.
3.2. Ostiomeatal unit pattern
Ostiomeatal unit pattern reflects the obstruction of all
drainage systems in the middle meatus. As a consequence, it
is heralded by maxillary, frontal, and anterior ethmoid sinusi-
tis. Aspecific mucosal thickenings as well as nasal polyps
most commonly induce ostiomeatal unit pattern; concha bullosa
and marked septal deviation are anatomic predisposing factors.
Additionally, lesions arising from the lateral nasal wall, such as
inverted papilloma, may cause this model.
3.3. Spheno-ethmoid recess pattern
Spheno-ethmoid recess pattern is rather rare; it consists of
sphenoid sinusitis and (not infrequently) posterior ethmoiditis,
374 R. Maroldi et al. / European Journal of Radiology 66 (2008) 372–386
secondary to spheno-ethmoid recess obstruction. Obliteration
of the recess and inflammatory mucosal thickenings are better
depicted with axial CT.
3.4. Pattern of nasal polyposis
This pattern is characterized by the involvement – mostly
bilateral – of middle meati, ethmoid infundibula (often widened)
and nasal cavity. Most inflammatory polyps originate in rela-
tion to sinus outlets, from the mucosa investing ostia, clefts and
recesses in the ostiomeatal complex, the ethmoid infundibulum,
and the uncinate process. Less commonly, they may originate
from the superior meatus, the frontal recess or the anterior
part of ethmoid bulla [17,18]. At CT, they appear as lobulated
lesions with soft-tissue attenuation filling ethmoid, nasal fos-
sae and sinusal cavities. CT attenuation may be elevated when
inspissated mucus is trapped within the mucosal folds. Bone
remodelling is associated, due to mechanical pressure exerted by
the polyps but also by the local release of inflammatory medi-
ators and by bacterial invasion of bone and periosteum [19].
As a result, thinning and displacement of subtle bone struc-
tures (such as ethmoid labyrinth and lamina papyracea) and
sclerosis of thicker sinusal walls (such as posterolateral max-
illary sinus wall) may be observed. Bone erosion is infrequent
and may be demonstrated in cases of long-standing, aggressive
polyposis.
Two additional signs are described as common features of
sinonasal polyposis: widening of ethmoid infundibulum, espe-
cially bilateral, and truncation of the more distal, bulbous
part of the middle turbinate (bilateral in up to 80% of the
cases).
MRI signal pattern reflect the stages of polyp growth (ede-
matous, cystic or fibrous). Most frequently it is composed of
hyper T2 signal and a combination of hyperintensity (mucosa)
and hypointensity (edematous stroma) on contrast-enhanced
T1.
Even though bone changes and bilateral pattern of growth
are quite typical, it must be emphasized that density pattern
of nasal polyps is not completely specific; therefore several
authors recommend thorough evaluation of surgical specimens
[20].
A peculiar variant of sinonasal polyp is represented by antro-
choanal polyp. This lesion arises in the maxillary sinus and
protrudes in the middle meatus through ethmoidal infundibulum
or through an accessory ostium, reaching typically the choana.
Usually, the intramaxillary portion is cystic (hypodensity on CT,
hyper T2 signal on MRI), while the intranasal portion is solid.
Sphenochoanal and ethmoidochoanal polyps are extremely
rare variants.
As a consequence of their growth through constrictive ostia,
all sino-choanal polyps are subject to strangling and vascular
compromise. When this occurs, the intranasal portion of the
sino-choanal polyp shows dilation and stasis of feeding ves-
sels, resulting in bright enhancement after contrast medium
administration (angiomatous polyp) [21,22]. Prolonged vascular
damage may induce necrosis of the polyp with autopolypectomy
[23].
3.5. Sporadic pattern
In the sporadic pattern, inflammatory changes of paranasal
sinuses are unrelated to impairment of any of mucociliary
drainage pathways. A wide list of different conditions, such
as isolated sinusitis, retention cyst, mucocele, post-surgical
changes are included in this group.
Mucosal thickenings are an extremely common finding in
maxillary and sphenoid sinuses; within ethmoid cells, it is often
impossible to differentiate them from inflammatory polyps or
retained secretions.
CT findings consist of partial or complete obliteration of a
sinusal cavity by thickened mucosa with smooth – occasionally
lobulated – surface and homogeneously low density, reflect-
ing chronic inflammatory edema of the submucosal layer. No
relevant bone changes are generally associated.
At MRI, thickened mucosa shows a uniformly bright signal
on SE T2 sequences, whereas SE T1 after contrast adminis-
tration demonstrates hyperintensity of the enhancing mucosa
combined with hypointense signal of the edematous submucosal
layer.
CT and MRI appearance of retained secretions is strictly
related to the composition of the entrapped fluid. Protein content
and viscosity of chronically retained secretions progressively
increase, resulting in higher CT density. Raised HU values are
also observed within pus or blood collections. At MRI, an inverse
correlation is observed between protein concentration and T2
signal (at 40–45% protein concentration the T2 signal becomes
black). On plain T1 sequence, signal rises to a peak at about
25–30% protein concentration and then progressively decreases
to hypointensity [24].
Retention cysts are more frequently observed in the maxil-
lary sinus (in the alveolar recess or at the level of the roof close
to infraorbital canal). They are secondary to obstruction of a
mucosal or minor salivary gland. At CT, retention cysts appear
as hypodense fluid-like lesions with smooth and convex bor-
ders, and variable size. MRI signal pattern is similar to the one
described for retained secretions.
Nonetheless, it must be emphasized that all mucosal thicken-
ings and retention cysts can be observed as incidental findings
in 30–50% of patients submitted to imaging studies of the head
for non-sinusal pathologies, with no significant correlation with
clinical symptoms [25–27].
Mucocele may be defined as an accumulation of prod-
ucts of secretion, desquamation, and inflammation within a
paranasal sinus with expansion of its bony walls. The devel-
opment of the lesion occurs as the result of sinus ostium
blockage. Imaging plays a crucial role in defining extension
of mucoceles, particularly towards orbit, anterior cranial fossa
and optic nerve canal [28]. Sinus expansion with bulging of
all its bony walls is the most typical presentation of muco-
cele. Nonetheless, these changes are often focal in post-operative
mucoceles, may be due to post-surgical sinusal compartmental-
ization [29] (Fig. 2). CT density and MRI intensity are largely
variable, according with the composition of entrapped material.
Peripheral rim enhancement is observed on both CT and MRI
images.
 R. Maroldi et al. / European Journal of Radiology 66 (2008) 372–386
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 middle
turbinate and lateral nasal wall which occludes the frontal recess (arrows). Reactive changes of right frontal sinus walls is well demonstrated. Bulla frontalis type IV
(arrowhead).
3.6. Imaging after endonasal surgery for chronic sinusitis
CT after endoscopic surgery is indicated in symptomatic
patients (headache, rhinoliquorrea, recurrence of pre-treatment
symptoms) and must be focused on critical areas, in order to
demonstrate the post-operative outcome and detect possible
recurrences and complications. Mucosal thickening or synechiae
into the fronto-nasal recess may cause frontal sinus blockage.
Dehiscences may occur in the lamina papyracea, in the sphenoid
sinus walls and in the ethmoid roof, due to direct penetration of
the endoscope or traction exerted on connected structures (i.e.,
turbinates). Although CT is the technique of choice in detect-
ing acute post-operative complications, MRI is mandatory when
CSF leak or meningo-(encephalo)-cele is suspected.
4. Aggressive inflammatory lesions
Fungal rhinosinusitis can be defined as an infection of
paranasal sinuses in which fungi play a role of primary pathogens
or cause an inflammation due to their presence.
According to the presence or lack of sinonasal mucosa inva-
sion [30], fungal rhinosinusitis is classified into:
- non-invasive forms: fungus ball and eosinophilic fungal rhi-
nosinusitis [31];
375
- invasive forms: acute fulminant rhinosinusitis, chronic inva-
sive fungal rhinosinusitis and granulomatous invasive fungal
rhinosinusitis.
In non-invasive fungal rhinosinusitis, the lesion is usually
confined by sinusal walls for a long time. Eventually, remodeling
and destruction of the walls occur, due to the mass-like growth
pattern of fungal debris and mucus within the sinus (fungus
ball, usually an isolated lesion) or to the mechanical pres-
sure exerted by diffuse accumulation of mucine (eosinophilic
fungal rhinosinusitis, frequently associated with sinonasal poly-
posis).
CT and MRI findings in non-invasive forms depend on the
high content of calcium, iron and manganese within fungal
hyphae. On CT, spontaneous hyperdensity and scattered cal-
cifications may be observed. Both iron and manganese cause
relevant shortening of T1 and T2. Therefore, on MRI, both fun-
gus ball and eosinophilic fungal rhinosinusitis will appear as
hypointense/signal-void lesions filling the naso-sinusal cavity.
Hyperintense signal on T1 has been shown in Bipolaris infection
[32]. As in the eosinophilic rhinosinusitis the mucosa is undam-
aged, the sinonasal cavities appeared bordered by the thickened
non-invaded mucosa, which has high SI on T2-weighted images
and enhances on post-contrast T1-weighted images [33]. Expan-
sion of sinusal walls and bone thinning are more commonly
observed in eosinophilic fungal rhinosinusitis [34] (Fig. 3),
376 R. Maroldi et al. / European Journal of Radiology 66 (2008) 372–386

Fig. 3. (a–d) Eosinophilic fungal rhinosinusitis. Axial CT (a and b), SE T1 before (c) and after Gd-DTPA administration (d). In (a and b) ethmoid cells are completely
filled by spontaneously hyperdense material. Bone remodelling and focal areas of pressure demineralization are depicted at the level of both laminae papyraceae
(arrows and arrowheads). In (c and d) fungal hyphae exhibit hypointense signal (asterisk), the mucosal lining is preserved.

whereas sclerosis of sinusal walls is more typical in a fungus
ball (Fig. 4).
Invasion of mucosa, bone and vessels is the hallmark
of invasive fungal rhinosinusitis. These forms are generally
encountered in immunocompromised patients. Acute fulminant
and chronic invasive fungal rhinosinusitis share common imag-
ing features; actually, the differential diagnosis is based on the
severity and rapidity of the clinical course, which, in the acute
fulminant form, is often lethal.
On MRI, due to the vascular invasion, the necrotic mucosa
does not enhance. It may show variable signal intensity on T2-
weighted images, probably reflecting different stages of tissue
ischemia (Fig. 5). Frequently, the infected, devascularized tissue
extends beyond the sinusal walls with involvement of the dura,
dural sinuses and the brain. Early extent into the orbital apex and
invasion of the skull base (with cavernous sinus involvement)
can be observed, particularly in the acute fulminant form [35].
Wegener’s granulomatosis is a chronic, granulomatous necro-
tizing vasculitis affecting the upper and lower respiratory tract
and the kidneys.
At imaging, sinonasal mucosal changes in the early stage of
the disease are non-specific and very similar to chronic inflam-
matory changes. Only in the late stage of the disease, signal
intensity of mucosa and submucosa switches to hypointensity
on both T2-weighted and T1-weighted sequences, with variable
degrees of contrast enhancement [36]. This is mostly due to sub-
mucosal granuloma formation. In advanced stages of the disease,
inflammatory infiltrate and granulomatous lesions within small
vessels walls lead to obliteration of the lumen and to avascu-
lar necrobiosis. This is the pathologic basis of bone destruction,
often involving midline structures like the nasal septum.
A similar pattern of bone destruction can be observed
in advanced cocaine abusers (midline destructive syndrome).
Unfortunately, Wegener’s granulomatosis and cocaine abuse
share overlapping histopathologic features and ANCA test-
ing may give positive results also in cocaine induced midline
destructive lesions.
Imaging may be useful for the differential diagnosis. In
cocaine abusers, not only the septum but also the adjacent
turbinates may be destroyed, in a sort of centrifugal pattern
[37]. In addition, differently from Wegener’s granulomatosis,
the destruction of hard and soft palate may occur, usually in late
stages.
Wegener’s granulomatosis may involve deep spaces of the
face and spread to central skull base. MR is decisive in identi-
fying the cause of nerve impairment:
- Direct granuloma extension into fissures or foramina of the
skull base, as the pterygopalatine fossa, the orbital fissure
or the vidian canal. On MRI, the granulomatous lesions
show hypointense signal on both T2-weighted and plain
T1-weighted sequences. Contrast enhancement is usually
observed. It ranges from mild inhomogeneous to hyperintense
[38].
 R. Maroldi et al. / European Journal of Radiology 66 (2008) 372–386 377

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 sinus
walls 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 sphenoid
sinus 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 bone
and extension of the disease into the pterygopalatine and infratemporal fossae (M).
378 R. Maroldi et al. / European Journal of Radiology 66 (2008) 372–386

- Perineural granulomatous spread along trigeminal/parasy-

mpathetic nerve branches. MR findings include asymmetri-
cal nerve thickening, enlargement and late destruction of the
related foramina and fissures [39].
- Central nervous system localization of the disease.

However, involvement of deep spaces of the face and/or per-

ineural spread is indistinguishable from malignant neoplasms,
like non-Hodgkin lymphoma.

5. Sinonasal tumors

The first step in the diagnostic work-up of both benign and

malignant sinus neoplasms consists of fiber-optic examination.
Endoscopy allows adequate demonstration of the superficial
spread of the lesion and may guide a biopsy. The discrimi-
nation between benign and malignant tumors and the precise
characterization of the lesion are, in most cases, far beyond
the capabilities of imaging. CT and MRI are better focused on
the precise mapping of deep lesion extension in all those areas
blinded at fiber-optic examination, especially anterior cranial
fossa, orbit, and pterygopalatine fossa.
In this setting, MRI is the technique of choice because it
clearly differentiates tumor from retained secretions; it allows
early detection of perivascular/perineural spread; it may accu-
rately grade orbital/dural invasion. On the other hand, the
strengths of CT consist of a superior definition of cortical bone
particularly in the case of subtle erosions; faster and easier acqui- Fig. 6. (a and b) Fibrous dysplasia. The disease involves the temporal, sphenoid
sitions; superior accessibility and inferior cost. and maxillary bone. Three different patterns of this bone disorder are shown
by CT in the same patient: pagetoid (sphenoid bone), sclerotic (temporal bone)
and cystic bone changes (maxillary bone). Pterygopalatine fossa (arrowheads),
5.1. Benign lesions
foramen rotundum (white arrow), pterygoid canal (black arrow).

A great variety of benign neoplasms and tumor-like lesions

may involve sinonasal region.
The capability of optimally display bony structures makes CT
superior to MRI in demonstrating fibro-osseous lesions, such as
osteoma, fibrous dysplasia, ossifying fibroma and aneurysmal
cysts.
Osteoma is the most frequent benign tumor of the nose and
paranasal sinuses, since it is found in 1% of patients under-
going plain sinus radiographs and in 3% of CT examinations
obtained for sinonasal symptoms About 80% of osteomas occur
in the frontal sinus, while ethmoid and maxillary sinuses are
affected in about 20% of cases [40]. Three histological categories
are described, regarding the type of bone which constitutes the
lesion: ivory or “eburnated” osteoma; osteoma spongiosum or
“mature osteoma”; mixed osteoma. According to the amount of
mineralized bone within the lesion, at CT scans osteomas may
exhibit very high density, resembling cortical bone, or a gradu-
ally decreasing density to a “ground-glass” pattern. All different
patterns can be found at once in the same lesion. CT multiplanar
reconstructions allow to precisely identify the site of origin of
the lesion, to fully depict course and patency of all sinus paths,
and to correctly assess the integrity of thin bony walls such as
the lamina papyracea or the cribriform plate.
Fibrous dysplasia and ossifying fibroma are two distinct
diseases. Fibrous dysplasia is a non-neoplastic disorder, char-
acterized by replacement of medullary bone by fibrous tissue
and immature woven bone (Fig. 6). Ossifying fibroma is a true
benign neoplasm with variable local aggressiveness (Fig. 7).
CT density pattern ranges from radiolucent to ground glass in
relation to the degree of mineralization of the fibrous tissue
within the lesion. This makes the differential diagnosis between
ossifying fibroma and fibrous dysplasia rather difficult. Site of
the lesion may be of help: isolated sphenoid or temporal bone
lesions as well as diffuse craniofacial involvement better apply to
fibrous dysplasia, whereas ossifying fibroma involves more fre-
quently zygomatic bone and mandible. Fronto-ethmoid lesions
are, conversely, rather unpredictable [41].
Among benign soft tissue lesions, inverted papilloma and
juvenile angiofibroma exhibit distinctive MRI features that, in
most cases allow a reliable diagnosis.
Inverted papilloma (IP) is an epithelial benign neoplasm char-
acterized by the infolding of the mucosa in the underlying stroma
without crossing the basement membrane. It is one of the most
common benign neoplasms of the sinonasal tract [42]. Its asso-
ciation with sinonasal malignancies, in particular squamous cell
carcinoma, is well established (the incidence ranging from 1.5
to 56%). In a recent review the prevalence of metachronous and
sinchronous carcinoma is reported to be 3.6 and 7.1%, respec-
tively [43]. IP may be suspected whenever an isolated, unilateral
 R. Maroldi et al. / European Journal of Radiology 66 (2008) 372–386 379

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 seen
in 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 (c
and 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.
380 R. Maroldi et al. / European Journal of Radiology 66 (2008) 372–386

polypoid lesion is detected by imaging studies. No pathog-
nomonic appearance has been shown on CT examination. At CT,
IP appears as a soft tissue density mass with non-homogeneous
contrast enhancement, and calcifications may be seen represent-
ing remnants of involved bone structures [44]. CT can predict
the site of attachment of inverted papilloma by detecting focal
hyperostosis on sinusal walls [45] (Fig. 8). MRI reveals the
presence of a pattern described as “septate striated appearance”
[42] or as “convoluted cerebriform pattern” [46]. On SE T2,
the epithelium shows hypointense signal (due to its high cel-
lularity), whereas the edematous stroma appears hyperintense.
On the other hand, on enhanced SE T1 the epithelium shows
mild enhancement, inferior to the underlying stroma. The jux-
taposition of several epithelial and stromal layers accounts for
the columnar pattern shown on both sequences (Fig. 8). Thin
SE T1 sections and acquisition of slices in the three planes of
the space improve the detectability of this peculiar pattern [47].
MRI can be useful to select cases in which endoscopic approach
is feasible, although the assessment of frontal sinus involve-
ment may be difficult and overestimation may occur at this
level.
Juvenile angiofibroma (JA) is a lesion composed of vascu-
lar and fibrous elements, which typically occurs in adolescent
males. It has been recently suggested that the lesion should be
considered a vascular malformation [48] (or hamartoma) rather
than a tumor. Peculiar findings of JA are its tendency to grow in
the submucosa and the early invasion of the cancellous bone at
the pterygoid root. From there, the lesion may further grow lat-

Fig. 9. (a–c) Juvenile angiofibroma. Axial TSE T2 image (a) shows soft tissue mass (white arrow) with intermediate signal and an intralesional flow-void (arrowhead).
Intense enhancement after Gd-DTPA injection is demonstrated on axial VIBE image (b). Coronal-enhanced SE T1 image (c) demonstrates upward displacement of
the sphenoid sinus floor (black arrows) with a small part of the tumor abutting into the left sphenoid sinus.
 R. Maroldi et al. / European Journal of Radiology 66 (2008) 372–386
erally into the greater wing of the sphenoid bone (Fig. 9). At CT,
intra-diploic spread may be demonstrated by differentiating the
normal medullary content from the strongly enhancing JA. On
MRI, this discrimination may be achieved by combining a plain
T1 with a post-contrast T1 without or with fat saturation. The
latter permits to easily distinguish the hyperintense-enhanced
JA from the suppressed signal of the surrounding bone mar-
row. From its site of origin in the pterygopalatine fossa, the JA
extends: (a) medially into the nasal cavity (and nasopharynx),
via enlargement and erosion of the sphenopalatine foramen; (b)
anteriorly with bowing of the maxillary sinus wall; (c) laterally,
via the pterygo-maxillary fissure; (d) superiorly into the apex of
the orbit through the inferior orbital fissure, and into the middle
cranial fossa via the superior orbital fissure.
Enhanced CT or MRI provide a precise mapping of the
extent into these spaces by detecting the enhancing “finger-like
projections” of the JA, characterized also by sharp and lobulated
margins.
Intracranial extent is mainly due to “finger-like projections”
running along canals or through foramina. Rarely does it occur
through the destruction of the inner table of the greater wing or
the lateral sphenoid sinus walls.
Follow-up is a crucial topic in imaging the juvenile angiofi-
broma. In fact, a high rate of persistence/recurrence is present
after surgery, especially in advanced lesions [49]. Contrast-
enhanced CT has been shown to be accurate in detecting residual
disease in the days after the resection [50]. In our experience,
early post-operative MRI is adequate in excluding un-resected
persistent disease.
A large spectrum of unusual lesions has been reported. They
may arise from minor salivary glands (such as pleomorphic
adenoma, monomorphic adenoma) or arise from soft tissues
(such as benign fibrous histiocytoma, hemangioma, pyogenic
granuloma, inflammatory myofibroblastic tumor, leiomyoma,
myxoma, paraganglioma, schwannoma). Information provided
by imaging rarely suggest the histologic diagnosis, but they
are essential to discriminate the liquid vs solid content of the
lesion, as well as its degree of vascularization (crucial for
safe biopsy planning). Moreover, imaging may detect con-
nection or extent to the anterior cranial fossa, crucial topic
in the planning of an endoscopic or an open surgical treat-
ment.
5.2. Essential information in managing naso-sinusal
malignancies
Although on overall infrequent, sinonasal neoplasms are
characterized by numerous different histotypes, a distinctive
feature which reflects the peculiar density of diverse anatomic
structures being present in this area. About 80% arise from the
maxillary sinus and up to 73% are squamous cell carcinoma.
Most of the remaining tumors arise from the ethmoid sinus
[51]: in this site adenocarcinoma, squamous cell carcinoma and
olfactory neuroblastoma are prevalent histotypes. As a result,
patterns of tumor spread may be generalized into two different
models, according to their site of origin (i.e., maxillary area vs.
naso-ethmoidal area).
381
5.3. Mapping naso-ethmoidal malignancies
In managing naso-ethmoidal neoplasm, the most critical
areas include the orbit (particularly the roof and the poste-
rior lamina papyracea, where most post-operative recurrences
occur), the floor of the anterior cranial fossa (ACF) and the
sphenoid sinus.
It is a widely accepted notion that orbit may be preserved
at surgery, even when its bony walls are completely eroded, on
condition that the periorbita is not (or minimally) invaded. In
fact, it has been demonstrated that a more aggressive approach
does not improve survival [52].
Displacement and distortion of orbital walls by ethmoid neo-
plasms occur frequently. The mineral content of the wall may
be partially or completely eroded leading to a questionable CT
evaluation. On MRI, when a thin and regular hypointensity is
still detectable on T2 images between neoplasm and orbital fat,
the periorbita should be considered intact [53] (Figs. 10 and 11).
Though definitive assessment of the integrity of the periorbita
is obtained in most cases intraoperatively, information provided
by MRI may be crucial for surgical planning.
Furthermore, if imaging suggests orbital infiltration, the
patient should be informed that an exenteratio orbitae might
be required.
Assessment of anterior cranial fossa floor invasion is also
relevant for treatment planning.
Similarly to orbital walls invasion, bone destruction of the
skull base is better demonstrated by CT.
However, at the skull base level imaging findings differ from
those observed in other bone interfaces of the paranasal sinuses
because when the skull base is invaded, the dura mater usu-
ally shows abnormal thickening and enhancement that can be
due either to neoplastic invasion or to an inflammatory, non-
neoplastic reaction.
Since dural invasion implies both a worse prognosis and a
wider surgical resection, imaging should focus on precising the
depth of skull base invasion [54,55].
MRI has been reported to be more accurate than CT. The
key aspect is the analysis of the MRI signal intensity of the
structures located at the interface between the ethmoid roof
(below) and brain (above): the cribriform plate and its double
periosteal covering (lower layer); the dura mater (middle layer);
the subarachnoid space (superior layer).
On enhanced sagittal and coronal SE T1 or 3D GE fat
sat T1 (VIBE) sequences the three layers compose a “sand-
wich” of different signals (bone–periosteum complex, dura
mater, CSF) [56]. When a sinonasal neoplasm abuts against the
cribriform plate interface, without interrupting its hypointense
signal, the lesion should be considered extracranial. Efface-
ment of the hypointense signal lower layer by tumor implies
bone–periosteum penetration. In this case, if an uninterrupted
thickened and enhancing dura mater (middle layer) is seen, the
neoplasm may be graded as intracranial-extradural (Fig. 12).
Conversely, focal or more extensive replacement of enhanced
thickened dura mater by tumor signal indicate intracranial-
intradural invasion (Fig. 13). Brain invasion is suspected in the
presence of edema.
382 R. Maroldi et al. / European Journal of Radiology 66 (2008) 372–386

Fig. 12. (a and b) Recurrent adenocarcinoma. Coronal and sagittal Gd-enhanced

VIBE images show a nodular lesion in the ethmoid roof with moderate enhance-
Fig. 10. (a and b) Recurrent adenocarcinoma. Coronal and axial TSE T2 images
ment. A thickened enhancing dura (arrows) separates the tumor from the brain
show a soft tissue mass abutting the right medial orbital wall. The demonstration
(intracranial extradural invasion).
of a hypointense line (arrows) in between the lesion and the orbital content
suggests that the perioribita is uninterrupted, thus the orbit is not invaded. On
the coronal T2 image, the crista galli and fovea ethmoidalis (arrowheads) are
invaded.

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 of Radiology 66 (2008) 372–386
Fig. 13. Squamous cell carcinoma. Sagittal Gd-enhanced T1 image shows a
mass with intracranial extension. The thickened and enhancing dura (arrow-
heads) is encroached by tumor (arrows), indicating intradural spread. No brain
edema is seen.
Patients with limited brain invasion treated by craniofacial
resection are reported to have non-significant decrease in sur-
vival compared to those with dural invasion only.
5.4. Mapping maxillary sinus malignancies
The critical areas of neoplasms arising from the maxillary
area include the posterior wall of maxillary sinus, the infratem-
poral and pterygopalatine fossa, the hard palate, and the orbital
floor. The main goal of imaging is to assess the integrity of the
bony–periosteal barrier. It is well known that MRI is less accu-
rate than CT in the assessment of focal bone erosions, since its
calcium content cannot be adequately detected [57]. Neverthe-
less, it is also known that the most effective barrier to spread
Fig. 14. (a and b) Adenoid cystic carcinoma. Coronal TSE T2 image (a) shows a soft tissue submucosal mass arising from the medial wall of the right maxillary.
The lesion causes lateral displacement of the maxillary sinus mucosa (white arrows). Enhanced VIBE image (b) demonstrates solid enhancing tissue into the
pterygopalatine fossa (black arrow).
383
of aggressive lesions beyond sinusal walls is the periosteum
rather than the mineralized bony walls. Therefore, neoplastic
spread beyond the periosteum of the sinusal walls is, in effect,
the critical information for therapeutic planning because related
to extrasinusal infiltration.
The thin sinusal walls appear hypointense in every MRI
sequence because of the reduced water content of the cortical
bone and of the periosteum. The entire thickness of the wall can
be appreciated when invested by thickened mucosa or when the
air on one/both side(s) has been replaced by mucous secretions
or neoplastic tissue. Of course, the proper frequency encod-
ing direction has to be selected in order to avoid asymmetric
appearance of cortical bone due to chemical shift artefact.
Posterior spread into the pterygopalatine fossa is a relevant
element in the treatment planning. On MRI, neoplastic inva-
sion of the pterygopalatine fossa is suspected whenever its fat
content has been replaced/effaced by soft tissue intensity [58]
(Fig. 14). Pterygoid canal and nerve, foramen rotundum and
maxillary nerve are well demonstrated on axial and coronal MRI
sequences.
5.5. Imaging of perineural spread
Although the term “perineural spread” should be limited
to tumor spreading along the perineurium which envelopes
the nerve bundles, the term actually encompasses either neo-
plasms invading all compartments and their neural sheaths or
tumor involving single compartments, as the space between the
epineurium and the nerve bundles, or single sheaths—mainly
the perineurium.
Nerve enhancement and nerve enlargement are the signs more
predictive of the perineural spread.
The tumor growth induces an increased permeability of the
endoneurial capillaries and, eventually, causes breakage of the
perineurium. The rupture of the blood–nerve barrier allows leak-
384 R. Maroldi et al. / European Journal of Radiology 66 (2008) 372–386
Fig. 15. (a–d) Adenoid cystic carcinoma. The tumor, located at the level of
the right choana (T), reaches the sphenopalatine foramen. In (a and b) tumor
extends into the pterygopalatine fossa (white arrows) from which it spreads both
antegradely along the infraorbital nerve (opposite arrows) and retrogradely along
the maxillary nerve (arrowheads), reaching the Meckel cave V2 (black arrows).
In (c and d) enhanced VIBE images show perineural spread along mandibular
nerve (white arrow), greater superficial petrosal nerve (black arrows), greater
(GP) and lesser (LP) palatine nerves.
age and accumulation of iodinated or paramagnetic contrast
agents, therefore accounting for segmental nerve enhancement
on MRI (Fig. 15).
In detecting segmental nerve enhancement MRI has been
demonstrated to be more sensitive than CT [59]. Several MRI
techniques have been proposed, with or without fat-saturation.
The use of high-spatial resolution post-contrast fat saturation
VIBE (with isotropic voxel ranging from 0.5 to 0.7 mm) permits
a detailed evaluation of skull base foramina without artifacts. Its
spatial resolution enables to clearly image the normal nerve and
the surrounding vascular plexus [60].
Segmental nerve enhancement, however, is not unique to per-
ineural spread. It can be present in several non-neoplastic lesions
which result in blood–nerve barrier disruption, as inflammation,
ischemia, infarct, trauma, demyelination, and axonal degenera-
tion. These conditions may account for false positive MRI.
Moreover, for segments as the V2, V3, XII and inferior
alveolar nerves crossing foramina/canals one should expect the
“target” or “tram-track-like” enhancement patterns to be nor-
mally present, and not to be interpreted as abnormal findings
[61]. Conversely, if these enhancement patterns are demon-
strated in the labyrinthine and/or mastoid segments of the facial
nerve, breakage of the blood–nerve barrier should be suspected
[62].
Abnormal enhancement of the central nerve on “target” or
“tram-track-like” patterns without nerve enlargement has been
correlated to minimal burden of perineural spread [63].
Further growth of tumor cells along the nerve gives rise
to increased nerve diameter (Fig. 15), which can be directly
demonstrated on MRI, with or without abnormal nerve enhance-
ment. Direct detection of an enlarged nerve is possible on CT,
on condition that the nerve is mainly surrounded by fat (i.e.,
the infraorbital nerve). Indirect signs at CT are widening and,
eventually, erosion of bony fissures and foramina.
However, the enlarged nerve may recover its normal diam-
eter while it runs along a bony canal instead of remodeling or
erode its inner bone surface, skipping the tract. Once it exits the
opposite side, perineural spread regains a macroscopic size. This
“resurfacing phenomenon” is a mechanism of perineural exten-
sion which deserves particular attention on CT and MRI. It can
be observed with hard or soft palate tumors which “resurface”
into the PPF.
Retrograde (central) spread may lead the tumor to the
Meckel’s cave (through V2 or V3) and to the cavernous sinus.
Replacement of fluid signal in the Meckel’s cave by solid
enhancing tissue and bulging and enlargement of the cavernous
sinus indicate neoplastic invasion (Fig. 15).
If an intravascular paramagnetic contrast agent is used and
high-definition post-contrast GE sequences (VIBE) is acquired
with a delay of about 2 min, the tumor can be better separated
from the venous signal within the cavernous sinus.
Furthermore, when perineural spread leads to the damage of a
motor branch of a cranial nerve, MRI can detect the changes into
the denervated muscles during both the acute phase (hyperinten-
sity in T2 images and abnormal enhancement) and the chronic
phase (atrophy and fat replacement).
5.6. Follow-up
During follow-up, role of MRI is to detect asymptomatic
extra-mucosal disease. The interpretation of post-treatment
imaging studies may be quite challenging because of anatomical
and functional changes induced by treatment(s). These changes
greatly reduce the differences both in morphology and signal
features between the persistent/recurrent disease and adjacent
tissues. Tissue changes secondary to resection can be predicted
based on the surgical report. As craniofacial resection is the sur-
gical treatment of choice, a thorough knowledge of the normal
appearance after open or endoscopic or combined craniofa-
cial resection is necessary. Since these surgical approaches are
indicated because a portion of the skull base floor is invaded,
recurrences are more frequently expected at the boundaries of
the resection and reconstruction. Hence, a detailed evaluation of
 R. Maroldi et al. / European Journal of Radiology 66 (2008) 372–386
the meningo-galeal complex, which replaces the anterior skull
base floor, has to be obtained. Both coronal and sagittal T2 and
post-contrast non-fat-suppressed T1 images are indicated. Focal
thickness changes and lost of the “multiple-layer aspect” of the
meningo-galeal complex during the follow-up are clues suggest-
ing neoplastic recurrence. When a local or revascularized flap
is used after orbital or maxillary resection, the regularity of the
interface between the flap and adjacent tissues must be assessed.
Reactive mucosal changes resulting from radiation-therapy or
bone resection and subperiosteal dissection may result difficult
to separate from recurrent disease, especially during the early
post-treatment phase [64]. In the late phase, progression toward
mature scar is suggested by hypointensity on T2 and absence of
enhancement [65].
The difficulty to discriminate between post-treatment
changes and residual/recurrent disease accounts for the rising
interest towards more sophisticated ways to interrogate tissues.
Dynamic contrast-enhanced MRI exploits the vascularization
and permeability of the endothelium of neoplastic microvessels
[66]. Diffusion-weighted imaging studies the diffusion motion
of water protons in the tissues. With this technique, signal is
related to the freedom of water molecules to move within the
intercellular spaces, thereby permitting to distinguish highly
cellular tissues (tumor), where movement of water molecules
is restricted, from inflammatory changes [67]. PET/CT may
demonstrate the increased glucidic metabolism of neoplastic
tissues.
Though all promising, none of the above-mentioned tech-
niques is still part of standardized follow-up protocols and their
role is still far to be established.
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