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Malignant Neoplasms 165
– Is there any invasion of the pterygopalatine
fossa?
– Is there any perineural spread?
– Is there any invasion of the alveolar process
and/or of the hard palate?
– Is there any invasion of the lateral nasopharyn-
geal wall?
Involvement of the orbit and lacrimal pathways:
– Is the periorbita intact or transgressed?
– If the periorbita is transgressed, does the tumor
invade the anterior and/or posterior segment of
the orbital content?
– Are the superior orbital fi ssure and/or the optic
canal invaded?
– Are the lacrimal pathways invaded?
Involvement of the anterior skull base:
– Is the tumor in contact with the anterior skull
base fl oor? Where is the contact area located
(Ethmoid roof? Cribriform plate? Roof of the
sphenoid sinus? Postero-superior wall of the
frontal sinus?)
– Is there any bony erosion?
– Is dura transgressed?
– Is brain invaded?
Involvement of the middle cranial fossa:
– Is the tumor in contact with the middle cranial
fossa fl oor? Where is the contact area located?
(Roof of the infratemporal fossa? Root of the
pterygoid process? Lateral wall of the sphenoid
sinus?)
– Is there any bony erosion?
– Is dura transgressed?
– Is brain invaded?
– Is there any sign of perineural spread?
Involvement of the nasal septum, contralateral
extent, nasal bones.
Involvement of the anterior, inferior and posterior
wall of the sphenoid sinus, nasopharynx, and/or
clivus
Involvement of the frontal sinus:
– Is there any bone erosion of sinusal walls?
(Anterior? Superior? Posterior? Medial?)
9.1.7
Imaging Strategies. Key Findings
Sinonasal malignant neoplasms are generally imaged
by CT or MR in two different clinical situations. The
fi rst scenario includes patients with nasal symptoms,
thus arising the suspect of chronic rhinosinusitis,
but unresponsive to medical therapy, whereas the
second one consists in the request of assessing the
local extent of a tumor already detected by clinical
examination.
Because CT is considered the technique of choice
in the clinical workup of chronic rhinosinusitis, it will
be the fi rst imaging technique used to examine patients with nasal or sinusal masses mimicking symptoms of chronic rhinosinusitis or causing blockage of
one or more sinusal cavities. It is worth remembering
that the detection of a unilateral nasal obstruction
on CT (Barnes 1986; Woodruff and Vrabec 1994)
should prompt, even in the absence of bone remodeling or destruction, a diagnosis alternative to chronic
rhinosinusitis (i.e., the presence of a nasal mass). In
this setting, two different strategies are available to
the radiologist. The fi rst consists in the administration of iodinated contrast agent. Generally, a relevant
enhancement of the mucosa lining both the nasal
structures and the sinusal walls will be obtained,
whereas the secretions entrapped within a blocked
sinus will not change their density. Therefore, it will
be possible to separate retained secretions from the
mass - its degree of enhancement varying according to several elements, as histotype, infl ammation,
and necrosis. Conversely, the differentiation between
the mass and the enhanced mucosa lining the nasal
structures may be very diffi cult or impossible.
Because of this limitation in contrast resolution
of CT, the second strategy consists in submitting the
patient to MR. In fact, the discrimination of tumor
from adjacent nasal structures and retained secretions results more feasible by combining T2, plain
and enhanced T1 sequences.
A thorough delineation of tumor extent towards
sinonasal bony framework, orbit, intracranial content, cranial nerves, and vessels as well as detailed assessment of neoplastic involvement of structures and
spaces adjacent to the sinonasal tract is the second
step in the diagnostic work-up.
As local spread of nasal and paranasal neoplasms
depends on their site of origin, the imaging features
of the two main patterns of growth (i.e., maxillary
and naso-ethmoidal tumors) are considered in detail.
Because most maxillary sinus tumors are squamous cell carcinoma and most naso-ethmoidal tumors are adenocarcinoma, these two histotypes are
used to illustrate the pattern of spread of epithelial
neoplasms arising in these sites. Some peculiar aspects of the pattern of growth and signal/density
abnormalities of the adenoid cystic carcinoma and
non-epithelial tumors, as olfactory neuroblastoma,
lymphomas, and sarcomas will be discussed in detail.
166
R. Maroldi et al.
9.1.7.1
Imaging to Assess the Patterns of Growth of
Maxillary Sinus Neoplasms
Progressive growth of maxillary sinus malignant
neoplasms leads to extra-sinusal spread through the
invasion of one or more of its fi ve bony walls: medial,
anterior, postero-lateral, inferior (alveolar recess), and
roof (Fig. 9.2). According to the direction of tumor
growth, different implications regarding treatment
and prognosis will result.
Invasion of the medial wall is certainly the less
critical pathway of spread as it leads to intra-nasal
extent where the lesion has to grow further prior to
involve critical structures, usually via ethmoid sinus
invasion. Nonetheless, once the tumor reaches the
choana and spreads along its lateral surface, there is
the risk of nasopharyngeal wall invasion with pos-
Fig. 9.2a,b. Squamous cell carcinoma of left maxillary sinus. On post-contrast CT images the lesion shows slight heterogeneous
enhancement. On the axial plane (a) the tumor is shown to invade the anterior (white arrows), the postero-lateral (arrowheads),
and the medial sinusal walls. Invasion of the pterygopalatine fossa is present (black arrows). On the coronal plane (b) intraorbital invasion with involvement of the inferior rectus muscle is detected (arrowheads). Marked sclerosis of the alveolar process
(black arrows) suggests reactive changes or intramedullary spread
a b
Fig. 9.3a,b. Squamous cell carcinoma of left maxillary sinus. On post-contrast CT in the axial plane (a), extensive involvement of
the masticator space (black arrows) with a residual bone fragment of the pterygoid laminae (black arrowheads) is demonstrated.
In addition, tumor invades the left nasopharyngeal wall and the pre-styloid compartment of the parapharyngeal space (white
arrowheads). Invasion of the pterygoid process with both erosion and sclerotic changes is shown (black arrows) in the coronal
plane (b). The left pterygoid canal is not detectable. Downward extent is associated with remodeling and lateral displacement
of the lateral pterygoid lamina (white arrows)
ba
Malignant Neoplasms 167
sible involvement of the opening of the Eustachian
tube (Fig. 9.3)
Because in the area of posterior fontanellae (behind natural sinusal ostium) the medial wall is thin
and very often dehiscent, in some cases its neoplastic invasion can be suggested on CT by the extent of
the mass into the nasal cavity, rather than by bone
destruction. Conversely, invasion of the anterior portion of the medial wall may be directly demonstrated
by bone erosion, eventually extended to the horizontal portion of the uncinate process and to the inferior
concha. Particular attention has to be placed to the
lacrimal pathways because their involvement – like
the invasion of pre-antral soft tissues through the
anterior wall - contraindicates the surgical approach
with midfacial degloving.
Tumor extent toward the alveolar process and into
the hard palate should be evaluated by means of
coronal (or sagittal) images (Fig. 9.2b, 9.4). A critical
pathway of spread may be observed when the posterior portion of the alveolar process is invaded, as the
neoplasm may involve the buccinator muscle and/or
the maxillary tuberosity, from which it may access
the pterygomandibular raphe.
Certainly, the two most critical bony boundaries are the postero-lateral wall, a pathway to spread
into the masticator space and pterygopalatine fossa,
and the maxillary sinus roof – i.e., the orbital fl oor
– because its involvement leads to orbital invasion.
In both settings, the main goal of imaging is to as-
sess the integrity of the bony-periosteal barrier
(Fig. 9.2b, 9.4).
As most malignant maxillary sinus tumors are
squamous cell carcinomas, this histotype is used to
describe the expected MR signal intensity of neoplasms in this site. Because of its highly cellular
composition, squamous cell carcinoma has usually
homogeneous intermediate-to-low signal intensity
on T2 sequences and moderate-to-relevant enhancement after contrast agent administration (Som et al.
1989) (Fig. 9.5).
The fi rst step in the assessment of neoplastic extent is the evaluation of the relationship of maxillary
sinus tumor with the sinusal walls. The sinusal walls
contacting the neoplasm may present various signal
patterns on imaging studies, ranging from infl ammatory changes to abnormalities indicating neoplastic
invasion.
On CT, chronic infl ammatory abnormalities of the
bony walls may be either due to long standing mucus
drainage impairment or represent reactive changes
induced by tumor contact. They appear as asymmetric thickening of sinusal walls. On MR, both T2 and
T1 sequences show thicker hypointense sinusal walls,
even though focal areas of signal hyperintensity may
be observed (Maroldi et al. 1996) (Fig. 9.5b). The
presence of a double shape, due to a hypointense line
parallel to the outer surface of the wall, represents
periosteal thickening. Infl ammatory changes of the
sinusal mucosa are frequently associated. They usu-
Fig. 9.4a,b. Squamous cell carcinoma of left maxillary sinus, post-contrast coronal multislice CT (a) and VIBE (b). Both tech-
niques demonstrate the sub-periosteal and sub-mucosal spread of tumor, which is covered by residual mucosa both in the maxillary sinus (black arrows) and in the left nasal fossa fl oor. The precise extent of submucosal spread into the hard palate is clearly
defi ned by MR (short white arrows). Both CT and MR show invasion of the bony nasal septum (black arrowhead). Whereas on
CT the medial left maxillary sinus wall appears undetectable, as the mineralized component is reabsorbed, its residual bony
framework is still detectable on MR (white arrowheads). On CT, enlargement of the infraorbital foramen is shown (white arrow
on a). At this level, MR shows regular and smooth thickening of the periorbita (long white arrows on b)
ba
168
Fig. 9.5a,b. Squamous cell carcinoma of right maxillary sinus. a On TSE T2 the tumor (T) has heterogeneous hypointense inten-
sity signal, lower than fl uid and mucosa within the sinus. Apart for the invasion of pterygopalatine fossa and pterygoid process
(arrows), the path of neoplastic spread progresses posteriorly (b) with involvement of masticator space (white arrowheads)
where tumor abuts the mandibular nerve (black thick arrows). While part of the lesion is still confi ned by the posterolateral
wall (black arrowheads), invasion of the choana with spread into the lateral nasopharyngeal wall is present (white thick arrows).
Thickening of left maxillary sinus walls is particularly evident along the postero-lateral wall (white thin arrows), where focal
hyperintense areas are also present (black thin arrows)
R. Maroldi et al.
ba
ally appear as diffuse and lobulated thickening, hypodense on CT, homogeneously hyperintense on T2
sequences, hypointense on plain T1. After contrast
agent administration, the thin superfi cial mucosal
layer enhances – a fi nding more easily demonstrated
on MR – whereas the liquid content within the submucosa does not (Som et al. 1988).
Among the different patterns of bone changes
due maxillary sinus neoplasms, remodeling may be
observed, even though less frequently than cortical
destruction, permeative bone invasion with subperiosteal and submucosal spread (Fig. 9.4), which may
be more thoroughly mapped by MR (see Chapter 4).
9.1.7.1.1
Imaging Findings of Pterygopalatine Fossa, Root of
Pterygoid Process, and Cavernous Sinus Invasion
Fat tissue surrounding nerves and vessels inside fossae and fi ssures is a key point to assess neoplastic invasion, both on CT and MR. As an example of this, the
sphenopalatine artery is a useful landmark to early
detect neoplastic involvement of the pterygopalatine
fossa. The artery appears as a twisted signal void
surrounded by fat tissue on both T1 and TSE T2 se-
quences, easily detectable in all planes. After contrast
agent administration, it can be demonstrated as an
enhanced vessel on axial and coronal high resolution
CT or enhanced VIBE sequences. Neoplastic invasion
of the pterygopalatine fossa is suspected whenever
the fat tissue surrounding the vessel is replaced by
soft tissue density/intensity and/or the vessel is encased or not recognizable (Woodruff et al. 1986;
To mu r a et al. 1999) (Fig. 9.6).
Once the pterygopalatine fossa has been invaded,
the tumor may progress toward the adjacent pterygoid process of the sphenoid bone, and from this
structure further spread intracranially. On CT and
MR imaging, the pterygoid process is a key anatomic
structure to detail the actual extent of neoplastic tissue not only for its strategic position but also for its
complex architecture (Yu et al. 2000). In fact, both
its cortical and medullary bone components are traversed - or serve as fl oor - for canals (Vidian canal)
and grooves (foramen rotundum) along which run
nerves surrounded by tiny vessels and fat. When tumor invades the pterygoid process, cortical destruction, intra-medullary growth, and permeative invasion are patterns that may be observed, on occasion
simultaneously (Fig. 9.3b). Conversely, sclerosis of its
Malignant Neoplasms 169
a b
Fig. 9.6a,b. Adenoid cystic carcinoma of left (a) and right (b) maxillary sinus with pterygopalatine fossa invasion on enhanced
coronal T1 images. a Normal right pterygopalatine artery is indicated by white arrows. On left side fat surrounding the ptery-
gopalatine artery is replaced by solid tissue (short black arrows). Invasion of medial pterygoid plate is detectable (long black
arrows). b Tumor arises from right side, solid enhancing tumor tissue surrounds the pterygopalatine artery (black arrows). Short
white arrows indicate normal pterygopalatine artery on left side. Invasion of the superior orbital fi ssure with spread along the
sphenoid wing is demonstrated (long white arrows)
c d
Fig. 9.7a-d. Cavernous sinus invasion by adenoid cystic carcinoma arising from right maxillary sinus. a–d Coronal enhanced
T1 images (a–d) show tumor (T) invading (a) the pterygoid process and superior orbital fi ssure (black arrows) with perineural
spread along the maxillary nerve (V2). Perineural spread along vidian nerve is suggested by enlargement of the vidian canal fi lled
by enhancing tissue which surrounds a thin, hypointense, and probably compressed nerve (white arrow on b and c). Sclerotic
changes in the diploic bone of the right sphenoid are indicated by replacement of the normal fat content by hypointense signal.
The invaded right cavernous sinus appears enlarged, with a more convex lateral outline on b and c. Intracavernous tumor tissue
splays the third cranial nerve (III) from internal carotid artery (c). d Tumor reaches the Meckel cave (white arrow), whose walls
are thickened compared with the contralateral. Mandibular branch of trigeminal nerve (black arrows on c)
ba
170
R. Maroldi et al.
medullary bone component does not always indicate
neoplastic bone involvement, apart for adenoid cystic carcinoma and lymphoma (Yasumoto et al. 2000).
Once the osseous structure of the pterygoid process
is replaced by tumor, intracranial spread may occur
via the cavernous sinus (superiorly) or the foramen
lacerum (posteriorly).
The MR fi ndings of cavernous sinus invasion include enlargement and lateral bulging of the sinus
and replacement of the hyperintense venous signal
by the intermediate tumor tissue on either coronal
and axial T2 or enhanced T1 sequences (Laine et al.
1990). Neoplastic encasement of the internal carotid
artery at the cavernous sinus may be detected by MR,
either on TSE T2 or T1 sequences. Reliable signs of
vessel infi ltration include enhancement of the thickened vessel wall and encasement of the internal carotid artery greater than two thirds of its circumference (Komiyama 1990; Cottier et al. 2000)
In addition to bone penetration, maxillary tumor
extending into the pterygopalatine fossa may enter
the middle and posterior skull base via perineural
spread along maxillary and vidian nerves, respectively, or may directly invade the orbit via the superior orbital fi ssure (Maroldi et al. 1997).
CT and MR fi ndings indicating perineural spread
are discussed in detail in section 9.2.1
vide a direct route through middle skull base fl oor
via perineural spread or foramen ovale invasion.
Furthermore, the mandibular nerve - and foramen
ovale - serve as landmarks for separating the masticator space from the adjacent prestyloid compartment
of parapharyngeal space, the middle layer of the deep
cervical fascia – separating the two spaces - being not
detectable by imaging techniques.
The mandibular nerve may be identifi ed on CT
and MR axial planes starting at the foramen ovale
where it should be evaluated by mean of thin slices
(Marsot-Dupuch et al. 1990). At this level, it appears as a hypointense oval structure on TSE T2,
partially surrounded by enhanced signal on 0.5 mm
VIBE sequences, probably refl ecting the presence of
a perineural vascular plexus besides the accompanying accessory meningeal artery (Wi l li am s 1999).
After exiting the foramen, its separation into three
branches may be appreciated only on VIBE thin partitions, whereas standard TSE T2 and T1 usually permit detecting at least the inferior alveolar nerve, its
largest branch (Fig. 9.8). Along its course inferiorly
directed toward the opening of the mandibular canal,
the inferior alveolar nerve can be identifi ed running
medially both to the lateral (nerve’s superior tract)
and to the medial (nerve’s inferior tract) pterygoid
muscles.
9.1.7.1.2
Masticator Space Invasion
Neoplastic growth beyond the postero-lateral wall of
the maxillary sinus gives tumor access into the masticator space. Tumor invasion of this space may also be
caused by spread from the pterygopalatine fossa via
the pterygomaxillary fi ssure. Effacement of fat and
invasion of structures belonging to the space are the
fi ndings to be demonstrated by imaging. Important
anatomical landmarks are the pterygoid muscles, the
internal maxillary and middle meningeal arteries, the
mandibular nerve and the inferior alveolar nerve.
They are better visualized by MR than by CT (Paling
et al. 1987). Detection of normal signal intensity of
pterygoid muscles or of a residual fat layer surrounding the nerves helps to rule out neoplastic infi ltration
(Matzko et al. 1994; Curtin 1998) (Fig. 9.3, 9.5).
A combination of axial and coronal high resolution TSE T2 and enhanced T1 are recommended to
precisely demonstrate both normal structures and
subtle abnormal fi ndings within masticator space.
Particularly, one should carefully evaluate the relationship between tumor tissue invading the space
and the mandibular nerve, as the latter may pro-
9.1.7.2
Imaging to Assess the Pattern of Growth of
Naso-Ethmoidal Neoplasms
Neoplasms arising from ethmoid sinus or nasal cavity do not usually have a well defi ned bony box to
completely fi ll before extending through its walls
to become symptomatic, as in maxillary sinus neoplasms. Unilateral or bilateral nasal obstruction, possibly leading earlier to endoscopic or CT examination, is more frequently observed than in maxillary
tumors (Fig. 9.9). Therefore, imaging fi ndings may
range from the detection of a nasal polypoid lesion
to the demonstration of a large naso-ethmoidal mass
abutting the bony framework of a complex bony box
including in its boundaries the lamina papyracea,
the lacrimal pathways, the medial maxillary wall, the
nasal septum, and the anterior cranial fossa fl oor. In
addition, naso-ethmoidal tumors may extend into the
frontal sinus and involve nasal bones – anteriorly – or
into the sphenoid sinus – posteriorly. Less frequently,
the nasopharynx or the soft palate are invaded via
the choana.
More often than in maxillary sinus tumors, a
naso-ethmoidal neoplasm has already invaded the
Malignant Neoplasms 171
ba
c
e
Fig. 9.8a–f. Mandibular nerve demonstrated on 0.5 mm enhanced VIBE images. A–d Four different axial levels show the course and
some of the major branches of the mandibular nerve (V3). The left mandibular nerve (a) is imaged at the level of the foramen ovale,
the right immediately below, where three branches are detectable, probably accounting for medial pterygoid (1), temporomasseteric
(2), and middle deep temporal (3) nerves. Middle meningeal artery (MMA) b Two branches of the mandibular nerve are imaged on
left side, while on right side the morphology of the nerve changes to give off (c) a large anterior trunk (black arrowheads), more clearly
demonstrated on left side (black arrowheads on d), which is probably the lingual nerve. d Inferior alveolar nerve (IAN) is the largest
trunk of the nerve; it gives off other small branches (black arrows on d). Right pterygopalatine artery (white arrowheads on a–d). e
Coronal MPR shows the mandibular nerve (V3) surrounded by enhancing venous plexus. Meckel cave (arrowheads) and third cranial
nerve (III) within the cavernous sinus are shown. f The sagittal MPR shows part of the extracranial course of the mandibular nerve
(V3): lingual nerve (black arrow); inferior alveolar nerve (arrowheads); internal carotid artery (ICA); internal jugular vein (IJV)
d
f
Fig. 9.9. Adenocarcinoma of left nasal fossa. Coronal plane CT dem-
onstrates a soft tissue mass occupying the left nasal cavity. Erosion
of the perpendicular plate and lateral displacement of the medial
wall of the left maxillary sinus suggest the presence of a tumor
172
R. Maroldi et al.
contralateral nasal fossa and ethmoid at diagnosis
(Fig. 9.10).
Small lesions may be very diffi cult to demonstrate
with imaging techniques. Moreover, their precise site
of origin may become apparent only at surgery, particularly when the nasal fossa is completely fi lled by
tumor.
Regarding orbital invasion, recent evidence in the
medical literature supports a more conservative approach on condition that the periorbita is not invaded,
ab c
as in this occurrence the eye can be spared without
increasing local recurrences or survival and adequate
postoperative function can be maintained (Roux et
al. 1997; Imola and Schramm 2002). Therefore, the
fi rst priority of imaging consists in assessing the
integrity of the periorbita (Curtin and Rabinov
1998). In case of ambiguous fi ndings of orbital invasion on imaging studies, it will be necessary to clearly
inform the patient about the potential need of orbital
clearance, although only intra-operative mapping of
d
Fig. 9.10a–d. Adenocarcinoma of right ethmoid sinus. TSE
T2 (a), plain and enhanced T1 (b–c) images obtained in the
axial plane show a non homogeneous soft tissue mass which
has both focal and large areas of hyperintensity on TSE T2
(asterisk). The tumor projects into the right sphenoid sinus
(white arrow) causing sinus blockage. Dehydrated mucus has
intermediate signal on all sequences; it is separated from the
bony walls by thickened smooth mucosa. The adenocarcinoma
causes focal displacement of the medial wall of the right maxillary sinus (arrowheads). Nasal septum invasion with contralateral extent is better shown on enhanced T1 (black arrows).
On coronal plane (d) the tumor causes focal bulging of the
medial wall of right maxillary sinus (arrows). Cribriform plate
is normal, suggesting possible endonasal approach
Malignant Neoplasms 173
the orbital wall(s) - with gross examination and frozen sections - provides clear-cut information. In this
setting, it should be noticed that the negative predictive value of MR (Maroldi et al. 1996) is higher than
its positive predictive value, recently reported to be
about 80% by Eisen et al. (2000) (Fig. 9.11).
The second priority of imaging consists in assessing the relationship between the lesion and the
anterior cranial fossa fl oor. Findings provided by
CT and MR are relevant in predicting the need for
craniofacial resection. Coronal TSE T2 sequences
are indicated to assess the integrity of the hypointense interface between sinonasal and intracranial
structures, which corresponds to bone/periosteum
independently from the grade of bone mineralization (Fig. 9.12–9.16). Enhanced SE T1 on sagittal
and coronal planes are particularly useful to grade
intracranial extent (Fig. 9.17) , and to differentiate
between extra-dural and trans-dural invasion (El-
Beltagi et al. 2002; Ishida et al. 2002) (see chapter
4).
In evaluating the relationship between a naso-ethmoidal tumor mass and orbit/anterior cranial fossa
fl oor, one should consider that these structures are
mostly made by thin osseous layers, easily displaced
and remodeled, particularly the lamina papyracea
and the cribriform plate. However, displacement and
Fig. 9.11. Large adenocarcinoma arising from left ethmoid,
invading both nasal fossae and left maxillary sinus. On fat sat
coronal T2 marked displacement and remodeling of left lamina papyracea is shown. A residual hypointense, continuous,
interface separates tumor from orbital content indicating that
the lesion is confi ned by the periorbita (arrowheads)
ba
Fig. 9.12. a Schematic drawing of a naso-ethmoidal mass non-contacting the ethmoid roof. In this setting, if the histological type
does not contraindicate surgery, micro-endoscopic endonasal approach is feasible. b Adenocarcinoma (intestinal type) of right
ethmoid (T) separated from the ethmoid roof by a small mucocele (M), which causes focal remodeling of the planum sphenoidale (arrowheads). Olfactory tracts (long white arrows); fl uid retention within both posterior ethmoid sinuses (asterisks)
174
ba
Fig. 9.13. a Schematic drawing of a naso-ethmoidal mass contacting the ethmoid roof. In this setting, if the histological type does
not contraindicate surgery, micro-endoscopic endonasal approach is feasible. b Recurrent adenocarcinoma of right ethmoid
abutting the lamina cribrosa and the fovea ethmoidalis (black arrowheads), whose signal is normal. The tumor also abuts the
lamina papyracea (white arrowheads), not transgressed. A focal area of neoplastic involvement is seen in the inferior aspect
of the lamina papyracea (thin white arrows). A residual hypointense signal still separates tumor from intraorbital fat, possibly
consisting with non-invaded periorbita. Defi nitive intraoperative assessment is necessary
R. Maroldi et al.
b
a
c
Fig. 9.14a–c. a Schematic drawing of a naso-ethmoidal mass partially
eroding the ethmoid roof. In this setting, if the histological type does not
contraindicate surgery, micro-endoscopic endonasal approach is feasible.
Defi nitive intraoperative assessment is necessary. b Recurrent adenocarcinoma (intestinal type) of left ethmoid extended into the sphenoid sinus (T).
Focal thinning of the hypointense interface corresponding to the planum
sphenoidale (arrowheads) indicates partial erosion of bone by the tumor,
still confi ned by the bone/periosteal barrier. Olfactory tracts (white arrows).
The area included in the white box is magnifi ed on an enhanced T1 image
(c). The different signals of the bone/periosteal layer (short black arrows),
thickened dura (white short arrows), and CSF (arrowheads) are shown in
detail. When compared with TSE T2, the residual bone/periosteal layer appears thinner because it enhances. The dura overlying the focal bulging is
homogeneously thickened (white arrows) and has signal intensity slightly
lower than the underlying tumor and enhancing periosteum
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