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34
D. Tomenzoli
morphology. Further research into craniofacial form
and development needs to be done before the exact
role of the paranasal sinuses in humans can be defi nitively clarifi ed or established. It is encouraging
that the more recent studies have emphasized the
importance of differential sinuses (Takahashi 1984;
Blaney 1986). With the advent of new imaging techniques much accurate data about paranasal sinus size
and morphology can be collected and further differential growth studies performed.
References
Allison DJ, Powis DA (1971) Adrenal catecholamine secretion
during stimulation of the nasal mucous membrane in the
rabbit. J Physiol (Lond) 217:327-339
Angell JJ, Daly MB (1972) Refl ex respiratory and cardiovas-
cular effects of stimulation of receptors in the nose of the
dog. J Physiol (Lond) 220:673-696
Biggs NL, Blanton PL (1970) The role of paranasal sinuses
as weight reducers of the head determined by electromyography of postural neck muscles. J Biomech 3:255262
Blaney SPA (1986) An allometric study of the frontal sinus in
gorilla, pan and pongo. Folia Primatol 47:81-96
Blaney SPA (1990) Why paranasal sinuses? J Laryngol Otol
104:690-693.
Blanton PL, Biggs NL (1969) Eighteen hundred years of contro-
versy: the paranasal sinuses. Am J Anat 124:135-147
Braune W, Clasen FE (1877) Die Nebenhöhlen der Mensch-
lichen Nase in ihre Bedeutung für den Mechanismus des
Riechens. Z Anat Entwicklungsgesch 2:1-15
Cauna N (1970) Electron microscopy of the nasal vascular bed
and its nerve supply. Ann Otol 79:443-450
Cloquet H (1830) A system of human anatomy. Machlachlan
and Steward, Edinburgh
Cole P (1998) Physyology of the nose and paranasal sinuses.
Clin Rev Allergy Immunol 16:25-54
Dahl R, Migynd N (1998) Anatomy, physiology and function
of the nasal cavities in health and disease. Adv Drug Deliv
Rev 5:3-12
Eckel W (1963) Untersuchungen zur Grössenentwicklung der
Kieferhöhlen. Arch Ohren Nasen Kehlkopfheilkd 182:479484
Flottes L, Clerc P, Rui R et al (1960) La physiologie des sinus.
Libraire Arnette, Paris
Howell HP (1917) Voice production from the standpoint of the
laryngologist. Ann Otol Rhinol Laryngol 26:643-655
Ingelstedt S, Toremalm NG (1961) Air fl ow pattern and heat trans-
fer within the respiratory tract. Acta Physiol Scand 51:1-4
Laffort P, Patte F, Etcheto M (1974) Olfactory coding on the
basis of physiochemical properties. Ann NY Acad Sci
237:193-208
Muir DCF (1972) Clinical aspects of inhaled particles. Heine-
mann, London
Mygind N (1978) Nasal allergy. Blackwell Scientifi c, Oxford
Negus V (1958) The comparative anatomy and physiology of
the nose and paranasal sinuses. Livingstone, London
Nishihira S, McCaffrey TV (1987) Refl ex control of nasal blood
vessels. Otolaryngol Head Neck Surg 96:273-277
Paulsson B, Dolata J, Larsson I, Ohlin P, Lindberg S (2001) Para-
nasal sinus ventilation in healthy subjects and in patients
with sinus disease evaluated with the 133-xenon washout
technique. Ann Otol Rhinol Laryngol 110:667-674
Proetz AW (1953) Applied physiology of the nose, 2nd edn.
Annals Publishing, St Louis
Rice DH, Gluckman JL (1995) Physyology. In: Donald PJ,
Gluckman JL, Rice DH (eds) The sinuses. Raven Press, New
York, pp 49-56
Rui L (1960) Contribution a l’étude du role des sinus parana-
saux. Rev Laryngol Otol Rhinol (Bordeaux) 81:796-839
Skillen RH (1920) Accessory sinuses of the nose, 2nd edn. Lip-
pincott Company, Philadelphia
Takahashi R (1984) The formation of paranasal sinuses. Acta
Otolaryngol Suppl (Stockh) 408:1-28
Wright J (1914) A history of laryngology and rhinology, 2nd
edn. Lea and Febiger, New York
Neoplastic Invasion of Bone, the Orbit and Dural Layers: Basic and Advanced CT and MR Findings 35
4 Neoplastic Invasion of Bone, the Orbit and Dural
Layers: Basic and Advanced CT and MR Findings
CONTENTS
4.1 Introduction 35
4.2 Patterns of Bone Invasion on CT and MR 36
4.2.1 Bone Remodeling 36
4.2.2 Cortical Destruction 37
4.2.3 Intra-diploic/Medullary Growth 37
4.2.4 Permeative Invasion 37
4.2.5 Sclerosis 38
4.3 CT and MR Findings of Orbital Invasion 39
4.4 CT and MR Findings of Skull Base and
Dura Mater Invasion 42
References 46
Roberto Maroldi, Davide Farina, Giuseppe Battaglia
4.1
Introduction
In the sinonasal area several thick or thinner bony
laminae divide the nasal cavity and paranasal sinuses
from the orbit and the brain. These bone structures
act as a barrier against tumor spread.
Conventional radiology and CT obtained fi ndings
suggesting bone invasion upon changes of the normal appearance of these interfaces (Som and Shugar
1980; Som et al. 1991; Lloyd et al. 2000). However, the
single absence (lysis) of the mineral content of the
lamina papyracea per se does not correctly predict,
for example, orbital invasion at CT.
In fact, it is well known that the most effective barrier to the spread of neoplastic or infl ammatory aggressive lesions beyond sinusal walls is the per iosteum
rather than the mineralized bony wall (Kimmelman
and Korovin 1988). Therefore, neoplastic extent be-
R. Maroldi, MD
Professor, Department of Radiology, University of Brescia,
Piazzale Spedali Civili 1, Brescia, BS, 25123, Italy
D. Fa ri na , MD; G. Battaglia, MD
Department of Radiology, University of Brescia, Piazzale
Spedali Civili 1, Brescia, BS, 25123, Italy
yond the periosteum of the sinusal walls is critical for
therapeutic planning.
Nevertheless, the limitation of CT in assessing
the presence of a residual demineralized barrier
(the periosteum) does not necessarily apply to MR.
In fact, though the mineral content does not give
up signal on MR, the cortical bone – its periosteal
covering included – can be adequately demonstrated using high resolution matrix and thin voxels, because it appears as a homogeneous hypointense structure (Som et al. 1987) (Fig. 4.1).
This signal actually results from the sum of both
cortical bone and its investing thin fi brous periosteal
layers. It can be recognized on MR independently of
the degree of bone mineralization (Maroldi et al.
1996).
For all these reasons, the information provided
by imaging should not simply regard the state of the
mineralized wall, but it should be refocused on assessing the normality of the periosteum lining the
bony “box.”
In addition, the bony interfaces between the sinonasal cavities and brain have a more complex
structure, because the intracranial surface of these
bones is covered by a specialized connective layer:
the dura mater. Like the periosteum, this layer prevents intra-cranial invasion by neoplasms or aggressive infl ammatory lesions. The dura mater
differs from the periosteum because in most cases
it reacts in front of the advancing lesion by signifi cantly increasing its thickness and vascularization
(Eisen et al. 1996).
As a result, the assessment of the relationships
between tumor and the adjacent bony walls – lined
by periosteum or by the dura – will include basic
(regular vs. irregular demineralization) and more
advanced fi ndings (demonstration of the periosteum, changes of the dura mater layer).
As both focal invasion and the simple contact between tumor and the periosteum/dura mater layer
signifi cantly infl uence the treatment planning, the
meticulous assessment of these fi ndings is a relevant part of the imaging work up.
36
R. Maroldi et al.
a
Fig. 4.1a,b. Coronal CT and TSE T2 MR of right ethmoid inverted papilloma. Moderate lateral displacement and reabsorption
of the lamina papyracea (1) well detectable on MR image because of replacement of the air content within the ethmoid cells
by thickened mucosa and tumor. Thinning of the fovea ethmoidalis (2) is correctly shown by the two techniques. Laterally, the
orbital plate of the frontal bone (3) appears completely demineralized, its border undetectable. On MR, a thin hypointense line
suggests that the lesion is still confi ned by the periosteal/dural interface. Similarly, the thin lamella reaching the anterior ethmoid
canal (arrowhead) and part of the medial maxillary sinus wall (4) are better shown by MR. Middle left concha (5)
4.2
Patterns of Bone Invasion on CT and MR
b
the mineral content of the remodeled bone (Som and
Shugar 1980) (Fig. 4.2). Whereas demineralization
of thin cortical interfaces cannot be detected by MR,
In the sinonasal area, the bone framework is composed not only of thin laminae (as the lamina papyracea or the lamina cribrosa) but also of thick osseous
structures as the zygomatic bone or the pterygoid
process and the great wing of the sphenoid.
The interaction between thin laminae or thick
medullary bones and lesions with variable degrees
of aggressiveness results in four patterns of bone
changes.
wall displacement and integrity of the periosteum
may be demonstrated on condition that the wall does
not contact air on one of its surfaces (Maroldi et al.
1996) (Fig. 4.1).
Basically, in normal sinuses there are two differ-
ent physiological and anatomic conditions: air on one
side, fat/fl uid on the opposite one (lamina papyracea
and orbital fat, cribriform plate and CSF); air on both
sides (medial maxillary sinus wall).
In the fi rst condition, the displaced and deminer-
alized medial orbital wall or cribriform plate – with
4.2.1
Bone Remodeling
Bone remodeling consists of displacement and – usually – thinning of bony walls. In most cases, it is observed in tumors contacting very thin walls as cribriform plate, lamina papyracea, turbinates, and medial
maxillary sinus wall. Bone remodeling is a continuously occurring adaptive dynamic process involving
both osteoblasts and osteoclasts (Giacchi et al. 2001).
Activation of this process is triggered by mechanical
stress – exerted by expansile lesions – as well as by
chemical mediators – released in both infectious and
non-infectious infl ammatory conditions. Bone remodeling is a sort of balance between the activity of
osteoblasts and osteoclasts. As a result, thinning and
displacement of subtle bone structures may be observed mixed with sclerosis of thicker sinusal walls.
The high spatial and contrast resolution of CT en-
ables the detection of even subtle abnormalities in
Fig. 4.2. Bone remodeling of the posterolateral (black arrows),
anterior, and medial maxillary sinus wall in an inverted papilloma. White arrows point to demineralization of the inferior
concha.
Neoplastic Invasion of Bone, the Orbit and Dural Layers: Basic and Advanced CT and MR Findings 37
their periosteal layers – can be detected by MR as hypointense (absent) linear signals enclosed in a sort of
sandwich between the lesion (on one side) and the orbital fat and CSF (or dura and subarachnoid spaces),
respectively, on the other side (Ishida et al. 2002)
(Fig. 4.3). Of course, the proper frequency encoding
direction has to be selected in order to avoid asymmetric appearance of cortical bone due to chemical
shift artifact (Dick et al. 1988).
In the second condition, remodeling of the medial
maxillary sinus wall or of the sphenoid sinus fl oor
may be shown by MR if a suffi ciently thick mucosal
layer invests the opposite surface or retained secretions fi ll the sinus (Maroldi et al. 1996).
The bone remodeling pattern can be observed in
benign neoplasms and in some chronic infl ammatory
lesions as the mucocele and polyposis, less frequently
in malignant neoplasms.
plasms as inverted papilloma and juvenile angiofi broma and in malignant tumors (Som et al. 1991)
(Fig. 4.4).
Fig. 4.4. Squamous cell carcinoma of the left maxillary sinus.
Irregular destruction of the posterolateral wall (1). Tumor
spreads into the fat content of the infratemporal fossa and
inferior orbital fi ssure (2). Arrowheads indicate the extent
into the inferior limit of the superior orbital fi ssure. Sclerotic
changes of the alveolar process (3)
Fig. 4.3. Adenocarcinoma of the ethmoid, TSE T2 sequence.
Even if the lamina papyracea is laterally displaced, a continuous sharp hypointense interface separates the orbital fat from
the mass (black arrows), indicating absence of periorbital penetration. The horizontal (white arrow) and lateral (vertical)
cribriform plate are demonstrated because tumor and mucous
fi lling the frontal sinus contact the bone from below
4.2.2
Cortical Destruction
Cortical destruction is detected at CT as a break of
the mineralized bone through its whole thickness,
whereas on MR a defect of the continuous hypointense thickness of the cortex, replaced by solid tissue,
implies invasion also of the periosteum (Maroldi et
al. 1996). It can be observed in aggressive infl ammatory lesions (both non-invasive and invasive fungal
rhinosinusitis), some benign, but aggressive, neo-
4.2.3
Intra-diploic/Medullary Growth
Intra-diploic/medullary growth relates to the characteristic path of intra-osseous spread demonstrated
by malignant tumors and the juvenile angiofi broma
(Fig. 4.5). The density and signal of the spongiosa is
replaced by solid tissue characterized by trabecular
destruction on plain CT and fat replacement on MR
(Lloyd et al. 1999). This intra-osseous tissue usually enhances like the primitive tumor mass. For
instance, the typical high enhancement of juvenile
angiofi broma can be detected within the diploe
(Fig. 4.6).
4.2.4
Permeative Invasion
Permeative invasion with or without sclerosis is a peculiar pattern observed mostly in lymphomas and in
adenoid cystic carcinoma (Suei et al. 1994; Yasumoto
et al. 2000). In this pattern, the most relevant fi nding is
the extensive replacement of the medullary bone even
in the absence of evident cortical erosion.
38
R. Maroldi et al.
a
c
b
d
Fig. 4.5a–d. Recurrent myxosarcoma.
TSE T2 (a), plain CT (b), enhanced T1 (c),
and enhanced CT (d). Intraspongiotic
spread within the greater wing, pterygoid process, lateral sinus wall and fl oor
of the left sphenoid bone. Whereas plain
CT shows lysis of cortical and diploic
mineral content of the bone, TSE T2
demonstrates a hypointense interface
(1) still separating the tumor from the
subarachnoid spaces, indicating that the
lesion is confi ned to the dura. Neoplastic
erosion extends into the lateral portion
of the greater wing (opposite arrows).
Because of sclerotic changes, the medullary bone within the intersinusal sphenoid septum and the residual sphenoid
sinus fl oor is more hypointense on TSE
T2 and enhanced T1 (2) than the ad-
jacent pterygoid process (4). Residual
pterygoid canal content (3), internal
carotid artery (5), anterior clinoid with
cortical rim and medullary content
(target-like appearance) (6), maxillary
nerve (7)
Fig. 4.6. Persistent juvenile angiofi broma. In the GE Gd-enhanced coronal image, the persistent lesion replaces the medullary bone of the greater wing of the right sphenoid (white
arrows), and projects into the sphenoid sinus, the superior
orbital fi ssure, and into the choana (black arrows). Foramen
rotundum (FR), pterygoid (vidian) canal (VC)
In this setting, a very subtle moth-eaten appearance of the hypointense cortical/periosteal lining can
be detected only if proper CT and MR techniques
are used. This model of sub-periosteal spread can be
missed on plain and enhanced CT, particularly in adenoid cystic carcinomas, because only faint areas of
denser spongious bone may be present. Conversely,
MR is more sensitive because it combines the information provided by different sequences: on both T2
and plain T1, the fat tissue is replaced by hypointense
signal; moreover, non homogeneous areas of enhancement can be demonstrated after contrast application, more evident when the fat-sat technique is
applied (Fig. 4.7).
4.2.5
Sclerosis
Sclerosis is characterized on MR by the above-mentioned changes on T2 and plain T1 sequences, usually
without any contrast enhancement. Extensive sclerosis can be, of course, obvious on CT (Fig. 4.5). This
is a chronic infl ammatory reaction of the spongiosa
Neoplastic Invasion of Bone, the Orbit and Dural Layers: Basic and Advanced CT and MR Findings 39
a
c
e
b
d
f
Fig. 4.7a-f. MR and CT of subperiosteal bone invasion. Recurrent adenoid cystic carcinoma of the hard palate. MR sequences: TSE
T2 (a), Gd-enhanced VIBE (b), plain (c) and Gd-enhanced T1 (d). Bone window CT, plain study (e), enhanced CT (f). The anterior,
medial, and posterolateral walls of left maxillary sinus are invaded through subperiosteal spread. Apart from areas of focal erosion (1), subperiosteal spread results in rather subtle CT changes: diffuse demineralization of maxillary sinus walls, and minimal
soft tissue thickening along the external surfaces of the walls (2). Conversely, MR clearly shows tumor spread on both the inner
and outer surfaces of the sinus, leaving the residual walls (hypointense on all sequences) between two layers of neoplastic signal
(arrowheads in b). On TSE T2, subperiosteal spread presents as a plaque-like lesion with a multilayer appearance with a double
hypointense layer (neoplastic) investing both sides of the bony walls, the inner being covered by the mucosa (intermediate-tohyperintense signal layer). This pattern is clearly shown at the medial maxillary sinus wall (arrows), where the the diffuse bulging
of the mucosa on left side is due to subperiosteal/submucosal invasion. The plaque-like neoplastic layer, which is hypointense on
plain T1, enhances after Gd admministration on T1 and VIBE, similarly to the mucosa. Erosion and intramedullary invasion of the
left petrygoid process is also shown (3). Mandibular nerve (4). Extent into the left nasopharyngeal wall is shown (5)
present in a wide range of infl ammatory and neoplastic conditions (Chang et al. 1992).
carcinomas) or the medial wall (ethmoid adenocarcinomas). The other walls are less frequently involved by primitive tumors. In fact, it is more likely
to observe this path of orbital invasion by recurrent
neoplasms or metastases. Apart from the infrequent
4.3
CT and MR Findings of Orbital Invasion
event of perineural spread along the infraorbital
nerve, rarely tumors extend into the orbit through
the fi ssures or canals.
Most nasosinusal neoplasms invade the orbit
through the fl oor (maxillary sinus squamous cell
As both the medial wall and the orbital fl oor are
very thin, they are often displaced by tumors arising
40
Fig. 4.8. Adenocarcinoma of left ethmoid abutting the lamina
papyracea. Mild sclerotic changes combined with focal areas
of erosion are shown
in the adjacent sinuses (Fig. 4.8). Chronic pressure
exerted by the mass is usually associated with thinning and demineralization of the wall or erosion.
Surgical strategy is controversial in the presence of
erosion of the lamina papyracea. According to some
authors this condition indicates orbital exenteration
(Ketcham et al. 1973). Nevertheless, criteria defi ning
the indications for orbital preservation or exenteration have changed throughout the last three decades.
Recent evidence in the surgical literature supports a
conservative approach even in the presence of bone
erosion on condition that the periorbita is not invaded (Lund et al. 1998; Cantu et al. 2000). More re-
R. Maroldi et al.
cently, data provided by other investigators (Tiwari
et al. 2000 Imola and Schramm 2002; ) advocate
more advanced criteria for orbital preservation. An
additional distinct fascial layer surrounding the
periocular fat and separating it from the periorbita
has been reported by Tiwari et al. (1998). Invasion
of the fascia prevents orbital preservation. In the series by Imola and Schramm (2002), full thickness
periorbital invasion was treated by microscopically
assisted dissection, enabling even limited removal of
the orbital fat.
Thus, imaging the periorbita is crucial for CT
and MR. Prediction of orbital invasion has been
based on the detection of positive findings graded
through progressive steps: tumor contacting the
periorbita (sensitivity of CT and MR 90%); fat
obliteration (positive predictive value: CT 86%,
MR 80%); extraocular muscle involvement (positive predictive value of MR 100%) (Eisen et al.
2000). Overall, CT proved to be more accurate
than MR. By comparison, in our series of 49 sinonasal malignancies the absence of orbital invasion has been correctly predicted in 40 orbits with
tumor contacting the wall more than 10 mm of
length (negative predictive value of CT 75%, MR
100%) (Maroldi et al. 1996, 1997). Detection of
a hypointense/absent linear signal indicating the
periorbita was the more specific predictor with
overall accuracy of MR significantly better than
CT (95.4% vs 81%) (Fig. 4.9–4.13).
a
Fig. 4.9a-c. Squamous cell carcinoma of left maxillary sinus. On coronal TSE T2 (a) and VIBE (b), upward displacement of the
orbital fl oor by the tumor is observed. A hypointense interface between the mass and the orbital fat can be recognized (long
arrows). Tumor invades the middle meatus (short arrows) blocking the anterior ethmoid. Hypointense fl uid (high protein con-
centration) within the ethmoid bulla (asterisk). On sagittal GD-enhanced T1 (c) a hypointense interface cannot be demonstrated,
only the sharp limits suggest that the lesion is limited by the periorbita
b
c
Neoplastic Invasion of Bone, the Orbit and Dural Layers: Basic and Advanced CT and MR Findings 41
a
Fig. 4.10a-d. Spindle cell naso-ethmoid carcinoma. The hypointensity of the lamina papyracea/periorbita can be appreciated
only in its anterior third (black arrowheads). In the posterior two thirds of the medial orbital wall, neoplastic spread through
the lamina papyracea/periorbita (black arrows) appears as several short solid fi nger-like projections into the orbital fat. An
ethmoid cell wall – same thickness of the papyracea – can be adequately detected by MR (white arrowheads). Invasion of the
right nasal bone (white long arrow). In the same patient as (a), TSE T2 (b), Gd-enhanced T1 (c) and VIBE (c) coronal planes
show invasion of the medial orbital wall with solid - and enhancing - tissue (arrowheads) replacing the orbital fat medially to
the rectus inferior muscle (1). Invasion of the lateral orbital fl oor (small white arrows on b and opposite arrows on c) is also
present. The signal void of the infraaorbital artery is surrounded by tumor (2). Ophthalmic artery (3), minimal dural thickening at the fovea ethmoidalis (4)
b d
c
Fig. 4.11. Adenocarcinoma of right ethmoid sinus invading the
orbit (arrows) through the erosion of the lamina papyracea and
lacrimal bone. NLD, nasolacrimal duct
a
Fig. 4.12a–c. Sinonasal non-Hodgkin lymphoma. Permeative pattern of invasion through the lamina papyracea (black arrows)
and extent into the maxillary sinus along the bony walls (white arrows). The horizontal and lateral (vertical) lamella of the
cribriform plate are well demonstrated on TSE T2 [short black arrow on (a)]. Focal dural enhancement is appreciated on (b) at
the level of the orbital plate of the frontal bone (white arrow). Lacrimal sac dilatation (asterisk)
b
c
42
R. Maroldi et al.
Fig. 4.13a,b. Squamous cell carcinoma
of left nasal cavity with extensive orbital infi ltration. Invasion through the
bony/periosteal hypointense interface
of the fovea ethmoidalis (1) with minimal enhancement of the dural layer.
Residual vertical lamella of the middle
torbinate (2)
a
b
Although preoperative imaging may aid in surgical planning, in ambiguous cases of orbital invasion the intra-operative mapping of the orbital
wall, with gross examination or frozen sections, is
necessary.
Orbital invasion is considered a negative prognostic factor, even though some authors specify that decrease in survival may refl ect the wider extension of
lesions invading the orbit (Shah et al. 1997).
4.4
CT and MR Findings of Skull Base and Dura
Mater Invasion
Assessment of the deep extent of sinonasal tumors
toward the dural layer is one of the issues that signifi cantly infl uence the treatment planning.
Like in the invasion of orbital walls, bone destruction of the skull base is better demonstrated
by CT. However, here the imaging fi ndings differ
from those observed in the other bone interfaces
of the sinonasal area because when the skull base
is invaded, the dura mater usually shows abnormal
thickening and enhancement that can be due either
to neoplastic invasion or to infl ammatory, non-neoplastic reaction.
Since dural invasion implies both a worse prognosis and a surgical resection not limited to the
eroded bone, the goals of imaging focus on establishing the depth of skull base invasion (Kraus et
al. 1992b; Shah et al. 1997).
MR has been reported to be more precise than
CT. Early observations emphasized the usefulness
of T2 (and T1 sequences) in separating the low signal of bone from the high signal of CSF (Fig. 4.14).
Thickening and enhancement of the dura mater
invaded by tumor were mentioned by Weissman
and Curtin (1994). Other investigators reported
that enhanced MR sequences could demonstrate
leptomeningeal invasion (Volle et al. 1989; Kraus
et al. 1992a). Moreover, in the series by Ishida et
Fig. 4.14. Naso-ethmoidal adenocarcinoma, intestinal-type,
TSE T2. Upward displacement of the right fovea ethmoidalis
(1) due to a small mucocele underneath (showing hyperintense signal) secondary to tumor (that shows homogeneous
intermediate intensity). The tumor abuts the right medial orbital wall, remodeled, but not invaded (2). Because of fl uid
retention within the contralateral posterior ethmoid cells, the
papyracea/periorbita is well demonstrated (3). Opposite ar-
rows point to the right residual vertical lamella of the middle
concha. Olfactory tract (4)
Neoplastic Invasion of Bone, the Orbit and Dural Layers: Basic and Advanced CT and MR Findings 43
al. (2002), as well as in our own, specifi c changes
in the appearance of the hypointense/absent signal
of bone and the overlying dura proved to correctly
predict dural invasion.
A key diagnostic observation concerns the signal intensity of the three structures located at the
interface between the ethmoid roof and brain at
the anterior cranial fossa: cribriform plate and its
double periosteal covering, dura mater, subarachnoid space.
On enhanced sagittal and coronal MR spin echo
T1 or 3D GE fat sat T1 sequences the three layers
give rise to a “sandwich” of different signals (boneperiosteum complex, dura, CSF) (Ishida et al.
2002).
If a malignant sinonasal neoplasm approaches
the ACF fl oor, three different conditions may occur: (a) the neoplasm appears in close contact with
an uninterrupted, hypointense cribriform plate
or fovea ethmoidalis (Fig. 4.15); (b) the neoplasm
erases the hypointensity of the cribriform plate, extends into the ACF and displaces an uninterrupted,
hyperintense and thickened dura (Fig. 4.16); (c)
the neoplasm encroaches the dural hyperintensity without erasing the hypointense signal of CSF
(Fig. 4.17, 4.18); (d) the neoplasm extends beyond
the dura encroaching the hypointense CSF and invades brain tissue (Fig. 4.19).
This last sign is easier to detect if the signal intensity of the neoplasm is lower than the enhanced
dura surrounding the invaded segment (Maroldi
et al. 1997).
Resectability of tumors invading the brain does
not stand only upon the assessment by imaging of
the depth of tumor extent into the brain or on the
detection of bilateral brain invasion. It requires a
thorough evaluation of several other issues, the
most important being the histotype and patient’s
performance status. Patients with limited brain
invasion treated by craniofacial resection are reported to have non-signifi cant decrease in survival
compared to those with dural invasion only.
Contraindications to surgery other than brain
invasion are considered to be the involvement of
the internal carotid artery or of the cavernous sinus
(Shah et al. 1997) (Fig. 4.20)
a b
Fig. 4.15a,b. Ethmoidal adenocarcinoma, intestinal-type, plain (a) and Gd-enhanced T1 (b). The black signal of the planum eth-
moidalis/fovea is continuous and regular [opposite white arrows on (a)]. Mild and uniform enhancement of the dura is detected
after Gd administration [white arrows on (b)]. Invasion of medial wall and part of the fl oor of the orbit (black arrows)
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