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Anatomy and Diseases of the Greater
Wings of the Sphenoid Bone
Renata Cochinski, MD
Mohit Agarwal, MD
Jessica Albuquerque, MD
Carolina A. de Almeida, MD
Rafaela P. Stricker, MD
Marcela F. Uberti, MSc
Ana Paula K. Casqueiro, MD
Gabriel S. Mendonça, MD
Galba R. S. do Nascimento, MD
Fernanda Miraldi, MSc
Marcos Decnop, MD
Abbreviations: GWS = greater wings of
the sphenoid bone, WHO = World Health
Organization
RadioGraphics 2022; 42:1177–1195
https://doi.org/10.1148/rg.210094
Content Codes:
From the Department of Radiology, Instituto
Nacional de Câncer (INCA), Praça Cruz Ver-
melha 23, Rio de Janeiro, RJ, Brazil 20230-130
(R.C., J.A., C.A.d.A., R.P.S., M.F.U., A.P.K.C.,
G.S.M., G.R.S.d.N., F.M., M.D.); and De-
partment of Radiology, Medical College of
Wisconsin, Milwaukee, Wis (M.A.). Presented
as an education exhibit at the 2020 RSNA An-
nual Meeting. Received March 29, 2021; revi-
sion requested July 22 and received September
28; accepted October 5. For this journal-based
SA-CME activity, the authors, editor, and re-
viewers have disclosed no relevant relationships.
Address correspondence to R.C. (e-mail:
renatacochinski@gmail.com).
©
RSNA, 2022
SA-CME LEARNING OBJECTIVES
After completing this journal-based SA-CME
activity, participants will be able to:
Identify the anatomy of the sphenoid
„ especially in relation to the skull base foramina and the neurovascular
bone and its greater wings.
Characterize the main imaging aspects
„ able. In this article, we describe a systematic approach to understand-
of GWS lesions.
List conditions that should be included
„
in the differential diagnosis of lesions in
the GWS.
See rsna.org/learning-center-rg.
1177
NEURORADIOLOGY
The greater wings of the sphenoid bone (GWS) comprise the com-
ponents of the sphenoid bone that make up most of the posterior
orbital wall and form the anterior and medial parts of the floor
of the middle cranial fossa. Many important skull base foramina,
which transmit vital neurovascular structures, are present in these
paired wings on either side of the central body of the sphenoid
bone. A wide variety of diseases can affect the GWS, ranging from
benign osseus lesions to malignant primary and secondary bone ab-
normalities. The complex three-dimensional curved (winged) shape
of the GWS and the wide array of pathologic entities that affect this
bone can make it challenging for the radiologist to report the imag-
ing findings accurately, especially in relation to the important skull
base foramina. The authors describe a systematic approach to un-
derstanding the three-dimensional anatomy of the GWS and review
important diseases, with the aid of imaging examples. Useful imag-
ing “pearls” that can help in making specific diagnoses are provided
throughout the article.
©
RSNA, 2022 • radiographics.rsna.org
Introduction
The greater wings of the sphenoid bone (GWS) are the components of
the sphenoid bone that project laterally from the central body and
form the anterior and medial portions of the floor of the middle
cranial fossa. Many skull base foramina in the GWS transit important
neurovascular structures.
As an osseous structure, the GWS can be affected by numerous be-
nign and malignant primary or secondary bone lesions. Several nonos-
seous diseases can also affect the GWS, either through direct involve-
ment (such as from an adjacent schwannoma) or through contiguous
extension (such as from perineural spread from a cancer of the head
or neck). For accurate reporting of abnormalities affecting the GWS,
structures, an understanding of the anatomy of the GWS is indispens-
ing the anatomy and pathologic conditions of the GWS.
Anatomy and Embryology of the Sphenoid Bone
The skull base has an intricate anatomy that is not directly accessible
to clinical evaluation and is composed of five bones: the ethmoid,
frontal, sphenoid, temporal, and occipital bones.
The central portion of the skull base, which is posterior to the
frontal and ethmoid bones and anterior to the occipital and tempo-
ral bones, is formed by the sphenoid bone. The term sphenoid is de-
rived from the Greek sphenoeides (ie, wedge-shaped). The sphenoid
bone mainly comprises a central body and a pair of large lateral
triangular wings that are arranged in a way that resembles the shape
of a butterfly (1,2). It also has two smaller anterolateral wings and two
anteroinferior pterygoid processes (Figs 1–4).
1178  July-August 2022 radiographics.rsna.org
TEACHING POINTS
„ The greater wings of the sphenoid bone (GWS) are the com-
ponents of the sphenoid bone that project laterally from the
central body and form the anterior and medial portions of the
floor of the middle cranial fossa. Many skull base foramina in
the GWS transit important neurovascular structures.
„ Although cortical involvement associated with an extraosse-
ous soft-tissue component is highly suspicious for malignancy,
there are some benign exceptions such as spheno-orbital me-
ningiomas and eosinophilic granulomas.
„ CT is the best imaging tool for characterizing the typical os-
seous changes of spheno-orbital meningiomas and helping
to discern them from other hyperostotic conditions (mainly
fibrous dysplasia). Although more than one pattern of hyper-
ostosis may be found in this subgroup of meningiomas, the
periosteal pattern is the most typical and useful because it is
not expected in fibrous dysplasia, which does not induce peri-
osteal new bone formation. Surface irregularity of the hyper-
ostotic bone is also characteristic of meningiomas.
„ Some imaging features of metastases to the GWS may be
related to the primary site of the tumor. Osteoblastic lesions
are typically described in patients with breast and prostate
cancers, sometimes mimicking benign sclerotic entities such
as meningiomas and Paget disease. When a single and ex-
pansive (“blowout”) lesion is found, renal cell and thyroid car-
cinomas should be suspected. However, this pattern may also
be present in patients with other primary malignancies, such
as breast and lung cancers.
„ The proximity of the GWS to vital structures such as the
cavernous sinus and its intimate relationship with the skull
base foramina and the nerves and vessels it contains make
it important for radiologists to have a mental checklist of im-
aging findings for which to search and on which to report.
Involvement of the nerves in the lateral wall of the cavernous
sinus and encasement of the cavernous internal carotid artery
are features that can alter the surgical approach or affect plan-
ning for radiation therapy. Also, involvement of the skull base
foramina can lead to anterograde or retrograde spread of the
tumors and has the potential to change patient care. Such
features also help in determining the prognosis for patients
with these lesions.
The central body contains the sphenoid sinus
and has a superior component known as the sella
turcica, which contains an open cavity that houses
the pituitary gland. The body of the sphenoid bone
also forms the medial aspect of the optic canal,
through which the optic nerve and the ophthal-
mic artery traverse (3,4). Laterally, the vidian (ie,
pterygoid) canal can be found along the line of
fusion of the pterygoid process and the body of
the sphenoid bone, allowing passage to the vidian
nerve and artery (5). The lesser wings partially
separate the anterior cranial fossa from the middle
cranial fossa and form the other border of the op-
tic canal. The greater wings are lateral projections
from the sphenoid body that make up most of the
posterior wall of the orbits and the anterior and
medial aspects of the floor of the middle cranial
fossa (1,6). The cleft between the lesser and the
greater wings is the superior orbital fissure, which
transmits the nerves for extraocular muscle move-
ment (cranial nerves III, IV, and VI), the ophthal-
mic division of the trigeminal nerve (V1), and the
superior ophthalmic vein (4).
Several other foramina are seen in the GWS
(Table 1). The most medial of these and the
closest to the sphenoid body is the foramen
rotundum, which transmits the maxillary division
of the trigeminal nerve (V2) from the cavern-
ous sinus to the pterygopalatine fossa. Accessory
variant openings that are found in 6%–16% of
individuals can sometimes be seen connecting
this foramen to the infratemporal fossa and are
presumed to contain emissary veins (3).
A relatively wide posteromedial opening of the
GWS that serves as a communication between the
middle cranial fossa and the infratemporal fossa
is an oval foramen aptly known as the foramen
ovale, which allows passage to the mandibular
division of the trigeminal nerve (V3) and the ac-
cessory meningeal artery (1,6). Anatomic varia-
tions in the shape (eg, round vs oval) or size of the
foramen ovale are commonly found. A posterolat-
eral groove for the accessory meningeal artery is
sometimes present. In rare cases, the medial wall
of the foramen ovale is absent, allowing its com-
munication with the sphenopetrosal fissure and
confluence with an adjacent foramen (eg, sphe-
noidal emissary foramen or foramen spinosum).
Anteromedial to the foramen ovale is the sphe-
noid emissary foramen or the foramen of Vesalius,
which transmits an emissary vein connecting the
cavernous sinus to the pterygoid venous plexus
(Fig 5). The most common variants of this fora-
men are asymmetry (unilateral), duplication, and
confluence with the foramen ovale (3).
Posterolateral to the foramen ovale is a small
rounded foramen, the foramen spinosum,
through which the meningeal branch of the
mandibular nerve (ie, nervus spinosus) and the
middle meningeal artery and vein traverse. When
the foramen spinosum is absent, a variation that
occurs unilaterally in 0.4%–1% of cases, the
middle meningeal artery originates directly from
a persistent stapedial artery (Fig 6) (7).
A small canal called canaliculus innominatus is
inconsistently present and is located between the
foramen ovale and the foramen spinosum, allow-
ing passage to some facial nerve fibers and the
small superficial (or lesser) petrosal nerve, which is
derived from the glossopharyngeal nerve (3).
The anatomic complexity of the sphenoid bone
results from the union of embryologically distinct
structures. The cephalic mesoderm forms the ba-
sipostsphenoids and the orbitosphenoids. The ba-
sipresphenoids originate from the neural crest cells,
as do the alisphenoids (the ossification centers that
are the precursors of the GWS) (1,3) (Fig 7).
RG  •  Volume 42  Number 4 Cochinski et al  1179

Figures 1–4.  The anatomy of the greater wings of the sphenoid bone (GWS). Illustrations show the anterior (1A, 1B), posterior (2A,
2B), superior (3A, 3B), and inferior (4A, 4B) views of the sphenoid bone, with the GWS in oil blue.

Because of its large size, polymorphic shape,
and central location, the sphenoid bone articu-
lates with several bones (eg, frontal, parietal, eth-
moid, zygomatic, temporal, occipital, palatal, and
vomer bones) by fibrous joints known as sutures.
Its relationship with the ethmoid and frontal
bones provides rigidity and stability to the skull,
thus contributing to protecting the brain.
General Approach to Imaging Lesions
of the GWS
The benign and malignant lesions affecting the
GWS can be intrinsic or extrinsic in origin. A few
general features can help in differentiating the
origin of the lesion (Table 2).
Radiologically, primary lesions of the GWS
(and bones in general) are classified on the basis
1180  July-August 2022 radiographics.rsna.org

Table 1: Main Foramina Found in the GWS and Anatomic Variations

Vessels Passing
Foramen Through Nerves Passing Through Anatomic Variations
Rotundum Artery of the fora- Maxillary division of the Accessory variant openings
men rotundum trigeminal nerve (V2) Asymmetry in size
and emissary vein Lateral or inferior
Ovale Accessory menin- Mandibular division of the Asymmetry in size or shape
geal artery trigeminal nerve (V3) Abnormal location
Sphenoid emissary Lesser petrosal nerve (if Confluence with the foramen spinosum or
vein canaliculus innomina- Vesalius
tum is absent) Absence
Spinosum Middle meningeal Meningeal branch of V3 Confluence with the foramen ovale
artery and vein Duplication
Absence
Vesalius Emissary vein None Asymmetry
Duplication
Confluence with the foramen ovale
Absence
Canaliculus None Lesser petrosal nerve Presence
 innominatum Facial nerve fibers
Vidian canal (me- Vidian artery Vidian nerve Variable relation to sphenoid sinus
dial to GWS)

of their biologic behavior. This can be ascertained

by distinguishing imaging features that suggest
aggressive (usually malignant) or nonaggressive
(usually benign) behavior, such as (a) the zone of
transition between a lesion and the adjacent bone,
(b) the pattern of periosteal reaction, (c) cortical
integrity, and (d) the presence of an associated
soft-tissue component. The last of these is best
evaluated with MRI, but CT is the best modality
to assess the osseous characteristics of the lesion.
The zone of transition represents the change
from pathologic to normal bone, thus defining
the sharpness of the margin of the lesion. Clas-
sically shown on radiographs, this feature can be
used to determinate the aggressiveness of intra- Figure 5.  Axial CT image (bone window) shows the
foramen spinosum (arrowhead), foramen ovale (*), and
medullary diseases (8). Aggressive lesions have a sphenoidal emissary foramen (Vesalius) (arrow).
broad zone of transition, whereas a narrow transi-
tion zone, often with sclerotic borders, suggests a
benign nature (9). both expanded and sclerotic. When the GWS is
An aggressive medullary lesion that grows rap- hyperostotic, some benign conditions should be
idly without allowing enough time for periosteal considered in the differential diagnosis, such as
osteogenesis to occur results in cortical destruc- fibrous dysplasia, meningiomas, and Paget dis-
tion. However, some osteogenic tissue can be ease. Distinct patterns of hyperostosis have been
produced if the tumor grows slowly, causing the described and may in fact coexist: periosteal,
bone to progressively expand, with cortical in- three-layer, diploic, and homogeneous patterns.
volvement being absent or featured subsequently Extrinsic lesions can also affect the GWS in
(10). Although cortical involvement associated different patterns, depending on how aggres-
with an extraosseous soft-tissue component is sive they are. Benign tumors have a tendency to
highly suspicious for malignancy, there are some cause remodeling of the adjacent bone, whereas
benign exceptions such as spheno-orbital menin- malignancies usually cause osseous destruction.
giomas and eosinophilic granulomas. (11,12). It Exceptions include juvenile angiofibroma and
is also important to define the term hyperostosis, skull base infections, which tend to be destructive
which is generally used to describe the bone, and infiltrating, respectively.
RG  •  Volume 42  Number 4 Cochinski et al  1181
Developmental and Anatomic Variants
Pneumatization of the Lateral Recess
The pneumatization process of the paranasal
sinuses is variable (13). The sphenoid sinus, one
of the most variable, is a small cavity at birth,
and mostly develops after puberty. In addi-
tion to being the least accessible sinus, its close
relationship with vital neurovascular structures
such as the optic nerve and the internal carotid
artery poses a challenge for endoscopic surgery
(14). Anatomic variations of the pneumatization
Figure 6.  Illustration shows the su-
perior view of the central skull base
and the GWS (oil blue) and its fo-
ramina, with important nerves and
arteries.
Figure 7.  Illustration shows the ossification
centers of the central skull base with the alisphe-
noids, which are precursors of the GWS, in oil
blue.
process can range from minimal to consider-
able (15), as it can extend to the lesser wings,
and laterally into the GWS, the pneumatized
lateral recess (13). In these cases, the sphenoid
sinus projects laterally beyond an imaginary line
connecting the foramen rotundum to the vidian
canal (Fig 8).
Arrested Pneumatization
During normal development, there is a progres-
sive replacement of the red bone marrow with
adipose tissue. Studies indicate that bones that
1182  July-August 2022 radiographics.rsna.org

Table 2: How to Discern Each Group of Lesions Affecting the GWS

Type of Lesion Intrinsic Origin Extrinsic Origin

Benign Intraosseous lesion with well-defined, often sclerotic Extraosseous lesion causing bone
margins* and a small or no zone of transition remodeling†
May show bone expansion
Malignant Intraosseous lesion with ill-defined borders Extraosseous lesion causing bone de-
May show cortical breakthrough and a soft-tissue struction, moth-eaten appearance
component, wide zone of transition
* Exception: eosinophilic granuloma.
†
Exceptions: skull base osteomyelitis, fungal infection, and juvenile angiofibroma.

go through the process of pneumatization show

fat substitution at an earlier stage of develop-
ment than bones in which pneumatization does
not occur. Thus, if this process is not completed,
and bone atypically contains yellow marrow into
adulthood, this phenomenon is described as
arrested pneumatization (16,17). Typically found
in the sphenoid bone as an incidental radiologic
finding, it is not a true lesion but, in fact, a benign
developmental variation. However, to be diag- Figure 8.  Lateral recess pneumatization in a 32-year-old
nosed as such, four specific criteria must be met: woman. Coronal CT image (bone window) shows lateral recess
(a) location in a place of normal (or of recognized pneumatization (*) beyond the limits of an imaginary plane con-
accessory) pneumatization, (b) fatty content, necting the round foramen to the pterygoid canal (dotted line).
(c) no mass effect, and (d) normal appearance
of the associated skull base foramina. On CT
images, the area should also have sclerotic and
well-circumscribed margins and internal curvi-
linear calcifications (Fig 9); on MR images, these
pseudolesions do not enhance with intravenous
contrast media (16–18).

Benign Lesions

Intrinsic Benign Lesions Figure 9.  Arrested pneumatization in a 53-year-old woman.

Fibrous Dysplasia.—Skull base and facial bones
are commonly affected by fibrous dysplasia and
are the second most common site of involve-
ment in the body. Craniofacial fibrous dyspla-
sia accounts for approximately 25% of cases
(19,20). Fibrous dysplasia is a congenital (not
hereditary) condition that may involve a single
(monostotic form) or more than one (polyos-
totic form) bone.
Histopathologically, there is replacement of
normal marrow and cancellous bone by an ex-
tensive fibrocellular matrix with scattered small
irregular trabeculae of immature osseous tissue
(19). As a result, fibrous dysplasia typically ap-
pears on CT images as an expanded medullary
bone with ground-glass opacity, causing endos-
teal scalloping and cortical thinning. Depending
on the proportion of the osseous and fibrous
components and the presence or absence of
Coronal CT image (bone window) shows a nonexpansile in-
traosseous area, with fatty content and internal curvilinear cal-
cifications, extending from the body to the left GWS (arrows).
hemorrhage and/or cystic degeneration, there
are three different patterns of fibrous dyspla-
sia that have been described: homogeneously
sclerotic (typically showing diffuse ground-glass
opacity), lytic (or predominantly lytic), and
mixed (ie, basipostsphenoid) fibrous dysplasia
(Fig 10) (Table 3) (21,22).
Although classic low signal intensity from the
osseous components is seen at MRI, this is not
always present and the appearance is commonly
confusing, especially at T1-weighted gadolin-
ium-enhanced MRI, with heterogeneous and
avid enhancement from the fibrous component
masquerading as a tumor (21). Correlation with
CT images is always useful when the MRI ap-
pearance is confusing or inconclusive.
RG  •  Volume 42  Number 4 Cochinski et al  1183

Figure 10.  Fibrous dysplasia in two patients. (A) Axial CT image (bone window) in a 37-year-old woman shows an
expansile lesion affecting the sphenoid bone, with a ground-glass appearance, mainly in the body and the right GWS,
which is a typical finding of fibrous dysplasia. (B) Axial CT image (bone window) in a 58-year-old woman shows a diffusely
enlarged right GWS, with thick pseudotrabeculae and a “cotton” appearance, representing a mixture of osteolytic and
osteoblastic areas. Cortical pseudothickening is also seen. These findings are consistent with pagetoid fibrous dysplasia.

Venous Malformation.—Formerly known as plaque from intraosseous meningiomas is often

intraosseous hemangioma, intraosseous venous
malformation is a nontumorous slow-growing
vascular anomaly that can involve any skull bone,
including the GWS. It is composed of angioma-
tous channels between thickened osseous tra-
beculae, resulting in the characteristic “sunburst”
or “honeycomb” pattern seen on CT images.
T2-weighted MRI shows the typical “bunch of
grapes” appearance from the hypointense tra-
beculae and the hyperintense vascular channels,
which are also responsible for progressive con-
trast enhancement (Fig 11) (23,24).
Meningiomas.—Meningiomas are the most
common primary intracranial tumors and occur
predominantly in women, with an increasing
incidence with age. Most (up to 90%) menin-
giomas are benign and typical (World Health
Organization [WHO] grade I). Intratumoral
cystic changes, edema and/or contrast enhance-
ment in the adjacent brain parenchyma, and
the presence of a draining vein are predictive
findings of atypical meningiomas (WHO grades
II and III) (25).
Approximately 50% of meningiomas are
located at the skull base, and the GWS are one
of the common sites affected. The portion of
the GWS that forms the posterolateral orbital
wall is commonly involved, and these menin-
giomas are more aptly known as spheno-orbital
meningiomas (26,27). Spheno-orbital menin-
giomas can be primarily intraosseous or can
originate from the adjacent meninges. In both
cases, neoplastic meningothelial cells infiltrate
the bone and can result in hyperostosis. Bone
involvement is usually disproportionate in this
morphologic subgroup of meningiomas, even
when they are derived from the meninges, which
typically results in a thickened sheet-like pattern
(ie, en plaque meningiomas). Differentiating en
impossible and of little importance, if any, from
a surgical perspective (12,26,28).
CT is the best imaging tool for characterizing
the typical osseous changes of spheno-orbital me-
ningiomas and helping to discern them from other
hyperostotic conditions (mainly fibrous dysplasia).
Although more than one pattern of hyperostosis
may be found in this subgroup of meningiomas,
the periosteal pattern is the most typical and use-
ful because it is not expected in fibrous dysplasia,
which does not induce periosteal new bone forma-
tion. Surface irregularity of the hyperostotic bone
is also characteristic of meningiomas (12).
Both intraorbital and intracranial soft-tissue
components of spheno-orbital meningiomas are
best evaluated with gadolinium-enhanced MRI.
Typically, meningiomas are isointense when com-
pared with gray matter at T1- and T2-weighted
MRI, showing intense, often homogeneous,
contrast enhancement. An enhancing dural tail is
also a quintessential feature of meningiomas. The
lesions may spread to the frontotemporal vault,
the cavernous sinus, or the orbits.
Cavernous sinus extension may simply involve
the lateral wall, variably affecting the III, IV, V1,
and V2 nerves, or may also invade the medial
compartment(ie, the cavernous sinus itself), with
variable encasement of the internal carotid artery.
There may be invasion of the optic canal and the
superior orbital fissure, with involvement of the
structures traversing through it. Direct extension
along the posterolateral orbital wall may involve
the extraconal orbit or the extraocular muscles.
The intracranial component usually causes mass
effect on the adjacent brain parenchyma. Higher-
grade tumors may involve the brain parenchyma,
in which altered signal intensity and contrast en-
hancement may be seen. Extracranial extension is
also possible, in which a soft-tissue mass involves
the masticator space (27,29) (Fig 12).
1184  July-August 2022 radiographics.rsna.org

Table 3: Imaging Features of Benign Lesions of the GWS

Lesion Type Main Imaging Features Pearls to Remember

Intrinsic
 Fibrous CT: expanded medullary bone with ground-glass at- CT: fibrous component may en-
dysplasia tenuation; lytic or pagetoid pattern may also occur hance like an aggressive mass;
MRI: variable signal intensity and contrast enhancement acquire CT images when in doubt
  Venous malfor- CT: characteristic “sunburst” or “honeycomb” pattern CT: “do not touch” lesion
mation MRI: “bunch of grapes” pattern on T2-weighted images
 Meningioma CT: diffuse hyperostosis CT: periosteal hyperostosis with sur-
MRI: soft-tissue component that is isointense face irregularity (to differentiate it
compared with gray matter and intense contrast from fibrous dysplasia)
enhancement; it may extend to the orbit, cavernous MRI: enhancing dural tail
sinus, skull base foramina, and masticator space
  Langerhans cell CT: “punched-out” appearance Affects young children
histiocytosis T1-weighted MRI: signal hypointensity compared
with the gray matter
T2-weighted MRI: signal hyperintensity, avid contrast
enhancement
Extrinsic
 Osteodural CT: osseous defect Frequently associated with elevated
  defects MRI: spontaneous lateral sphenoid cephalocele and intracranial pressure
arachnoid pits that show signal intensity similar to Look for cerebrospinal fluid signal
that of cerebrospinal fluid intensity at MRI
 Schwannoma CT: bone remodeling Trigeminal nerve is the second most
MRI: well-defined mass with high T2-weighted signal common cranial nerve involved
intensity and moderate-to-intense contrast en- (following the vestibulocochlear
hancement nerve)
 Sphenoid Isolated or associated with a plexiform neurofibroma Association with neurofibromatosis
dysplasia deformity type 1
Hypoplasia and displacement of the GWS
 Juvenile CT and MRI: avidly enhancing and locally aggressive Typical patient is a male teenager
angiofibroma mass originating at or near the sphenopalatine fora-
men; multiple flow voids at MRI
  Infectious and CT: bone erosion or sclerosis Often secondary to bacterial otitis
inflammatory MRI: soft-tissue infiltrative process involving the skull externa
diseases base foramina

Excision of meningiomas involving the medial Langerhans Cell Histiocytosis.—Formerly known

compartment of the cavernous sinus cannot be
achieved without causing morbidity. So, during
the preoperative MRI evaluation, it is crucial to
determinate whether the tumor is restricted to the
lateral compartment of the cavernous sinus and to
identify its relationship with the cavernous internal
carotid artery. It is critical to determine whether
the tumor involves the anterior clinoid process; in
these cases, an anterior clinoidectomy is required.
Residual tumor in the medial compartment should
be managed with observation or radiation therapy,
depending on cellular atypia, the proliferative in-
dex, patient age, and clinical condition. The tumor
portion that infiltrates the superior orbital fissure
can be followed and treated with radiation therapy
(30). Although it is described in this section, simi-
lar guiding principles govern the surgical approach
in other GWS lesions that may involve the cavern-
ous sinuses or the orbits.
as histiocytosis X, Langerhans cell histiocytosis is
a rare disorder with a peak incidence in patients
aged 1–3 years that is characterized by monoclonal
growth of bone marrow–derived Langerhans cells.
Bone lesions are either solitary (eg, eosinophilic
granuloma) or multiple and lead to osseous expan-
sion, and eventually, cause a cortical breach (31).
Craniofacial involvement is common, especially of
the calvaria, followed by the skull base and maxil-
lofacial bones (32). Lesions affecting the GWS
demonstrate a nonsclerotic “punched-out” appear-
ance on CT images. At T1-weighted MRI, they are
hypointense when compared with gray matter, and
at T2-weighted MRI, they are hyperintense and
exhibit avid contrast enhancement (31,33). The
soft-tissue component of the tumor grows toward
both the middle cranial fossa and the orbital cavity.
Because of the dural displacement, a tapering rim
of dural enhancement is formed (ie, the “dural
RG  •  Volume 42  Number 4 Cochinski et al  1185

Figure 11.  Intraosseous venous malformation in a 42-year-old man. (A) Coronal T2-weighted MR image shows a hyperintense
expansile lesion (arrows) affecting the left GWS with the typical “bunch of grapes” appearance. (B) Coronal T1-weighted gadolinium-
enhanced fat-suppressed MR image shows avid and heterogeneous enhancement (arrows).

Figure 12. Spheno-orbital me-

ningioma in a 48-year-old woman.
(A) Axial CT image (bone window)
shows the typical periosteal pattern
of hyperostosis found in this set of
meningiomas (arrow). (B) Axial gad-
olinium-enhanced T1-weighted MR
image with fat suppression shows
both orbital (*) and intracranial (ar-
row) extraosseous extension.

tail” sign, a finding typical of but not exclusive to
meningiomas). When it affects the orbital wall, the
mass typically invades the extraconal compart-
ment, and sometimes, the extrinsic eye muscula-
ture and the lacrimal gland (31) (Fig 13).
scattered in the medullary cavity at T1-weighted
MRI are helpful findings in differentiating Paget
disease from other similar diffuse conditions (34).
Extrinsic Benign Lesions

Other Benign Bone Lesions.—Except for intraos-
seous spheno-orbital meningiomas, primary
benign tumors of the GWS are rare. They may be
classified as bone forming (eg, osteoblastoma or
ossifying fibroma), cartilage forming (eg, chon-
droblastoma or chondromyxoid fibroma), or with
neither an osteoid nor chondroid matrix. The
last group encompasses the spectrum of giant-
cell lesions, which include giant cell granulomas,
brown tumors, giant cell tumors, and other un-
common lesions that can be found in the GWS,
such as dermoid cysts (Fig 14) (23,34).
Diffuse osseus processes may affect the GWS.
These disease processes include melorheostosis, os-
teopetrosis (Fig 15), and Paget disease, among oth-
ers. Paget disease is most often multifocal and, like
fibrous dysplasia, exhibits a wide range of imaging
patterns, ranging from well-defined lytic areas to
sclerotic changes, with thickening of both the med-
ullary cavity and the cortical bone. Hyperintensities
Osteodural Defects.—The term cephalocele is
used generically to describe herniation of intra-
cranial contents through a defect of the skull base
or calvarial bones. The herniated material could
be meninges and cerebrospinal fluid (menin-
gocele), brain parenchyma (encephalocele), or a
combination of both (meningoencephalocele). The
cause can be classified as congenital (ie, failure
of the skull to close normally), acquired (ie, due
to trauma, surgery, tumor, dysplasia, or osteora-
dionecrosis), or spontaneous (ie, no clear cause)
(17,35). A spontaneous cephalocele of the base
of the skull is currently regarded as a multifacto-
rial process caused by a combination of osseous
thinning and elevated intracranial pressure. When
it is off the midline of the sphenoid bone, it is
called spontaneous lateral sphenoid cephalocele,
and can be classified as type 1 or type 2. Type
1 occurs when there is a defect of the bone in a
pneumatized lateral recess (Fig 16), while type 2
1186  July-August 2022 radiographics.rsna.org

Figure 13.  Langerhans cell histiocytosis in an 11-year-old boy. Axial (A) and coronal (B) gadolinium-enhanced
T1-weighted MR images with fat suppression show an expansile and destructive lesion affecting the left GWS
that protrudes into the temporal fossa (arrowhead in B), the middle cranial fossa, and the orbital cavity, pushing
the left lateral rectus muscle (* in A). Note the dural tail sign (arrow in B).

Figure 14.  Small circumscribed fat-containing

lesion (presumed to be an intraosseous dermoid
cyst) in the right GWS in a 38-year-old man.
(A) Axial CT image (bone window) shows a non-
aggressive lytic lesion with well-defined margins.
(B) Corresponding axial CT image (soft-tissue win-
dow) shows fat attenuation.

develops as an osseous dehiscence in a nonpneu-

matized GWS (17). CT and MRI are able to show
the bone defect and the content of the herniation,
respectively (35).
Aberrant arachnoid granulations (ie, arach-
noid pits) can also be seen along the GWS,
especially among patients with elevated intracra-
nial pressure (Fig 16).
Figure 15.  Osteopetrosis in a 2-year-old child. Axial CT image
Schwannoma.—Schwannomas are benign tumors (bone window) shows a diffusely attenuating skull base.
that arise from the sheath of any of the multiple
nerves that pass through the foramina in or ad-
jacent to the GWS, and they usually have typical are detected with T2-weighted MRI, where lesions
benign imaging features such as well-defined mar- show characteristic findings of high signal intensity
gins, displacement of adjacent structures (instead and moderate to intense contrast enhancement.
of invasion), and osseous remodeling. Among Lesions, especially if they are large, can be partially
the cranial nerves involved by schwannomas, the cystic. Intratumoral microhemorrhage, which is
vestibulocochlear nerve accounts for the most seen as areas of low signal intensity on T2-weighted
schwannomas, followed by the trigeminal nerve. MR images, may be present and is better shown on
When they arise from V2 or V3, there can be en- susceptibility-weighted MR images (36).
largement of the foramen rotundum and foramen
ovale, respectively (Fig 17). Enlarged bone foram- Sphenoid Dysplasia.—Although it is one of the
ina can be seen with CT; however, most tumors diagnostic criteria for neurofibromatosis type 1,
RG  •  Volume 42  Number 4 Cochinski et al  1187

Figure 16.  Spontaneous lateral sphenoid cephalocele in a 33-year-old woman. (A, B) Axial T2-weighted (A) and T1-
weighted (B) gadolinium-enhanced fat-suppressed MR images show an extensive nonenhanced cerebrospinal fluid–
like cystic lesion in the sphenoid sinus, including the right lateral recess (arrow in A) and protruding through the sphe-
noethmoidal recess (arrowhead in A). (C, D) Coronal CT images (bone window) show the defect in the posterosuperior
wall of the right sphenoid sinus (arrow in C) and some arachnoid pits along the inner table of both greater sphenoid
wings (arrowheads in D). Other findings supporting the diagnosis of intracranial idiopathic hypertension as the underly-
ing cause for spontaneous lateral sphenoid cephalocele include enlarged Meckel caves (* in A), bilateral distention of
the perioptic subarachnoid space, and vertical tortuosity of the optic nerves (not shown).

sphenoid dysplasia occurs in only 4%–11% of
cases. Sphenoid dysplasia can be isolated or can
be due to extension of a plexiform neurofibroma
to the vicinity of the bone, which induces osse-
ous changes that progress over time. In addition
to deformity and hypoplasia of the GWS, ante-
rior displacement of the GWS and elevation of
the lesser wing can occur, thus causing enlarge-
ment of the middle cranial fossa, proptosis, and
widening of the superior orbital fissure (37,38)
(Fig 18).
Juvenile Angiofibroma.—Juvenile angiofibroma
is a locally aggressive, although benign, vascular
neoplasm originating at or near the sphenopala-
tine foramen. The typical patient who presents
clinically with juvenile angiofibroma is a teenage
boy with a nasal obstruction and epistaxis and
the imaging appearance of a hypervascularized
mass centered at the sphenopalatine foramen
(Fig 19). As in many diseases of the skull base,
CT is helpful for demonstrating bone changes,
whereas MRI is used to better differentiate the
tumor from sinonasal secretions and to evaluate
intracranial extension and bone marrow invasion.
MRI shows an avidly enhancing richly vascular
mass with multiple flow voids. Although different
growth patterns are described, juvenile angiofi-
broma frequently spreads anterolaterally through
the pterygopalatine fossa, filling it and causing
bowing of the posterior wall of the maxillary si-
nus. As it continues to grow, the tumor may reach
the infratemporal fossa and the inferior orbital
fissure, may erode the sphenoid bone (includ-
ing the GWS), and may even invade the middle
cranial fossa (39).
Infectious and Inflammatory Diseases.—Infec-
tions that reach the GWS are usually advanced
and life threatening. Osteomyelitis of the skull
base is an important clinical entity, not only be-
cause of its local aggressiveness but also because
the diagnosis is often delayed, and most patients
with it are immunocompromised. The process
is usually secondary to bacterial otitis externa.
Through the vertical fissures in the cartilaginous
external auditory canal (ie, the fissures of San-
torini), the infection reaches the adjacent supra-
hyoid neck spaces and then may affect various
cranial nerves and may spread along the skull
base foramina (40) (Fig 20). It can also spread to
the floor of the middle cranial fossa and result in
cavernous sinus thrombosis.
Some noninfectious inflammatory processes
may also invade or arise from the central skull
base (eg, sarcoidosis, granulomatosis with poly-
angiitis, and immunoglobulin G4–related dis-
ease). Like skull base osteomyelitis, these entities
have a propensity to spread along the skull base
foramina (41).
1188  July-August 2022 radiographics.rsna.org

Figure 17.  Schwannoma in a 58-year-old woman. (A) Coronal gadolinium-enhanced T2-weighted MR image
with fat suppression shows a large well-circumscribed mass that is causing substantial enlargement of the left
round foramen, which is consistent with a schwannoma arising from V2 (arrowhead). (B) Axial CT image (bone
window) shows remodeling of the left GWS (arrow).

Figure 18.  Neurofibromatosis type 1 in a 2-year-old

boy. (A) Axial gadolinium-enhanced T2-weighted fat-
suppressed MR image shows an orbital and periorbital
plexiform neurofibroma (arrow). Note the prominence
of the cerebrospinal fluid anterior to the temporal lobe
(*). (B, C) Axial (bone window) (B) and three-dimen-
sional reconstruction (C) CT images show dysplasia and
anterior displacement of the GWS (arrowhead), eleva-
tion of the lesser wing (*), and widening of the superior
orbital fissure.

Malignant Lesions

Intrinsic Malignant Lesions well-defined margins and the characteristic “rings

Several bone lesions with aggressive behavior can
affect the GWS, such as sarcomas, hematologic
malignancies, and metastases (Table 4).
Sarcomas.—Although they are uncommon,
sarcomas can affect the GWS and should be
considered in the differential diagnosis of an
aggressive mass, especially when there is a soft-
tissue component.
Chondrosarcomas are malignant lesions with a
cartilaginous matrix. Only 2% of them are found
in the skull base, with the petroclival synchon-
drosis being the most common site of origin. In
some instances, chondrosarcomas may arise from
the GWS (42). Histologically, these tumors can
be classified by subtype (ie, conventional, mesen-
chymal, clear-cell, or dedifferentiated) and grade
(ie, high-, intermediate-, or low-grade). Conven-
tional low-grade chondrosarcomas typically show
and arcs’’ calcifications (mineralized chondroid
matrix) on CT images (Fig 21). On the other
hand, the nonmineralized chondroid matrix can
be identified at T2-weighted MRI as a high-sig-
nal-intensity component, while calcifications ex-
hibit low signal intensity. Gadolinium-enhanced
T1-weighted MRI may show a characteristic
pattern of curvilinear enhancement, reflecting
fibrovascular bundles surrounding cartilaginous
areas (42–44). Aggressive lesions (eg, high-grade
chondrosarcomas) tend to exhibit a “moth-eaten”
or permeative pattern of lytic destruction on CT
images, and a heterogeneous pattern of contrast
enhancement (43,44).
Craniofacial osteosarcomas are much rarer than
those arising in the appendicular skeleton. The
maxillomandibular complex is more commonly
affected than is the skull base, and the GWS are
an uncommon site of origin. These tumors can be
RG  •  Volume 42  Number 4 Cochinski et al  1189

Figure 19.  Juvenile angiofibroma in a 16-year-old adolescent boy. (A) Axial CT image (bone window) shows a large
mass widening the left pterygopalatine fossa (*). (B) Coronal gadolinium-enhanced T1-weighted fat-suppressed MR
image shows massive destruction of the sphenoid bone, mainly on the left side (*), where there is invasion of the
intracranial compartment. Flow voids (arrowhead) can be seen because of the vascular nature of the lesion.

Figure 20.  Osteomyelitis of the skull base in a 54-year-old man. Coronal (A) and axial (B) T1-weighted MR
images with fat suppression after gadolinium administration show an aggressive inflammatory process originat-
ing from the external auditory canal and compromising the infratemporal fossa (arrow). From this region, it
reaches the pterygopalatine fossa (arrowhead in B) and foramen ovale (*) and then spreads to the dura mater
(arrowhead in A).

Table 4: Types of Malignant Lesions of the GWS

Lesion Type Main Imaging Features Pearls to Remember

Intrinsic
 Sarcoma CT and MRI: well- to ill-defined borders (depending Osteosarcomas of the GWS
on histologic grade; attenuation and signal intensity usually do not cause periosteal
depend on the matrix reaction
Look for pulmonary metastasis
 Lymphoma CT: permeative lytic lesion causing little or no cortical MRI for early diagnosis and pre-
destruction diction of treatment outcome
MRI: T2-weighted signal isointensity compared with
gray matter; restricted diffusion
 Plasmacytoma CT: hyperattenuating mass, with destructive behavior Associated with or progressing to
MRI: T2-weighted signal hypointensity with restricted multiple myeloma
diffusion
 Metastases CT: circumscribed or diffuse; attenuation depends on Primary neoplastic malignancies
the primary origin are lung, breast, and prostate
MRI: T1-weighted signal hypointensity, T2-weighted cancers in adults and sarcomas
signal intensity and variable contrast enhancement and neuroblastoma in children
Extrinsic (head and CT: bone destruction (direct extension), foraminal MRI is the best imaging modality
neck malignan- widening (perineural spread) to identify perineural spread
cies) MRI: invasive mass (direct extension), T1-weighted
hypointensity, T2-weighted heterogeneous signal in-
tensity with variable contrast enhancement, perineu-
ral spread, foraminal contrast enhancement
1190  July-August 2022 radiographics.rsna.org

Figure 21.  Mesenchymal chondrosarcoma in a 12-year-old girl. Axial (A) and sagittal (B) CT images (bone window)
show a conventional low-grade chondrosarcoma affecting the left GWS, with well-defined margins and chondroid
calcifications (arrows).

Figure 22.  Chondroblastic osteosarcoma in a 36-year-old woman. (A) Axial CT image (bone window) shows a sphe-
noid lesion destroying the GWS (arrow) and the body, with chondroid calcifications (arrowhead). (B) Axial gadolinium-
enhanced T1-weighted fat-suppressed MR image shows dural invasion with contrast enhancement (arrow).

primary or secondary to radiation therapy, fibrous
dysplasia, Paget disease, trauma, osteomyelitis, os-
sifying fibroma, or giant cell tumors. Lesions can be
intramedullary, intracortical, periosteal, parosteal,
or extraosseous. Histologically, they could be osteo-
blastic, chondroblastic, fibroblastic, telangiectatic,
or osteoclastic and could exhibit high, intermediate,
or low histologic grade (43). As a result, a spec-
trum of bone changes can be found on CT images,
ranging from well- to ill-defined borders, depending
on the histologic grade, and from lytic to sclerotic,
depending on the extent of matrix mineralization.
Although variable, the typical CT pattern is of an
ill-defined sclerotic mass with cortical breakthrough
and extension to the soft tissues (44,45). Except
for those affecting the jaw, craniofacial osteosarco-
mas usually do not cause periosteal reactions (44).
In the chondroblastic variant, typical chondroid
calcifications can be found (Fig 22). MRI is more
accurate for assessing the soft-tissue component for
surgical planning (42).
Other types of sarcomas affecting the GWS
are described in the literature, but they are rare
malignancies.
Hematologic Malignancies.—Primary lymphomas
of the bone are an uncommon subgroup of ex-
tranodal lymphomas, usually of the non-Hodgkin
type, which sometimes affect the GWS. Although
sclerotic and mixed patterns have been described,
the typical appearance on CT images is that of
a permeative lytic lesion extending beyond the
bone but causing little cortical destruction. MRI
allows better evaluation of bone marrow replace-
ment and soft-tissue involvement, thus allowing
early diagnosis and prognostication of treatment
outcome, respectively (46). The characteristic
high cellularity of lymphomas accounts for their
signal isointensity compared with gray matter at
T2-weighted MRI, their low signal intensity on
apparent diffusion coefficient maps, and their
high attenuation at noncontrast CT, which are
findings that raise diagnostic suspicion (47).
Composed of malignant monoclonal plasma
cells, plasmacytomas are solitary or multiple
bone or soft-tissue tumors with variable mass
effect and may be associated with or progress to
multiple myeloma. As for imaging findings, high
cellularity and a low nucleocytoplasmic ratio
explain the hyperattenuating appearance on CT
images and signal hypointensity on T2-weighted
MR images. Restricted diffusion on diffusion-
weighted MR images is also likely because of the
high cellular nature of these lesions. Contrast
enhancement is typically intense, and destructive
behavior is usually evident (48).
RG  •  Volume 42  Number 4 Cochinski et al  1191

Figure 23.  Metastasis of adenocarcinoma of the lung

to the GWS (both wings) in a 48-year-old man. Axial
CT image (bone window) shows aggressive lytic lesions
affecting the central skull base. Note the circumscribed
geographic pattern on the right side (arrow) and a more
aggressive involvement on the left (arrowheads), with a
permeative “moth-eaten” appearance across the spheno-
squamosal suture.

Figure 24.  Metastatic adenocarcinoma of the prostate in a 72-year-old man. (A) Axial contrast-enhanced CT image
(soft-tissue window) shows diffuse metastatic involvement of the central skull base, with an extraosseous component
arising from the GWS (both wings). (B) Axial CT image (bone window) shows no bone sclerosis, unlike most cases
of skeletal prostate metastases.

Metastases.—Metastases to the skull base can
be found in approximately 4% of all patients with
cancer, occurring most commonly secondary to
prostate, breast, or lung malignancies in adults and
to neuroblastoma or sarcomas in children (49,50).
They arise by hematogenous spread of neoplastic
cells to the bone marrow and, depending on the
histopathologic type and location of the primary
tumor, lytic or blastic lesions may be seen (51).
Metastatic disease affecting the GWS can
be described on the basis of the number of le-
sions (ie, single or multiple), osseous extension
(ie, circumscribed or diffuse, depending on the
spread across sutures), extraosseous extension
(ie, whether there is extension to the orbital cav-
ity or middle cranial fossa), and the nature of the
lesions (ie, sclerotic, lytic, or mixed) (49,51,52).
CT and MRI have complementary roles in
the evaluation of metastases to the GWS. Al-
though they are considered appropriate to assess
lytic lesions with cortical erosion (Fig 23) and
sometimes allow identification of extraosseous
extension (Fig 24), CT is less sensitive than MRI
for detection of multiplicity of the lesions, dural
invasion, intracranial extension, and cranial nerve
invasion. At T1-weighted MRI, the normal signal
intensity of bone marrow is replaced by the ab-
normal signal hypointensity of metastatic tissue,
which has a variable appearance at T2-weighted
MRI, with different patterns of contrast enhance-
ment ranging from markedly avid to virtually
absent (common in osteoblastic lesions) (49,52).
Some imaging features of metastases to the
GWS may be related to the primary site of the
tumor. Osteoblastic lesions are typically described
in patients with breast and prostate cancers, some-
times mimicking benign sclerotic entities such as
meningiomas and Paget disease. When a single
and expansive (“blowout”) lesion is found, renal
cell and thyroid carcinomas should be suspected.
However, this pattern may also be present in
patients with other primary malignancies, such as
breast and lung cancers (49,51).
Extrinsic Lesions: Malignancies of the
Head and Neck
The GWS can also be affected by local ex-
tension of aggressive disease arising from the
surrounding regions. In addition to infectious
entities such as invasive fungal sinusitis and
osteomyelitis, several head and neck malignan-
cies can extend to the GWS.
Contiguous involvement of malignancies aris-
ing in the suprahyoid neck and facial structures
account for most of the aggressive lesions affect-
ing the skull base, including the GWS. They can
result from direct extension, perineural spread
through the GWS foramina, or both (34).
1192  July-August 2022 radiographics.rsna.org

Figure 25.  Parameningeal rhabdomyosarcoma in an 8-year-old girl. (A) Coronal T2-weighted fat-suppressed MR im-
age shows a large lesion that arises from the masticator space, causing destruction of the GWS and protrusion toward
the sphenoid sinus (*) and the middle cranial fossa (arrowhead). (B) Axial CT image (bone window) shows destruction
of the left GWS.

Figure 26.  Adenoid cystic carcinoma of the right maxillary sinus in a 50-year-old man. Axial (A) and coronal (B)
gadolinium-enhanced fat-suppressed T1-weighted MR images show an extensive tumor spreading through the inferior
orbital fissure (white arrow in A) and the foramen rotundum (dashed arrow in B), reaching the cavernous sinus (solid
black arrow in A), the Meckel cave (arrowhead in A) and the orbital apex (arrowhead in B), with dural infiltration
(dashed black arrow in A).

In children, parameningeal rhabdomyosarco- Lymphomas more commonly affect the GWS by

mas from the nasopharynx, parapharyngeal space,
masticator space, or paranasal sinuses may affect
the GWS directly, because of the proximity to the
skull base (Fig 25), and may spread along V2 and
V3 in the foramen rotundum and foramen ovale,
respectively. Orbital rhabdomyosarcomas can
invade the orbital fissures and the GWS (47).
Because they occur frequently, cutaneous
and mucosal squamous cell carcinomas account
for most cases of perineural spread among head
and neck malignancies. However, adenoid cystic
carcinoma (from both minor and major salivary
glands) is the histopathologic type that is most
likely to develop this complication (53) (Fig 26).
Nasopharyngeal carcinomas may reach the sphe-
nopalatine foramen, gaining access to the ptery-
gopalatine fossa, and then extend along V2 (Fig
27). When these tumors invade the masticator
space, perineural spread along V3 is of concern
(Fig 28). Malignancies can also involve the V3
through its cutaneous branches or through the
auriculotemporal nerve that runs in the parotid
gland in the stylomandibular tunnel (Fig 29).
contiguous extension rather than arising primar-
ily from the GWS (34).
Checklist for Reporting GWS Lesions
The proximity of the GWS to vital structures
such as the cavernous sinus and its intimate
relationship with the skull base foramina and
the nerves and vessels it contains make it impor-
tant for radiologists to have a mental checklist
of imaging findings for which to search and on
which to report (Table 5). Involvement of the
nerves in the lateral wall of the cavernous sinus
and encasement of the cavernous internal carotid
artery are features that can alter the surgical ap-
proach or affect planning for radiation therapy.
Also, involvement of the skull base foramina can
lead to anterograde or retrograde spread of the
tumors and has the potential to change patient
care. Such features also help in determining the
prognosis for patients with these lesions. Simi-
larly, extension into the orbit, optic canal, and
superior orbital fissure is essential to be evaluated
if orbital salvage is being considered at surgery.
RG  •  Volume 42  Number 4 Cochinski et al  1193

Figure 27.  Nasopharyngeal carcinoma in a 42-year-old man. Axial (A) and coronal (B) T1-weighted MR images
with fat suppression after gadolinium administration show an enhancing lesion enlarging the sphenopalatine foramen
(arrow in A) and reaching the pterygopalatine fossa (* in A). From this point, it spreads along the foramen rotundum
(arrow in B). Also, there is direct erosion of the body of the sphenoid bone (arrowhead in B) and the medial portion
of the right GWS.

Figure 28.  Nasopharyngeal carcinoma in a 45-year-old woman. (A) Coronal T1-weighted MR image with fat suppres-
sion after gadolinium administration shows the tumor extending laterally and ascending through the foramen ovale
(*). (B) Axial bone window CT image better demonstrates the foraminal enlargement (*). Note that the left foramen
lacerum is also enlarged by the lesion in comparison with the right side (arrowheads).

Figure 29.  Squamous cell carcinoma of the skin in a 53-year-old man. Axial gadolinium-enhanced T1-weighted
fat-suppressed MR images show diffuse infiltration of the facial skin, subcutaneous tissue, and parotid gland on the
right side (arrows in A). Through the auriculotemporal nerve (arrowhead in A), there is perineural spread to V3
(dashed arrow in B).

The presence and extent of involvement of the
temporal fossa could determine and guide the
surgical approach for optimal cosmesis in qualify-
ing cases. Aggressive lesions may involve the sub-
jacent brain parenchyma, and it is essential for
radiologists to search for and report on abnormal
signal intensity and/or enhancement in the brain.
Given the three-dimensional curved shape of
the GWS, the size of a lesion can be difficult to
measure accurately. Lesions, therefore, should be
measured in all three planes (axial, coronal, and
sagittal) as best as possible.
Conclusion
It is essential for the radiologist to be familiar with
the complex anatomy of the GWS to better iden-
tify incidental or suspected lesions affecting the
GWS, whether with MRI or CT. By defining the
behavior (benign or malignant) and origin (intrin-
sic or extrinsic) and other imaging characteristics
1194  July-August 2022 radiographics.rsna.org

Table 5: Checklist for Reporting of GWS Lesions

Structure to Be Evaluated Imaging Findings

Orbit Orbital bony walls
Orbital fat
Extraocular muscles
Optic canal/nerve
Superior orbital fissure
Cavernous sinus Involvement of lateral wall or entire sinus
Encasement of the internal carotid artery
Skull base foramina Anterograde or retrograde perineural tumor spread along the cranial nerves
Brain Abnormal T2-weighted fluid-attenuation inversion-recovery signal intensity
Enhancement
Mass effect
Dural involvement
Temporal fossa/masticator space Involvement of muscles of the masticator space
Involvement of temporalis fascia

of such lesions, one can narrow the differential
diagnosis and accurately define the extent of
involvement (Table 5).
Acknowledgments.—The authors would like to thank Soraia
Ale Souza, PhD, MD, and Raphael Machado Reali, MD, for
the courtesy of some CT and MR images and Bruno Baldissara
Moreira for collaboration in preparing the medical illustrations.
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