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Imaging Spectrum of Cavernous
Sinus Lesions with Histopathologic
Correlation
Harsha Vardhan Mahalingam, MD
Sunithi E. Mani, MD
Bimal Patel, MD
Krishna Prabhu, MCh
Mathew Alexander, DM
Girish M. Fatterpekar, MD
Geeta Chacko, MD
Abbreviations: CCF = carotid-cavernous fis-
tula, CSF = cerebrospinal fluid, FLAIR = fluid-
attenuated inversion recovery, ICA = internal
carotid artery, IgG4 = immunoglobulin G4,
WHO = World Health Organization
RadioGraphics 2019; 39:795–819
https://doi.org/10.1148/rg.2019180122
Content Codes:
From the Departments of Radiology (H.V.M.,
S.E.M.), Pathology (B.P., G.C.), Neurosurgery
(K.P.), and Neurology (M.A.), Christian Medi-
cal College, Ida Scudder Road, Vellore, Tamil
Nadu 632004, India; and the Department of
Radiology, NYU Langone Medical Center, New
York, NY (G.M.F.). Presented as an education
exhibit at the 2017 RSNA Annual Meeting. Re-
ceived March 31, 2018; revision requested May
24 and received July 15; accepted July 20. For
this journal-based SA-CME activity, the authors,
editor, and reviewers have disclosed no relevant
relationships. Address correspondence to
S.E.M. (e-mail: sunithi.mani@cmcvellore.ac.in).
©
RSNA, 2019
SA-CME LEARNING OBJECTIVES
After completing this journal-based SA-CME
activity, participants will be able to:
■■Describe the anatomy of the cavernous
sinus.
■■Identify the imaging features of a wide
variety of cavernous sinus lesions.
■■Recognize imaging clues for differential
diagnosis, and avoid pitfalls in interpreta-
tion.
See rsna.org/learning-center-rg.
795
NEUROLOGIC/HEAD AND NECK IMAGING
Cavernous sinuses are paired interconnected venous plexuses situ-
ated in the floor of the middle cranial fossa on either side of the
sella turcica and sphenoid sinus. They are lined by dura mater and
consist of multiple venous channels within. The cavernous sinuses
are intimately related to the internal carotid artery and its associ-
ated sympathetic plexus, the oculomotor nerve, the trochlear nerve,
the abducens nerve, and the ophthalmic nerve. Cavernous sinuses
are connected to the orbit, the pterygopalatine fossa, the infratem-
poral fossa, the nasopharynx, and the posterior cranial fossa by
various foramina, fissures, and canals in the skull base. A multitude
of structures in close relation to the cavernous sinus give rise to a
myriad of possible pathologic conditions that can be broadly classi-
fied into (a) neoplastic, (b) vascular, (c) infective or inflammatory,
or (d) miscellaneous lesions. These pathologic conditions can have
overlapping clinical manifestations. Hence, imaging plays a cru-
cial role in identifying the disease, assessing its extent, providing a
pertinent differential diagnosis to guide further management, and
suggesting a site or route for biopsy. MRI is the modality of choice
to depict the cavernous sinuses, with CT and digital subtraction an-
giography playing supplementary roles in certain situations. In this
article, the cavernous sinus lesions encountered in our institution
during a 10-year period are reviewed. The purpose of the article
is to (a) describe the anatomy of the cavernous sinus; (b) dem-
onstrate the multimodality imaging spectrum of a wide variety of
pathologic conditions involving the cavernous sinus, correlating
with the histopathologic findings; (c) highlight important imaging
clues for differential diagnosis; and (d) help the reader overcome
potential pitfalls in interpretation.
Online supplemental material is available for this article.
©
RSNA, 2019 • radiographics.rsna.org
Introduction
Cavernous sinuses are paired complex venous spaces situated on
either side of the sphenoid sinus and the sella turcica and are at the
crossroads of many crucial neurovascular structures. The internal
carotid artery (ICA) and the abducens nerve travel within the cavity
of the cavernous sinus; and the oculomotor nerve (cranial nerve III),
the trochlear nerve (cranial nerve IV), and the ophthalmic nerve
(cranial nerve V1) travel in the lateral wall of the cavernous sinus.
The maxillary nerve (cranial nerve V2) courses just inferior to the
796  May-June 2019 radiographics.rsna.org
TEACHING POINTS
■■ Cavernous sinuses are paired complex venous spaces situated
on either side of the sphenoid sinus and the sella turcica and
are at the crossroads of many crucial neurovascular structures.
The internal carotid artery (ICA) and the abducens nerve trav-
el within the cavity of the cavernous sinus; and the oculomo-
tor nerve (cranial nerve III), the trochlear nerve (cranial nerve
IV), and the ophthalmic nerve (cranial nerve V1) travel in the
lateral wall of the cavernous sinus.
■■ The cavernous sinus can be affected by neoplasms (benign
or malignant), infection or inflammation, vascular pathologic
conditions, and congenital lesions, among others. Diverse
pathologic conditions of this region can, however, have simi-
lar clinical features; and imaging plays a crucial role in con-
firming the presence of disease, assessing its extent, guiding
further investigations, and planning therapy (medical man-
agement, microsurgery, endovascular surgery, or radiation
therapy). MRI is the imaging modality of choice for assess-
ment of the cavernous sinus, owing to the superior contrast
resolution of MRI. CT and digital subtraction angiography are
useful in certain cases.
■■ Common neoplasms that involve the cavernous sinus include
pituitary adenoma, meningioma, nerve sheath tumors, head
and neck malignancies such as nasopharyngeal carcinoma,
and metastases. These neoplasms can be classified on the ba-
sis of the origin or epicenter of the lesion as (a) lesions that
arise primarily within the cavernous sinus, (b) lesions that
invade the cavernous sinus from adjacent structures, and
(c) metastatic or hematologic disease.
■■ Vascular lesions of the cavernous sinus—namely, cavernous
sinus thrombosis, ICA aneurysm, and CCF—are great clinical
mimics, with a wide variety of clinical manifestations varying
from trivial to life threatening. Among this category of cavern-
ous sinus lesions, septic thrombosis is the most common and
is managed primarily by controlling the source of sepsis with
medical and surgical means. Digital subtraction angiography
plays an important role in the management of CCF and ICA
aneurysm.
■■ Considerable overlap exists in the radiologic findings of cav-
ernous sinus involvement in infective or inflammatory diseas-
es; the most common findings encountered are a bulky cav-
ernous sinus and increased enhancement, which may extend
to the orbit or the adjacent dura. Imaging clues that point to
infection or inflammation as the possible cause, as compared
with neoplasms, are a sheetlike configuration of the abnormal
soft tissue and T2 hypointensity. However, certain neoplasms,
such as lymphoma and en plaque meningioma, can mimic
these findings. Among this spectrum of infective and inflam-
matory disorders, Tolosa-Hunt syndrome is a diagnosis of
exclusion; other disease processes are diagnosed by specific
serum or histopathologic biomarkers.
junction of the lateral and medial walls of the
cavernous sinus. Pathologic conditions of the
cavernous sinus can have various clinical conse-
quences, ranging from subtle to devastating, and
including headache, ophthalmoplegia, exophthal-
mos (proptosis), chemosis, vision loss, trigeminal
neuralgia, and, rarely, cerebral infarction owing
to ICA involvement. The cavernous sinus can
be affected by neoplasms (benign or malignant),
infection or inflammation, vascular pathologic
conditions, and congenital lesions, among others.
Diverse pathologic conditions of this region
can, however, have similar clinical features; and
imaging plays a crucial role in confirming the
presence of disease, assessing its extent, guid-
ing further investigations, and planning therapy
(medical management, microsurgery, endovascular
surgery, or radiation therapy). MRI is the imaging
modality of choice for assessment of the cavernous
sinus, owing to the superior contrast resolution of
MRI. CT and digital subtraction angiography are
useful in certain cases. A thorough knowledge of
anatomy, awareness of the imaging appearance of
the wide variety of lesions that can possibly involve
this region, and correlation with clinical and
histopathologic features are essential for providing
appropriate patient care. We review the anatomy
of the cavernous sinus, along with the imaging
technique, the multimodality imaging features of
individual pathologic conditions of the cavernous
sinus correlating with histopathologic findings,
an algorithmic imaging approach to differential
diagnosis, and imaging pitfalls.
Anatomy
Each of the paired cavernous sinuses is a ve-
nous lake situated lateral to the sella turcica,
the pituitary gland, and the sphenoid sinus and
medial to the medial aspect of the temporal lobe
of the brain. The term cavernous sinus was first
used by Winslow in 1734 owing to the multiple
filaments, or septa, within, which gave it a cavern-
ous or plexiform appearance. However, this term
has courted controversy because the cavernous
sinus has certain anatomic differences from other
dural venous sinuses. It is extradural in location,
contains fat, and is continuous with the epidural
space (extradural space) of the spine (by way of
the periosteum of the skull base) and the orbital
space, in contrast to other dural venous sinuses
that are located between the two dural layers.
Parkinson (1) has argued that the cavernous si-
nus should be more accurately called “the lateral
sellar compartment.” Because the term cavernous
sinus is well established in the medical literature,
it continues to be used widely to refer to this
anatomic compartment.
The cavernous sinus has been described as
an “anatomic jewel box” owing to its complex-
ity. Figure 1 is a diagram of a coronal section
through the cavernous sinuses. The cavernous
sinus extends from the superior orbital fissure
anteriorly to the petrous apex and the dorsum
sellae posteriorly. The cavernous sinus is said
to have a shape resembling a boat and is nar-
rowest anteriorly and widest posteriorly. It is
bounded by dura and has five walls: (a) lateral;
(b) medial; (c) superior, or roof; (d) anterior;
and (e) posterior (2). The medial wall is the
RG  •  Volume 39  Number 3 Mahalingam et al  797
only one that consists of a single dural layer; the
other walls consist of two dural layers—an outer
meningeal dural layer and an inner periosteal
dural layer (1,3).
The medial wall is the weakest one and sepa-
rates the cavernous sinus from the lateral wall of
the sphenoid sinus inferiorly and the pituitary
gland superiorly. The part of the medial wall that
separates the cavernous sinus from the pituitary
gland is continuous with the diaphragma sel-
lae (3). Inherent weakness of this wall makes
the cavernous sinus susceptible to invasion from
pituitary tumors. Although the two dural layers
of the lateral cavernous sinus wall may not be
discernible as separate structures at imaging, they
are important for the neurosurgical approach to
the cavernous sinus. These two layers can be dis-
sected apart, and cranial nerves can be accessed
without entering the venous compartment of the
cavernous sinus because cranial nerves III, IV,
Figure 1.  Diagram of a coronal section through
the cavernous sinuses and the sella turcica. Note
that the medial wall of the cavernous sinus (CS) is
constituted by only a single layer of the dura ma-
ter. ACA = anterior cerebral artery, ICA = cavern-
ous segment of the ICA, III = oculomotor nerve,
IV = trochlear nerve, MCA = middle cerebral ar-
tery, OC  = optic chiasm, PIT  = pituitary gland,
SS = sphenoid sinus, VI = abducens nerve, V1 =
ophthalmic nerve, V2  = maxillary nerve, black
arrowhead = inner periosteal layer of the dura,
white arrowhead = outer meningeal layer of the
dura, * = subarachnoid space.
Figure 2.  Diagram of the segments and major
branches of the cavernous segment of the ICA.
Light blue structure represents the cavernous si-
nus (CS). The segments of the cavernous carotid
artery from proximal to distal are the posterior
vertical  (PV), the posterior genu (PG), the hori-
zontal (HORZ), the anterior genu (AG), and the
anterior vertical (AV). ACP = anterior clinoid pro-
cess, DDR  = distal dural ring, OA  = ophthalmic
artery, PDR  = proximal dural ring, PLL  = petro­
lingual ligament.
and V1 are located within the inner dural layer of
the lateral cavernous sinus wall. The lateral and
medial walls merge inferiorly with each other at
the superior margin of cranial nerve V2 (2).
The ICA within the cavernous sinus bends
to form an S shape, as seen in both coronal and
sagittal sections. The ICA is divided into five
segments on the basis of its course: posterior
vertical, posterior genu, horizontal, anterior
genu, and anterior vertical (Fig 2). Although the
ICA is firmly adherent at its point of entry and
exit, the intervening segment is unsupported
and can have a variable degree of tortuosity (4).
The intracavernous ICA commonly gives rise to
two branches—namely, the meningohypophy-
seal trunk and the inferolateral trunk. The ICA
divides the cavernous sinus into four venous
spaces: (a) the medial (between the ICA and
the medial wall of the cavernous sinus), (b) the
anteroinferior (relative to the posterior genu),
798  May-June 2019 radiographics.rsna.org
(c) the posterosuperior (between the ICA and the
posterior part of the roof of the cavernous sinus),
and (d) the lateral (between the ICA and the
ophthalmic nerve) (2).
The oculomotor nerve and the trochlear nerve
pierce the roof of the cavernous sinus in the ocu-
lomotor triangle to enter the cavernous sinus, and
the abducens nerve enters through the posterior
wall. The oculomotor nerve (cranial nerve III),
the trochlear nerve (cranial nerve IV), and the
ophthalmic division of the trigeminal nerve (or
ophthalmic nerve) (cranial nerve V1) lie in the
lateral wall of the cavernous sinus in that order
from superior to inferior. The maxillary division of
the trigeminal nerve (or maxillary nerve) (cra-
nial nerve V2) lies just inferior to the junction of
the lateral and medial wall dura of the cavernous
sinus. The abducens nerve (cranial nerve VI) and
the sympathetic plexus around the carotid artery,
on the contrary, lie within the cavity of the cavern-
ous sinus in close relation to the ICA. The abdu-
cens nerve courses in the lateral venous space (2).
The venous connections of the cavernous
sinus are illustrated in Figure 3. Each cavernous
sinus communicates with its counterpart on the
opposite side by way of intercavernous commu-
nications—these are the anterior, inferior, and
posterior intercavernous communications and the
basilar venous plexus (2).
Apart from the venous blood, the cranial nerves,
and the ICA, each cavernous sinus also contains
variable amounts of fat and fibrous tissue. The
structures within the cavernous sinus are embed-
ded in a weblike fibrous skeleton. Adipose tissue is
predominantly located adjacent to the lateral wall
of the cavernous sinus medial to the cranial nerves
(5). Multiple foramina and fissures act as a con-
duit of structures from the cavernous sinus to the
surrounding spaces, including the orbits, the face,
the pterygopalatine fossa, the nasopharynx, the
infratemporal fossa, and the middle and posterior
cranial fossae. These fissures and foramina and the
veins and nerves passing through the cavernous
sinus also act as pathways for the spread of disease
to and from the cavernous sinus. Figure 4 illustrates
these anatomic relationships and pathways.
Clinical Manifestations of Cavernous
Sinus Lesions (Cavernous Sinus
Syndrome)
The classic manifestations described are ophthal-
moplegia, ptosis, exophthalmos, chemosis, Horner
syndrome (characterized by partial ptosis and
miosis, with or without anhidrosis), facial pain or
loss of sensation in the trigeminal nerve distribu-
tion, and headache. These symptoms may occur
individually or in combination, depending on the
location of the lesion in the cavernous sinus. Le-
Figure 3.  Diagram of the venous connections of the cavern-
ous sinus (CS). BasVP = basilar venous plexus, ICC = intercavern-
ous communication, IJV = internal jugular vein, IOV = inferior
ophthalmic vein, IPS = inferior petrosal sinus, PteryVP = ptery-
goid venous plexus, SOV = superior ophthalmic vein, SphPS =
sphenoparietal sinus, SPS = superior petrosal sinus, SS = sig-
moid sinus.
sions of the anterior part of the cavernous sinus
manifest with ophthalmoplegia and ptosis and
usually do not involve the lower two trigeminal
nerve divisions. Blurring of vision or vision loss
can occur when the lesion extends anteriorly
to involve the orbital apex. The combination of
lateral rectus muscle palsy and Horner syndrome
is highly specific for cavernous sinus pathologic
conditions and usually indicates a lesion located
within the cavernous sinus, as opposed to a lateral
wall lesion. Pain is usually unilateral, localized to
the orbitofrontal region, and dull aching or boring
in character. The presence or absence of pain,
however, does not provide any clue with regard to
the nature of the underlying lesion (6,7). Other
less common manifestations include hypotha-
lamic-pituitary axis impairment, seizures caused
by irritation of the adjacent cortex, and stroke
owing to ICA involvement. Onset can be insidious
(usually with neoplastic and chronic inflamma-
tory causes) or sudden (with acute inflammatory
and vascular causes), but considerable overlap in
symptoms exists among the various causes. Clini-
cal manifestations specific to a particular lesion are
highlighted in the respective sections. A practical
classification of different causes of cavernous sinus
lesions is presented in Figure 5.
Imaging Protocol
MRI is the mainstay of imaging the cavernous
sinus because of the superior soft-tissue contrast
RG  •  Volume 39  Number 3 Mahalingam et al  799

Figure 4.  Anatomic pathways related to the cavernous sinuses and the regional bone anatomy. Blue areas represent the position of
the cavernous sinuses in the floor of the middle cranial fossa. Yellow lines outline the anatomic region set in boldface in each label.
ACP = anterior clinoid process, OC = optic canal, PCP = posterior clinoid process, PPF = pterygopalatine fossa (outlined in orange on
image at far left).

Figure 5.  Etiologic classification of cavernous sinus lesions. IgG4 = immunoglobulin G4.

resolution of MRI and its multiplanar capa-
bilities. In our institution, a typical basic MRI
protocol is followed for suspected cavernous
sinus lesions (Table 1). The coronal thin-section
high-spatial-resolution T2-weighted sequence
and the thin-section fat-suppressed T1-weighted
sequence in the axial and coronal planes before
and after injection of intravenous gadolinium-
based contrast material are the mainstay for
interpretation. The coronal thin-section MR im-
ages should cover from the orbits anteriorly to
the brainstem posteriorly. Additional sequences
that can be useful in certain situations are the
three-dimensional heavily T2-weighted sequence
and time-of-flight angiography. Contrast-en-
hanced constructive interference in steady-state
800  May-June 2019 radiographics.rsna.org

Table 1: Basic 3-T MRI Protocol for Suspected Cavernous Sinus Lesions

Section
TE TR Thickness Flip Fat
Sequence (msec) (msec) (mm) Field of View Matrix Angle (°) Suppression
Axial T2 weighted 80 3000 6 230 × 184 512 90/180 SPIR
Coronal thin-section T2 weighted 80 3000 3 150 × 150 512 90/180 NA
FLAIR (TI = 2800 msec) 125 11 000 6 230 × 184 512 90/180 NA
T1 weighted 3.9 8.4 0.8 230 × 230 512 8 NA
Susceptibility weighted 21 15 1 230 × 230 512 15–20 NA
Diffusion weighted 68 2132 5 230 × 230 256 90/180 SPIR
Nonenhanced and contrast agent–en- 2.3 4.7 0.9 395 × 278 432 10 SPAIR
hanced T1 weighted fat suppressed
Driven equilibrium* 185 1500 1 140 × 148 800 90/180 NA
Note.—FLAIR = fluid-attenuated inversion recovery, NA = not applicable, SPAIR = spectral attenuated inver-
sion recovery, SPIR = spectral presaturation with inversion recovery, TE = echo time, TI = inversion time, TR =
recovery time.
*DRIVE (Philips Healthcare, Andover, Mass).

imaging can clearly delineate the intracavernous
course of the cranial nerves (8).
CT plays an adjunctive role in imaging of the
cavernous sinus. Plain helical CT with a thin-
section (<1 mm) axial acquisition and multi-
planar reconstruction is useful for studying the
osseous relationship of cavernous sinus masses
before surgery and for evaluating osseous ero-
sion or sclerosis. CT angiography performed
with a bolus-tracking technique after injecting
60–80 mL of intravenous iodinated contrast
material at a rate of 3–5 mL/sec can be used
to assess the relationship of the ICA to cavern-
ous sinus mass lesions and in the evaluation of
suspected vascular lesions of the cavernous sinus
such as aneurysm, carotid-cavernous fistula
(CCF), or cavernous sinus thrombosis. CT
scanning in cases of cavernous sinus thrombosis
requires attention to the scan delay, with a mini-
mum recommended delay of at least 45 seconds
after contrast material injection (9). Contrast-
enhanced CT is also used in planning for
stereotactic radiosurgery in certain cavernous
sinus lesions such as meningioma and cavernous
hemangioma.
Neoplasia
Common neoplasms that involve the cavernous
sinus include pituitary adenoma, meningioma,
nerve sheath tumors, head and neck malignancies
such as nasopharyngeal carcinoma, and metasta-
ses. These neoplasms can be classified on the basis
of the origin or epicenter of the lesion as (a) le-
sions that arise primarily within the cavernous
sinus, (b) lesions that invade the cavernous sinus
from adjacent structures, and (c) metastatic or
hematologic disease.
Tumors Arising within the Cavernous
Sinuses
Meningioma.—Meningiomas are one of the most
common lesions to involve the cavernous sinus.
They constituted 41% of all cavernous sinus le-
sions in one large series (10). Advanced age (peak
incidence in the 5th to 7th decade) and female
sex are identified risk factors for development of
meningioma (11). Multiple meningiomas may be
encountered in the setting of neurofibromatosis
type 2. Meningiomas arise from the arachnoid
cap cells of the dura. About 80%–90% of menin-
giomas are well-circumscribed benign neoplasms
(World Health Organization [WHO] grade I),
with grade II (atypical, clear cell, and chordoid)
and grade III (anaplastic, rhabdoid, and papil-
lary) lesions being rare. Brain invasion, necrosis,
prominent nucleoli, sheeting, hypercellularity,
and small cell formation can be seen in atypical
meningiomas; and anaplastic meningiomas are
frankly malignant and can have areas resembling
carcinoma, sarcoma, or melanoma at histopatho-
logic examination (12).
Cavernous sinus meningiomas arise from the
dura of the cavernous sinus (more specifically,
the lateral wall dura) or arise from the adjacent
dura in the petroclival region, the sphenoid
ridge, or the clinoid process with extension to the
cavernous sinus. Meningiomas also differ in the
extent of their cavernous sinus involvement. They
can be (a) predominantly exophytic, projecting
laterally from the lateral dura of the cavernous
sinus; (b) localized to the lateral wall, growing in
between the two dural layers of the lateral wall in
the “interdural plane”; or (c) invading the cav-
ernous sinus proper. Meningiomas invading the
RG  •  Volume 39  Number 3 Mahalingam et al  801

Figure 6.  Cavernous sinus meningioma in a 50-year-old woman who presented with left-sided facial pain
and numbness, which had been present for 2 years, and diplopia, which had been present for 2 months. At
physical examination, the patient had bilateral papilledema, left ophthalmoparesis, an absent corneal reflex on
the left side, and left-sided deviation of the jaw. (a) Axial contrast-enhanced fat-suppressed T1-weighted MR
image shows a homogeneously enhancing mass involving the left cavernous sinus. Note the markedly narrowed
flow void of the left ICA (arrow). (b) Photomicrograph shows sheets of meningothelial cells with mild nuclear
pleomorphism, prominent nucleoli, and eosinophilic cytoplasm, as well as a mitotic figure (arrow). Whorling
is inconspicuous. The features are those of an atypical meningioma. (Hematoxylin-eosin [H-E] stain; original
magnification, 3400.)

cavernous sinus proper can encase the cavernous
segment of the ICA, causing its narrowing, or can
even invade the ICA wall (13).
Meningiomas are iso- to hypo­intense to gray
matter on T1- and T2-weighted MR images and
show homogeneous intense enhancement on
gadolinium-enhanced MR images. The cellular
nature of these tumors manifests as hyperat-
tenuation at nonenhanced CT and as restricted
diffusion at MRI. Although generally homoge-
neous in appearance, tumor heterogeneity can
be seen owing to calcification, tumor-associated
vascularity, cystic areas, and, rarely, hemorrhage.
The dural tail sign and hyperostosis of adjacent
bone, if depicted, can provide a clue to diagnosis.
Luminal narrowing of the ICA (Fig 6a) can be
seen if it is encased by tumor (14).
Schwannoma.—Schwannomas are benign nerve
sheath tumors arising from Schwann cells. Cav-
ernous sinus schwannomas most commonly arise
from the trigeminal nerve. Oculomotor schwan-
nomas are less common. Schwannomas arising
from the abducens nerve and the sympathetic
plexus around the ICA are extremely rare, with
only a few cases reported (15,16). Most lesions
occur sporadically, are solitary, and are encoun-
tered most commonly in patients in the 5th and
6th decades. Patients with neurofibromatosis type
2 develop multiple schwannomas at an earlier
age. Histologically, these tumors are composed of
spindle cells, which can be arranged in two pat-
terns: (a) Antoni type A, the compact or neuri-
lemoma pattern; or (b) Antoni type B, the loose
pattern (17). Verocay bodies and degenerative
changes are common. This results in a heteroge-
neous appearance of schwannomas at imaging,
especially when they are large.
On T2-weighted MR images, schwannomas
are heterogeneously hyperintense; and on T1-
weighted MR images, the lesions are hypointense.
Schwannomas demonstrate heterogeneous en-
hancement on gadolinium-enhanced T1-weighted
MR images (Fig 7). Cystic areas are common.
Fluid-fluid levels and hemorrhage can be seen
within the lesion. These lesions tend to have an
ovoid shape when they are restricted to the cav-
ernous sinus but assume a classic dumbbell shape
when they extend into the posterior cranial fossa,
the orbit, or the infratemporal fossa (18). Heavily
T2-weighted thin-section MR images are useful
to directly depict the cranial nerves and assess
their relation to the tumor. However, it may be
difficult to localize the origin to a particular cra-
nial nerve, especially when the lesion is restricted
to the confines of the cavernous sinus.
802  May-June 2019 radiographics.rsna.org

Figure 7.  Cavernous sinus schwannoma in a 55-year-

old woman presenting with a holocranial headache,
which had been present for 1.5 years, and diplopia,
which had been present for 1 year. The patient had
bilateral papilledema, right temporalis wasting, an ab-
sent right corneal reflex, and right lateral rectus palsy.
(a) Axial fat-suppressed T2-weighted MR image shows
a hyperintense lesion in the right cavernous sinus, with
an anterior cystic component (arrow). (b) Axial contrast-
enhanced fat-suppressed T1-weighted MR image shows
enhancement in the solid component. (c) Photomicro-
graph shows fascicles of spindle-shaped cells arranged
compactly (at left) and loosely (at right), with wavy
mildly pleomorphic nuclei, inconspicuous nucleoli, and
eosinophilic cytoplasm. (H-E stain; original magnifica-
tion, 3100.)

Plexiform Neurofibroma.—Plexiform neurofi- thought to arise from the pericytes surrounding

bromas are seen almost exclusively in the set-
ting of neurofibromatosis type 1. These lesions
most commonly occur in the distribution of the
ophthalmic or maxillary divisions of the trigemi-
nal nerve in young adults. The involved cranial
nerves become diffusely enlarged. Histologically,
there is a multinodular pattern from the involve-
ment of multiple fascicles, which are expanded
by tumor cells and wisps of collagen. Lesions
typically show peripheral T2 hyperintensity and
central hypointensity, a finding that has been la-
beled as the “target sign” (Fig E1). Other features
of neurofibromatosis type 1, such as sphenoid
wing dysplasia, can provide additional clues to
the diagnosis. The amount of enhancement after
administration of a gadolinium-based contrast
agent can be variable. Pointers to malignant
change in a plexiform neurofibroma are rapid
growth, an irregular infiltrative outline, loss of
the target sign, disproportionate erosion of bone,
a peripheral enhancement pattern, peritumoral
edema, and intratumoral cysts (19,20).
Solitary Fibrous Tumor/Hemangiopericytoma.—
These are rare mesenchymal neoplasms that are
the capillaries and precapillary venules. In the
central nervous system, these neoplasms usually
arise from the dura. Previously known as simply
hemangiopericytoma, this tumor has been reclassi-
fied into the category of a combined entity termed
solitary fibrous tumor/hemangiopericytoma in the
2016 update to the fourth edition of the WHO
classification of central nervous system neoplasms
because of the similarities in the genetic makeup of
these tumors (21). At histopathologic examination,
the tumor exhibits a spectrum of two patterns.
The classic solitary fibrous tumor–like pattern is a
patternless architecture of hypo- and hypercellular
areas of spindle-shaped to oval cells separated by
thick bands of keloid-like or amianthoid-like col-
lagen. The other pattern is that of a classic heman-
giopericytoma, with high cellularity composed of
ovoid cells with a haphazard pattern and a charac-
teristic branching “staghorn” pattern of vascula-
ture. In the WHO classification, these tumors are
graded in a three-tier system, with grade I tumors
being considered as benign and with grade II and
grade III tumors considered as malignant. Most of
these neoplasms harbor a genomic inversion at the
12q13 locus that fuses the NGFI-A binding pro-
RG  •  Volume 39  Number 3 Mahalingam et al  803

Figure 8.  Cavernous hemangioma in a 40-year-old woman with decreased vision in the
left eye that had been present for 6 months. No other clinically important cranial nerve
deficits were seen. (a) Axial T2-weighted MR image shows a homogeneous hyperintense
mass (arrow) in the left cavernous sinus and the left trigeminal cave (Meckel cave). The
superior orbital fissure (arrowhead) is not involved. (b) Axial T1-weighted MR image
obtained 2 minutes after contrast agent injection shows central enhancement within the
lesion. (c) Axial T1-weighted MR image obtained 9 minutes after contrast agent injection
shows complete fill-in of contrast agent, with homogeneous enhancement. (Note that
the gadolinium-enhanced images in b and c have a different axial orientation, compared
with the axial T2-weighted image in a.) (d) Scintigraphic image obtained after adminis-
tration of technetium 99m (99mTc) pertechnetate–labeled red blood cells shows accumu-
lation of the tracer within the lesion in the left cavernous sinus (arrow).

cavernous sinus or cerebellopontine angles and

tein 2 gene, NAB2, and the signal transducer and
activator of transcription 6 gene, STAT6, leading
to STAT6 nuclear expression (22).
The imaging features of solitary fibrous tumor/
hemangiopericytoma closely mimic those of me-
ningiomas. Some of the clues that are suggestive
of a diagnosis of solitary fibrous tumor/heman-
giopericytoma are a narrow base of attachment
to the dura, erosion of the adjacent bone, and
the presence of associated flow voids (Fig E2).
On the other hand, meningiomas usually have a
broad base of attachment to the dura, hyperosto-
sis of adjacent bone, and intratumoral calcifica-
tion. Solitary fibrous tumor/hemangiopericytoma
also occurs in a younger age group, compared
with meningiomas, which occur in patients in the
5th to 7th decades (23).
Cavernous Hemangioma.—Cavernous heman­
g­iomas are not true neoplasms and are better
described as vascular malformations. In the
central nervous system, they are encountered
most commonly in the brain parenchyma. Extra-
axial hemangiomas are rare and can occur in the
have clinical behavior and imaging features dif-
ferent from their intra-axial counterparts (24,25).
Extra-axial hemangiomas occur more commonly
in middle-aged women. Microscopically, these le-
sions consist of numerous dilated vascular chan-
nels lined by endothelial cells.
At MRI, cavernous hemangiomas are charac-
terized by high signal intensity on T2-weighted
and FLAIR MR images. Dynamic contrast-
enhanced T1-weighted MR images show char-
acteristic progressive “fill-in” of contrast agent,
with intense homogeneous enhancement on
late gadolinium-enhanced MR images (Fig 8).
Hemangiomas encasing the cavernous segment
of the ICA usually do not cause luminal nar-
rowing of the ICA, in contrast to meningiomas,
which tend to cause luminal narrowing of the
ICA. Scintigraphic imaging after administration
of 99mTc pertechnetate–labeled red blood cells
demonstrates accumulation of tracer within the
lesion, a finding that is said to be specific for
making the diagnosis of cavernous hemangioma
(25). Digital subtraction angiography may show
hypertrophic branches from the ICA and the ex-
ternal carotid artery, as well as variable vascular
blush (26). Establishing the diagnosis of cavern-
ous hemangioma before surgery is of paramount
importance, because these tumors are notorious
for causing profuse and often uncontrollable
intraoperative hemorrhage.
804  May-June 2019 radiographics.rsna.org

Figure 9.  Cavernous sinus melanoma in a 36-year-old woman who presented with headache,
which had been present for 3 years, numbness on the left side of the face, difficulty in chewing
on the left side, and diplopia, which had been present for 6 months. The patient had left lateral
rectus palsy, mild ptosis, left temporalis and masseter wasting, and an absent left corneal reflex.
(a) Axial nonenhanced CT image at the level of the cavernous sinuses shows a heterogeneous
mass with peripheral hyperattenuation in the left cavernous sinus. (b) Coronal T1-weighted
MR image shows the T1 hyperintensity of the mass (arrow). (c) Photomicrograph shows sheets
and nests of spindle-shaped to polygonal cells that are heavily pigmented and show moderate
nuclear pleomorphism and some prominent nucleoli. (H-E stain; original magnification, 3400.)

Melanocytoma or Melanoma.—Primary melano-

cytic tumors are said to arise from melanocytes in
the leptomeninges. These tumors can be benign
(represented by melanocytoma) or malignant
(melanoma). Malignant melanoma of the central
nervous system can be primary or metastatic. At
histopathologic examination, these tumors are
made up of polygonal to spindle-shaped cells.
Mitotic activity and nucleoli are inconspicuous in
melanocytomas but are prominent in melanomas.
Other pigmented neoplasms of the central nervous
system, such as melanocytic meningiomas and
melanocytic schwannomas, can mimic melanoma
at histopathologic examination.
Common sites of occurrence for melano-
cytoma or melanoma in the central nervous melanocytosis of the first and second divisions
system are the posterior fossa, the trigeminal of the trigeminal nerve (28).
cave (Meckel cave), and the cervical and tho-
racic spinal canal. Most patients with primary Tumors That Arise from Adjacent
me­ningeal melanocytoma are in the 5th decade Structures and Secondarily Invade
of life (27). Melanoma of the cavernous sinus is the Cavernous Sinus
a rare entity. These lesions are hyperattenuating
on CT images. At MRI, the lesions demonstrate Pituitary Adenoma.—Pituitary adenomas are
characteristic hyperintensity on T1-weighted the most common lesion to involve the cavern-
MR images and heterogeneous signal inten- ous sinus. They are primarily tumors of adults.
sity on T2-weighted MR images, with areas These tumors can be functional or clinically and
of hypointensity ascribed to the paramagnetic biochemically silent. Although prolactinomas
effects of melanin (Fig 9). Enhancement of a and corticotroph adenomas are more frequent in
melanoma of the cavernous sinus after admin- women, growth hormone–secreting adenomas are
istration of a gadolinium-based contrast agent more often found in men. Around a quarter of
can be variable, ranging from no enhancement all adenomas are the null-cell type (29). Around
to intense enhancement. This tumor can also 6%–10% of all pituitary adenomas invade the
be associated with cutaneous nevus of Ota and cavernous sinus.
RG  •  Volume 39  Number 3 Mahalingam et al  805

Figure 10.  Juvenile nasopharyngeal angiofibroma in a 15-year-old male patient presenting with recur-
rent epistaxis and nasal obstruction, which had been present for 3 years. (a) Axial gadolinium-enhanced
fat-suppressed T1-weighted MR image shows an intensely enhancing mass lesion centered in the left
pterygopalatine fossa, causing its expansion, with anterior bowing of the posterior wall of the left maxil-
lary sinus (white arrow). A normal right pterygopalatine fossa (black arrow) is also depicted. (b) Axial
gadolinium-enhanced fat-suppressed T1-weighted MR image obtained at a more cranial level than a
shows involvement of the left cavernous sinus and orbit by the lesion.

Invasion of the cavernous sinus is an impor-
tant prognostic factor with regard to surgery for
pituitary adenomas, with a higher incidence of
both intraoperative ICA injury and postoperative
leakage of cerebrospinal fluid (CSF) when cav-
ernous sinus invasion is present. Hence, preoper-
ative identification of cavernous sinus invasion is
of paramount importance. The lateral part of the
dural sac of the pituitary gland forms the medial
wall of the cavernous sinus, and its perforation
by the tumor indicates cavernous sinus invasion.
However, this thin dural layer is not depicted
with routine CT or MRI; and hence, indirect
signs have been proposed to predict cavernous
sinus invasion. Knosp et al (30) used medial,
median, and lateral intercarotid lines to classify
pituitary adenomas invading the cavernous sinus;
and Cottier et al (31) used the percentage of
ICA circumference contacting the tumor and the
invasion of five venous compartments around the
ICA. These two classification systems are repre-
sented in Figure E3 (30,31). Greater than 67%
circumferential contact with the ICA indicates
invasion, and less than 25% contact and the tu-
mor not crossing the medial intercarotid line have
high negative predictive values for invasion.
occur almost exclusively in adolescent male pa-
tients. Recurrent spontaneous epistaxis is the usual
presenting symptom. Histologically, these tumors
consist of stellate and staghorn-shaped blood ves-
sels embedded in an irregular fibrous stroma with
interspersed spindle-shaped fibroblasts. Cavernous
sinus invasion by juvenile nasopharyngeal angio-
fibroma can occur owing to skull base erosion or
extension by way of the skull base foramina.
Juvenile nasopharyngeal angiofibromas are
generally hyperintense to muscle on T2-weighted
MR images and iso- to hypointense on T1-
weighted MR images. Flow voids can be observed
within the lesion, reflecting its highly vascular
nature. Juvenile nasopharyngeal angiofibromas
exhibit intense enhancement on gadolinium-
enhanced MR images (Fig 10). Expansion of the
pterygopalatine fossa is an important diagnostic
clue to a diagnosis of juvenile nasopharyngeal
angiofibroma. The lesion characteristically
causes anterior bowing of the posterior wall of
the maxillary sinus. These tumors have a notori-
ous tendency to bleed profusely when dissected.
Hence, preoperative endovascular embolization
of the tumor is a part of routine management of
these lesions (32,33).

Juvenile Nasopharyngeal Angiofibroma.—These Chondrosarcoma.—Cranial chondrosarcomas

lesions are locally aggressive, histologically benign usually arise from the skull base, most com-
neoplasms that arise in the nasal cavity or naso- monly at the site of the petro-occipital synchon-
pharynx near the sphenopalatine foramen. They drosis, and can extend to involve the cavernous
806  May-June 2019 radiographics.rsna.org

Figure 11.  Chondrosarcoma in a 25-year-old man who presented with numbness on the left side of
the face, difficulty in chewing, diplopia on looking to the left, and a left-sided headache, which had been
present for 2 years. The patient had left lateral rectus palsy, left temporalis wasting, and an absent left
corneal reflex. (a) Axial nonenhanced CT image shows a mass causing expansion of the left petrous apex.
Note the large calcified component of the mass anteriorly (arrow). (b) Axial fat-suppressed T2-weighted
MR image shows a markedly hyperintense mass lesion (arrow) involving the posterior part of the left
cavernous sinus.

sinus. These lesions are usually slow growing
but invasive lesions. Cranial chondrosarcomas
can be encountered in any age group, with the
average age of occurrence being in the 4th and
5th decades (34). On the basis of the histo-
pathologic findings, cranial chondrosarcomas
are subdivided into three types: classic, mesen-
chymal, and dedifferentiated. The classic type
is the most common and consists of large cells
with abundant pale cytoplasm in a chondroid
background matrix.
MRI characteristically demonstrates high
signal intensity in chondrosarcomas on T2-
weighted MR images because of the chondroid
matrix. Regions of low signal intensity can
be depicted owing to calcifications. The le-
sions usually show marked enhancement on
gadolinium-enhanced MR images (35). CT
demonstrates matrix calcification in a chondroid
pattern (“ring and arc” pattern) and helps in the
assessment of bone destruction (Fig 11).
Chordoma.—Chordomas are locally aggressive
neoplasms of the axial skeleton, with around
one-third occurring in the clivus. Chordomas
are mostly encountered in patients who are in
the 4th decade of life (36). Chordomas arise
from notochordal cell rests. The clival chordo-
mas arise from the spheno-occipital junction.
On the basis of the histopathologic findings,
chordomas can be classified into classic and
chondroid types. The classic type of chordoma
consists of lobules containing highly vacuolated
physaliferous cells and pools of mucin sepa-
rated by fibrous septa. The chondroid variety
of chordoma may have histopathologic features
closely resembling those of chondrosarcomas,
and analysis of immunohistochemical markers is
often required for accurate distinction between
these two entities. Chordomas are positive for
epithelial markers such as cytokeratin and epi-
thelial membrane antigen, but chondrosarcomas
are not (37). Chordomas are typically located in
the midline of the skull base.
At imaging of chordomas, CT shows a well-de-
fined soft-tissue mass with lytic destruction of the
bone. At MRI, the signal intensity characteristics
of chordomas parallel those of chondrosarcoma.
The T2 hyperintensity of chordomas is ascribed
to the high fluid content of the physaliferous cells.
The chondroid variant of chondrosarcoma more
commonly has calcifications within (36). Differ-
entiation of chordomas from chondrosarcomas
can be difficult at imaging, especially if the lesion
grows in a position off the midline.
Nasopharyngeal Carcinoma.—Nasopharyn-
geal carcinomas are the most common primary
malignancy of the nasopharynx and the most
common extracranial malignancy to invade the
cavernous sinus. Nasopharyngeal carcinomas
are encountered in patients in the 5th and 6th
decades of life. Nasopharyngeal carcinomas can
be of two pathologic types: (a) the keratinizing
RG  •  Volume 39  Number 3 Mahalingam et al  807
type, which is similar in behavior to other head
and neck squamous cell carcinomas; and (b) the
non­keratinizing type, which is strongly associ-
ated with Epstein-Barr virus infection. Cavernous
sinus involvement occurs by perineural spread or
by direct invasion of the skull base (38). Cavern-
ous sinus involvement occurs late in the course of
the disease and represents T4 disease in the TNM
staging of nasopharyngeal carcinoma. The signal
intensity characteristics of nasopharyngeal car-
cinomas at MRI are nonspecific—iso- to hypo­
intense on T1-weighted MR images, hyperintense
on T2-weighted MR images, and heterogeneous
enhancement on gadolinium-enhanced MR im-
ages. Bulky metastatic cervical lymphadenopathy
is usually seen (Fig E4).
Adenoid Cystic Carcinoma.—Adenoid cystic
carcinomas are malignant tumors of the mi-
nor and major salivary glands, with a marked
propensity for perineural spread. These lesions
account for about one-third of all minor salivary
gland tumors (33). Common sites of origin in
the head and neck are the palate, nasopharynx,
parapharyngeal space, buccal mucosa, and the
tongue. Adenoid cystic carcinomas can occur in
a wide range of age groups, with a peak rate of
occurrence in the 5th and 6th decades. Adenoid
cystic carcinomas have an apparently indolent
course but have aggressive long-term behavior,
with high rates of recurrence. On the basis of
their architecture, adenoid cystic carcinomas
can be divided into three types—tubular, crib-
riform, and solid, in order of increasing aggres-
siveness (39).
MRI is the modality of choice for staging
adenoid cystic carcinomas, owing to its superior
delineation of perineural extension. Gadolin-
ium-enhanced fat-suppressed MR images are
useful for this purpose (Fig E5). Although the
presence of a small primary carcinoma with
extensive perineural spread may provide a clue
to this diagnosis, this feature is not specific
and may be seen in other malignancies, such
as squamous cell carcinoma, mucoepidermoid
carcinoma, melanoma, and lymphoma (40).
Sinonasal Carcinoma.—Carcinoma of the
paranasal sinus can involve the cavernous sinus
by way of direct invasion and bone destruction.
Sphenoid sinus carcinoma, although rare and
accounting for less than 1% of all sinonasal car-
cinomas, is the most common of the sinonasal
carcinomas to invade the cavernous sinus, owing
to its anatomic proximity (33).
Rhadomyosarcoma.—Rhabdomyosarcoma is a
tumor of the pediatric age group, with around
40% of rhabdomyosarcomas occurring in the
head and neck region. Common sites of occur-
rence in the head and neck region include the
nasopharynx, the parapharyngeal and mastica-
tor spaces, the paranasal sinuses, and the orbits.
Rhabdomyosarcoma often manifests as a solitary
bulky heterogeneous mass (41). Rhabdomyosar-
coma can invade the cavernous sinus by way of
bone destruction or perineural extension.
Suprasellar Neoplasms.—A wide spectrum of
lesions can arise in the suprasellar region and
secondarily involve the cavernous sinus. More
common among these lesions are (a) germ cell
tumors and (b) craniopharyngiomas.
Intracranial germ cell tumors are a heteroge-
neous group of lesions that occur in the pineal
and suprasellar region. Of these lesions, 90%
occur in patients before the age of 20 years
(42). Intracranial germ cell tumors are broadly
divided into germinomatous and nongermino-
matous tumors (namely, embryonal carcinoma,
yolk sac tumor, and choriocarcinoma). Supra-
sellar germinomas classically manifest with
diabetes insipidus, emaciation, or precocious
puberty. Peculiar to germ cell tumors is the se-
cretion of protein markers, such as α-fetoprotein
and the beta subunit of human chorionic go-
nadotropin, that can be detected in the serum
and CSF. The combination of extremely high
levels of these proteins and the presence of a
suprasellar mass virtually clinches the diagnosis
of germ cell tumor. These tumors have a varied
appearance at imaging; germinomas usually are
solid, and nongerminomatous lesions are said
to be more heterogeneous, with cystic and solid
areas. Nongerminomatous lesions tend to be
more invasive (Fig E6). Imaging features are not
specific enough to be used to distinguish be-
tween germinomatous and nongerminomatous
germ cell tumors. Teratomas can manifest as a
heterogeneous cystic mass with fat and calcifica-
tion (43).
Craniopharyngiomas are sellar and/or supra-
sellar tumors that arise from remnants of the
craniopharyngeal duct. Cavernous sinus inva-
sion is rare. Craniopharyngioma has a bimodal
age distribution, with peaks in the 2nd decade
and in the 4th to 6th decades. Craniopharyngio-
mas are divided into two types: (a) the adaman-
tinomatous type, which occurs predominantly in
children and is characterized by the presence of
wet keratin, stellate reticulum, and cholesterol
granuloma; and (b) the papillary type, which
occurs in adults and shows more squamous
differentiation. Adamantinomatous craniopha-
ryngiomas have a T1-hyperintense component
owing to “motor oil cysts” (“machine oil cysts”)
808  May-June 2019 radiographics.rsna.org

Figure 12.  Lymphoma in a 61-year-old man who presented with left-sided fa-
cial pain, diplopia, weight loss, and fever, which had been present for 2 months.
(a) Axial T2-weighted fat-saturated MR image shows isointense soft tissue involv-
ing and expanding the left cavernous sinus (arrow). (b, c) Axial diffusion-weighted
MR image (b) and apparent diffusion coefficient map (c) show diffusion restric-
tion within the mass lesion (arrow on b) in the left cavernous sinus. (d) Axial PET/
CT fusion image shows intense uptake of fluorine 18 fluorodeoxyglucose (FDG)
within the mass (arrow). Multiple other lesions with intense FDG uptake were also
found in the lungs, kidneys, liver, and multiple lymph nodes (not shown). The
findings from histopathologic examination of the specimen from biopsy disclosed
high-grade non-Hodgkin lymphoma.

and are frequently calcified; papillary craniopha-

ryngiomas are solid and are not calcified (44).

Systemic Neoplasia

Lymphoma.—Systemic lymphoma and leukemia

can involve the cavernous sinus either by direct
extension from adjacent structures, such as the
marrow of surrounding bones or the nasophar-
ynx, or by hematogenous dissemination. Most of
these lesions represent non-Hodgkin lymphoma.
A primary lymphomatous lesion of the cavern-
ous sinus without evidence of systemic disease
is exceedingly rare (45). At MRI, lymphoma-
tous lesions often are T2 hypointense and show
diffusion restriction owing to their high cel-
lularity. On gadolinium-enhanced MR images,
these lesions demonstrate intense enhancement.
Lymphoma can mimic Tolosa-Hunt syndrome
clinically and radiologically (46). PET plays an
important role in assessing the extent of sys-
temic disease involvement (Fig 12).
Myeloma or Plasmacytoma.—Cavernous sinus
involvement can be due to invasion from adja-
cent bone marrow disease (myeloma) or can be
due to extramedullary plasmacytoma occurring
within the cavernous sinus (47,48). Patients
with primary extramedullary plasmacytoma
may go on to develop multiple myeloma later.
Imaging features are nonspecific and mimic
those seen in other aggressive neoplasms, such
as lymphoma and metastasis.
Histiocytosis.—Histiocytosis is the term applied
to a group of disorders that are characterized by
proliferation of macrophages and dendritic cells
and that occur predominantly in children. Ac-
cording to the WHO classification, these disor-
ders are divided into three groups: (a) dendritic
cell disorders, such as Langerhans cell histio-
cytosis and Erdheim-Chester disease; (b) mac-
rophage disorders, such as Rosai-Dorfman
disease; and (c) malignant histiocytic disorders.
The most commonly encountered entity among
these disorders is Langerhans cell histiocytosis
(49). Lan­ger­hans cell histiocytosis is character-
ized histologically by myeloid dendritic cells that
are positive for CD1a and demonstrate Birbeck
granules at electron microscopic examination.
These cells are accompanied by lymphocytes
RG  •  Volume 39  Number 3 Mahalingam et al  809

Figure 13.  Cavernous sinus thrombosis in a 24-year-old woman who presented with headache, which
had been present for 2 weeks, left-sided exophthalmos, and multiple episodes of seizures during the
previous 24 hours. (a) Coronal T2-weighted MR image shows a bulky left cavernous sinus with a convex
lateral margin (arrow). (b) Axial contrast-enhanced fat-suppressed T1-weighted MR image shows filling
defects in the left cavernous sinus (arrow) and in the left superior ophthalmic vein (arrowhead). Also note
the abnormal enhancement of the retro-orbital fat, with enhancing soft-tissue thickening in the preseptal
space of the left orbit.

and eosinophils. These disorders can occasion-
ally involve the cavernous sinus, either owing to
contiguous invasion from a skull base lesion or
owing to dural disease. These lesions have been
described as being hypointense on T2-weighted
MR images and demonstrate variable contrast
enhancement (50) (Fig E7).
Metastasis.—Metastasis to the cavernous sinus
can occur by way of hematogenous, perineural,
or direct vascular spread. Head and neck ma-
lignancies are the most common ones to me-
tastasize to the cavernous sinus. Distant tumors
that metastasize to the cavernous sinus are lung,
breast, renal, and gastric malignancies (14). An
aggressive cavernous sinus lesion in the presence
of a known malignancy at another site often
clinches the diagnosis of metastatic disease.
However, cavernous sinus syndrome owing to
metastatic involvement may occasionally be the
presenting symptom of an occult malignancy.
Diagnosis of a metastatic lesion should be given
consideration especially when a lesion with ag-
gressive features, such as bone destruction, is
encountered.
Vascular Conditions
Vascular lesions of the cavernous sinus—namely,
cavernous sinus thrombosis, CCF, and ICA an-
eurysm—are great clinical mimics, with a wide
variety of clinical manifestations varying from
trivial to life threatening. Among this category
of cavernous sinus lesions, septic thrombosis is
the most common and is managed primarily by
controlling the source of sepsis with medical and
surgical means. Digital subtraction angiography
plays an important role in the management of
CCF and ICA aneurysm.
Cavernous Sinus Thrombosis
Cavernous sinus thrombosis most often occurs
as a complication of bacterial or fungal sepsis in
the paranasal sinuses, the face, the orbits, and
the skull base. The tributaries of the cavernous
sinus do not possess any valves and allow bidirec-
tional flow, thus predisposing the sinus to septic
involvement (51). The clinical manifestations of
cavernous sinus thrombosis are often dramatic
and are characterized by sudden-onset painful
ophthalmoplegia, exophthalmos, and vision loss.
Cavernous sinus thrombosis is more common in
patients with diabetes and those with an immu-
nocompromised status.
Imaging signs of cavernous sinus thrombosis
include a bulky cavernous sinus, a convex con-
figuration of the lateral wall, and filling defects
within the sinus. Pitfalls in interpretation of cav-
ernous sinus filling defects are highlighted in the
section, “Pitfalls in Interpretation and Pseudole-
sions.” Indirect signs that support the diagnosis
of cavernous sinus thrombosis are back pressure
changes such as an engorged or thrombosed
superior ophthalmic vein manifest as a loss of
its flow void, ipsilateral retro-orbital fat strand-
ing, bulky extraocular muscles, and exophthal-
mos (52) (Fig 13). T1 and T2 signal intensity
810  May-June 2019 radiographics.rsna.org

Figure 14.  CCF in a 20-year-old man with a history of head injury 1 month ago and progressive left exophthalmos during the previ-
ous 2 weeks. (a) Axial fat-suppressed T2-weighted MR image shows a bulky and hypointense left cavernous sinus (black arrowhead)
with left-sided exophthalmos. Also note the stranding of the retrobulbar fat and the prominent extraocular muscles in the left orbit
(white arrowheads). (b) Coronal T2-weighted MR image of the orbits shows a dilated left superior ophthalmic vein (arrow). (c) Digi-
tal subtraction angiographic image of the left ICA obtained in the lateral view shows opacification of the left cavernous sinus (arrow)
and its tributaries in the early arterial phase. SOV = superior ophthalmic vein.

is not reliable for the diagnosis of cavernous ICA Aneurysm

sinus thrombosis in isolation, because the signal
intensity of a normal cavernous sinus is variable.
Diffusion-weighted MRI can be especially useful
in the acute stages of cavernous sinus throm-
bosis and can demonstrate diffusion restriction
within the sinus itself (Fig E8).
Carotid-Cavernous Fistula
CCF represents an abnormal communication
from the carotid artery to the cavernous sinus; this
communication can be either direct or indirect by
way of the branches of the carotid artery. CCF can
be traumatic or spontaneous, with the traumatic
type being more common, representing 75% of all
CCFs (53). Most of the posttraumatic CCFs are
encountered in young male subjects. In contrast,
spontaneous CCFs are more common in older fe-
male subjects. The clinical manifestations of CCF,
especially the direct type, tend to be dramatic,
with progressive pulsatile exophthalmos, chemosis,
and diplopia. The indirect type of CCF has a more
insidious onset and can mimic an inflammatory
cause, with a waxing and waning course.
The reference standard for diagnosis of CCF
is digital subtraction angiography. Features
of CCF at routine MRI include a bulky ipsi-
lateral cavernous sinus, exaggerated adjacent
flow voids, a dilated superior ophthalmic vein,
stranding of the retro-orbital fat, and bulky ex-
traocular muscles (Fig 14). CT angiography has
been shown to be equivalent to digital subtrac-
tion angiography and better than MR angiogra-
phy in the detection of CCFs (54). Transarterial
or transvenous endovascular embolization is the
preferred method of treatment.
Aneurysms arising from the cavernous segment
of the intracranial ICA constitute around 2%–
9% of all intracranial aneurysms and around 5%
of giant aneurysms (>2.5 cm) (55). Most cav-
ernous ICA aneurysms are asymptomatic and
are incidentally detected at imaging, most often
in women older than 50 years (56). When these
aneurysms are symptomatic, the most common
manifestation is diplopia and headache owing to
mass effect. Rupture can rarely occur and can
manifest with symptoms unique to the location
of these aneurysms, such as epistaxis, spontane-
ous CCF, subarachnoid hemorrhage, and cere-
bral infarction owing to distal embolization.
At CT, cavernous ICA aneurysms are mildly
hyperattenuating compared with brain paren-
chyma and can show peripheral curvilinear
calcifications. The signal intensity within the
aneurysm on MR images can be highly variable
and depends on the patency of and flow rate
through the aneurysm. On T2-weighted MR
images, the aneurysm can be seen as a flow void
or can be heterogeneously hyperintense ow-
ing to slow flow or partial thrombosis (Fig 15).
Pulsation artifacts can also be seen. Completely
thrombosed aneurysms generally demonstrate
iso- to hyperintense signal intensity on both
T1- and T2-weighted MR images (57) (Fig E9).
Digital subtraction angiography plays an impor-
tant role in planning management of cavernous
ICA aneurysms. It is important to note that the
signal intensity of the lesion on MR images can
be misleading, and the clue to diagnosis is the
round shape of the lesion and its continuity with
the ICA.
RG  •  Volume 39  Number 3 Mahalingam et al  811

Figure 15.  ICA aneurysm in a 50-year-old woman with a history of occasional headache for 2 years who
presented with right hemiparesis, which had been present for 1 day after an episode of loss of conscious-
ness. (a) Axial fat-suppressed T2-weighted MR image shows a rounded heterogeneous lesion in the left
cavernous sinus. The heterogeneous signal intensity within the lesion is due to turbulent flow. A few small
acute infarcts were seen in the left frontal lobe in the territory of the middle cerebral artery (not shown).
(b) Digital subtraction angiographic image of the left ICA obtained in the lateral view shows a large an-
eurysm involving the cavernous segment of the ICA.

Infective and invasive, and chronic granulomatous invasive

Inflammatory Conditions
A wide spectrum of infective and inflammatory
disorders can affect the cavernous sinus, includ-
ing fungal infections (acute or chronic), tuber-
culosis, actinomycosis, sarcoidosis, immuno-
globulin G4 (IgG4)–related disease, idiopathic
hypertrophic pachymeningitis, granulomatosis
with polyangiitis, and Tolosa-Hunt syndrome.
Considerable overlap exists in the radiologic
findings of cavernous sinus involvement in infec-
tive or inflammatory diseases; the most common
findings encountered are a bulky cavernous si-
nus and increased enhancement, which may ex-
tend to the orbit or the adjacent dura. Imaging
clues that point to infection or inflammation as
the possible cause, as compared with neoplasms,
are a sheetlike configuration of the abnormal
soft tissue and T2 hypointensity. However,
certain neoplasms, such as lymphoma and en
plaque meningioma, can mimic these findings.
Among this spectrum of infective and inflam-
matory disorders, Tolosa-Hunt syndrome is a
diagnosis of exclusion; other disease processes
are diagnosed by specific serum or histopatho-
logic biomarkers. Individual disease processes
are reviewed in the following paragraphs, with
an emphasis on multidisciplinary evaluation.
Fungal Infection
Cavernous sinus involvement with fungal infec-
tion is due to spread from an invasive fungal
infection of the paranasal sinus. Invasive fungal
infection is classified into acute invasive, chronic
types on the basis of histologic criteria (58).
The acute invasive, or fulminant, subtype of
invasive fungal infection occurs in the setting
of immunocompromise, such as uncontrolled
diabetes mellitus or posttransplant immunosup-
pression, and is characterized by a painless, ne-
crotic black nasal septal or palatal ulcer that rap-
idly progresses into full-blown cavernous sinus
syndrome and ICA thrombosis, with extremely
high mortality rates. Angioinvasion by fungal
hyphae is characteristic of this disease. The
previously described imaging features of cavern-
ous sinus thrombosis are seen. MRI can be used
to assess the extent of disease much better than
CT. Bone erosion, although a specific feature
suggestive of invasive disease, often occurs late
in the course of the disease. The infarcted tissue
characteristically has a nonenhancing T2-hy-
pointense nature; in the nasal turbinate, this fea-
ture has been called the “black turbinate sign”
(Fig 16) (59). Diffusion-weighted MRI can
show infarction of the optic nerve or the brain
parenchyma either owing to direct parenchymal
invasion or ICA invasion and thrombosis.
The chronic invasive and chronic granu-
lomatous invasive subtypes of invasive fungal
infection generally occur in immunocompetent
patients, although diabetes mellitus and steroid
therapy are risk factors. The disease evolves
during a period of months to years and is
characterized by dense accumulation of fungal
hyphae and mixed bone erosion and sclerosis
(60). CT shows hyperattenuating soft tissue
812  May-June 2019 radiographics.rsna.org

Figure 16.  Acute invasive fungal infection in a 62-year-old man with uncontrolled diabetes mellitus
who presented with right facial pain, which had been present for 1 week, loss of vision in the right eye,
and a fever, which had been present for 2 days. The level of hemoglobin A1c at admission was 13.6 g/
dL. (a) Coronal contrast-enhanced T1-weighted MR image shows mucosal thickening involving the right
maxillary sinus (white arrow) and nonenhancing nasal turbinates (black arrow) on the right side. (b) Axial
contrast-enhanced fat-suppressed T1-weighted MR image shows a filling defect in the right cavernous
sinus (black arrowhead), as well as right exophthalmos (white arrowhead). (c) Photomicrograph shows
necrotic debris with occasional broad aseptate basophilic fungal hyphae (arrow). Fungal culture (not
shown) grew Aspergillus flavus and Rhizopus arrhizus. (H-E stain; original magnification, 3200.)

in the sinuses, which demonstrates markedly

T2-hypointense signal intensity attributed to
the accumulation of paramagnetic ions in the
fungal hyphae. These chronic invasive subtypes
are great mimics of the noninfective inflamma-
tory spectrum of diseases, both clinically and
at imaging. Moreover, if corticosteroid therapy
is inadvertently administered to a patient with
invasive fungal disease, the therapy can cause
rapid worsening of the disease. Histopathologic
examination hence plays a central role in diag-
nosing invasive fungal disease.

Tuberculosis
Tuberculosis is an infectious disease caused by
Mycobacterium tuberculosis that can rarely involve
the cavernous sinus, with both acute (61) and
chronic cavernous sinus syndrome (62) being
reported in the literature. Disease manifestation
of the chronic form can mimic meningioma and
other chronic inflammatory disorders, with the
diagnosis being established by histopathologic
demonstration of granulomatous inflamma-
tion with caseous necrosis (Fig E10). Culture of
M tuberculosis from the biopsy sample is the only
definitive proof of diagnosis but is often elusive.
Sarcoidosis
Sarcoidosis is a multisystem granulomatous
disorder of unknown etiology. Cavernous sinus
involvement is rare. It can occur as part of sys-
temic disease or rarely as isolated cavernous sinus
disease. Elevated serum angiotensin-converting
enzyme levels may provide a clue to the diagno-
sis, although this finding is not specific or sensi-
tive. The results of histopathologic examination
show noncaseating granulomas, with no organ-
isms or other causes of granulomatous reaction
(63) (Fig 17).
IgG4-related Disease
IgG4-related disease is a recently recognized
multisystemic fibroinflammatory disease entity
characterized by lesions with a dense IgG4-
positive lymphoplasmacytic infiltrate, storiform
fibrosis, and elevated serum IgG4 levels (64). Al-
though first recognized in the context of autoim-
RG  •  Volume 39  Number 3 Mahalingam et al  813

Figure 17.  Sarcoidosis in a 64-year-old man who presented with cognitive impairment, which had been present
for 1 year, polyuria, and polydipsia, which had been present for 2 months. There were no cranial nerve deficits.
(a) Coronal T2-weighted MR image shows T2-hypointense soft tissue (arrow) involving the right sphenoid sinus and
the right cavernous sinus. (b) Photomicrograph shows a supraclavicular lymph node with its architecture partially
effaced by discrete granulomas composed of epithelioid histiocytes admixed with few lymphocytes, and Langhans-
type (white arrows) and foreign body–type (straight black arrow) multinucleate giant cells. Basophilic concentric
lamellar bodies (curved black arrow), resembling Schaumann bodies, are depicted. Serum angiotensin-converting
enzyme levels were within normal limits. (H-E stain; original magnification, 3100.)

mune pancreatitis, IgG4-related disease has now
been reported to involve almost all organ systems.
Similar to sarcoidosis, it is a unifying histologic
diagnosis for diverse clinical syndromes. Ume-
hara et al (65) have proposed comprehensive
diagnostic criteria for this disease on the basis of
serum IgG4 levels and histologic criteria. Cav-
ernous sinus involvement is often accompanied
by orbital and dural disease characterized by
T2-hypointense thickening of involved tissue and
marked enhancement after administration of a
gadolinium-based contrast agent (Fig E11). The
nerves of the cavernous sinus may show thicken-
ing and enhancement (66).
Granulomatosis with Polyangiitis
Formerly known as Wegener granulomatosis,
granulomatosis with polyangiitis is a necrotizing
small-vessel vasculitis characterized by involve-
ment of the nose and/or paranasal sinuses, the
lungs, and the kidneys. The findings at histo-
pathologic examination reveal leukocytoclastic
vasculitis with necrosis and palisading histiocytes
(67). The levels of cytoplasmic antineutrophil
cytoplasmic antibody (c-ANCA) are often but
not always elevated. Cavernous sinus involvement
is uncommon and can occur because of contigu-
ous extension from the orbit or paranasal sinus or
because of de novo dural disease.
Tolosa-Hunt Syndrome
Tolosa-Hunt syndrome is a syndrome of painful
ophthalmoplegia caused by a nonspecific inflam-
mation of the superior orbital fissure–cavernous
sinus region on one side. Considerable overlap
of the histopathologic findings exists with those
of idiopathic hypertrophic pachymeningitis
and inflammatory pseudotumor, with only
the involved location being different. Tolosa-
Hunt syndrome is a diagnosis of exclusion that
requires careful ruling out of alternative diagno-
ses. Common clinical features include orbital or
retro-orbital pain, paresis of the cavernous sinus
nerves, Horner syndrome, symptoms lasting for
a period of days to weeks, an absence of a sys-
temic or CSF inflammatory reaction, occasional
spontaneous remissions, and dramatic improve-
ment with administration of corticosteroid
therapy (68). In contrast to other inflammatory
disorders, biopsy is not essential to establish the
diagnosis. Biopsy is restricted to patients with
rapidly progressive disease and a lack of re-
sponse to corticosteroid therapy.
In patients with Tolosa-Hunt syndrome, MRI
shows enhancing soft-tissue thickening of the
cavernous sinus and superior orbital fissure (Fig
E12). The thickening is usually isointense to
gray matter on T1-weighted MR images and iso-
to hypointense on T2-weighted MR images (69).
The cavernous ICA may show mild narrowing.
More important, imaging plays a crucial role
in demonstrating a lack of disease outside the
region of the cavernous sinus, superior orbital
fissure, and orbital apex region, as well as in
ruling out mimics such as mass lesions (68). Be-
cause the diagnosis is made only on the basis of
the clinical and imaging features, close follow-
up is usually recommended for at least 2 years
after establishing the diagnosis of Tolosa-Hunt
syndrome (70).
814  May-June 2019 radiographics.rsna.org

Figure 18.  Epidermoid cyst in a 9-year-old girl who presented

with intermittent headache, which had been present for 4 years,
and preferential use of the left eye. (a) Axial fat-suppressed T2-
weighted MR image shows a T2-hyperintense lesion (arrow) in the
right cavernous sinus; the lesion was depicted medial to the lateral
dura of the cavernous sinus. (b, c) Axial diffusion-weighted MR im-
age (b) and apparent diffusion coefficient map (c) show diffusion
restriction within the lesion. No enhancement was demonstrated
(image not shown). (d) Photomicrograph shows the cyst wall
composed of fibrocollagenous tissue lined by stratified squamous
epithelial cells and lamellated keratin. Adnexal structures are not
present. (H-E stain; original magnification, 3100.)

Congenital and Miscellaneous

Lesions

Epidermoid and Dermoid Cysts

Epidermoid cysts and dermoid cysts are con-
genital lesions that occur because of a disorder
in the cleavage of cutaneous elements from the
neuroectoderm. Both of these types of cysts are
lined by stratified squamous epithelium and
filled with desquamated skin cells. An epider-
moid cyst is distinguished from a dermoid cyst
by the lack of dermal elements and append-
ages (sebaceous glands, apocrine glands, and
hair). Dermoid and epidermoid cysts are slow
growing and manifest in an insidious manner.
Rarely, they can rupture, with resultant chemical
meningitis (71).
A parasellar location is the second most com-
mon location, after the cerebellopontine angle,
for intracranial epidermoid cysts. On the basis
of their location, they can be classified into
(a) extra­cavernous (most commonly arising
from the trigeminal cave) with cavernous sinus
invasion, (b) interdural (between the two layers
of the lateral wall of the cavernous sinus), or
(c) true intracavernous (tending to encase the
ICA and push the nerves laterally). Interdural
lesions are adherent to the nerves and usually
cannot be resected completely (72). The features
of epidermoid cysts of the cavernous sinus at
MRI are characteristic. The lesions are T2 hy-
perintense, with signal intensity equal to that of
the CSF, and T1 hypointense; they show partial
suppression of signal intensity on FLAIR MR
images; they show diffusion restriction; and they
do not enhance (Fig 18). High-spatial-resolution
steady-state or heavily T2-weighted MR images
help to clearly outline the wall of the lesion.
Occasional lesions have T1-hyperintense signal
intensity and have been described as “white
epidermoids” (71).
Dermoid cysts are around 3–10 times less
common than epidermoid cysts (73). Simi-
lar to epidermoid cysts, dermoid cysts can be
extra­dural or interdural in location. Extradural
lesions tend to have adjacent skull base erosion
and encase the ICA; interdural lesions do not
show skull base erosions and tend to displace
the ICA medially. The signal intensity character-
istics of dermoid cysts generally parallel those of
fat at MRI, owing to their cholesterol content.
Dermoid cysts are hyperintense on T1-weighted
MR images and are of variable signal intensity
on T2-weighted MR images. Thin peripheral
enhancement can be seen (71).
RG  •  Volume 39  Number 3 Mahalingam et al  815

Figure 19.  CSF pseudocyst in a 55-year-old

woman who presented with diplopia, which
had been present for 2 months. She had un-
dergone surgery for a pituitary macroadenoma
11 years ago. (a) Coronal T2-weighted MR
image shows a thin-walled T2-hyperintense
lesion (arrow) occupying the right cavernous
sinus and the right side of the sella. (b) Coro-
nal gadolinium-enhanced T1-weighted MR im-
age shows no associated enhancement in the
lesion (arrow). (c)  Coronal contrast-enhanced
T1-weighted MR image obtained 11 years ago
(before the previous surgery) shows a hypoen-
hancing pituitary macroadenoma (arrow) with
right cavernous sinus invasion and complete
encasement of the right ICA.

Arachnoid Cyst CSF signal intensity and showed no enhancement

Arachnoid cysts are benign congenital CSF-
containing unilocular cysts that are lined by a
thin collagenous membrane and arachnoid cells.
Arachnoid cyst of the cavernous sinus is extremely
rare, with only a few case reports in the literature
(74,75). The cranial nerves in the lateral wall
of the cavernous sinus are sheathed by separate
arachnoid membranes, and an arachnoid cyst may
form when CSF gets trapped within these mem-
branes. The signal intensity of the lesions parallels
that of the CSF with use of all MRI sequences,
and the lesions do not enhance. Heavily T2-
weighted MR images are useful in demonstrating
the wall of the lesion.
CSF Pseudocyst
Intracranial collections of CSF can occur after sur-
gery or trauma. Such lesions can occasionally oc-
cur in the cavernous sinus and cause symptoms by
exerting mass effect on the nerves. We encountered
a patient who had undergone surgery for a pitu-
itary macroadenoma in the remote past and now
presented with diplopia. Imaging showed a cystic
lesion in a sellar-parasellar location; the lesion had
(Fig 19). This lesion was surgically decompressed,
and the patient had an uneventful recovery.
Pitfalls in Interpretation
and Pseudolesions
Asymmetry
The cavernous sinuses are not always bilater-
ally symmetric at imaging. This finding could be
either related to the imaging technique (owing
to unintended obliquity in the plane of acquisi-
tion) or related to the patient (owing to actual
difference in the shape and width of the cavern-
ous sinus). Asymmetry of the cavernous sinuses
is a natural variation that can be mistaken for a
lesion, especially on the contrast-enhanced im-
ages, when the contrast material opacification
within the cavernous sinus and within the ICA is
equal. One of the cavernous sinuses can appear
comparatively bulky. This finding needs to be
correlated with the patient’s symptoms. Other
ways of resolving this issue are (a) reviewing the
T2-weighted axial and coronal MR images that
clearly show a more tortuous course of the ICA
816  May-June 2019 radiographics.rsna.org

Table 2: Clues to the Differential Diagnosis of Cavernous Sinus Lesions on the

Basis of Their Imaging Appearance

Imaging Clue Diagnosis

T2 hypointensity Chronic inflammation, fungal infection, Langerhans cell histio-
cytosis, lymphoma, aneurysm with flow void
Marked T2 hyperin- Cavernoma, hemangioma, chondrosarcoma
tensity
T1 hyperintensity Dermoid cyst, melanoma, adenoma with hemorrhage, aneu-
rysm with thrombosis and/or slow flow, lipoma
Calcifications Chondrosarcoma, chordoma
CT hyperattenuation Meningioma, melanoma, highly cellular neoplasms, throm-
bosed aneurysm
Hyperostosis Meningioma
Hemorrhage Adenoma, schwannoma
Intense homogeneous Meningioma, lymphoma, cavernous hemangioma, aneurysm,
enhancement juvenile nasopharyngeal angiofibroma, chronic inflammatory
disease
Diffusion restriction Lymphoma, epidermoid cyst
Dural disease Meningioma, inflammatory disease
Perineural extension Neurogenic tumors, adenoid cystic carcinoma, nasopharyngeal
carcinoma, melanoma, lymphoma
Constriction of the Meningioma, inflammatory lesions
ICA
Flow voids Hemangiopericytoma, juvenile nasopharyngeal angiofibroma,
CCF
Dilated superior oph- CCF, cavernous sinus thrombosis
thalmic vein

within the bulky-appearing cavernous sinus and
(b) assessing the lateral border of the cavernous
sinus—this border remains straight or concave
even if the cavernous sinus is apparently bulky
owing to natural variation, as compared with a
convex lateral margin when the cavernous sinus is
involved by a lesion (Fig E13).
Fat in the Cavernous Sinus
Fat can normally be seen within the cavernous si-
nus, more commonly in the anterior part near the
superior orbital fissure and in the region posterior
to the ICA. The results of microanatomic stud-
ies have shown that intracavernous adipose tissue
has a dumbbell-shaped configuration between the
ICA and the cranial nerves (5). At CT, promi-
nent fat attenuation can be depicted in patients
with Cushing syndrome or can even be a normal
variant (76). This finding should not be mistaken
for a mass lesion. At CT, inexperienced readers
can mistake fat within the cavernous sinus for air
owing to its low attenuation; this problem is easily
resolved by using a wide window setting.
Gas in the Cavernous Sinus
At head CT, air attenuation in the cavernous sinus
can occasionally be depicted. This finding occurs
probably as a result of venous air emboli from in-
travenous catheters or owing to trauma. In patients
without symptoms of cavernous sinus syndrome,
this finding is not of much clinical importance (77).
Incomplete Opacification of the
Cavernous Sinus
The cavernous sinuses are opacified at a later
time than other dural venous sinuses. First-pass
multidetector CT angiographic images often show
inadequate contrast opacification of the cavern-
ous sinus (9). Even at delayed phase imaging
performed with a time delay of 40 seconds, not all
images show adequate cavernous sinus opacifica-
tion. Moreover, first-pass images can show partial
opacification of the cavernous sinus, mimicking
thrombosis (Fig E14). Thus when cavernous sinus
thrombosis is suspected, delayed phase imaging
(scanning delay of at least 45 seconds after con-
trast material injection) is required to definitively
rule out filling defects (78). Acquisition can also be
planned in the craniocaudal direction, which pro-
vides some extra time for cavernous sinus filling.
Clues to Differential Diagnosis and
Algorithmic Approach
Although in certain cases, imaging features are
pathognomonic, considerable overlap often exists
among the imaging findings of the various patho-
RG  •  Volume 39  Number 3 Mahalingam et al  817
Figure 20.  Diagram of a diagnostic algorithm for an imaging-based differential diagnosis of cavernous sinus lesions. CS = cavernous
sinus, JNA = juvenile nasopharyngeal angiofibroma, LCH = Langerhans cell histiocytosis, PPF = pterygopalatine fossa.
logic conditions described in this article. Imaging
clues can point toward one group of diseases, thus
helping to provide a more targeted clinical ap-
proach to diagnosis. These clues are highlighted
in Table 2. A stepwise algorithmic approach to
differential diagnosis that is based on imaging is
highlighted in Figure 20.
Conclusion
Cavernous sinus syndrome can manifest with
ophthalmoplegia, ptosis, exophthalmos, chemo-
sis, vision loss, Horner syndrome, facial pain, or
headache. A wide range of conditions can cause
cavernous sinus syndrome, including neoplasms,
infection, inflammation, and vascular pathologic
conditions. Knowledge of the imaging clues is es-
sential to arrive at a workable set of possible diag-
noses. Although a few conditions have a pathog-
nomonic imaging appearance that can clinch
their diagnosis, a multidisciplinary approach is
often necessary to arrive at the final diagnosis in
most scenarios.
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