AJR 2003; 181:583-590
© American Roentgen Ray Society
Cavernous Sinus Syndrome: Clinical Features and Differential Diagnosis with MR Imaging
Jeong Hyun Lee1,
Ho Kyu Lee1,
Ji Kang Park2,
Choong Gon Choi1 and
Dae Chul Suh1
1 Department of Radiology, Asan Medical Center, University of Ulsan College of
Medicine, 388-1 Poongnap-dong, Songpa-gu, Seoul, Korea.
2 Department of Radiology, Ulsan University Hospital, University of Ulsan
College of Medicine, 1290-3 Jeonha-dong, Dong-gu, Ulsan, 682-060, Korea.
Received July 29, 2002;
accepted after revision January 2, 2003.
Address correspondence to H. K. Lee.
Presented at the annual meeting of the Radiological Society of North
America, Chicago, November 2001.
Introduction
The cavernous sinus is a small but complex structure consisting of a venous
plexus, the carotid artery, cranial nerves, and sympathetic fibers. Broad
categories of diseases involving the cavernous sinus can cause the so-called
cavernous sinus syndrome; these diseases include bacterial or fungal
infections, noninfectious inflammation, vascular lesions, and neoplasms. In
this report, we briefly review the normal anatomy of the cavernous sinus,
illustrate a variety of the primary pathologic conditions that can affect this
structure, and discuss the imaging features that help to make the differential
diagnosis of these diseases.
Normal Anatomy of the Cavernous Sinus
The cavernous sinuses consist of extradural venous plexuses surrounded by a
dural fold. The intracavernous internal carotid artery with its periarterial
sympathetic plexus runs between the venules of the parasellar venous plexus
(Fig. 1A,
1B). The abducens nerve runs
lateral to the internal carotid artery, but medial to the oculomotor and
trochlear nerves and the ophthalmic and maxillary divisions of the trigeminal
nerve, which run superior to inferior within the lateral dural border of the
cavernous sinus [1].

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Fig. 1A. Anatomic diagrams of cavernous sinus. Drawings of coronal (A)
and lateral (B) views show structure of cavernous sinus. 1 = carotid
artery, 2 = oculomotor nerve, 3 = trochlear nerve, 4 = ophthalmic nerve, 5 =
maxillary nerve, 6 = abducens nerve, 7 = pituitary gland, 8 = sympathetic
nerve, 9 = mandibular nerve.
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Fig. 1B. Anatomic diagrams of cavernous sinus. Drawings of coronal (A)
and lateral (B) views show structure of cavernous sinus. 1 = carotid
artery, 2 = oculomotor nerve, 3 = trochlear nerve, 4 = ophthalmic nerve, 5 =
maxillary nerve, 6 = abducens nerve, 7 = pituitary gland, 8 = sympathetic
nerve, 9 = mandibular nerve.
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Cavernous Sinus Syndrome
Cavernous sinus syndrome is characterized by multiple cranial neuropathies.
The clinical presentation includes impairment of ocular motor nerves, Horner's
syndrome, and sensory loss of the first or second divisions of the trigeminal
nerve in various combinations. The pupil may be involved or spared or may
appear spared with concomitant oculosympathetic and parasympathetic
involvement. Various degrees of pain may be involved
[1].
Infectious Diseases
Cavernous Sinus Thrombophlebitis
Thrombophlebitis of the cavernous sinus potentially is a lethal condition
usually caused by bacterial or fungal invasion complicating sinusitis in
patients with poorly controlled diabetes or immunosuppression. The diagnosis
is based primarily on clinical data. CT and MR imaging can provide diagnostic
information with direct signs, including changes in signal intensity and in
the size and contour of the cavernous sinus, and indirect signs, including
dilatation of the tributary veins, exophthalmos, and increased dural
enhancement along the lateral border of the cavernous sinus
[2] (Figs.
2A,
2B,
2C and
3A,
3B).

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Fig. 2A. Cavernous sinus thrombophlebitis caused by paranasal sinusitis in
62-year-old woman with right ocular pain and diplopia due to oculomotor,
trochlear, and abducens nerve palsy. Coronal T2-weighted image shows
asymmetric bulging of right cavernous sinus (arrows). Note
hyperintense thick mucosa of right sphenoidal sinus due to sinusitis.
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Fig. 2B. Cavernous sinus thrombophlebitis caused by paranasal sinusitis in
62-year-old woman with right ocular pain and diplopia due to oculomotor,
trochlear, and abducens nerve palsy. Contrast-enhanced coronal (B) and
axial (C) T1-weighted images show diffuse enhancement of right orbital
contents due to orbital cellulitis and ophthalmitis. Note nonenhancing acute
thrombus (arrows, C) in right cavernous sinus.
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Fig. 2C. Cavernous sinus thrombophlebitis caused by paranasal sinusitis in
62-year-old woman with right ocular pain and diplopia due to oculomotor,
trochlear, and abducens nerve palsy. Contrast-enhanced coronal (B) and
axial (C) T1-weighted images show diffuse enhancement of right orbital
contents due to orbital cellulitis and ophthalmitis. Note nonenhancing acute
thrombus (arrows, C) in right cavernous sinus.
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Fig. 3A. Cavernous sinus thrombophlebitis and skull base osteomyelitis in
58-year-old woman with left ocular pain and diplopia due to left abducens
nerve palsy after tooth extraction. Contrast-enhanced coronal (A) and
axial (B) T1-weighted images show enlarged cavernous sinuses with
lateral convexity and luminal narrowing of right carotid artery
(arrow, A). Note multiple filling defects due to thrombosis in
cavernous sinuses (solid arrows, B) and in left inferior
ophthalmic vein (open arrows, B), which is one tributary of
cavernous sinus. Also note heterogeneous enhancement of clival fat marrow (C,
A).
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Fig. 3B. Cavernous sinus thrombophlebitis and skull base osteomyelitis in
58-year-old woman with left ocular pain and diplopia due to left abducens
nerve palsy after tooth extraction. Contrast-enhanced coronal (A) and
axial (B) T1-weighted images show enlarged cavernous sinuses with
lateral convexity and luminal narrowing of right carotid artery
(arrow, A). Note multiple filling defects due to thrombosis in
cavernous sinuses (solid arrows, B) and in left inferior
ophthalmic vein (open arrows, B), which is one tributary of
cavernous sinus. Also note heterogeneous enhancement of clival fat marrow (C,
A).
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Actinomycosis
Actinomycosis is a rare disease. Most patients are immunocompetent, and men
are affected more often than women. The bacteria are generally considered to
gain access to the central nervous system by direct extension from the ear or
sinuses or hematogenous spread from a distant source. Radiographically,
actinomycosis may appear as an irregularly marginated, rim-enhancing abscess;
as meningoencephalitis; or as a mass lesion
[3] (Fig.
4A,
4B,
4C).

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Fig. 4A. Actinomycosis in 27-year-old man with severe frontal headache and
decreased visual acuity. Axial T1-weighted (A) and T2-weighted
(B) images show ill-defined isointense lesion (arrows,
A) in left anterior cavernous sinus and orbital apex.
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Fig. 4B. Actinomycosis in 27-year-old man with severe frontal headache and
decreased visual acuity. Axial T1-weighted (A) and T2-weighted
(B) images show ill-defined isointense lesion (arrows,
A) in left anterior cavernous sinus and orbital apex.
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Fig. 4C. Actinomycosis in 27-year-old man with severe frontal headache and
decreased visual acuity. Coronal contrast-enhanced T1-weighted image shows
intense and homogeneous enhancement of lesion. Note encasement of left carotid
artery with luminal narrowing (arrow).
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Rhinocerebral Mucormycosis
Fungi of the order Mucorales have minimal intrinsic pathogenicity but can
cause fulminant infection in immunocompromised and diabetic patients. After
inhalation into the nasal cavity and paranasal sinuses, the fungi cause
necrotizing vasculitis, thrombosis, or infarction of the nose and sinuses and
can then rapidly extend into the orbits, deep face, and cranial cavity
[4]. The central nervous system
may be invaded directly by extension through the skull base or indirectly
through involvement of the carotid artery and cavernous sinus (Fig.
5A,
5B).

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Fig. 5A. Rhinocerebral mucormycosis in 61-year-old diabetic man with diplopia
due to right oculomotor and trochlear nerve palsy. On contrast-enhanced CT
scan, right cavernous sinus does not enhance by contrast agent
(arrows). CT scan also reveals acute infarction of anterior temporal
lobe (T).
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Fig. 5B. Rhinocerebral mucormycosis in 61-year-old diabetic man with diplopia
due to right oculomotor and trochlear nerve palsy. Contrast-enhanced coronal
T1-weighted image shows nonenhancing isointense lesion filling adjacent right
sphenoidal sinus due to fungal sinusitis and luminal narrowing of right
carotid artery.
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Aspergillosis
Aspergillosis arises most commonly as a result of hematogenous spread and
occasionally by direct extension of infection from the paranasal sinuses,
middle ear, or orbit. Most cases occur in immunocompromised patients
[5]. As with fungi of the order
Mucorales, Aspergillus species tend to invade vessels. Decreased
signal intensity on T1-weighted imaging and very low signal intensity on
T2-weighted imaging are characteristic findings in paranasal sinus
aspergillosis and are attributed to paramagnetic elements by hemorrhage or
aspergillus fungal colonies, mainly iron and magnesium
[5] (Fig.
6A,
6B,
6C).

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Fig. 6A. Aspergillosis in 55-year-old man with diplopia due to oculomotor
nerve palsy. He had been treated for biliary sepsis. Axial T2-weighted image
(A) shows hypointense lesion (straight arrows, A) in
left cavernous sinus, which is isointense on T1-weighted image (B).
Normal signal void of carotid artery is replaced by acute thrombus (curved
arrows).
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Fig. 6B. Aspergillosis in 55-year-old man with diplopia due to oculomotor
nerve palsy. He had been treated for biliary sepsis. Axial T2-weighted image
(A) shows hypointense lesion (straight arrows, A) in
left cavernous sinus, which is isointense on T1-weighted image (B).
Normal signal void of carotid artery is replaced by acute thrombus (curved
arrows).
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Fig. 6C. Aspergillosis in 55-year-old man with diplopia due to oculomotor
nerve palsy. He had been treated for biliary sepsis. On coronal
contrast-enhanced T1-weighted image, thrombus extends into distal internal
carotid artery (curved arrow). Within sphenoidal sinus, isointense
fungal mass (straight arrows) surrounded by enhanced mucosa is
identified.
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Noninfectious Inflammation
Tolosa-Hunt Syndrome
Tolosa-Hunt syndrome is a recurrent painful ophthalmoplegia due to
nonspecific granulomatous inflammation in the anterior cavernous sinus,
superior orbital fissure, or orbital apex. The diagnosis is based on findings
of painful ophthalmoplegia accompanied by variable deficits of the oculomotor
through the abducens nerves, excellent response to corticosteroid therapy, and
exclusion of other lesions [6].
Reported MR findings include nonspecific inflammatory lesions isointense to
T1- and T2-weighted images in the anterior cavernous sinus, the superior
orbital fissure, or the orbital apex with contrast enhancement
[6] (Fig.
7A,
7B).

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Fig. 7A. Tolosa-Hunt syndrome in 21-year-old woman with painful
ophthalmoplegia. Unenhanced (A) and contrast-enhanced (B) axial
T1-weighted images reveal homogeneous infiltrating lesion (arrows)
narrowing carotid artery in orbital apex and in anterior cavernous sinus,
which shows homogeneous intense enhancement.
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Fig. 7B. Tolosa-Hunt syndrome in 21-year-old woman with painful
ophthalmoplegia. Unenhanced (A) and contrast-enhanced (B) axial
T1-weighted images reveal homogeneous infiltrating lesion (arrows)
narrowing carotid artery in orbital apex and in anterior cavernous sinus,
which shows homogeneous intense enhancement.
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Inflammatory Pseudotumor
Inflammatory pseudotumors are idiopathic inflammatory lesions in which
skull base involvement is rare. These pseudotumors include a diverse group of
lesions characterized by inflammatory cell infiltration and variable fibrotic
responses according to the chronicity of the lesion. Typical MR findings
include soft-tissue lesions infiltrating the skull base with intracranial
dural involvement, bone destruction, iso- to hypointensity on T2-weighted
images according to the fibrosis and high cellularity, and contrast
enhancement [7] (Fig.
8A,
8B,
8C).

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Fig. 8A. Inflammatory pseudotumor in 64-year-old woman with right oculomotor
nerve palsy. Axial T2-weighted (A) and T1-weighted (B) images
show infiltrative mass (arrows) in right cavernous sinus, sphenoid
bone, posterior clival dura, and infratemporal fossa with encasement of
carotid artery. Note marked hypointensity on T2-weighted image.
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Fig. 8B. Inflammatory pseudotumor in 64-year-old woman with right oculomotor
nerve palsy. Axial T2-weighted (A) and T1-weighted (B) images
show infiltrative mass (arrows) in right cavernous sinus, sphenoid
bone, posterior clival dura, and infratemporal fossa with encasement of
carotid artery. Note marked hypointensity on T2-weighted image.
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Fig. 8C. Inflammatory pseudotumor in 64-year-old woman with right oculomotor
nerve palsy. On coronal contrast-enhanced T1-weighted image, lesion is
strongly enhanced (solid arrows). Note thick enhancement of dura
(open arrows) along right cerebral convexity.
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Vascular Lesions
Aneurysm of the Internal Carotid Artery
Vascular ectasia and distal internal carotid artery aneurysms (Fig.
9A,
9B,
9C) are the most common
nonneoplastic parasellar masses in adults. The imaging appearance of these
aneurysms is variable depending on the presence and age of the thrombus and
various flow parameters. Diagnosis of a parasellar aneurysm is clinically
important because performing surgery on an aneurysm misdiagnosed as a tumor
can have a fatal outcome.

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Fig. 9A. Bilateral saccular aneurysms of internal carotid arteries in
cavernous sinuses in 67-year-old woman with diplopia. Axial T2-weighted image
shows large signal void (arrows) due to aneurysm of internal carotid
artery in both cavernous sinuses.
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Fig. 9B. Bilateral saccular aneurysms of internal carotid arteries in
cavernous sinuses in 67-year-old woman with diplopia. Coronal
contrast-enhanced T1-weighted image shows crescent isointense thrombus
(black arrow) in right aneurysm and intense enhancement of left one
(white arrows).
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Fig. 9C. Bilateral saccular aneurysms of internal carotid arteries in
cavernous sinuses in 67-year-old woman with diplopia. Digital subtraction
angiogram of both internal carotid arteries shows partially thrombosed
aneurysms of internal carotid artery of right cavernous sinus (large
arrow) and another aneurysm of internal carotid artery of left one
(small arrow).
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CarotidCavernous Fistula and Dural Arteriovenous Fistula
Carotidcavernous fistula and dural arteriovenous fistula (Fig.
10A,
10B) may present with similar
clinical symptoms and signs, and on a cursory glance, the angiographic
appearance may seem to be similar in both conditions. Carotidcavernous
fistula can result from traumatic laceration of the carotid artery or from
rupture of an aneurysm into the surrounding venous sac establishing a direct
arteriovenous fistula between the internal carotid artery and the venous
spaces of the cavernous sinus. However, dural arteriovenous fistula of the
cavernous sinus is most easily understood as simply a dural arteriovenous
fistula in a specific location
[8]. On CT or MR imaging, the
diagnosis depends on morphologic changes such as exophthalmos and enlargement
of the superior ophthalmic veins, cavernous sinus, or extraocular muscles. MR
imaging is able to depict flow voids in the involved cavernous sinus.

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Fig. 10A. Dural arteriovenous fistula in 61-year-old woman with exophthalmos
and ocular pain. Axial T1-weighted image shows enlargement of both cavernous
sinuses. Structures other than internal carotid artery that exhibit signal
void (arrows) are noted in right cavernous sinus.
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Fig. 10B. Dural arteriovenous fistula in 61-year-old woman with exophthalmos
and ocular pain. Digital subtraction angiogram of right external carotid
artery reveals multiple fine feeders from distal branches of right maxillary
artery (arrowhead), opacification of cavernous sinus (large solid
arrow), and draining into inferior petrosal (open arrow) and
sphenoparietal (small solid arrow) sinuses. Distal internal carotid
artery (curved arrow) and its branches are also opacified.
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Neoplasm
The most common neoplastic lesions in the cavernous sinus are caused by
direct invasion of intracranial tumors such as pituitary adenoma, perineural
spread of head and neck malignancy, or hematogenous spread from distant
lesions (Fig. 11A,
11B). However, primary tumors
such as meningioma, neurogenic tumors, and hemangioma can also arise from the
cavernous sinus itself (Fig.
12A, 12B,
12C).

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Fig. 11A. Perineural spread of adenoid cystic carcinoma of parotid gland in
36-year-old woman with diplopia and left-sided hemifacial pain. Coronal
contrast-enhanced T1-weighted image shows strongly enhancing infiltrating mass
in left parapharyngeal space (arrows) extending into cavernous sinus
through widened foramen ovale.
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Fig. 11B. Perineural spread of adenoid cystic carcinoma of parotid gland in
36-year-old woman with diplopia and left-sided hemifacial pain.
Contrast-enhanced CT scan obtained at level of parotid glands shows enhancing
mass in deep lobe of left parotid gland that is infiltrating into
parapharyngeal space through stylomandibular tunnel (arrows).
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Fig. 12B. Cavernous hemangioma (cavernoma) in 56-year-old woman with severe
headache. Coronal T1-weighted image shows isointensity of mass. Note encased
lumen of internal carotid artery is not narrowed, despite large size of
mass.
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Conclusion
Cavernous sinus syndrome can be caused by various disease entities.
Understanding the characteristic clinical features and their implications as
well as the characteristic imaging findings will assist in the differential
diagnosis focused on this small but complex structure, the cavernous
sinus.
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