DOI:10.2214/AJR.07.7015
AJR 2007; 189:S64-S75
© American Roentgen Ray Society
Radiologic Diagnosis of Cerebral Venous Thrombosis: Pictorial Review
Colin S. Poon1,2,
Ja-Kwei Chang1,
Amar Swarnkar1,
Michele H. Johnson2 and
John Wasenko1
1 1Department of Radiology, State University of New York Upstate
Medical University, 750 E Adams St., Syracuse, NY 13210.
2 Department of Diagnostic Radiology, Yale University School of Medicine, New
Haven, CT.
Received May 31, 2007;
accepted after revision June 11, 2007.
Address correspondence to C. S. Poon
(poonc{at}upstate.edu).
Abstract
Objective
Cerebral venous thrombosis is often associated with nonspecific clinical
complaints. In addition, the imaging findings are often subtle. Underdiagnosis
or misdiagnosis of cerebral venous thrombosis can lead to severe consequences,
including hemorrhagic infarction and death.
Conclusion
This article reviews the radiologic findings and diagnostic pitfalls of
cerebral venous thrombosis. After completing this article, the readers should
have an improved ability to diagnose cerebral venous thrombosis accurately,
using the optimal imaging tools to achieve this goal.
Keywords: brain imaging cerebral venous thrombosis CT MRI neuroradiology
Introduction
Cerebral venous thrombosis (CVT) is often underdiagnosed because it is an
uncommon disease, it is associated with a wide spectrum of etiologic factors,
clinical presentation is often nonspecific, and the diagnostic imaging
features can be subtle.
The correct diagnosis of CVT relies on neurologic imaging. Radiologists
play a crucial role in patient care by providing early diagnosis through
interpretation of imaging studies. Early diagnosis leads to prompt treatment
that can be effective. Delayed diagnosis is associated with high morbidity and
mortality.
The purpose of this article is to review the clinical presentation and
basic pathophysiology of the disease; review the approach for radiologic
investigation, including emerging technology such as CT venography; review the
imaging features of CVT; and show common pitfalls associated with the
radiologic evaluation of this diagnosis. We have included many cases to
illustrate the radiologic features of CVT. Whenever possible, findings on
different imaging techniques are correlated and compared.
Predisposing Factors
The list of factors associated with CVT is too extensive to be memorized
[1–7].
A more manageable approach is to understand that they may involve one or more
of the following mechanisms: direct involvement of the dural sinuses (e.g.,
infection, trauma, neoplastic infiltration), possibly with damage to the
vascular endothelium; venous stasis; hypercoagulable states; and increased
blood viscosity.
The frequency of these etiologic factors depends on age. Often, the cause
is multifactorial. In neonates, acute systemic illness, such as shock or
dehydration, may be the cause. Frequent causes in older children include local
infection, such as mastoiditis, and coagulopathy. In adults, intrinsic or
acquired coagulopathies become the most important factors, contributing to as
many as 70% of cases. Infection contributes to less than 10% of cases in
adults [1,
3]. In women of childbearing
age, oral contraceptive use and pregnancy are strong risk factors. CVT
actually occurs more often in puerperium than during the pregnancy. Although
pregnancy-related CVT occurs more often in older women, age per se is not a
risk factor.
The pathogenesis of CVT is complex and remains poorly understood. In
20–35% of cases, the cause remains unknown; therefore, one should remain
suspicious, even in the absence of known risk factors
[1–3].
Clinical Presentation
The clinical presentation of CVT is often nonspecific
[1–6]
(Table 1). Common presentation
includes headache, focal neurologic deficits, seizures, and altered
consciousness. A syndrome of intracranial hypertension (headache and
papilledema) accounted for 40% of cases in a series, so CVT needs to be
excluded in patients considered for the diagnosis of benign intracranial
hypertension [1]. Although
subarachnoid hemorrhage is a rare presentation of CVT, cases have also been
reported [1,
8]. There is also a wide
distribution in the mode of onset of symptoms, with approximately 28% acute
(< 48 hours), 42% subacute (between 48 hours and 30 days), and 30% chronic
(> 30 days) [1]. The
teaching point is that CVT may have an atypical presentation or even an
absence of clinical symptoms. The evaluation for evidence of CVT should be
included in the diagnostic checklist in every neuroradiologic case.

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Fig. 1C —5-year-old boy with severe headache and eye pain. Thrombosis
was found in right lateral sinus (arrows). Enhanced CT images show
same structure as filling defect with enhancing rim (empty delta sign).
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Fig. 1D —5-year-old boy with severe headache and eye pain. Thrombosis
was found in right lateral sinus (arrows). Enhanced CT images show
same structure as filling defect with enhancing rim (empty delta sign).
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Fig. 2A —Cord sign in cortical venous thrombosis in a young woman.
Unenhanced CT scans show dense cortical veins (white arrows,A), an uncommon direct sign of cerebral venous thrombosis (CVT)
known as cord sign. Note also indirect signs of CVT, including subcortical
hemorrhagic infarction (black arrows), diffuse brain swelling, and
small ventricular size.
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Fig. 2B —Cord sign in cortical venous thrombosis in a young woman.
Unenhanced CT scans show dense cortical veins (white arrows,A), an uncommon direct sign of cerebral venous thrombosis (CVT)
known as cord sign. Note also indirect signs of CVT, including subcortical
hemorrhagic infarction (black arrows), diffuse brain swelling, and
small ventricular size.
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Fig. 3A —38-year-old woman with history of pseudotumor cerebri who
presented with headache and decreased consciousness. Diagnosis was thrombosis
of superior sagittal sinus, straight sinus, and internal cerebral veins.
(Long white arrows indicate superior sagittal sinus; short white
arrows, straight sinus; black arrows, Rosenthal's veins).
Unenhanced CT scans show dense thrombosis. Note nonhemorrhagic infarction in
basal ganglia, thalami, and internal capsules, which is typically seen in deep
cerebral venous thrombosis.
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Fig. 3B —38-year-old woman with history of pseudotumor cerebri who
presented with headache and decreased consciousness. Diagnosis was thrombosis
of superior sagittal sinus, straight sinus, and internal cerebral veins.
(Long white arrows indicate superior sagittal sinus; short white
arrows, straight sinus; black arrows, Rosenthal's veins).
Unenhanced CT scans show dense thrombosis. Note nonhemorrhagic infarction in
basal ganglia, thalami, and internal capsules, which is typically seen in deep
cerebral venous thrombosis.
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Fig. 3C —38-year-old woman with history of pseudotumor cerebri who
presented with headache and decreased consciousness. Diagnosis was thrombosis
of superior sagittal sinus, straight sinus, and internal cerebral veins.
(Long white arrows indicate superior sagittal sinus; short white
arrows, straight sinus; black arrows, Rosenthal's veins). Axial
T2-weighted MR image shows replacement of signal void by thrombus
(arrow) in superior sagittal sinus. Veins at internal capsules are
engorged.
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Fig. 3D —38-year-old woman with history of pseudotumor cerebri who
presented with headache and decreased consciousness. Diagnosis was thrombosis
of superior sagittal sinus, straight sinus, and internal cerebral veins.
(Long white arrows indicate superior sagittal sinus; short white
arrows, straight sinus; black arrows, Rosenthal's veins).
Sagittal contrast-enhanced T1-weighted image (D) shows filling defects
in sagittal and straight sinuses, correlating with absence of flow on 2D phase
contrast MR venography (E).
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Fig. 3E —38-year-old woman with history of pseudotumor cerebri who
presented with headache and decreased consciousness. Diagnosis was thrombosis
of superior sagittal sinus, straight sinus, and internal cerebral veins.
(Long white arrows indicate superior sagittal sinus; short white
arrows, straight sinus; black arrows, Rosenthal's veins).
Sagittal contrast-enhanced T1-weighted image (D) shows filling defects
in sagittal and straight sinuses, correlating with absence of flow on 2D phase
contrast MR venography (E).
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Fig. 3F —38-year-old woman with history of pseudotumor cerebri who
presented with headache and decreased consciousness. Diagnosis was thrombosis
of superior sagittal sinus, straight sinus, and internal cerebral veins.
(Long white arrows indicate superior sagittal sinus; short white
arrows, straight sinus; black arrows, Rosenthal's veins). After
catheter-directed thrombolysis, flow was partially reestablished.
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Neuroradiology
Unenhanced CT remains the technique of choice for screening patients with
nonspecific clinical presentation and a low suspicion of CVT.
Contrast-enhanced CT provides a more accurate diagnosis of CVT. MRI and MR
venography have been the noninvasive imaging techniques of choice
[4–6,
9] and are often used as the
initial diagnostic test for suspicious cases. CT venography is now emerging as
a competing technique. It has been shown to be comparable to MR venography
and, in some situations, to provide better diagnostic information
[10].
Unenhanced CT
Direct signs of CVT are uncommon and are seen in only one third of cases.
Direct visualization of thrombosis in dural sinus may give a "dense clot
sign" (Fig. 1A,
1B,
1C,
1D). The cord sign represents
direct visualization of a thrombosed cortical vein that is seen as linear
hyperdensity (Fig. 2A,
2B).
More often, unenhanced CT shows only the indirect signs of CVT. These are
often nonspecific and may include diffuse brain edema, leading to hypodensity
of the brain (seen in 20–50% of cases) or decreased ventricular size. In
young patients, the pathologic decrease in ventricular size may be difficult
to differentiate from the normally small ventricles commonly seen in young
patients.
Venous infarction is the most specific indirect sign on unenhanced CT
images. An infarction not conforming to a major arterial vascular territory,
such as the presence of multiple isolated lesions, involvement of a
subcortical region with sparing of the cortex, and extension over more than
one arterial distribution, is highly suspicious for a venous cause. The
infarction may be hemorrhagic (Fig.
2A,
2B) or nonhemorrhagic
(Fig. 3A). The location of the
infarction with respect to the expected course of venous drainage may give a
clue to the venous structure involved. Thrombosis in the sagittal sinus often
leads to impaired venous drainage and, therefore, parenchymal change in the
parasagittal region. Thrombosis in Labbé's vein should lead to
infarction in the temporal lobe. Bilateral or unilateral infarction in the
thalami, basal ganglia, and internal capsule is typically seen in deep venous
thrombosis (Fig. 3A,
3B,
3C,
3D,
3E,
3F).

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Fig. 4A —16-year-old girl with multiple traumatic injuries in head.
Initial unenhanced CT (not shown) showed hyperdensity in right internal
jugular vein (IJV) and sigmoid sinus that was suspicious for venous
thrombosis. Findings were confirmed on CT venography, MRI, and conventional
venography. Axial source images from CT venography. Thrombus in IJV
(asterisk, A) and sigmoid sinus (black arrow,B) is clearly shown as filling defect. Note collateral veins
(white arrow, A) arising from right IJV.
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Fig. 4B —16-year-old girl with multiple traumatic injuries in head.
Initial unenhanced CT (not shown) showed hyperdensity in right internal
jugular vein (IJV) and sigmoid sinus that was suspicious for venous
thrombosis. Findings were confirmed on CT venography, MRI, and conventional
venography. Axial source images from CT venography. Thrombus in IJV
(asterisk, A) and sigmoid sinus (black arrow,B) is clearly shown as filling defect. Note collateral veins
(white arrow, A) arising from right IJV.
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Fig. 4C —16-year-old girl with multiple traumatic injuries in head.
Initial unenhanced CT (not shown) showed hyperdensity in right internal
jugular vein (IJV) and sigmoid sinus that was suspicious for venous
thrombosis. Findings were confirmed on CT venography, MRI, and conventional
venography. Sagittal planar reconstruction of CT venography shows thrombus
extending from right IJV (asterisk) into sigmoid sinus
(arrow), correlating well with findings on conventional venography
(E).
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Fig. 4D —16-year-old girl with multiple traumatic injuries in head.
Initial unenhanced CT (not shown) showed hyperdensity in right internal
jugular vein (IJV) and sigmoid sinus that was suspicious for venous
thrombosis. Findings were confirmed on CT venography, MRI, and conventional
venography. T1-weighted MR image shows sigmoid sinus thrombosis
(arrow) as seen on CT (B).
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Fig. 4E —16-year-old girl with multiple traumatic injuries in head.
Initial unenhanced CT (not shown) showed hyperdensity in right internal
jugular vein (IJV) and sigmoid sinus that was suspicious for venous
thrombosis. Findings were confirmed on CT venography, MRI, and conventional
venography. Venogram (E) shows thrombus as filling defects. Note
collateral veins at region of right IJVs, also seen in A. Venogram
after suction thrombectomy (F) shows improved patency in right IJV and
lateral sinus. Asterisk, right internal jugular vein; solid arrow, sigmoid
sinus; open arrow, torcular Herophili.
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Fig. 4F —16-year-old girl with multiple traumatic injuries in head.
Initial unenhanced CT (not shown) showed hyperdensity in right internal
jugular vein (IJV) and sigmoid sinus that was suspicious for venous
thrombosis. Findings were confirmed on CT venography, MRI, and conventional
venography. Venogram (E) shows thrombus as filling defects. Note
collateral veins at region of right IJVs, also seen in A. Venogram
after suction thrombectomy (F) shows improved patency in right IJV and
lateral sinus. Asterisk, right internal jugular vein; solid arrow, sigmoid
sinus; open arrow, torcular Herophili.
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Contrast-Enhanced CT
Direct evidence of CVT on contrast-enhanced CT includes the empty delta
sign, which may be seen 5 days to 2 months from onset. This sign represents a
filling defect (thrombus) in the dural sinus, with peripheral enhancement
possibly secondary to the development of collaterals (Fig.
1A,
1B,
1C,
1D).
Indirect evidence of CVT may be seen as contrast enhancement of the falx
and tentorium secondary to venous stasis and hyperemia of the dura mater,
which is seen in approximately 20% of cases.
One should be aware that in 10–30% of cases of CVT, the findings on
either unenhanced or contrast-enhanced CT are negative. Therefore, in highly
suspicious cases, further evaluation with CT venography, or MRI with MR
venography, is warranted.
CT Venography
A more recent tool that can be used to evaluate CVT is CT venography
[10–12].
CT venography allows direct visualization of thrombus as filling defects (Fig.
4A,
4B,
4C,
4D,
4E,
4F).
MRI
On MRI, venous thrombus may be directly visualized. On conventional MRI
sequences, patent dural sinuses are often seen as a flow void. This is
particularly well seen when the imaging plane is orthogonal to the blood flow
direction (e.g., coronal images are best for visualization of the superior
sagittal, transverse, and sigmoid sinuses). The effect of a flow void may be
reduced in a plane parallel to the dural sinus, although such an imaging plane
often offers a better depiction of the complete extent of thrombosis in the
dural sinus. For example, a sagittal T1-weighted image may show the complete
extent of the superior sagittal sinus thrombosis as an abnormally bright
signal filling the sinus. The thrombus may manifest as absence of a flow void,
which is often best seen on FLAIR images and T2-weighted spin-echo images. The
abnormal signal intensity follows the signal characteristics of intracranial
hemorrhage and may evolve through the stages of oxyhemoglobin,
deoxyhemoglobin, methemoglobin, and hemosiderin
[4]. On T1-weighted images,
thrombus with methemoglobin is seen as hyperintensity. On T2*-weighted
gradient-echo images, exaggerated signal loss is often seen because of the
increased susceptibility effect of deoxyhemoglobin, methemoglobin, or
hemosiderin.

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Fig. 6A —Middle-aged woman (exact age unknown) with history of
multiple myeloma. Axial unenhanced CT images show subdural hemorrhage at right
cerebellar convexity that mimics thrombosis of right transverse sinus.
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Fig. 6B —Middle-aged woman (exact age unknown) with history of
multiple myeloma. Axial unenhanced CT images show subdural hemorrhage at right
cerebellar convexity that mimics thrombosis of right transverse sinus.
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Fig. 6C —Middle-aged woman (exact age unknown) with history of
multiple myeloma. Axial FLAIR image (C), coronal FLAIR image
(D), and unenhanced CT scan (E) at location adjacent to B
show similar finding of subdural hemorrhage (white arrow, E)
medial to right transverse sinus (black arrow, E).
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Fig. 6D —Middle-aged woman (exact age unknown) with history of
multiple myeloma. Axial FLAIR image (C), coronal FLAIR image
(D), and unenhanced CT scan (E) at location adjacent to B
show similar finding of subdural hemorrhage (white arrow, E)
medial to right transverse sinus (black arrow, E).
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Fig. 6E —Middle-aged woman (exact age unknown) with history of
multiple myeloma. Axial FLAIR image (C), coronal FLAIR image
(D), and unenhanced CT scan (E) at location adjacent to B
show similar finding of subdural hemorrhage (white arrow, E)
medial to right transverse sinus (black arrow, E).
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Fig. 6F —Middle-aged woman (exact age unknown) with history of
multiple myeloma. Contrast-enhanced MR venogram shows patent dural venous
sinuses. Right transverse sinus (arrows) is smaller and slightly
irregular compared with left, possibly secondary to mass effect from adjacent
subdural hematoma.
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Indirect evidence of venous thrombosis is often secondary to parenchymal
change as a result of venous occlusion. This is similar to the findings on CT,
including brain swelling and hemorrhagic or nonhemorrhagic infarction.
Conventional MRI sequences often provide sufficient information to raise
the suspicion or to make a diagnosis of CVT. The diagnosis can then be further
confirmed on MR venography or CT venography.
MR Venography
MR venography may be performed without the use of a contrast agent using
the time-of-flight (TOF) technique or the phase contrast technique. Because
these techniques use MR flow phenomena for contrast generation, they are
subject to flow-related image artifacts.
Similar to CT venography, contrast-enhanced MR venography takes advantage
of luminal filling by contrast material rather than relying on the MR flow
phenomena as in TOF or phase contrast MR venography. Therefore,
contrast-enhanced MR venography is less likely to be affected by complex flow.
Recently, gadolinium-enhanced MR venography has been shown to be superior to
TOF MR venography [13,
14] and may offer the best
evaluation using MRI. The various MR venography techniques are summarized in
Table 2.

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Fig. 7A —7-year-old girl with closed head injury. Unenhanced CT scans
on first day show subdural hemorrhage along tentorium cerebelli and skull
fracture. Subtle density is seen in right lateral sinus (arrows,B and C) that was not well appreciated initially.
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Fig. 7B —7-year-old girl with closed head injury. Unenhanced CT scans
on first day show subdural hemorrhage along tentorium cerebelli and skull
fracture. Subtle density is seen in right lateral sinus (arrows,B and C) that was not well appreciated initially.
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Fig. 7C —7-year-old girl with closed head injury. Unenhanced CT scans
on first day show subdural hemorrhage along tentorium cerebelli and skull
fracture. Subtle density is seen in right lateral sinus (arrows,B and C) that was not well appreciated initially.
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Comparison of MR Venography and CT Venography
A comparison of CT venography and MR venography is summarized in
Table 3.
CT venography has been shown to be superior to traditional MR venography
techniques based on 2D TOF or phase contrast techniques
[10]. However, a direct
comparison between CT venography and contrast-enhanced MR venography is not
yet available. These two techniques probably provide comparable performance,
and preference will be dictated by the experience and resources of the
individual institutions.

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Fig. 8A —4-month-old girl with seizure. Unenhanced CT scans show
subdural hemorrhage along falx and tentorium cerebelli, simulating sagittal
and transverse sinus thrombosis. Note pseudo empty delta sign (arrow,
A). Empty delta sign of cerebral venous thrombosis is applicable only
on contrast-enhanced CT. Hyperdensity along posterior parietal convexity
simulates transverse sinus thrombosis (black arrow, B).
Extension of hyperdensity beyond expected location of transverse sinus
suggests this is actually subdural hematoma (white arrow, B)
[8].
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Fig. 8B —4-month-old girl with seizure. Unenhanced CT scans show
subdural hemorrhage along falx and tentorium cerebelli, simulating sagittal
and transverse sinus thrombosis. Note pseudo empty delta sign (arrow,
A). Empty delta sign of cerebral venous thrombosis is applicable only
on contrast-enhanced CT. Hyperdensity along posterior parietal convexity
simulates transverse sinus thrombosis (black arrow, B).
Extension of hyperdensity beyond expected location of transverse sinus
suggests this is actually subdural hematoma (white arrow, B)
[8].
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Fig. 9A —29-year-old woman woman with headache. Contrast-enhanced
T1-weighted image (A), source image of 2D time-of-flight (TOF) MR
venography (B), and maximum-intensity-projection of 2D TOF MR
venography image (C) show fenestration of straight sinus
(arrow). On basis of A alone, sinus thrombosis is difficult to
exclude. However, other imaging series, including unenhanced T1-weighted and
FLAIR images (not shown), fail to show abnormal signal intensity to suggest
presence of a true thrombus, raising suspicion that this may have another
cause. Two-dimensional TOF MR venogram (B) shows fenestration. Note
small vessels representing fenestration are round and positioned on opposite
sides of expected course of straight sinus. This appearance is unusual for
residual patent lumen of dural venous sinus filled with thrombus because
residual lumen tends to be irregular or crescent-shaped.
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Fig. 9B —29-year-old woman woman with headache. Contrast-enhanced
T1-weighted image (A), source image of 2D time-of-flight (TOF) MR
venography (B), and maximum-intensity-projection of 2D TOF MR
venography image (C) show fenestration of straight sinus
(arrow). On basis of A alone, sinus thrombosis is difficult to
exclude. However, other imaging series, including unenhanced T1-weighted and
FLAIR images (not shown), fail to show abnormal signal intensity to suggest
presence of a true thrombus, raising suspicion that this may have another
cause. Two-dimensional TOF MR venogram (B) shows fenestration. Note
small vessels representing fenestration are round and positioned on opposite
sides of expected course of straight sinus. This appearance is unusual for
residual patent lumen of dural venous sinus filled with thrombus because
residual lumen tends to be irregular or crescent-shaped.
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Fig. 9C —29-year-old woman woman with headache. Contrast-enhanced
T1-weighted image (A), source image of 2D time-of-flight (TOF) MR
venography (B), and maximum-intensity-projection of 2D TOF MR
venography image (C) show fenestration of straight sinus
(arrow). On basis of A alone, sinus thrombosis is difficult to
exclude. However, other imaging series, including unenhanced T1-weighted and
FLAIR images (not shown), fail to show abnormal signal intensity to suggest
presence of a true thrombus, raising suspicion that this may have another
cause. Two-dimensional TOF MR venogram (B) shows fenestration. Note
small vessels representing fenestration are round and positioned on opposite
sides of expected course of straight sinus. This appearance is unusual for
residual patent lumen of dural venous sinus filled with thrombus because
residual lumen tends to be irregular or crescent-shaped.
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Fig. 10 —Superior sagittal sinus thrombosis in young woman (exact age
unknown) on T1-weighted image. Sagittal T1-weighted images can be useful for
depiction of extensive superior sagittal sinus thrombosis. However, bright
signal of thrombus with methemoglobin (arrow) may mimic patent sinus
on contrast-enhanced T1-weighted images and time-of-flight MR venography.
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Fig. 11A —25-year-old woman with headache. Black arrows indicate left
transverse and sigmoid sinuses; white arrows indicate right transverse and
sigmoid sinuses. Axial phase contrast MR venogram shows loss of flow signal
(arrow).
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Fig. 11B —25-year-old woman with headache. Black arrows indicate left
transverse and sigmoid sinuses; white arrows indicate right transverse and
sigmoid sinuses. Axial T1-weighted image fails to show thrombus.
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Fig. 11C —25-year-old woman with headache. Black arrows indicate left
transverse and sigmoid sinuses; white arrows indicate right transverse and
sigmoid sinuses. Axial T1-weighted gadolinium-enhanced image shows smooth
enhancement in hypoplastic left transverse and sigmoid sinuses.
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Fig. 11D —25-year-old woman with headache. Black arrows indicate left
transverse and sigmoid sinuses; white arrows indicate right transverse and
sigmoid sinuses. Coronal reformations of CT venography, from posteriorly to
anteriorly, show smooth enhancement in hypoplastic left transverse and sigmoid
sinuses. Hypoplasia of ipsilateral jugular foramen also serves as important
corroborative evidence of hypoplastic dural sinus.
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Fig. 11E —25-year-old woman with headache. Black arrows indicate left
transverse and sigmoid sinuses; white arrows indicate right transverse and
sigmoid sinuses. Coronal reformations of CT venography, from posteriorly to
anteriorly, show smooth enhancement in hypoplastic left transverse and sigmoid
sinuses. Hypoplasia of ipsilateral jugular foramen also serves as important
corroborative evidence of hypoplastic dural sinus.
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Fig. 11F —25-year-old woman with headache. Black arrows indicate left
transverse and sigmoid sinuses; white arrows indicate right transverse and
sigmoid sinuses. Coronal reformations of CT venography, from posteriorly to
anteriorly, show smooth enhancement in hypoplastic left transverse and sigmoid
sinuses. Hypoplasia of ipsilateral jugular foramen also serves as important
corroborative evidence of hypoplastic dural sinus.
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Diagnostic Pitfalls
Pitfalls are associated with all imaging techniques
[15]. To improve diagnostic
accuracy, it is important to be aware of these pitfalls. Always correlate
findings on multiple imaging sequences. If in doubt, other imaging techniques
should be used to confirm the findings.
Pitfalls on Unenhanced CT
Hyperdense blood in patent dural sinuses may mimic thrombosis. Hyperdense
blood may be seen in children, particularly neonates and infants, and in
patients with a hemoconcentration of the blood, as might be present in
polycythemia or dehydration. At times, hyperdense blood may be difficult to
differentiate from true dural venous thrombosis, but symmetry of involvement,
homogeneity of the hyperdensity, and involvement of virtually all visualized
dural venous sinuses and major venous structures should suggest that
hyperdense blood is present rather than venous thrombosis (Figs.
5A and
5B). The presence of normal
flow void in the venous sinuses should confirm the presence of patent sinuses.
Hyperdense blood may also mimic subdural hemorrhage on CT, but the symmetry of
apparent involvement, the limitation of the hyperdensity in the expected lumen
of the dural sinuses, and a negative MRI study would effectively exclude this
possibility (Figs. 5C and
5D).
Subdural hematoma may mimic CVT (Figs.
6A,
6B,
6C,
6D,
6E,
6F and
8A,
8B). The clue to the correct
interpretation is that the abnormal signal of the subdural hematoma is located
more medial than the expected location of the transverse sinus. Figure
6A,
6B,
6C,
6D,
6E,
6F shows the abnormal FLAIR
signal extending too far inferiorly and medially, beyond the expected location
of the normal transverse and sigmoid sinuses. Contrast-enhanced MR venography
(Fig. 6F) confirms patent
dural venous sinuses and no evidence of thrombosis.
CVT may mimic subdural hematoma (Fig.
7A,
7B,
7C,
7D,
7E,
7F,
7G). CVT should be confined
entirely in the expected lumen of the dural venous sinuses. On the contrary,
subdural hemorrhage is seen exterior to the dural venous sinuses. Patients
with subdural hemorrhage in the posterior fossa may be at risk for CVT
(possibly as a result of direct injury of the dural venous sinuses or venous
stasis). In a patient with preexisting subdural hematoma, increasing density
at the location of the dural venous sinuses should prompt consideration of the
possibility of CVT (Fig. 7A,
7B,
7C,
7D,
7E,
7F,
7G).

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Fig. 12B —74-year-old man with headache and mastoiditis.
Maximum-intensity-projection of contrast-enhanced MR venography using sagittal
3D spoiled gradient-recalled echo (SPGR) sequence. Diagnosis is suggested by
presence of normal patent flow immediately proximal and distal to filling
defects, continuity of defects with dural surface, localized round or
lobulated appearance, and central enhancement.
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Fig. 13A —Arachnoid granulations simulating thrombus in dural venous
sinuses. In conventional angiography of 16-year-old boy with developmental
venous anomaly (long arrow), persistent filling defect is seen in
right transverse sinus (short arrow).
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Fig. 13B —Arachnoid granulations simulating thrombus in dural venous
sinuses. Contrast-enhanced T1-weighted image in same patient as in A
shows soft-tissue structure (black arrow) at corresponding location.
This structure is round and well defined, consistent with arachnoid
granulation.
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Fig. 13C —Arachnoid granulations simulating thrombus in dural venous
sinuses. Coronal T2-weighted image in different patient, 40-year-old man,
shows typical round arachnoid granulation in left transverse sinus
(arrow) that is abutting superior medial wall of transverse sinus.
Normal flow void is seen adjacent to this structure (at arrow tip) and in
consecutive images (not shown), further supporting this is an arachnoid
granulation.
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Retained contrast material from previous radiologic examinations due to
severely slow flow, such as might occur after ligation of the internal jugular
vein, may mimic CVT. However, these conditions may also predispose the patient
to developing thrombosis, so a contrast-enhanced study should be performed to
clarify the findings.
Pitfalls on Contrast-Enhanced CT
An empty delta sign may be mimicked by intrasinus septa or by a split or
fenestrated dural sinus, which may manifest as false-positive filling
defects.
Pitfalls on MRI
Intrasinus septa or a split or fenestrated dural sinus may also mimic CVT
on MR images (Fig. 9A,
9B,
9C). Acute and early subacute
hemorrhage may show hypointensity on T2-weighted MR images, mimicking the flow
void that would normally be seen in a patent venous sinus. Thrombus with
methemoglobin may mimic a patent sinus on contrast-enhanced T1-weighted MR
images (Fig. 10). Slow flow
leading to loss of flow void may mimic thrombosis.

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Fig. 14B —6-year-old boy with neuroblastoma. Contrast-enhanced
T1-weighted image shows enhancing lesion (black arrow) is dural
extension of neuroblastoma, compressing lateral sinus (white arrow).
Mass lesion is also seen posterior to torcular Herophili, compressing and
displacing it anteriorly. Note mass lesion at lateral wall of left orbit.
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Fig. 15B —42-year-old woman with headache. Sagittal gadolinium-enhanced
T1-weighted image shows extensive filling defects in superior sagittal sinus,
straight sinus, and torcular Herophili (arrows).
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Fig. 15C —42-year-old woman with headache. Coronal gadolinium-enhanced
T1-weighted image confirms that loss of flow void in A represents
thrombosis of superior sagittal sinus. Note filling defect of thrombus, giving
rise to empty delta sign (arrow).
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Pitfalls on MR Venography
Signal loss on unenhanced MR venography may result from in-plane flow,
extremely slow flow, or complex flow, mimicking thrombosis.
Thrombus with methemoglobin may show hyperintensity and mimic patent flow
on TOF MR venography (Fig.
10). If in doubt, phase contrast venography (which depends only on
blood flow characteristics and is not affected by the hyperintensity of
methemoglobin) can be performed to clarify the findings.
Pitfalls on All Techniques
A hypoplastic or aplastic dural sinus may mimic CVT. Figure
11A,
11B,
11C,
11D,
11E,
11F shows a hypoplastic left
transverse sinus. MR venography (Fig.
11A) can be misleading if it is interpreted in isolation. The
significant change in blood flow dynamics in stenotic or hypoplastic dural
venous sinuses can give rise to loss of flow signal
(Fig. 11A). Unenhanced
T1-weighted images (Fig. 11B)
fail to show thrombus, which should be evident given the severe narrowing of
the left dural sinuses. On the contrary, conventional gadolinium-enhanced
T1-weighted images (Fig. 11C)
show smooth enhancement in the hypoplastic left transverse and sigmoid
sinuses, which is subsequently confirmed on CT venography (Figs.
11D,
11E,
11F). Hypoplasia of the
ipsilateral jugular foramen (Figs.
11E and
11F) also serves as important
corroborative evidence of a hypoplastic dural sinus. The case illustrated in
Figure 11A,
11B,
11C,
11D,
11E,
11F highlights the importance
of correlating MR venography or CT venography with conventional imaging
findings.
Intrasinus arachnoid granulation may mimic thrombus (Figs.
12A,
12B and
13A,
13B,
13C). Figure
12A,
12B shows arachnoid
granulations in the bilateral transverse sinuses. These granulations are also
known as pacchionian granulations. In a series of autopsies of 10 patients
with no known venous disease, giant arachnoid granulations were found in two
patients, suggesting they are quite common
[16]. Arachnoid granulation
may show central and inhomogeneous contrast enhancement
[16] (Fig.
13A,
13B,
13C).
Tumor invasion or tumor compression of dural sinuses may mimic CVT (Fig.
14A,
14B). However, tumor invasion
or compression is a predisposing factor in the development of CVT, so this
possibility should be explicitly excluded in these circumstances.
Subarachnoid hemorrhage can be one presentation of dural venous thrombosis
[1,
8] (Fig.
15A,
15B,
15C). In such cases, careful
review of the images may show abnormal signal in the lumen of the affected
dural sinus, consistent with concurrent venous thrombus. MR venography can be
used to confirm the presence of extensive dural sinus thrombosis by showing
loss of flow void and filling defects.
Conclusion
The clinical presentation of CVT is nonspecific. To avoid a delay in
diagnosis, radiologists need to be aware of the various imaging features of
CVT, which can be subtle. Diagnostic pitfalls are associated with all imaging
techniques, but can be avoided by careful correlation of all imaging
findings.
Patients with low clinical suspicion of an intracranial abnormality can be
screened with unenhanced CT. If in doubt, further workup may include CT
venography or MRI with MR venography. CT venography and contrast-enhanced MR
venography are probably comparable in accuracy for evaluating CVT, and the
technique of choice will depend on the experience and resources of individual
institutions. Conventional angiography is usually reserved for difficult cases
or performed in conjunction with neurointervention.
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