AJR Integrative Imaging
LIFELONG LEARNING
Radiologic Diagnosis of Cerebral Venous Thrombosis:
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Pictorial Review
Colin S. Poon1,2, Ja-Kwei Chang1, Amar Swarnkar1, Michele H. Johnson2, John Wasenko1
Objective
Cerebral venous thrombosis is often associated with non-
specific clinical complaints. In addition, the imaging find-
ings are often subtle. Underdiagnosis or misdiagnosis of ce-
rebral 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 diag-
nose cerebral venous thrombosis accurately, using the opti-
mal imaging tools to achieve this goal.
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 non-
specific, 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 diag-
nosis 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 presenta-
tion and basic pathophysiology of the disease; review the ap-
proach for radiologic investigation, including emerging technol-
ogy such as CT venography; review the imaging features of CVT;
and show common pitfalls associated with the radiologic evalua-
tion 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 [17]. A more manageable approach is to un-
derstand that they may involve one or more of the following
Keywords: brain imaging, cerebral venous thrombosis, CT, MRI, neuroradiology
DOI:10.2214/AJR.07.7015
Received May 31, 2007; accepted after revision June 11, 2007.
Department of Radiology, State University of New York Upstate Medical University, 750 E Adams St., Syracuse, NY 13210. Address correspondence to C. S. Poon (poonc@upstate.edu).
1
Department of Diagnostic Radiology, Yale University School of Medicine, New Haven, CT.
2
AJR 2007;189:S64S75 0361803X/07/1886S64 American Roentgen Ray Society
S64 AJR:189, December 2007
FOR RADIOLOGY
mechanisms: direct involvement of the dural sinuses (e.g.,
infection, trauma, neoplastic infiltration), possibly with
damage to the vascular endothelium; venous stasis; hyperco-
agulable 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. Fre-
quent causes in older children include local infection, such as
mastoiditis, and coagulopathy. In adults, intrinsic or acquired
coagulopathies become the most important factors, contrib-
uting 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 fac-
tors. CVT actually occurs more often in puerperium than dur-
ing 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 2035% of cases, the cause remains unknown;
therefore, one should remain suspicious, even in the absence
of known risk factors [13].
Clinical Presentation
The clinical presentation of CVT is often nonspecific [16]
(Table 1). Common presentation includes headache, focal neuro-
logic 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 pa-
tients considered for the diagnosis of benign intracranial hyper-
tension [1]. Although subarachnoid hemorrhage is a rare presen-
tation of CVT, cases have also been reported [1, 8]. There is also
a wide distribution in the mode of onset of symptoms, with ap-
proximately 28% acute (< 48 hours), 42% subacute (between 48
hours and 30 days), and 30% chronic (> 30 days) [1]. The teach-
ing 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 neu-
roradiologic case.
 Cerebral Venous Thrombosis
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A B C

Fig. 15-year-old boy with severe headache and eye pain. Thrombosis was found in right lateral sinus (arrows).
A and B, Unenhanced CT images show thrombosis as hyperdensity (dense clot sign).
C and D, Enhanced CT images show same structure as filling defect with enhancing rim (empty delta sign).

Fig. 2Cord sign in cortical venous thrombosis in a

young woman.
A and B, 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 sub-
cortical hemorrhagic infarction (black arrows), dif-
fuse brain swelling, and small ventricular size.
A B

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A B C

D E F

Fig. 338-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, Rosen-
thals veins).
A and B, 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.
C, Axial T2-weighted MR image shows replacement of signal void by thrombus (arrow) in superior sagittal sinus. Veins at internal capsules are engorged.
D and E, Sagittal contrast-enhanced T1-weighted image (D) shows filling defects in sagittal and straight sinuses, correlating with absence of flow on 2D phase con-
trast MR venography (E).
F, After catheter-directed thrombolysis, flow was partially reestablished.

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 venogra-
phy have been the noninvasive imaging techniques of choice
[46, 9] and are often used as the initial diagnostic test for
suspicious cases. CT venography is now emerging as a com-
peting 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 du-
ral sinus may give a dense clot sign (Fig. 1). The cord sign
represents direct visualization of a thrombosed cortical
vein that is seen as linear hyperdensity (Fig. 2).
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
2050% 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 unen-
hanced CT images. An infarction not conforming to a major
arterial vascular territory, such as the presence of multiple iso-
lated lesions, involvement of a subcortical region with sparing
of the cortex, and extension over more than one arterial distri-

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A B C

D E F

Fig. 416-year-old girl with multiple traumatic injuries in head. Initial unenhanced CT (not shown) showed hyperdensity in right internal jugular vein (IJV) and sig-
moid sinus that was suspicious for venous thrombosis. Findings were confirmed on CT venography, MRI, and conventional venography.
A and B, 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.
C, 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).
D, T1-weighted MR image shows sigmoid sinus thrombosis (arrow) as seen on CT (B).
E and F, 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.

bution, is highly suspicious for a venous cause. The infarction
may be hemorrhagic (Fig. 2) 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 im-
paired venous drainage and, therefore, parenchymal change in
the parasagittal region. Thrombosis in Labbs 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. 3).
the dural sinus, with peripheral enhancement possibly sec-
ondary to the development of collaterals (Fig. 1).
Indirect evidence of CVT may be seen as contrast enhance-
ment of the falx and tentorium secondary to venous stasis
and hyperemia of the dura mater, which is seen in approxi-
mately 20% of cases.
One should be aware that in 1030% of cases of CVT, the find-
ings 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.

Contrast-Enhanced CT CT Venography
Direct evidence of CVT on contrast-enhanced CT includes A more recent tool that can be used to evaluate CVT is
the empty delta sign, which may be seen 5 days to 2 months CT venography [1012]. CT venography allows direct visu-
from onset. This sign represents a filling defect (thrombus) in alization of thrombus as filling defects (Fig. 4).

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A B C

Fig. 54-day-old neonatal boy after idiopathic cardiac arrest.

A and B, Axial unenhanced CT scans show normal, hyperdense blood commonly seen in neonates and in-
fants.
C and D, T1- (C) and T2-weighted (D) MR images show normal findings.

MRI
On MRI, venous thrombus may be directly visualized. On
TABLE 1: Signs and Symptoms of Cerebral
conventional MRI sequences, patent dural sinuses are often Venous Thrombosis
seen as a flow void. This is particularly well seen when the
Presentation Frequency (%)
imaging plane is orthogonal to the blood flow direction (e.g.,
coronal images are best for visualization of the superior sag- Headache 75
ittal, transverse, and sigmoid sinuses). The effect of a flow Papilledema 49
void may be reduced in a plane parallel to the dural sinus, Seizures 37
although such an imaging plane often offers a better depic- Motor or sensory deficit 34
tion of the complete extent of thrombosis in the dural sinus. Mental status changes 30
For example, a sagittal T1-weighted image may show the
Dysphasia 12
complete extent of the superior sagittal sinus thrombosis as
Cranial nerve palsies 12
an abnormally bright signal filling the sinus. The thrombus
may manifest as absence of a flow void, which is often best Cerebellar incoordination 3
seen on FLAIR images and T2-weighted spin-echo images. Bilateral or alternating cortical signs 3
The abnormal signal intensity follows the signal characteris- Nystagmus 2
tics of intracranial hemorrhage and may evolve through the Hearing loss 2
stages of oxyhemoglobin, deoxyhemoglobin, methemoglo- NotePercentages total > 100% because patients may have multiple presentations.
bin, and hemosiderin [4]. On T1-weighted images, thrombus Adapted from [1].

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A B C

D E F

Fig. 6Middle-aged woman (exact age unknown) with history of multiple myeloma.
A and B, Axial unenhanced CT images show subdural hemorrhage at right cerebellar convexity that mimics thrombosis of right transverse sinus.
CE, 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).
F, 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.

with methemoglobin is seen as hyperintensity. On T2*-weighted MR Venography

gradient-echo images, exaggerated signal loss is often seen
because of the increased susceptibility effect of deoxyhemo-
globin, methemoglobin, or hemosiderin.
Indirect evidence of venous thrombosis is often second-
ary to parenchymal change as a result of venous occlusion.
This is similar to the findings on CT, including brain swell-
ing and hemorrhagic or nonhemorrhagic infarction.
Conventional MRI sequences often provide sufficient in-
formation 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 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 sub-
ject to flow-related image artifacts.
Similar to CT venography, contrast-enhanced MR venog-
raphy 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

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A B C

D E F

Fig. 77-year-old girl with closed head injury.

AC, Unenhanced CT scans on first day show subdural hemorrhage along tentorium cerebelli and skull frac-
ture. Subtle density is seen in right lateral sinus (arrows, B and C) that was not well appreciated initially.
D and E, On next day, repeat CT scan shows dense thrombus in right lateral sinus (arrows) mimicking sub-
dural hematoma (compare E with A).
F and G, On sagittal T1-weighted MR images, normal flow void is seen in left lateral sinus (arrow, F), but note
isodense thrombus on right (arrow, G).
G

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.
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 con-
trast techniques [10]. However, a direct comparison between
CT venography and contrast-enhanced MR venography is not
yet available. These two techniques probably provide compa-
rable performance, and preference will be dictated by the expe-
rience and resources of the individual institutions.

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TABLE 2: Comparison of MR Venography Techniques

Technique Advantages Disadvantages
Time-of-flight Shorter imaging time More prone to false-positive results from in-plane flow
False-negatives due to methemoglobin
Phase contrast Better background suppression More sensitive to motion artifacts and turbulent flow
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Can detect flow in all three orthogonal planes

Better flow quantification
No false-negatives due to methemoglobin
Gadolinium-enhanced Less likely to give false-positives due to slow or Potential false-negatives due to methemoglobina or
complex flow enhancing chronic thrombosis
a
But less likely than with time-of-flight.

Fig. 84-month-old girl with seizure.

A and B, Unenhanced CT scans show subdural
hemorrhage along falx and tentorium cerebelli,
simulating sagittal and transverse sinus thrombo-
sis. Note pseudo empty delta sign (arrow, A). Empty
delta sign of cerebral venous thrombosis is appli-
cable only on contrast-enhanced CT. Hyperdensity
along posterior parietal convexity simulates trans-
verse sinus thrombosis (black arrow, B). Extension
of hyperdensity beyond expected location of trans-
verse sinus suggests this is actually subdural he-
matoma (white arrow, B) [8].
A B

A B C

Fig. 929-year-old woman woman with headache.

AC, 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 venog-
raphy 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 op-
posite 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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 Poon et al.

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 im-
aging sequences. If in doubt, other imaging techniques
should be used to confirm the findings.
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Fig. 10Superior sagittal sinus thrombosis in young woman (exact age un-
known) on T1-weighted image. Sagittal T1-weighted images can be useful for
depiction of extensive superior sagittal sinus thrombosis. However, bright sig-
nal of thrombus with methemoglobin (arrow) may mimic patent sinus on con-
trast-enhanced T1-weighted images and time-of-flight MR venography.
Pitfalls on Unenhanced CT
Hyperdense blood in patent dural sinuses may mimic
thrombosis. Hyperdense blood may be seen in children, par-
ticularly neonates and infants, and in patients with a hemo-
concentration of the blood, as might be present in poly-
cythemia or dehydration. At times, hyperdense blood may
be difficult to differentiate from true dural venous throm-
bosis, but symmetry of involvement, homogeneity of the
hyperdensity, and involvement of virtually all visualized
dural venous sinuses and major venous structures should

A B C

D E F

Fig. 1125-year-old woman with headache. Black arrows indicate left transverse and sigmoid sinuses; white arrows indicate right transverse and sigmoid sinuses.
A, Axial phase contrast MR venogram shows loss of flow signal (arrow).
B, Axial T1-weighted image fails to show thrombus.
C, Axial T1-weighted gadolinium-enhanced image shows smooth enhancement in hypoplastic left transverse and sigmoid sinuses.
DF, Coronal reformations of CT venography, from posteriorly to anteriorly, show smooth enhancement in hypoplastic left transverse and sigmoid sinuses. Hypopla-
sia of ipsilateral jugular foramen also serves as important corroborative evidence of hypoplastic dural sinus.

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 Cerebral Venous Thrombosis

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 involve-
ment, the limitation of the hyperdensity in the expected
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nuses. Contrast-enhanced MR venography (Fig. 6F) confirms
patent dural venous sinuses and no evidence of thrombosis.
CVT may mimic subdural hematoma (Fig. 7). CVT should be
confined entirely in the expected lumen of the dural venous si-
nuses. On the contrary, subdural hemorrhage is seen exterior to
the dural venous sinuses. Patients with subdural hemorrhage in

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. 6 and 8). The
clue to the correct interpretation is that the abnormal signal of
the subdural hematoma is located more medial than the expect-
ed location of the transverse sinus. Figure 6 shows the abnormal
FLAIR signal extending too far inferiorly and medially, beyond
the expected location of the normal transverse and sigmoid si-
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 consid-
eration of the possibility of CVT (Fig. 7).
Retained contrast material from previous radiologic ex-
aminations due to severely slow flow, such as might occur af-
ter ligation of the internal jugular vein, may mimic CVT.

Fig. 1274-year-old man with headache and mas-

toiditis.
A, Contrast-enhanced T1-weighted image shows fill-
ing defects (arrows) in bilateral transverse sinuses.
B, Maximum-intensity-projection of contrast-en-
hanced MR venography using sagittal 3D spoiled
gradient-recalled echo (SPGR) sequence. Diagnosis
is suggested by presence of normal patent flow im-
mediately proximal and distal to filling defects, con-
tinuity of defects with dural surface, localized round
or lobulated appearance, and central enhancement.
A B

A B C

Fig. 13Arachnoid granulations simulating thrombus in dural venous sinuses.

A, 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).
B, 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.
C, Coronal T2-weighted image in different patient, 40-year-old man, shows typical round arachnoid granulation in left transverse sinus (arrow) that is abutting supe-
rior 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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 Poon et al.

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 sep-
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MR images (Fig. 10). Slow flow leading to loss of flow void may
mimic thrombosis.
Pitfalls on MR Venography
Signal loss on unenhanced MR venography may result
from in-plane flow, extremely slow flow, or complex flow,

ta or by a split or fenestrated dural sinus, which may mani- mimicking thrombosis.

fest 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. 9). Acute and early sub-
acute 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
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
11 shows a hypoplastic left transverse sinus. MR venography

Fig. 146-year-old boy with neuroblastoma.

A, T1-weighted image shows isointense lesion (ar-
row) at region of left transverse sinus, simulating
sinus thrombosis.
B, Contrast-enhanced T1-weighted image shows
enhancing lesion (black arrow) is dural extension of
neuroblastoma, compressing lateral sinus (white ar-
row). Mass lesion is also seen posterior to torcular
Herophili, compressing and displacing it anteriorly.
Note mass lesion at lateral wall of left orbit.

A B

A B C

Fig. 1542-year-old woman with headache.

A, Coronal FLAIR image shows hyperintensity in subarachnoid space, consistent with subarachnoid hemorrhage.
B, Sagittal gadolinium-enhanced T1-weighted image shows extensive filling defects in superior sagittal sinus, straight sinus, and torcular Herophili (arrows).
C, Coronal gadolinium-enhanced T1-weighted image confirms that loss of flow void in A represents thrombosis of superior sagittal sinus. Note filling defect of throm-
bus, giving rise to empty delta sign (arrow).

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 Cerebral Venous Thrombosis
TABLE 3: Comparison of MR Venography and CT Venography
Technique Advantages
MR venography No radiation risk
Better established
CT venography Short imaging time
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Less prone to motion artifacts
Generally better availability
More accessible for critical patients
Better depiction of small vessels
Easy to interpret
(Fig. 11A) can be misleading if it is interpreted in isolation. The
significant change in blood flow dynamics in stenotic or hyp-
oplastic 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 nar-
rowing 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 sig-
moid sinuses, which is subsequently confirmed on CT venogra-
phy (Figs. 11 D11F). Hypoplasia of the ipsilateral jugular fora-
men (Figs. 11E and 11F) also serves as important corroborative
evidence of a hypoplastic dural sinus. The case illustrated in
Figure 11 highlights the importance of correlating MR venogra-
phy or CT venography with conventional imaging findings.
Intrasinus arachnoid granulation may mimic thrombus
(Figs. 12 and 13). Figure 12 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. 13).
Tumor invasion or tumor compression of dural sinuses
may mimic CVT (Fig. 14). However, tumor invasion or com-
pression is a predisposing factor in the development of CVT,
so this possibility should be explicitly excluded in these cir-
cumstances.
Subarachnoid hemorrhage can be one presentation of
dural venous thrombosis [1, 8] (Fig. 15). In such cases, care-
ful review of the images may show abnormal signal in the
lumen of the affected dural sinus, consistent with concur-
rent venous thrombus. MR venography can be used to con-
firm 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 vari-
ous 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.
AJR:189, December 2007 S75
Disadvantages
Cannot be used in patients with contraindication to MRI
Unenhanced techniques more prone to flow-related image artifacts, leading to
higher incidence of false-positive results
Requires iodinated contrast agent
Patients with low clinical suspicion of an intracranial ab-
normality 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 evaluat-
ing CVT, and the technique of choice will depend on the expe-
rience and resources of individual institutions. Conventional
angiography is usually reserved for difficult cases or performed
in conjunction with neurointervention.
References
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