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1 Department of Diagnostic Radiology, State University of New York Upstate
Medical University, Syracuse, NY.
2 Department of Diagnostic Radiology, Yale University School of Medicine, New
Haven, CT.
3 Department of Radiology, University of Washington, Box 354755, 4245 Roosevelt
Way NE, Seattle, WA 98105.
Received August 30, 2007;
accepted after revision August 30, 2007.
Address correspondence to F. S. Chew
(fchew{at}u.washington.edu).
Abstract
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Keywords: brain imaging cerebral venous thrombosis CT MRI neuroradiology
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REQUIRED READING (available at www.arrs.org)
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Solution to Question 1
Infection contributes to fewer than 10% of cerebral venous thrombosis (CVT)
cases in adults [1,
2]. Option A is not the best
response. CVT occurs more often in puerperium than during the pregnancy.
Option B is not the best response. Although pregnancy-related CVT occurs more
often in older women, aging per se is not a risk factor. Option C is not the
best response. In 20–35% of cases, the cause remains unknown, so one
should remain suspicious even in the absence of known risk factors
[1–3].
Option D is the best response. The pathogenesis of CVT is complex and
is poorly understood.
Solution to Question 2
Common presentations include headache, focal neurologic deficits, seizures,
and altered consciousness. Options A, B, and D are not the best responses. A
syndrome of intracranial hypertension (headache and papilledema) accounts 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 subdural
hemorrhage has not been associated with CVT, cases of subarachnoid hemorrhage
as a rare presentation of CVT have been reported
[1,
4]. Option C is the best
response. 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) presentation
[1]. Option A, which is true,
is not the best response. The teaching point is that CVT may present with an
atypical presentation or even an absence of clinical symptoms.
Solution to Question 3
An infarction not conforming to a major arterial vascular territory, such
as the presence of multiple isolated lesions, involvement of the subcortical
region with sparing of the cortex, or extension over more than one arterial
distribution, is highly suspicious for a venous cause. The infarction may be
hemorrhagic or nonhemorrhagic. Option A is not the best response. The empty
delta sign may be seen on contrast-enhanced CT and represents a filling defect
(thrombus) in the dural sinus, with peripheral enhancement possibly secondary
to the development of collaterals. The empty delta sign may be seen 5 days to
2 months from onset [5].
Option B is the best response. 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. This is seen in approximately 20% of cases.
Option C is not the best response. The "dense clot sign" and the
dense cord sign represent direct visualization of the thrombosed cortical vein
or the venous sinus in short and long axes, respectively, but are seen in only
one third of cases. Option D is not the best response.
Solution to Question 4
An infarction not conforming to a major arterial vascular territory
strongly suggests CVT. The location of an infarction with respect to the
expected course of venous drainage may provide a clue to the venous structure
involved [6]. Thrombosis in the
sagittal sinus often leads to impaired venous drainage and, therefore,
parenchymal change in the parasagittal region. Options A and B are not the
best responses. Thrombosis in Labbé's vein should lead to infarction in
the temporal lobe. Option C is not the best response. Bilateral or unilateral
infarction in the thalami, basal ganglia, and internal capsule is typically
seen in deep venous thrombosis. Option D is the best response.
Solution to Question 5
Venous thrombus may be directly visualized on MRI
[7]. On conventional MRI
sequences, patent dural sinuses are often seen as flow voids; thus, the
absence of signal in the dural sinuses is an indication that CVT is absent.
Option C is the best response because it is not a sign of CVT. The
thrombus may manifest as absence of a flow void, which is often best seen on
FLAIR 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
[8]. On T1-weighted images,
thrombus with methemoglobin is seen as hyperintensity replacing the normal
flow void. Option A is not the best response. Thrombus with deoxyhemoglobin is
seen as an isointense or slightly hypointense signal replacing the normal flow
void. Option B is not the best response. On T2*-weighted gradient-echo images,
exaggerated signal loss (very hypointense) is often seen as a result of the
increased susceptibility effect of deoxyhemoglobin, methemoglobin, or
hemosiderin. Option D is not the best response.
Solution to Question 6
Normal hyperdense blood is commonly seen in newborns or infants and, at
times, may be difficult to differentiate from true dural venous thrombosis.
However, imaging features such as symmetry, homogeneity, and involvement of
virtually all visualized dural venous sinuses and major venous structures
would argue against true venous thrombosis. Option A is not the best response.
Subarachnoid hemorrhage can be a presentation of dural venous thrombosis
[4]. Therefore, cases in which
subarachnoid hemorrhage is found should be carefully reviewed for direct and
indirect signs of underlying dural sinus thrombosis. Option B is not the best
response. Arachnoid granulations (also known as pacchionian granulations) may
simulate dural sinus filling defects when found in or adjacent to a venous
sinus. Arachnoid granulation may show central and inhomogeneous contrast
enhancement [9]. The true
diagnosis is suggested by the presence of normal patent flow immediately
proximal and distal to the filling defects, the continuity of the defects with
the dural surface, a localized round or lobulated appearance, and central
enhancement. Option C is not the best response. The cord sign represents
direct visualization of a thrombosed cortical vein, seen as linear
hyperdensity, and is therefore not a pitfall in diagnosis. Option D is the
best response. A hypoplastic dural sinus may be misleading if interpreted
in isolation [10]. The
significant change in blood flow dynamics in stenotic or hypoplastic dural
venous sinuses can give rise to a loss of flow signal, suggesting occlusion by
thrombus. Lack of visualization of the thrombus on conventional MRI, a small
jugular foramen on the ipsilateral side, and the visualization of diffuse
smooth narrowing of the sinus on enhanced CT, enhanced MRI, CT venography, or
MR venography should lead one to the correct diagnosis. Option E is not the
best response.
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