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Diagnosis of Cerebral Venous Thrombosis With Echo-Planar T2*-Weighted Magnetic Resonance Imaging
Magdy Selim, MD, PhD;
John Fink, FRACP;
Italo Linfante, MD;
Sandeep Kumar, MD;
Gottfried Schlaug, MD;
Louis R. Caplan, MD
Arch Neurol. 2002;59:1021-1026.
ABSTRACT
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Background Magnetic resonance (MR) signal changes suggestive of cerebral venous
thrombosis (CVT) on T1- and T2-weighted images may be subtle and their identification
requires a high degree of suspicion. Magnetic resonance venography remains
essential for definitive diagnosis. Recent reports have shown that T2*-weighted MR sequence is more sensitive than T1-weighted, T2-weighted,
and fluid-attenuated inversion recovery (FLAIR) images in detecting subarachnoid
and intracerebral hemorrhages, both of which can be seen in association with
CVT. The value of T2*-weighted magnetic resonance imaging (MRI)
in diagnosing CVT has not been well studied.
Objectives To investigate and describe T2*(susceptibility-weighted)
MRI findings in 5 patients with CVT.
Methods We reviewed our stroke database from May 1, 1997, through May 31, 2001.
The diagnosis of CVT was made in 6 patients, 5 had an MRI with T2* sequence.
We examined T2*/susceptibility-weighted images for these 5 patients
to determine their ability, relative to T1-weighted, T2-weighted, and FLAIR
sequences, to detect CVT.
Results On T2*-weighted images, we were able to detect areas of hypointensities
in the affected veins and/or sinuses in all 5 patients. Thrombosed veins and/or
sinuses were more easily seen on T2*-weighted images than on any
other MR sequence. The T2* sequence also allowed visualization
of associated hemorrhagic venous infarcts, which were considerably less obvious
on other MR sequences.
Conclusions The T2*-weighted MR sequence can be useful in rapid detection
of CVT and may enable the diagnosis to be made prior to MR venography. This
is particularly important in clinically unsuspected patients, in whom MR venography
is rarely obtained.
INTRODUCTION
CEREBRAL VENOUS thrombosis (CVT) can lead to devastating disability,
and even death, if not timely diagnosed and treated.1
Diagnosing CVT often challenges physicians owing to the nonspecific symptoms
and the broad spectrum of presentation.2 Some
cases of CVT may be unrecognized. Radiological studies are crucial in establishing
the diagnosis. Computed axial tomography (CT) cannot reliably diagnose CVT
in many cases, especially if contrast is not given. A nonenhanced CT shows
no abnormality in about 20% of the patients with CVT3-4;
and CT findings of CVT may be misinterpreted as subarachnoid hemorrhage or
intraparenchymal hemorrhage.3, 5
Alterations in blood flow and hemoglobin degradation products in thrombosed
veins may produce signal changes on magnetic resonance (MR) T1- and T2-weighted
images, which may suggest the diagnosis of CVT.6-8
However, conventional T1- and T2-weighted MR images (MRIs) are relatively
insensitive since such signal changes are often subtle.5
Gadolinium administration can increase the sensitivity of the MRI,9 but cerebral angiography remains essential for the
definite diagnosis of CVT. Of late, MR venography (MRV) has surpassed conventional
angiography as the imaging modality most widely used to establish the diagnosis
of CVT.5, 10
Thus, the diagnosis of CVT can be missed, particularly in clinically
unsuspected cases, if only routine nonenhanced T1- and T2-weighted MRI sequences
are performed without angiography. Because MRV and gadolinium enhancement
are not routinely performed in most MRI protocols, delays of serious consequences
can occur in the diagnosis of CVT. Recent reports have confirmed high sensitivity
of echo-planar T2*(susceptibility)-weighted MRIs (SWI) for detecting the magnetic
susceptibility effect of blood products such as deoxyhemoglobin, in patients
with acute subarachnoid hemorrhage and intraparenchymal hemorrhage.8, 11 The utility of T2*/SWI for detecting
CVT is unknown. A T2*-weighted sequence has been a routine part of our stroke
MRI protocol for several years. We have performed a retrospective analysis
of MRI findings in patients with CVT to assess the feasibility of T2*/SWI
sequence for the detection of CVT.
SUBJECTS AND METHODS
PATIENT SELECTION
We reviewed our computerized stroke database from May 1, 1997, through
May 31, 2001. Over this period, the diagnosis of CVT was made in 6 patients
who all had brain MRI, MRV, and CT. Two patients also had conventional angiography
(DSA). Five of the 6 patients had T2*-weighted sequences as a part of their
MRI. These 5 patients were included in this study.
MRI PROTOCOL
The MRI protocol used in our institution routinely includes diffusion-weighted
MRI (DWI), SWI, and T1- and T2-weighted images, non–echo-planar FLAIR
images, and MR angiography of the intracranial vessels. The imaging parameters
for SWI, echo-planar imaging gradient echo are as follows: repetition time,
0.8 milliseconds; echo time, 60 milliseconds; flip angle, 60°; number
of slices, 20; slice thickness, 7 mm; acquisition matrix, 96 x 128 pixels;
field of view, 240 cm; and acquisition time, 2 seconds. Parameters for other
sequences have been previously reported.8
REPORT OF CASES
CASE 1
Figure 1 highlights MRI findings
in patient 1 and shows signal loss (darkening) in the sagittal sinus, vein
of Galen, left transverse sinus, and straight sinus confluence on T2*-weighted
images. This patient is a 38-year-old man who presented with acute change
in mental status in the setting of a 4-day history of "flulike illness," headaches,
vomiting, and lethargy. On examination, he was inattentive, abulic, and had
papilledema. The findings from the remainder of his neurological and general
physical examinations showed no abnormality. The National Institute of Health
Stroke Scale (NIHSS) score was 4. A CT of the head, plain and contrasted,
suggested "subarachnoid hemorrhage vs cortical venous occlusion in the left
posterior occipital region." Diffusion-weighted MRI showed restricted diffusion
abnormalities in frontal regions, a right-sided thalamic infarct, and a left-sided
occipital hemorrhagic infarct. Magnetic resonance venography showed poor flow
in the sagittal sinus, internal cerebral veins, vein of Galen, septal and
thalamic veins, transverse sinuses, and straight sinus confluence (Figure 1D). Conventional angiography confirmed
thrombosis in these veins and showed occlusions of both internal jugular veins.
He was initially treated with intravenous heparin sulfate but rapidly became
somnolent. He received intrasinus recombinant tissue-type plasminogen activator
(rt-PA), followed by stenting of the left internal jugular vein and systemic
anticoagulation. His condition rapidly improved. He was diagnosed as having
polycythemia vera.
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Figure 1. Case 1. Magnetic resonance image
(MRI). C, T2*/susceptibilty-weighted MRI with the arrows pointing to blood
products (darkening) in the sagittal sinus, vein of Galen, left transverse
sinus, and straight sinus confluence, which is not easily seen on comparable
T1-weighted (A) and T2-weighted (B) MRI slices. D, Views of the MR venography
(MRV), nonenhanced computed tomographic scan (CT), and diffusion-weighted
image (DWI) of the same patient. Note the filling defects in the superior
sagittal sinus (arrows) on MRV in comparison to that in Figure 4 from a healthy
control subject.
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CASE 2
Figure 2 highlights MRI findings
in patient 2 and shows susceptibility effect in the vein of Galen, sagittal
sinus, and left-sided lateral sinus complex on T2* images. He was a 36-year-old
man who had left-sided facial pain for 1 week, then suddenly developed severe
headache, nausea, and vomiting. He was found "unresponsive" and had urinary
incontinence. On examination, he was intubated and comatose with decerebrate
posturing. Brainstem reflexes were intact. His pupils were equal and reactive
to light. Fundoscopic examination showed papilledema. Neurological examination
showed no focal signs; NIHSS score was 37. The findings of his general physical
examination showed no abnormality. A CT of the head showed multiple foci of
high signal in the left temporoparietal-occipital junction and outlining gyri;
this was interpreted as intraparenchymal and subarachnoid hemorrhages (Figure 2D). Brain MRI revealed similar findings
on T1-weighted, T2-weighted, and FLAIR images; MRV revealed absent flow in
the superior sagittal, straight, and left transverse sinuses. Conventional
angiography confirmed the presence of diffuse CVT involving the sagittal,
bilateral transverse, and deep venous systems and thrombosis of the left internal
jugular vein. He was treated with intrasinus rt-PA, followed by systemic anticoagulant
therapy. His condition rapidly improved, with a near-complete recovery. His
evaluation for possible underlying cause was normal except for an elevated
serum homocysteine level.
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Figure 2. Patient 2. Magnetic resonance
image (MRI). C, Note that T2*/susceptibilty-weighted MRI shows the abnormalities
(arrows), as low signal, within the left parieto-occipital region (hemorrhage)
and sagittal, transverse, and straight sinuses (blood degradation products
of the intravenous thrombus) more clearly than the the corresponding T1-weighted
(A), T2-weighted (B), and fluid-attenuated inversion recovery (FLAIR) (D)
images. Magnetic resonance venography (MRV) shows absent flow in the superior
sagittal sinus (arrows).
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CASE 3
Figure 3A depicts the T2*/SWI
findings in patient 3 and shows a susceptibility effect within the vein of
Galen and left sinus complex. This 62-year-old woman presented with new onset
of right-sided focal motor seizure with secondary generalization after a 3-day
history of worsening headaches. Her medications included estrogen replacement
therapy. On examination, she was inattentive and hypophonic. She had a right
Babinski sign and a slow shuffling gait; NIHSS score was 0. Plain head CT
showed "an unusual increased signal at the inferior sagittal sinus"; a contrast-enhanced
MRI did not support CVT. Brain MRI showed restricted diffusion abnormalities
in the basal ganglia and thalami; MRV confirmed CVT involving the internal
cerebral veins, vein of Galen, and straight, sigmoid, and left transverse
sinuses. Her symptoms resolved with the administration of systemic anticoagulant
therapy and the cessation of hormonal replacement therapy.
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Figure 3. Patients 3 through 5. T2*-weighted magnetic resonance (MR) imaging and MR venography rows A
through C. The arrows point to the abnormalities, susceptibility effect on
T2*, and filling defects on MR venography.
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CASE 4
Figure 3B shows T2* areas
of hypointensities within the left transverse and sigmoid sinuses of patient
4. 42-year-old man, he had presented with acute onset of severe headache.
Neurological and general physical examination findings showed no abnormality;
NIHSS score was 0. A CT of the head showed a left posterior temporal hyperdensity,
interpreted as "hemorrhage vs vascular malformation." Brain MRI, T1- and T2-weighted
images, suggested the presence of a hyperintense signal within the left transverse
and sigmoid sinuses; MRV confirmed occlusion of the left transverse and sigmoid
sinuses. He was treated with heparin, then warfarin sodium. His headache rapidly
resolved.
CASE 5
Figure 3C shows a large area
of susceptibility effect in the right temporoparietal region and within the
right transverse sinus of patient 5. A 53-year-old woman, she had had sudden
onset of severe headaches and vomiting. She had 2 witnessed generalized tonic-clonic
seizures en route to our hospital. On physical examination, she was somnolent;
had bilateral papilledema, left visual field cut, and left-sided hemiparesis.
The NIHSS score was 6. A CT of the head showed a right parietal hemorrhage,
interpreted as "amyloid angiopathy vs hypertensive hemorrhage." Brain MRI
showed "a large area of hemorrhage with edema within the right temporoparietal
cortex" on T1-weighted and T2-weighted images. Gadolinium administration showed
a thrombus within the right transverse sinus; MRV confirmed occlusion of the
right transverse and sigmoid sinuses. She was found to have persistent protein
C deficiency. She was treated with systemic anticoagulant therapy that resulted
in the improvement of her condition.
RESULTS
The diagnosis of CVT was made by stroke-experienced neurologists and
neuroradiologists on the basis of history, clinical examination results, and
radiological findings. The definite diagnosis was confirmed by MRV in all
5 patients.
We were able to detect areas of hypointensities in the affected veins
and/or sinuses, indicating the presence of intravenous clots, on T2*-weighted
sequence. In all 5 patients, thrombosed veins and sinuses were more easily
seen on T2*-weighted images than on any other nonangiographic MR sequence.
In patients 1 and 2, the associated hemorrhagic venous infarcts were easily
visualized on T2*-weighted images, but not T1- or T2-weighted images.
Figure 4 shows MRV and T2*
MRI of a healthy control subject for comparisons. The results of CT or DSA
are not shown for all patients since the purpose of this study is not to compare
CT vs MRI or MRV vs DSA.
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Figure 4. Control subject. Magnetic resonance
venography (MRV) and T2*-weighted magnetic resonance imaging sequence of a
healthy control subject.
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COMMENT
To our knowledge, the use of T2*/SWI in diagnosing CVT has not been
previously evaluated. Our study shows that the gradient echo T2*-weighted
images are able to detect the presence of the intravenous clot. The clot is
directly visualized as an area of hypointensity in the affected vein and/or
sinus. Although not quantitatively assessed, the sensitivity of T2*/SWI for
detecting CVT far exceeded that of routine T1- and T2-weighted images. Thrombosed
veins and sinuses were more easily visualized on SWI than on any other MR
sequence in all 5 patients.
Several studies have confirmed the usefulness of MRI for the diagnosis
of CVT.3, 5, 9 The
MRI features of CVT have been described in detail in numerous reports.5, 9 The main sign of CVT on a standard
MRI protocol is the lack of expected signal flow-void on standard spin echo
T1 and T2 sequences. The MR signal relies on proton (hydrogen nuclei) density
and T1 and T2 relaxation times.10-11
The different chemical products of blood breakdown in thrombosed veins and
sinuses result in signal changes on T1- and T2-weighted images. Thus, the
actual appearance and signal intensity of the intraluminal thrombus evolve
over time depending on the paramagnetic effects of hemoglobin breakdown products,
in a manner similar to that of intraparenchymal hemorrhage.6-8,12-13
The use of standard spin echo T1 and T2 sequences, in isolation, to
diagnose CVT has its shortcomings since their sensitivity for detection of
CVT is poor, especially in chronic cases, and the lateral and superior sagittal
sinuses are not seen well in axial sections.5
Magnetic resonance venography is almost always required to confirm the diagnosis
of CVT. Absence of flow signal on MRV suggests intraluminal thrombosis. However,
MRV is also subject to artifacts, which may result in a false-negative diagnosis.5
The MR properties of products of hemoglobin catabolism are well characterized.6-8 Hemoglobin becomes deoxygenated
when the arterial blood, with high oxygen saturation, passes into the venous
blood with lower oxygen saturation.14 This
results in the formation of deoxyhemoglobin, which possesses paramagnetic
properties. Decreased cerebral venous blood flow in CVT promotes a local shift
in the hemoglobin oxygenation curve toward the formation of deoxyhemoglobin.
Deoxyhemoglobin produces a nonuniform magnetic field and rapid dephasing of
proton spins and loss of T2*-weighted signal.11
This property of paramagnetic molecules, such as deoxyhemoglobin, is termed
"magnetic susceptibility effect" and results in signal loss (darkening) best
seen in T2*/SWI.13, 15-16
This magnetic susceptibility effect of hemoglobin degradation products within
the thrombosed veins accounts for our current results, showing that T2*/SWI
is the nonangiographic MR sequence that most clearly reveals CVT in all 5
patients. Simultaneous acquisition of MRV in all of our patients, besides
establishing the diagnosis of CVT, confirms that the susceptibility effect
seen within the veins and sinuses is consistent with blood clots and is not
an artifact.
We have previously shown that T2*/SWI is the most sensitive MR sequence
for detecting intracerebral hemorrhage.8 Thus,
T2*/SWI not only allows direct visualization of the involved sinuses that
are distended with proton-dense blood clots, but also of associated venous
infarcts that are frequently hemorrhagic.
Some have questioned the utility of MRI/MRV in detecting CVT since nonvisualization
of a sinus, which may be hypoplastic or absent, is not uncommon in normal
individuals.2 The ability of T2* sequence to
show an easy-to-visualize susceptibility effect within the involved sinus
is of added benefit in such questionable cases.
Although it is impossible to determine the exact time of onset of CVT
in all of our patients, the duration of symptoms imply that none could have
been longer than 9 days from presentation. Therefore, the sensitivity of T2*/SWI
for detecting chronic CVT remains unknown.
It is important to recognize that the susceptibility effect seen on
T2*/SWI does not always indicate intravascular thrombosis or blood products.
Arterial flow voids or calcifications commonly result in susceptibility artifacts.
Therefore, experienced readers, familiar with such artifacts, should interpret
signal changes on SWI. Also, the T2* signal may be hard to interpret at the
boundaries between tissues of differing magnetic susceptibility, such as bone
and soft tissue, where the bone surfaces of the skull causes areas of low
signal. Patient 3 (Figure 3A) provides
an example where the susceptibility within the left transverse sinus cannot
be easily distinguished from the low signal of the nearby bone. In such locations,
combining T2* with FLAIR or MRV may be advisable.
CONCLUSIONS
This study shows that T2*/SWI MR sequence can be useful in rapid detection
of CVT. It may enable the diagnosis to be made prior to MRV. This is particularly
important in clinically unsuspected cases, where MRV is rarely obtained, since
early diagnosis will help achieve better outcome. The T2*-weighted sequences
can be performed on standard MR scanners, with additional total scan time
of only 2 seconds. We recommend adding T2*-weighted sequence to
routine MRI protocols to screen for CVT. We recognize the limitations of the
retrospective nature and small sample size of this study. However, current
observations merit further prospective studies to assess the sensitivity and
specificity of T2*/SWIs in diagnosing CVT.
AUTHOR INFORMATION
Accepted for publication December 19, 2001.
Author contributions: Study concept and design (Drs Selim, Fink, Linfante, Kumar, Schlaug, and Caplan);
acquisition of data (Drs Selim, Fink, Linfante, Kumar, and
Schlaug); analysis and interpretation of data (Drs
Selim, Fink, Linfante, Schlaug, and Caplan); drafting of the manuscript (Drs Selim, Fink, and Schlaug); critical revision of the
manuscript for important intellectual content (Drs Fink,
Linfante, Kumar, and Schlaug); statistical expertise (Dr Schlaug); obtained funding (Dr Schlaug);
administrative, technical, and material support (Drs Selim,
Linfante, Kumar, and Schlaug); study supervision (Drs Linfante, Schlaug, and Caplan).
This study was supported in part by grants from the Fireman and Rubenstein
Foundations, Boston, Mass, and the Doris Duke Clinical Scientist Development
Award (Dr Schlaug); and by the New Zealand Neurological Foundation V. J. Chapman
Fellowship Grant, Auckland (Dr Fink).
Corresponding author: Magdy H Selim, MD, PhD, University of Massachusetts
Medical School, Department of Neurology, University of Massachusetts Memorial
Medical Center, 119 Belmont St, Worcester, MA 01605 (e-mail: selimm{at}ummhc.org).
From the Department of Neurology, Division of Cerebrovascular Diseases,
Beth Israel Deaconess Medical Center, Boston Mass. Dr Selim is now with the
Department of Neurology, University of Massachusetts Medical School, Worcester.
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