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(Stroke. 1998;29:2649-2652.)
© 1998 American Heart Association, Inc.
Case Reports |
From the Service d'Urgences Cérébro-Vasculaires, Groupe hospitalier Pitié-Salpétrière (J.C.C., R.M., M.L., Y.S., G.R.), and Service de Neuroradiologie Marsault, Groupe hospitalier Pitié-Salpétrière (C.O., D.D., C.M.), Paris, France.
Abstract
BackgroundDiffusion-weighted imaging (DWI) is the most sensitive MR sequence in acute arterial ischemic stroke but has not yet been evaluated in venous cerebral ischemia. We describe a patient with DWI performed at the acute phase of a venous ischemic stroke.
Case DescriptionA rapid cerebral MRI including DWI and fast fluid-attenuated inversion recovery (FLAIR) sequences was performed at the acute phase of a venous stroke confirmed by conventional angiography. DWI showed a slight decrease in apparent diffusion coefficient values 3 hours after onset (0.53±0.07x10-3 mm2/s) and was normal 48 hours later (0.064±0.15x10-3 mm2/s). Fast FLAIR sequences showed large left frontoparietal hyperintensities. The lack of a clear decrease in apparent diffusion coefficient values associated with marked FLAIR abnormalities may suggest prominent or early associated vasogenic edema. Physiopathological differences between arterial and venous ischemia may explain the different type of DWI FLAIR abnormalities during the acute phase as well as the better recovery of neurological deficit in venous stroke than in arterial ischemic stroke.
ConclusionsIn the context of an acute stroke, the contrast between marked FLAIR and subtle DWI abnormalities on MRI may reflect the venous mechanism of cerebral ischemia.
Key Words: cerebral veins magnetic resonance imaging magnetic resonance imaging, diffusion-weighted
The arterial origin of an ischemic stroke must be confirmed at the acute phase because thrombolysis indication depends on an early diagnosis and is proposed within 3 hours after onset.1 Although progress in neuroimaging makes the diagnosis of cerebral venous thrombosis (CVT) easier,2 3 4 the acute phase of a venous stroke may be difficult to differentiate from arterial ischemic stroke (AIS) because of the polymorphism of clinical presentation,2 5 which sometimes mimics an AIS. Diffusion-weighted imaging (DWI) is a new MR technique that shows early abnormalities within minutes after stroke onset, related to early cytotoxic edema in AIS.6 7 8 9 10 DWI performed at the acute phase of CVT has not yet been evaluated.
We describe a patient with CVT whose initial clinical presentation suggested AIS. The early DWI pattern was unusual for AIS, and the venous mechanism of ischemia was confirmed by angiography. The MR data are suggestive of prominent vasogenic edema, which may be the basis for the pathophysiology of venous ischemia.
Case Report
A 64-year-old woman was admitted to the hospital 2 hours and 30
minutes after the sudden onset of right hemiplegia and nonfluent
aphasia. On admission, this right-handed woman had right hemiplegia and
hypoesthesia and nonfluent aphasia. She was apyretic, and blood
pressure was 140/80 mm Hg with regular pulse of 70/min. CT scan
performed 2 hours and 50 minutes after onset was normal. Three hours
after deficit onset, a rapid MRI was obtained with a total acquisition
time of only 5 minutes. Two sequences were performed on 1.5-T MR
equipment (GE Signa Horizon Echospeed). The first sequence featured
multislice single-shot, spin-echo diffusion, echo-planar imaging with a
pair of diffusion gradients centered around the 180° pulse with 6-mm
axial slice thickness, 1.5-mm gap, 96x64 matrix, 28x21-cm field of
view, repetition time of 4000 ms, and effective echo time of 120 ms.
Five sets of 17 slices were acquired with 5 values of b (
=25 ms,
=28 ms), from b=0 to 800 s/mm2, with diffusion
gradients applied simultaneously in 3 orthogonal spatial
directions. The DW raw images were transferred to an independent
workstation. Dedicated software (Functool, GE) allowed the
quantification of the diffusion changes. Calculation of the apparent
diffusion coefficient (ADC) was based on the Stejskal and Tanner
equation11 as the negative slope of the linear regression
best fitting the point for b versus ln (SI), where SI is the signal
intensity from a region of interest of the images acquired at each b
value. Performing this calculation on a pixel-by-pixel basis created
maps of ADC. The second sequence featured fast fluid-attenuated
inversion recovery (FLAIR) acquisition with 5-mm axial interleaved
slices, 256x256 matrix, 24x24-cm field of view, repetition time of
10 002 ms, effective echo time of 148 ms, inversion time of 2200 ms,
and 32-kHz bandwidth; direction of the frequency encoding gradient was
superior to inferior.
DWI showed a discrete hypersignal limited to the left rolandic area in
only 1 slice (5 mm). There was a corresponding very slight
decrease of ADC values on the ADC maps
(0.53±0.07x10-3
mm2/s) compared with a matching location in the
uninvolved contralateral hemisphere (0.61±0.09x
10-3 mm2/s) (Figure 1
, left panel). This slight decrease of
ADC values contrasted with the clear ADC drop usually observed at the
acute phase of AIS. Conversely, the fast FLAIR sequences showed large
left frontoparietal hyperintensities visible on 7 slices (35 mm)
(Figure 1
, right panel).
|
The patient had a generalized seizure just after the MRI was performed.
She was therefore rejected for thrombolysis, and a
second MRI was performed 48 hours later. The hypersignal on DWI
completely disappeared, and ADC values returned to normal
(0.64±0.15x10-3
mm2/s) compared with the uninvolved contralateral
hemisphere (0.63±0.19x10-3
mm2/s) (Figure 2
).
Signal abnormalities on FLAIR sequences were unchanged.
|
These results, further supported by the generalized seizure, were
unusual for AIS and led us to suspect a venous stroke. This was
confirmed by MRI angiography and conventional angiography, which showed
extensive thrombosis of the superior sagittal and left lateral sinuses
(Figure 3
). D-dimer values
were >1000 ng/mL (enzyme-linked immunosorbent assay method). The
patient had a hemoglobin concentration of 61 g/L, with anemia related
to a previously unknown gastric ulcer. Platelets and leukocytes
were normal; coagulation tests, including normal levels of protein C,
protein S, and antithrombin III, were normal; and antinuclear and
antiphospholipid antibodies were negative. The patient's family later
reported a history of 8 days of continuous headaches preceding the
stroke. She was treated with intravenous heparin therapy
(adjusted according to partial thromboplastin time 2 to 3 times the
partial thromboplastin time before administration of heparin),
phenytoin 300 mg/d per os, omeprazole 20 mg/d, and eradication of
Helicobacter pylori. The patient's outcome was favorable,
with marked regression of neurological deficit within 3 days. She was
discharged 3 weeks later with only a moderate right ataxia.
|
Discussion
The context of a sudden neurological deficit with a normal initial CT scan was compatible, in this patient, with AIS in the left superficial middle cerebral artery territory. Initially, this patient was considered to have AIS and was admitted to our stroke center for possible inclusion in a thrombolysis protocol (European Cooperative Acute Stroke Study II).
A 5-minute MRI including DWI and a fast FLAIR sequence was obtained.
DWI, first developed by Le Bihan et al,6 is a new MR
technique based on the molecular motion of water. It is extremely
sensitive at the acute phase of AIS since abnormalities appear within
minutes after onset in animals,12 related to slower
diffusion motion in intracellular cytotoxic edema induced by
ischemia, resulting in a drop of ADC values.8 9 10
In our patient, the slight decrease of ADC values observed on DWI 3
hours after onset (Figure 1
, left panel) was
inconsistent with the clear ADC drop usually observed in
AIS.13 Moreover, ADC values returned to normal at 48 hours
after onset (Figure 2
), while they should reach minimum values
in AIS.9
FLAIR sequences, developed by Rydberg et al14 allow the acquisition of heavily T2-weighted, cerebrospinal fluidnulled images. These sequences are highly sensitive to ischemic strokes,15 16 but, as shown for conventional T2 sequence,17 FLAIR abnormalities may be delayed compared with DWI abnormalities in AIS. However, the hyperintensities were marked and larger than on DWI only 3 hours after the sudden clinical deficit, suggesting preexisting but clinically asymptomatic focal abnormalities. Overall, these data were compatible with a venous ischemic stroke developed on a preexisting cortical venous and superior sagittal sinuses thrombosis, as confirmed later by angiography.
The venous strokes share some common features with other types of focal ischemia, such as a reduced capillary perfusion pressure,18 19 increased cerebral blood volume,20 and decreased cerebral blood flow.21 However, venous ischemia also has specific characteristics, such as an early blood-brain barrier disruption and an increase of the net capillary filtration, that may result in early vasogenic edema.19 24 In our patient, the contrast between slight DWI abnormalities and marked FLAIR abnormalities may reflect prominent and early vasogenic edema associated with mild cytotoxic edema. This contrast may explain the excellent and rapid recovery of neurological deficit of most cases of venous stroke that is treated early.22 A relative preservation of neuronal tissue has also been documented recently by Hsu et al,23 using proton MR spectroscopy in a case of deep CVT. The authors suggested an impaired but viable tissue in that case.
Another argument for an important vasogenic rather than a pure cytotoxic component of the edema in venous ischemia is derived from the experimental rat model of CVT described by Röther et al 24 Although a strict comparison is difficult to make, the authors, who also used DWI, showed an early marked decrease of ADC values, followed by an increase during 48 hours. They concluded that early cytotoxic edema was closely followed by vasogenic edema.
To our knowledge, this is the first reported case of early DWI after onset of venous stroke in humans. Although the diversity of CVT patterns of presentation precludes definitive conclusions from a single case, the present findings clearly show that a 5-minute MRI protocol, which can easily be performed within the therapeutic window of cerebral ischemia, may greatly improve the accuracy of diagnosis in acute stroke. Moreover, our results suggest that new MR techniques may improve knowledge of the pathophysiology of cerebrovascular disorders.
Footnotes
Reprint requests to G. Rancurel, MD, Service d'Urgences Cérébro-Vasculaires, Groupe hospitalier Pitié-Salpétrière, 47 Boulevard de l'hôpital, 75631 Paris Cedex 13, France.
Received June 23, 1998; revision received July 31, 1998; accepted August 18, 1998.
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